Clinical and Prognostic Value of Molecular Markers of Diffuse Large B-Cell Lymphoma

SM Rastorguev1, DA Koroleva2, ES Boulygina1, SV Tsygankova1, NG Goncharov1, OS Naraikin1, NG Gabeeva2, EE Zvonkov2, AV Nedoluzhko1

1 National Research Center “Kurchatov Institute”, 1 Akademika Kurchatova sq., Moscow, Russian Federation, 123182

2 National Medical Hematology Research Center, 4а Novyi Zykovskii pr-d, Moscow, Russian Federation, 125167

For correspondence: Artem Valer’evich Nedoluzhko, PhD in Biology, 1 Akademika Kurchatova sq., Moscow, Russian Federation, 123182; Tel.: +7(916)670-55-95; e-mail: nedoluzhko@gmail.com

For citation: Rastorguev SM, Koroleva DA, Bulygina ES, et al. Clinical and Prognostic Value of Molecular Markers of Diffuse Large B-Cell Lymphoma. Clinical oncohematology. 2019:12(1):95–100.

DOI: 10.21320/2500-2139-2019-12-1-95-100


ABSTRACT

Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoid tumor in adults which is associated with approximately 30–40 % of all non-Hodgkin’s lymphomas. Diagnostic criteria include diffuse growth of large anaplastic tumor cells, expression of В-cell markers, and a high proliferative index. Due to the development of molecular genetic technologies it became obvious that underlying cause of clinical diversity is a huge amount of genetic failures which determine epigenetic modification of gene expression, activation variability of certain signaling pathways, and immunological properties of tumor cells. The study and systemization of molecular markers present a significant trend in DLBCL diagnosis and treatment. This review discusses most important molecular markers and current view on their clinical value.

Keywords: lymphoma, DLBCL, B-cells, transcriptomics, gene expression, epigenomics, genomics.

Received: July 3, 2018

Accepted: December 10, 2018

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REFERENCES

  1. Alizadeh AA, Eisen MB, Davis RE, et al. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling. Nature. 2000;403(6769):503–11. doi: 10.1038/35000501.

  2. Rosenwald A, Alizadeh AA, Widhopf G, et al. Relation of gene expression phenotype to immunoglobulin mutation genotype in B cell chronic lymphocytic leukemia. J Exp Med. 2001;194(11):1639–48. doi: 1084/jem.194.11.1639.

  3. Staudt LM, Dave S. The biology of human lymphoid malignancies revealed by gene expression profiling. Adv Immunol. 2005;87:163–208. doi: 10.1016/S0065-2776(05)87005-1.

  4. Звонков Е.Е., Морозова А.К., Кравченко С.К. и др. Восьмилетний опыт применения модифицированной программы NHL-BFM-90 в лечении взрослых больных первичной диффузной В-крупноклеточной лимфомой желудка. Гематология и трансфузиология. 2012;57(3):47–8.

    [Zvonkov EE, Morozova AK, Kravchenko SK, et al. Eight-year experience of using the modified NHL-BFM-90 program for treatment of adult patients with primary diffuse large B-cell gastric lymphoma. Gematologiya i transfuziologiya. 2012;57(3):47–8. (In Russ)]

  5. Магомедова А.У., Кравченко С.К., Кременецкая A.M. и др. Девятилетний опыт лечения больных диффузной В-крупноклеточной лимфосаркомой. Терапевтический архив. 2011;83(7):5–10.

    [Magomedova AU, Kravchenko SK, Kremenetskaya AM, et al. Nine-year experience in the treatment of patients with diffuse large B-cell lymphosarcoma. Terapevticheskii arkhiv. 2011;83(7):5–10. (In Russ)]

  6. Гаврилина О.А., Габеева Н.Г., Морозова А.К. и др. Роль высокодозной химиотерапии и трансплантации аутологичных стволовых клеток крови у пациентов с диффузной В-крупноклеточной лимфомой. Терапевтический архив. 2013;85(7):90–7.

    [Gavrilina OA, Gabeeva NG, Morozova AK, et al. Role of high-dose chemotherapy and autologous blood stem cell transplantation in patients with diffuse large B-cell lymphoma. Terapevticheskii arkhiv. 2013;85(7):90–7. (In Russ)]

  7. Габеева Н.Г., Королева Д.А., Беляева А.В. и др. Диффузная В-крупноклеточная лимфома с сочетанной реаранжировкой генов c-MYC и BCL6 с первичным поражением кожи: собственное наблюдение и обзор литературы. Терапевтический архив. 2017;89(7):85–92.

    [Gabeeva NG, Koroleva DA, Belyaeva AV, et al. Diffuse large B-cell lymphoma with concomitant c-MYC and BCL6 gene rearrangements with primary skin involvement: A case report and a review of literature. Terapevticheskii arkhiv. 2017;89(7):85–92. (In Russ)]

  8. Martelli M, Ferreri AJ, Agostinelli C, et al. Diffuse large B-cell lymphoma. Crit Rev Oncol Hematol. 2013;87(2):146–71. doi: 10.1016/j.critrevonc.2012.12.009.

  9. Cohen M, Vistarop AG, Huaman F, et al. Epstein-Barr virus lytic cycle involvement in diffuse large B cell lymphoma. Hematol Oncol. 2017;36(1):98–103. doi: 10.1002/hon.2465.

  10. Lenz G, Wright G, Dave SS, et al. Stromal gene signatures in large-B-cell lymphomas. N Engl J Med. 2008;359(22):2313–23. doi: 10.1056/NEJMoa0802885.

  11. Wright G, Tan B, Rosenwald A, et al. A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma. Proc Natl Acad Sci USA. 2003;100(17): 9991–6. doi: 10.1073/pnas.1732008100.

  12. Skryabin KG, Prokhortchouk EB, Mazur AM, et al. Combining Two Technologies for Full Genome Sequencing of Human. Acta Nat. 2009;1(3):102–7.

  13. Artemov AV, Boulygina ES, Tsygankova SV, et al. Study of Alzheimer Family Case Reveals Hemochromotosis-Associated HFE Mutation. Hum Gen Var. 2014;1(1):14004. doi: 10.1038/hgv.2014.4.

  14. Scelo G, Riazalhosseini Y, Greger L, et al. Variation in genomic landscape of clear cell renal cell carcinoma across Europe. Nat Commun. 2014;5(1):5135. doi: 10.1038/ncomms6135.

  15. Shipp MA, Ross KN, Tamayo P, et al. Diffuse large B-cell lymphoma outcome prediction by gene-expression profiling and supervised machine learning. Nat Med. 2002;8(1):68–74. doi: 10.1038/nm0102-68.

  16. Scherer F, Kurtz DM, Newman AM, et al. Distinct biological subtypes and patterns of genome evolution in lymphoma revealed by circulating tumor DNA. Sci Transl Med. 2016;8(364):364ra155. doi: 10.1126/scitranslmed.aai8545.

  17. Lawrie CH, Soneji S, Marafioti T, et al. MicroRNA expression distinguishes between germinal center B cell-like and activated B cell-like subtypes of diffuse large B cell lymphoma. Int J Cancer. 2007;121(5):1156–61. doi: 10.1002/ijc.22800.

  18. Malumbres R, Sarosiek KA, Cubedo E, et al. Differentiation stage–specific expression of microRNAs in B lymphocytes and diffuse large B-cell lymphomas. Blood. 2009;113(16):3754–64. doi: 10.1182/blood-2008-10-184077.

  19. Zhu D, Fang C, Li X, et al. Predictive analysis of long non-coding RNA expression profiles in diffuse large B-cell lymphoma. Oncotarget. 2017;8(14):23228–36. doi: 10.18632/oncotarget.15571.

  20. Peng W, Fan H, Wu G, et al. Upregulation of long noncoding RNA PEG10 associates with poor prognosis in diffuse large B cell lymphoma with facilitating tumorigenicity. Clin Exp Med. 2016;16(2):177–82. doi: 10.1007/s10238-015-0350-9.

  21. Peng W, Feng J. Long noncoding RNA LUNAR1 associates with cell proliferation and predicts a poor prognosis in diffuse large B-cell lymphoma. Biomed Pharmacother. 2016;77:65–71. doi: 10.1016/j.biopha.2015.12.001.

  22. Peng W, Wu J, Feng J. Long noncoding RNA HULC predicts poor clinical outcome and represents pro-oncogenic activity in diffuse large B-cell lymphoma. Biomed Pharmacother. 2016;79:188–93. doi: 10.1016/j.biopha.2016.02.032.

  23. Yan Y, Han J, Li Z, et al. Elevated RNA expression of long non-coding HOTAIR promotes cell proliferation and predicts a poor prognosis in patients with diffuse large B cell lymphoma. Mol Med Rep. 2016;13(6):5125–31. doi: 10.3892/mmr.2016.5190.

  24. Li L-J, Chai Y, Guo X-J, et al. The effects of the long non-coding RNA MALAT-1 regulated autophagy-related signaling pathway on chemotherapy resistance in diffuse large B-cell lymphoma. Biomed Pharmacother. 2017;89:939–48. doi: 10.1016/j.biopha.2017.02.011.

  25. Sun J, Cheng L, Shi H, et al. A potential panel of six-long non-coding RNA signature to improve survival prediction of diffuse large-B-cell lymphoma. Sci Rep. 2016;6(1):27842. doi: 10.1038/srep27842.

  26. Verma A, Jiang Y, Du W, et al. Transcriptome sequencing reveals thousands of novel long non-coding RNAs in B cell lymphoma. Gen Med. 2015;7(1):110. doi: 10.1186/s13073-015-0230-7.

  27. Gutierrez-Garcia G, Cardesa-Salzmann T, Climent F, et al. Gene-expression profiling and not immunophenotypic algorithms predicts prognosis in patients with diffuse large B-cell lymphoma treated with immunochemotherapy. Blood. 2011;117(18):4836–43. doi: 10.1182/blood-2010-12-322362.

  28. Schuetz JM, Johnson NA, Morin RD, et al. BCL2 mutations in diffuse large B-cell lymphoma. Leukemia. 2012;26(6):1383–90. doi: 10.1038/leu.2011.378.

  29. Greenough A, Moffitt A, Jima D, et al. Strand-Specific Total RNA Sequencing Establishes the Complete Transcriptome and Alternative Splicing Repertoire in Diffuse Large B Cell Lymphoma. Blood. 2014;124(21):864.

  30. Park HY, Lee SB, Yoo HY, et al. Whole-Exome and Transcriptome Sequencing of Refractory Diffuse Large B-Cell Lymphoma. Oncotarget. 2016;7(52): 86433–45. doi: 10.18632/oncotarget.13239.

  31. Dekker JD, Park D, Shaffer AL, et al. Subtype-Specific Addiction of the Activated B-Cell Subset of Diffuse Large B-Cell Lymphoma to FOXP1. Proc Natl Acad Sci USA. 2016;113(5):E577–86. doi: 10.1073/pnas.1524677113.

  32. Reddy A, Zhang J, Davis NS, et al. Genetic and Functional Drivers of Diffuse Large B Cell Lymphoma. Cell. 2017;171(2):481–94.e15. doi: 10.1016/j.cell.2017.09.027.

  33. Saez AI, Saez AJ, Artiga MJ, et al. Building an outcome predictor model for diffuse large B-cell lymphoma. Am J Pathol. 2004;164(2):613–22. doi: 10.1016/S0002-9440(10)63150-1.

  34. Campo E. MYC in DLBCL: partners matter. Blood. 2015;126(22):2439–40. doi: 10.1182/blood-2015-10-671362.

  35. Schmitz R, Wright GW, Huang DW, et al. Genetics and Pathogenesis of Diffuse Large B-Cell Lymphoma. N Engl J Med. 2018;378(15):1396–407. doi: 10.1056/NEJMoa1801445.

  36. Dubois S, Viailly PJ, Mareschal S, et al. Next-generation sequencing in diffuse large B-cell lymphoma highlights molecular divergence and therapeutic opportunities: a LYSA study. Clin Cancer Res. 2016;22(12):2919–28. doi: 10.1158/1078-0432.CCR-15-2305.

  37. Lohr JG, Stojanov P, Lawrence MS, et al. Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing. Proc Natl Acad Sci USA. 2012;109(10):3879–84. doi: 10.1073/pnas.1121343109.

  38. Morin RD, Mungall K, Pleasance E, et al. Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing. Blood. 2013;122(7):1256–65. doi: 10.1182/blood-2013-02-483727.

  39. Pasqualucci L, Trifonov V, Fabbri G, et al. Analysis of the coding genome of diffuse large B-cell lymphoma. Nat Genet. 2011;43(9):830–7. doi: 10.1038/ng.892.

  40. Roschewski M, Dunleavy K, Pittaluga S, et al. Circulating tumour DNA and CT monitoring in patients with untreated diffuse large B-cell lymphoma: a correlative biomarker study. Lancet Oncol. 2015;16(5):541–9. doi: 10.1016/S1470-2045(15)70106-3.

  41. Yeh P, Hunter T, Sinha D, Ftouni S, et al. Circulating tumour DNA reflects treatment response and clonal evolution in chronic lymphocytic leukaemia. Nat Commun. 2017;8:14756. doi: 10.1038/ncomms14756.

  42. Khare D, Goldschmidt N, Bardugo A, et al. Plasma microRNA profiling: Exploring better biomarkers for lymphoma surveillance. PLoS One. 2017;12(11):e0187722. doi: 10.1371/journal.pone.0187722.

  43. Meng Y, Quan L, Liu A. Identification of key microRNAs associated with diffuse large B-cell lymphoma by analyzing serum microRNA expressions. Gene. 2018;642:205–11. doi: 10.1016/j.gene.2017.11.022.

  44. Kurtz DM, Green MR, Bratman SV, et al. Noninvasive Monitoring of Diffuse Large B-Cell Lymphoma by Immunoglobulin High-Throughput Sequencing. Blood. 2015;125(24):3679–87. doi: 10.1182/blood-2015-03-635169.

  45. Cohen JD, Li L, Wang Y, et al. Detection and localization of surgically resectable cancers with a multi-analyte blood test. Science. 2018;359(6378):926–30. doi: 10.1126/science.aar3247.

  46. Shaknovich R, Melnick A. Epigenetics and B-Cell Lymphoma. Curr Opin Hematol. 2011;18(4):293–9. doi: 10.1097/MOH.0b013e32834788cf.

  47. Shaknovich R, Geng H, Johnson NA, et al. DNA methylation signatures define molecular subtypes of diffuse large B-cell lymphoma. Blood. 2010;116(20):e81–9. doi: 10.1182/blood-2010-05-285320.

  48. Lai AY, Fatemi M, Dhasarathy A, et al. DNA methylation prevents CTCF-mediated silencing of the oncogene BCL6 in B cell lymphomas. J Exp Med. 2010;207(9):1939–50. doi: 10.1084/jem.20100204.

  49. Kristensen LS, Hansen JW, Kristensen SS, et al. Aberrant Methylation of Cell-Free Circulating DNA in Plasma Predicts Poor Outcome in Diffuse Large B Cell Lymphoma. Clin Epigen. 2016;8(1):5. doi: 10.1186/s13148-016-0261-y.

  50. Wedge E, Hansen JW, Garde C, et al. Global hypomethylation is an independent prognostic factor in diffuse large B cell lymphoma. Am J Hematol. 2017;92(7):689–94. doi: 10.1002/ajh.24751.

  51. Krajnovic M, Jovanovic MP, Mihaljevic B, et al. Hypermethylation of p15 Gene in Diffuse – Large B‐Cell Lymphoma: Association with Less Aggressiveness of the Disease. Clin Transl Sci. 2014;7(5):384–90. doi: 10.1111/cts.12162.

  52. Chambwe N, Kormaksson M, Geng H, et al. Variability in DNA methylation defines novel epigenetic subgroups of DLBCL associated with different clinical outcomes. Blood. 2014;123(11):1699–708. doi: 10.1182/blood-2013-07-509885.

  53. Clozel T, Yang S, Elstrom RL, et al. Mechanism-based epigenetic chemosensitization therapy of diffuse large B-cell lymphoma. Cancer Discov. 2013;3(9):1002–19. doi: 10.1158/2159-8290.CD-13-0117.

  54. Pan H, Jiang Y, Boi M, et al. Epigenomic evolution in diffuse large B-cell lymphomas. Nat Commun. 2015;6(1):6921. doi: 10.1038/ncomms7921.

  55. Jing L, Su L, Ring BZ. Ethnic Background and Genetic Variation in the Evaluation of Cancer Risk: A Systematic Review. PLoS ONE. 2014;9(6):e97522. doi: 10.1371/journal.pone.0097522.

  56. Li Y, Wang Y, Wang Z, et al. Racial Differences in Three Major NHL Subtypes: Descriptive Epidemiology. Cancer Epidemiol. 2015;39(1):8–13. doi: 10.1016/j.canep.2014.12.001.

 

Correlation of CD34+ Hematopoietic Stem Cells and CFU in Peripheral Blood Apheresis Products in Patients with Malignant Lymphoproliferative Diseases Before and After Cryopreservation Prior to auto-HSCT

VA Balashova, VI Rugal’, SS Bessmel’tsev, SV Gritsaev, NYu Semenova, SV Voloshin, ZhV Chubukina, AV Shmidt, AD Garifullin, IM Zapreeva, AA Kuzyaeva, II Kostroma, AYu Kuvshinov, AV Chechetkin

Russian Research Institute of Hematology and Transfusiology, 16 2-ya Sovetskaya str., Saint Petersburg, Russian Federation, 191024

For correspondence: Valentina Andreevna Balashova, MD, PhD, 16 2-ya Sovetskaya str., Saint Petersburg, Russian Federation, 191024; Tel.: +7(812)717-19-37; e-mail: vbspb37@mail.ru

For citation: Balashova VA, Rugal’ VI, Bessmel’tsev SS, et al. Correlation of CD34+ Hematopoietic Stem Cells and CFU in Peripheral Blood Apheresis Products in Patients with Malignant Lymphoproliferative Diseases Before and After Cryopreservation Prior to auto-HSCT. Clinical oncohematology. 2018;11(4):368–77.

DOI: 10.21320/2500-2139-2018-11-4-368-377


ABSTRACT

Aim. To establish correlation between CD34+ autologous hematopoietic stem cell (HSC) count and colony-forming units (CFU) in the same peripheral blood apheresis product samples before and after cryopreservation in multiple myeloma and lymphoma patients, and to assess clinical value of these parameters.

Materials & Methods. Cell samples of peripheral blood cytapheresis product and cell cultures were studied before and after cryopreservation in 32 multiple myeloma and 25 lymphoma patients who underwent autologous HSC transplantation. The material was analyzed using culture technique and flow cytometry.

Results. The paper provides information on the relationship between CD34+ HSC count obtained by flow cytometry, and CFU in cell culture obtained by cytapheresis of the same peripheral blood samples. A direct correlation was confirmed between CD34+ count and all the CFUs before and after cryopreservation in lymphoma patients. Correlation between CD34+ count and granulocyte-macrophage CFUs was revealed in multiple myeloma and lymphoma patients before cryopreservation.

Conclusion. The parameter of colony-forming capacity used for the assessment of the functional HSC was shown to be equally reliable criterion for condition evaluation of autotransplant proliferative pool than CD34+ cells. Both methods should be applied for qualitative and quantitative evaluation of an autotransplant for multiple myeloma and lymphoma patients.

Keywords: CD34+ cells, CFU, CFU-GM, correlation, lymphoma, multiple myeloma, apheresis, auto-HSCT.

Received: April 11, 2018

Accepted: July 28, 2018

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REFERENCES

  1. Lansdorp PM. Self-renewal of stem cells. Biol Blood Marrow Transplant. 1997;3(4):171–8.

  2. Bryder D, Rossi DJ, Weissman IL. Hematopoietic stem cells: the paradigmatic tissue specific stem cell. Am J Pathol. 2006;169(2):338–46. doi: 10.2353/ajpath.2006.060312.

  3. Wodnar-Filipowicz A. Biological properties of haematopoietic stem cells. The EBMT Handbook, 6th edition; 2012. pp. 61–72.

  4. Moreb JS, Salmosinia D, Hsu J, et al. Long-term outcome after autologous stem cell transplantation with adequate peripheral blood stem cell mobilization using plerixafor and G-CSF in poor mobilizer lymphoma and myeloma patients. Adv Hematol. 2011;2011:1–8. doi: 10.1155/2011/517561.

  5. Птушкин В.В., Жуков Н.В., Миненко С.В. и др. Роль высокодозной химиотерапии с трансплантацией стволовых кроветворных клеток у больных с неходжкинскими лимфомами. Онкогематология. 2006;1–2:86–96.

    [Ptushkin VV, Zhukov NV, Minenko SV, et al. Role of high-dose chemotherapy with hematopoietic stem cell transplantation in patients with non-Hodgkin’s lymphomas. Onkogematologiya. 2006;1–2:86–96. (In Russ)]

  6. Avet-Loiseau H, Attal M, Moreau P, et al. Genetic abnormalities and survival in multiple myeloma: the experience of the Intergroup Francophone du Myeloma. Blood. 2007;109(8):3489–95. doi: 10.1182/blood-2006-08-040410.

  7. Avet-Loiseau H, Soulier J, Fermand JP, et al. Impact of high-risk cytogenetics and prior therapy on outcomes in patients with advanced relapsed or refractory multiple myeloma treated with lenalidomide plus dexamethasone. 2010;24(3):623–8. doi: 10.1038/leu.2009.273.

  8. Dabusti M, Lanza F, Campioni D, et al. CXCR4 expression on bone marrow CD34+ cells prior to mobilization can predict mobilization adequacy in patients with hematological malignancy. J Hematother Stem Cell Res. 2003;12(4):425–34. doi: 10.1089/152581603322286051.

  9. Ratip S. Mobilization failure in hematopoietic stem cell transplantation. XXXIX Ulusal Hematoloji Kongresi. Antalya, Turkey; 2013. рр. 106–10.

  10. Артюхина З.Е., Семенова Н.Ю., Балашова В.А. и др. Кроветворная ткань и стромальное микроокружение больных множественной миеломой. Вестник гематологии. 2017;13(1):15–8.

    [Artyukhina ZE, Semenova NYu, Balashova VA, et al. Hematopoietic tissue and stromal microenvironment in patients with multiple myeloma. Vestnik gematologii. 2017;13(1):15–8. (In Russ)]

  11. Бессмельцев С.С., Абдулкадыров К.М. Множественная миелома: руководство для врачей. М.: МК, 2016. 504 с.

    [Bessmel’tsev SS, Abdulkadyrov KM. Mnozhestvennaya mieloma: rukovodstvo dlya vrachei. (Multiple myeloma: manual for doctors.) Moscow: MK Publ.; 2016. 504 p. (In Russ)]

  12. Покровская О.С., Менделеева Л.П., Гальцева И.В. и др. Мобилизация гемопоэтических клеток крови у больных миеломной болезнью. Проблемы гематологии и переливания крови. 2003;2:55–65.

    [Pokrovskaya OS, Mendeleeva LP, Gal’tseva IV, et al. Mobilization of hematopoietic cells in myeloma patients. Problemy gematologii i perelivaniya krovi. 2003;2:55–65. (In Russ)]

  13. Покровская О.С. Кроветворная ткань и стромальное микроокружение в процессе интенсивной терапии и мобилизации гемопоэтических стволовых клеток у больных множественной миеломой: Автореф. дис.… канд. мед. наук. М., 2011.

    [Pokrovskaya OS. Krovetvornaya tkan’ i stromal’noe mikrookruzhenie v protsesse intensivnoi terapii i mobilizatsii gemopoeticheskikh stvolovykh kletok u bol’nykh mnozhestvennoi mielomoi. (Hematopoietic tissue and stromal microenvironment in intensive treatment and mobilization of hematopoietic stem cells in multiple myeloma ) [dissertation] Moscow; 2011. (In Russ)]

  14. Haizmann M, O’Meara AC, Moosmann PR, et al. Efficient mobilization of PBSC with vinorelbine/G-CSF in patients with malignant lymphoma. Bone Marrow Transplant. 2009;44(2):75–9. doi: 10.1038/bmt.2008.434.

  15. Haverkos BM, McBride A, O’Donnell L, et al. An effective mobilization strategy for lymphoma patients after failed upfront mobilization with plerixafor. Bone Marrow Transplant. 2014;49(8):1052–5. doi: 10.1038/bmt.2014.90.

  16. Lansdorp PM, Sutherland HJ, Eaves CJ. Selective expression of CD45 isoforms on functional subpopulations of CD34+ hemopoietic cells from human bone marrow. J Exp Med. 1990;172(1):363–6. doi: 10.1084/jem.172.1.363.

  17. Fritsch G, Buchinger P, Printz D, et al. Rapid discrimination of early CD34+ myeloid progenitors using CD45-RA analysis. Blood. 1993;1(9):2301–9.

  18. Fritsch G, Buchinger P, Printz D. Use of flow cytometric CD34 analysis to quantify hematopoietic progenitor cells. Leuk Lymphoma. 1993;10(6):443–51. doi: 10.3109/10428199309148201.

  19. Nissen-Druey C, Tichelli A, Mayer-Monard S. Human hematopoietic colonies in health and disease. Acta Haematol. 2005;113(1):5–10. doi: 10.1159/000081987.

  20. Takano H, Ema H, Sudo K, et al. Asymmetric division and lineage commitment at the level of hematopoietic stem cells: Inference from differentiation in daughter cell and granddaughter cell pairs. J Exp Med. 2004;199(3):295–302. doi: 10.1084/jem.20030929.

  21. Sieburg HB, Cho RH, Dykstra B, et al. The hematopoietic stem compartment consists of a limited number of discrete stem cell subsets. Blood. 2006;107(6):2311–6. doi: 10.1182/blood-2005-07-2970.

  22. Guo Y, Lubbert M, Engelhard M. CD34-hematopoietic stem cells: current concepts and controversies. Stem Cell. 2003;21(1):15–20. doi: 10.1634/stemcells.21-1-15.

  23. Donahue RE, Yang YC, Clark SC. Human P40 T-cell growth factor (interleukin-9) supports erythroid colony formation. Blood. 1990;75(12):2271–5.

  24. Ema H, Suda T, Miura Y, Nakauchi H. Colony formation of clone-sorted human haematopoietic progenitors. Blood. 1990;75(10):1941–6.

  25. Serke S, Sauberlich S, Huhn D. Multiparameter flow-cytometrical quantitation of circulating CD34+ cells: correlation to the quantitation of circulating haemopoietic progenitor cells by in vitro colony-assay. Br J Haematol. 2008;77(4):453–9. doi: 10.1111/j.1365-2141.1991.tb08609.x.

  26. Bensinger WI, Longin K, Appelbaum F, et al. Peripheral blood stem cells (PBSCs) collected after recombinant granulocyte colony stimulating factor (rhG-CSF): An analysis of factors correlating with the tempo of engraftment after transplantation. Br J Haematol. 1994;87(4):825–31. doi: 10.1111/j.1365-2141.1994.tb06744.x.

  27. Bensinger WI, Appelbaum F, Rowley S, et al. Factors that influence collection and engraftment of autologous peripheral blood stem cells. J Clin Oncol. 1995;13(10):2547–55. doi: 10.1200/jco.1995.13.10.2547.

  28. Weaver CH, Haselton B, Birch R, et al. An analysis of engrafment kinetics as a function of the CD34 content of peripheral blood progenitor cell collections in 692 patients after administration of myeloablative chemotherapy. Blood. 1995;86(10):3961–9.

  29. Weaver CH, Potz J, Redmond J, et al. Engraftment and outcomes of patients receiving myeloablative therapy followed by autologous peripheral blood cells with a low CD34+ cell content. Bone Marrow Transplant. 1997;19(11):1103–10. doi: 10.1038/sj.bmt.1700808.

  30. Watts MJ, Sullivan AM, Jamieson E, et al. Progenitor-cell mobilization after low-dose cyclophosphamide and granulocyte colony-stimulating factor, an analysis of progenitor-cell quantity and quality and factors predicting for these parameters in 101 pretreated patients with malignant lymphoma. J Clin Oncol. 1997;15(2):535–46. doi: 10.1200/jco.1997.15.2.535.

  31. Serke S, Watts M, Knudsen LM, et al. In-vitro clonogenity of mobilized peripheral blood CD34 expressing cells: inverse correlation to both relative and absolute number of CD34-expressing cells. Br J Haematol. 1996;95(2):234–40. doi: 10.1046/j.1365-2141.1996.d01-1918.x.

  32. Fritsch G, Emminger W, Buchinger P, et al. CD34-positive cell proportions in peripheral blood correlate with colony-forming capacity. Exp Hematol. 1991;19(11):1079–83.

  33. Fritsch G, Emminger W, Buchinger P, et al. CD34 analysis in peripheral blood correlates with colony-forming capacity. Progr Clin Biol Res. 1992;377:531–6.

  34. Scott MA, Ager S, Apperley JF, et al. Peripheral blood progenitor cell harvesting in multiple myeloma and malignant lymphoma. Leuk Lymphoma. 1995;19(5–6):479–84. doi: 10.3109/10428199509112208.

  35. Buzzi M, Granchi D, Bacci G, et al. CD34+ cells and clonogenicity of peripheral blood stem cells during chemotherapy treatment in association with granulocyte colony stimulating factor in osteosarcoma. J Chemother. 1999;11(4):293–300. doi: 10.1179/joc.1999.11.4.293.

  36. Андреева Л.Ю., Тупицын Н.Н., Овумян Г.Ш. и др. Гемопоэтические предшественники в крови онкологических больных: взаимосвязь колониеобразования и экспрессии CD Вестник РОНЦ им. Н.Н. Блохина РАМН. 2000;11(1):5–10.

    [Andreeva LYu, Tupitsyn NN, Ovumyan GSh, et al. Hematopoietic progenitors in blood of cancer patients: relationship between colony formation and CD34 expression. Vestnik RONTs im NN Blokhina RAMN. 2000;11(1):5–10. (In Russ)]

  37. Healy LE, Nirsimloo N, Scott M, et al. In vitro proliferation by cells mobilized into the peripheral blood for collection and autologous transplantation. Exp Hematol. 1994;22(13):1278–82.

  38. Magagnoli M, Spina M, Balzarotti M, et al. IGEV regimen and a fixed dose of lenograstim: an effective mobilization regimen in pretreated Hodgkin’s lymphoma patients. Bone Marrow Transplant. 2007;40(11):1019–25. doi: 10.1038/sj.bmt.1705862.

  39. Koutna I, Peterkova M, Simara P, et al. Proliferation and differentiation potential CD133+ and CD34+ populations from the bone marrow and mobilized peripheral blood. Ann Hematol. 2011;90(2):127–37. doi: 10.1007/s00277-010-1058-2.

  40. Балашова В.А., Ругаль В.И., Грицаев С.В. и др. Колониеобразующая способность гемопоэтических стволовых клеток мобилизованной периферической крови больных множественной миеломой до и после криоконсервирования. Трансфузиология. 2016;17(4):63–70.

    [Balashova VA, Rugal’ VI, Gritsaev SV, et al. Colony-forming capacity of hematopoietic stem cells of mobilized peripheral blood in multiple myeloma patients before and after cryopreservation. Transfuziologiya. 2016;17(4):63–70. (In Russ)]

  41. Балашова В.А., Ругаль В.И., Бессмельцев С.С. и др. Колониеобразующая способность гемопоэтических стволовых клеток мобилизованной периферической крови больных злокачественными лимфомами до и после криоконсервирования. Medline. 2018;19(3):45–54.

    [Balashova VA., Rugal VI., Bessmeltsev SS. et al. Colonyforming capacity of hematopoietic stem cells of mobilized peripheral blood in patients with malignant lymphomas before and after cryopreservation. Medline. 2018;19(3):45–54. (In Russ)]

Clinical Significance of the PRAME Gene Expression in Oncohematological Diseases

VA Misyurin

NN Blokhin National Medical Cancer Research Center, 24 Kashirskoye sh., Moscow, Russian Federation, 115478

For correspondence: Vsevolod Andreevich Misyurin, PhD, 24 Kashirskoye sh., Moscow, Russian Federation, 115478; Tel.: +7(985)436-30-19; e-mail: vsevolod.misyurin@gmail.com

For citation: Misyurin AV. Clinical Significance of the PRAME Gene Expression in Oncohematological Diseases. Clinical oncohematology. 2018;11(1):26–33.

DOI: 10.21320/2500-2139-2018-11-1-26-33


ABSTRACT

Although the PRAME activity was first discovered in solid tumors, this gene is very frequently expressed in oncohematological diseases. PRAME can be regarded as a reliable biomarker of tumor cells. Determination of PRAME transcripts is used in residual disease monitoring and molecular relapse diagnostics. Experimentation with PRAME expressing lines of leukemia cells yielded controversial results. Therefore, it is hardly possible to estimate the prognostic value of PRAME activity in oncohematological diseases. In chronic myeloproliferative disease and chronic myeloid leukemia, however, PRAME activity proves to be a predictor of negative prognosis, and on the contrary, it can be regarded as a positive prognostic factor in acute myeloid or lymphoid leukemia. Despite many clinical studies prognostic value of PRAME expression in some diseases requires further investigation. The present literature review contains the data concerning PRAME expression in oncohematological diseases.

Keywords: PRAME, leukemia, lymphoma, prognosis.

Received: September 14, 2017

Accepted: December 2, 2017

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REFERENCES

  1. Ikeda H, Lethe B, Lehmann F, et al. Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor. Immunity. 1997;6(2):199–208. doi: 10.1016/S1074-7613(00)80426-4.
  2. Greiner J, Ringhoffer M, Simikopinko O, et al. Simultaneous expression of different immunogenic antigens in acute myeloid leukemia. Exp Hematol. 2000;28(12):1413–22. doi: 10.1016/S0301-472X(00)00550-6.
  3. Epping MT, Wang L, Edel MJ, et al. The human tumor antigen PRAME is a dominant repressor of retinoic acid receptor signaling. Cell. 2005;122(6):835–47. doi: 10.1016/j.cell.2005.07.003.
  4. De Carvalho DD, Mello BP, Pereira WO, Amarante-Mendes GP. PRAME/EZH2-mediated regulation of TRAIL: a new target for cancer therapy. Curr Mol Med. 2013;13(2):296–304. doi: 10.2174/156652413804810727.
  5. Costessi A, Mahrour N, Tijchon E, et al. The tumour antigen PRAME is a subunit of a Cul2 ubiquitin ligase and associates with active NFY promoters. EMBO J. 2011;30(18):3786–98. doi: 10.1038/emboj.2011.262.
  6. Kim HL, Seo YR. Molecular and genomic approach for understanding the gene-environment interaction between Nrf2 deficiency and carcinogenic nickel-induced DNA damage. Oncol Rep. 2012;28(6):1959–67. doi: 10.3892/or.2012.2057.
  7. Yao J, Caballero OL, Yung WK, et al. Tumor subtype-specific cancer-testis antigens as potential biomarkers and immunotherapeutic targets for cancers. Cancer Immunol Res. 2014;2(4):371–9. doi: 10.1158/2326-6066.CIR-13-0088.
  8. van Baren N, Chambost H, Ferrant A, et al. PRAME, a gene encoding an antigen recognized on a human melanoma by cytolytic T cells, is expressed in acute leukaemia cells. Br J Haematol. 1998;102(5):1376–9. doi: 10.1046/j.1365-2141.1998.00982.x.
  9. Oehler VG, Guthrie KA, Cummings CL, et al. The preferentially expressed antigen in melanoma (PRAME) inhibits myeloid differentiation in normal hematopoietic and leukemic progenitor cells. Blood. 2009;114(15):3299–308. doi: 10.1182/blood-2008-07-170282.
  10. Roman-Gomez J, Jimenez-Velasco A, Agirre X, et al. Epigenetic regulation of PRAME gene in chronic myeloid leukemia. Leuk Res. 2007;31(11):1521–8. doi: 10.1016/j.leukres.2007.02.016.
  11. Ortmann CA, Eisele L, Nuckel H, et al. Aberrant hypomethylation of the cancer–testis antigen PRAME correlates with PRAME expression in acute myeloid leukemia. Ann Hematol. 2008;87(10):809–18. doi: 10.1007/s00277-008-0514-8.
  12. Gutierrez-Cosio S, de la Rica L, Ballestar E, et al. Epigenetic regulation of PRAME in acute myeloid leukemia is different compared to CD34+ cells from healthy donors: Effect of 5-AZA treatment. Leuk Res. 2012;36(7):895–9. doi: 10.1016/j.leukres.2012.02.030.
  13. Arons E, Suntum T, Margulies I, et al. PRAME expression in Hairy Cell Leukemia. Leuk Res. 2008;32(9):1400–6. doi: 10.1016/j.leukres.2007.12.010.
  14. Steinbach D, Schramm A, Eggert A, et al. Identification of a Set of Seven Genes for the Monitoring of Minimal Residual Disease in Pediatric Acute Myeloid Leukemia. Clin Cancer Res. 2006;12(8):2434–41. doi: 10.1158/1078-0432.CCR-05-2552.
  15. Matsushita M, Ikeda H, Kizaki M, et al. Quantitative monitoring of the PRAME gene for the detection of minimal residual disease in leukaemia. Br J Haematol. 2001;112(4):916–26. doi: 10.1046/j.1365-2141.2001.02670.x.
  16. Tajeddine N, Millard I, Gailly P, Gala JL. Real-time RT-PCR quantification of PRAME gene expression for monitoring minimal residual disease in acute myeloblastic leukaemia. Clin Chem Lab Med. 2006;44(5):548–55. doi: 10.1515/CCLM.2006.106.
  17. Schneider V, Zhang L, Rojewski M, et al. Leukemic progenitor cells are susceptible to targeting by stimulated cytotoxic T cells against immunogenic leukemia-associated antigens. Int J Cancer. 2015;137(9):2083–92. doi: 10.1002/ijc.29583.
  18. Гапонова Т.В., Менделеева Л.П., Мисюрин А.В. и др. Экспрессия опухолеассоциированных генов PRAME, WT1 и XIAP у больных множественной миеломой. Онкогематология. 2009;2:52–7. [Gaponova TV, Mendeleeva LP, Misyurin AV, et al. Expression of PRAME, WT1 and XIAP tumor-associated genes in patients with multiple myeloma. Onkogematologiya. 2009;2:52–7. (In Russ)]
  19. Абраменко И.В., Белоус Н.И., Крячок И.А. и др. Экспрессия гена PRAME при множественной миеломе. Терапевтический архив. 2004;74(7):77–81. [Abramenko IV, Belous NI, Kryachok IA, et al. Expression of PRAME gene in multiple myeloma. Terapevticheskii arkhiv. 2004;74(7):77–81. (In Russ)]
  20. Мисюрин В.А., Мисюрин А.В., Кесаева Л.А. и др. Новые маркеры прогрессирования хронического миелолейкоза. Клиническая онкогематология. 2014;7(2):206–12. [Misyurin VA, Misyurin AV, Kesayeva LA, et al. New molecular markers of CML progression. Klinicheskaya onkogematologiya. 2014;7(2):206–12. (In Russ)]
  21. van Baren N, Brasseur F, Godelaine D, et al. Genes encoding tumor-specific antigens are expressed in human myeloma cells. Blood. 1999;94(4):1156–64.
  22. Pellat-Deceunynck C, Mellerin M., Labarriere N, et al. The cancer germ-line genes MAGE-1, MAGE-3 and PRAME are commonly expressed by human myeloma cells. Eur J Immunol. 2000;30(3):803–9. doi: 10.1002/1521-4141(200003)30:3<803:AID-IMMU803>3.0.CO;2-P.
  23. Andrade VC, Vettore AL, Felix RS, et al. Prognostic impact of cancer/testis antigen expression in advanced stage multiple myeloma patients. Cancer Immun. 2008;8:2.
  24. Qin Y, Lu J, Bao L, et al. Bortezomib improves progression-free survival in multiple myeloma patients overexpressing preferentially expressed antigen of melanoma. Chin Med J (Engl). 2014;127(9):1666–71. doi: 10.3760/cma.j.issn.0366-6999.20132356.
  25. Proto-Siqueira R, Falcao RP, de Souza CA, et al. The expression of PRAME in chronic lymphoproliferative disorders. Leuk Res. 2003;27(5):393–6. doi: 10.1016/S0145-2126(02)00217-5.
  26. Proto-Siqueira R, Figueiredo-Pontes LL, Panepucci RA, et al. PRAME is a membrane and cytoplasmic protein aberrantly expressed in chronic lymphocytic leukemia and mantle cell lymphoma. Leuk Res. 2006;30(11):1333–39. doi: 10.1016/j.leukres.2006.02.031.
  27. Paydas S, Tanriverdi K, Yavuz S, Seydaoglu G. PRAME mRNA levels in cases with chronic leukemia: Clinical importance and review of the literature. Leuk Res. 2007;31(3):365–9. doi: 10.1016/j.leukres.2006.06.022.
  28. Kawano R, Karube K, Kikuchi M, et al. Oncogene associated cDNA microarray analysis shows PRAME gene expression is a marker for response to anthracycline containing chemotherapy in patients with diffuse large B-cell lymphoma. J Clin Exp Hematop. 2009;49(1):1–7. doi: 10.3960/jslrt.49.1.
  29. Mitsuhashi K, Masuda A, Wang YH, et al. Prognostic significance of PRAME expression based on immunohistochemistry for diffuse large B-cell lymphoma patients treated with R-CHOP therapy. Int J Hematol. 2014;100(1):88–95. doi: 10.1007/s12185-014-1593-z.
  30. Schmitt M, Li L, Giannopoulos K, et al. Chronic myeloid leukemia cells express tumor-associated antigens eliciting specific CD8+ T-cell responses and are lacking costimulatory molecules. Exp Hematol. 2006;34(12):1709–19. doi: 10.1016/j.exphem.2006.07.009.
  31. Qian J, Zhu Z.H, Lin J, et al. Hypomethylation of PRAME promoter is associated with poor prognosis in myelodysplastic syndrome. Br J Haematol. 2011;154(1):153–5. doi: 10.1111/j.1365-2141.2011.08585.x.
  32. Ding K, Wang XM, Fu R, et al. PRAME Gene Expression in Acute Leukemia and Its Clinical Significance. Cancer Biol Med. 2012;9(1):73–6. doi: 10.3969/j.issn.2095-3941.2012.01.013.
  33. Greiner J, Ringhoffer M, Taniguchi M, et al. mRNA expression of leukemia-associated antigens in patients with acute myeloid leukemia for the development of specific immunotherapies. Int J Cancer. 2004;108(5):704–11. doi: 10.1002/ijc.11623.
  34. Li L, Reinhardt P, Schmitt A, et al. Dendritic cells generated from acute myeloid leukemia (AML) blasts maintain the expression of immunogenic leukemia associated antigens. Cancer Immunol Immunother. 2005;54(7):685–93. doi: 10.1007/s00262-004-0631-8.
  35. Atanackovic D, Luetkens T, Kloth B, et al. Cancer-testis antigen expression and its epigenetic modulation in acute myeloid leukemia. Am J Hematol. 2011;86(11):918–22. doi: 10.1002/ajh.22141.
  36. Gerber JM, Qin L, Kowalski J, et al. Characterization of chronic myeloid leukemia stem cells. Am J Hematol. 2011;86(1):31–7. doi: 10.1002/ajh.21915.
  37. Qin YZ, Zhu HH, Liu YR, et al. PRAME and WT1 transcripts constitute a good molecular marker combination for monitoring minimal residual disease in myelodysplastic syndromes. Leuk Lymphoma. 2013;54(7):1442–9. doi: 10.3109/10428194.2012.743656.
  38. Steinbach D, Viehmann S, Zintl F, Gruhn B. PRAME gene expression in childhood acute lymphoblastic leukemia. Cancer Genet Cytogenet. 2002;138(1):89–91. doi: 10.1016/S0165-4608(02)00582-4.
  39. Steinbach D, Hermann J, Viehmann S, et al. Clinical implications of PRAME gene expression in childhood acute myeloid leukemia. Cancer Genet Cytogenet. 2002;133(2):118–23. doi: 10.1016/S0165-4608(01)00570-2.
  40. Spanaki A, Perdikogianni C, Linardakis E, Kalmanti M. Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia. Leuk Res. 2007;31(5):639–42. doi: 10.1016/j.leukres.2006.06.006.
  41. Steinbach D, Bader P, Willasch A, et al. Prospective Validation of a New Method of Monitoring Minimal Residual Disease in Childhood Acute Myelogenous Leukemia. Clin Cancer Res. 2015;21(6):1353–9. doi: 10.1158/1078-0432.CCR-14-1999.
  42. Paydas S, Tanriverdi K, Yavuz S, et al. PRAME mRNA levels in cases with chronic leukemia: Clinical Importance and Future Prospects. Am J Hematol. 2005;79(4):257–61. doi: 10.1002/ajh.20425.
  43. Steinbach D, Pfaffendorf N, Wittig S, Gruhn B. PRAME expression is not associated with down-regulation of retinoic acid signaling in primary acute myeloid leukemia. Cancer Genet Cytogenet. 2007;177(1):51–4. doi: 10.1016/j.cancergencyto.2007.05.011.
  44. Santamaria C, Chillon MC, Garcia-Sanz R, et al. The relevance of preferentially expressed antigen of melanoma (PRAME) as a marker of disease activity and prognosis in acute promyelocytic leukemia. Haematologica. 2008;93(12):1797–805. doi: 10.3324/haematol.13214.
  45. Qin Y, Zhu H, Jiang B, et al. Expression patterns of WT1 and PRAME in acute myeloid leukemia patients and their usefulness for monitoring minimal residual disease. Leuk Res. 2009;33(3):384–90. doi: 10.1016/j.leukres.2008.08.026.
  46. Мисюрин В.А., Лукина А.Е., Мисюрин А.В. и др. Особенности соотношения уровней экспрессии генов PRAME и PML/RARa в дебюте острого промиелоцитарного лейкоза. Российский биотерапевтический журнал. 2014;13(1):9–16. [Misyurin VA, Lukina AE, Misyurin AV, et al. A ratio between gene expression levels of PRAME and PML/RARA at the onset of acute promyelocytic leukemia and clinical features of the disease. Rossiiskii bioterapevticheskii zhurnal. 2014;13(1):9–16. (In Russ)]
  47. Liberante FG, Pellagatti A, Boncheva V, et al. High and low, but not intermediate, PRAME expression levels are poor prognostic markers in myelodysplastic syndrome at disease presentation. Br J Haematol. 2013;162(2):282–5. doi: 10.1111/bjh.12352.
  48. Goellner S, Steinbach D, Schenk T, et al. Childhood acute myelogenous leukaemia: Association between PRAME, apoptosis- and MDR-related gene expression. Eur J Cancer. 2006;42(16):2807–14. doi: 10.1016/j.ejca.2006.06.018.
  49. Tajeddine N, Louis M, Vermylen C, et al. Tumor associated antigen PRAME is a marker of favorable prognosis in childhood acute myeloid leukemia patients and modifies the expression of S100A4, Hsp 27, p21, IL-8 and IGFBP-2 in vitro and in vivo. Leuk Lymphoma. 2008;49(6):1123–31. doi: 10.1080/10428190802035933.
  50. Santamaria CM, Chillon MC, Garcia-Sanz R, et al. Molecular stratification model for prognosis in cytogenetically normal acute myeloid leukemia. Blood. 2009;114(1):148–52. doi: 10.1182/blood-2008-11-187724.
  51. Ercolak V, Paydas S, Bagir E, et al. PRAME Expression and Its Clinical Relevance in Hodgkin’s Lymphoma. Acta Haematol. 2015;134(4):199–207. doi: 10.1159/000381533.
  52. Luetkens T, Kobold S, Cao Y, et al. Functional autoantibodies against SSX‐2 and NY‐ESO‐1 in multiple myeloma patients after allogeneic stem cell transplantation. Cancer Immunol Immunother. 2014;63(11):1151–62. doi: 10.1007/s00262-014-1588-x.
  53. Gunn SR, Bolla AR, Barron LL, et al. Array CGH analysis of chronic lymphocytic leukemia reveals frequent cryptic monoallelic and biallelic deletions of chromosome 22q11 that include the PRAME gene. Leuk Res. 2009;33(9):1276–81. doi: 10.1016/j.leukres.2008.10.010.
  54. Mraz M, Stano Kozubik K, Plevova K, et al. The origin of deletion 22q11 in chronic lymphocytic leukemia is related to the rearrangement of immunoglobulin lambda light chain locus. Leuk Res. 2013;37(7):802–8. doi: 10.1016/j.leukres.2013.03.018.
  55. Staege MS, Banning-Eichenseer U, Weissflog G, et al. Gene expression profiles of Hodgkin’s lymphoma cell lines with different sensitivity to cytotoxic drugs. Exp Hematol. 2008;36(7):886–96. doi: 10.1016/j.exphem.2008.02.014.
  56. Kewitz S, Staege MS. Knock-Down of PRAME Increases Retinoic Acid Signaling and Cytotoxic Drug Sensitivity of Hodgkin Lymphoma Cells. PLoS One. 2013;8(2):e55897. doi: 10.1371/journal.pone.0055897.
  57. Bea S, Salaverria I, Armengol L, et al. Uniparental disomies, homozygous deletions, amplifications, and target genes in mantle cell lymphoma revealed by integrative high-resolution whole-genome profiling. Blood. 2009;113(13):3059–69. doi: 10.1182/blood-2008-07-170183.
  58. Liggins AP, Lim SH, Soilleux EJ, et al. A panel of cancer-testis genes exhibiting broadspectrum expression in haematological malignancies. Cancer Immun. 2010;10:8.
  59. Radich JP, Dai H, Mao M, et al. Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad Sci USA. 2006;103(8):2794–9. doi: 10.1073/pnas.0510423103.
  60. Luetkens T, Schafhausen P, Uhlich F, et al. Expression, epigenetic regulation, and humoral immunogenicity of cancer-testis antigens in chronic myeloid leukemia. Leuk Res. 2010;34(12):1647–55. doi: 10.1016/j.leukres.2010.03.039.
  61. Hughes A, Clarson J, Tang C, et al. CML patients with deep molecular responses to TKI have restored immune effectors and decreased PD-1 and immune suppressors. Blood. 2017;129(9):1166–76. doi: 10.1182/blood-2016-10-745992.
  62. Khateeb EE, Morgan D. Preferentially Expressed Antigen of Melanoma (PRAME) and Wilms’ Tumor 1 (WT 1) Genes Expression in Childhood Acute Lymphoblastic Leukemia, Prognostic Role and Correlation with Survival. Open Access Maced J Med Sci. 2015;3(1):57–62. doi: 10.3889/oamjms.2015.001.
  63. Zhang YH, Lu AD, Yang L, et al. PRAME overexpression predicted good outcome in pediatric B-cell acute lymphoblastic leukemia patients receiving chemotherapy. Leuk Res. 2017;52):43–9. doi: 10.1016/j.leukres.2016.11.005.
  64. McElwaine S, Mulligan C, Groet J, et al. Microarray transcript profiling distinguishes the transient from the acute type of megakaryoblastic leukaemia (M7) in Down’s syndrome, revealing PRAME as a specific discriminating marker. Br J Haematol. 2004;125(6):729–42. doi: 10.1111/j.1365-2141.2004.04982.x.
  65. Tanaka N, Wang YH, Shiseki M, et al. Inhibition of PRAME expression causes cell cycle arrest and apoptosis in leukemic cells. Leuk Res. 2011;35(9):1219–25. doi: 10.1016/j.leukres.2011.04.005.
  66. De Carvalho D.D, Binato R, Pereira W.O, et al. BCR-ABL-mediated upregulation of PRAME is responsible for knocking down TRAIL in CML patients. Oncogene. 2011;30(2):223–33. doi: 10.1038/onc.2010.409.
  67. Tajeddine N, Gala JL, Louis M, et al. Tumor-associated antigen preferentially expressed antigen of melanoma (PRAME) induces caspase-independent cell death in vitro and reduces tumorigenicity in vivo. Cancer Res. 2005;65(16):7348–55. doi: 10.1158/0008-5472.CAN-04-4011.
  68. Yan H, Zhao RM, Wang ZJ, et al. Knockdown of PRAME enhances adriamycin-induced apoptosis in chronic myeloid leukemia cells. Eur Rev Med Pharmacol Sci. 2015;19(24):4827–34. doi: 10.18632/oncotarget.9977.
  69. Xu Y, Yue Q, Wei H, Pan G. PRAME induces apoptosis and inhibits proliferation of leukemic cells in vitro and in vivo. Int J Clin Exp Pathol. 2015;8(11):14549–55.
  70. Xu Y, Rong LJ, Meng SL, et al. PRAME promotes in vitro leukemia cells death by regulating S100A4/p53 signaling. Eur Rev Med Pharmacol Sci. 2016;20(6):1057–63.
  71. Bullinger L, Schlenk RF, Gotz M, et al. PRAME-Induced Inhibition of Retinoic Acid Receptor Signaling-Mediated Differentiation – Possible Target for ATRA Response in AML without t(15;17). Clin Cancer Res. 2013;19(9):2562–71. doi: 10.1158/1078-0432.CCR-11-2524.

Application of Modern Genome Technologies in Treatment of Lymphomas

MV Nemtsova1, MV Maiorova2

1 Russian Medical Academy of Postgraduate Education, 2/1 Barrikadnaya str., Moscow, Russian Federation, 125993

2 PA Hertzen Moscow Oncology Research Institute, 3 2-y Botkinskii pr-d, Moscow, Russian Federation, 125284

For correspondence: Marina Vyacheslavovna Nemtsova, DSci, Professor, 2/1 Barrikadnaya str., Moscow, Russian Federation, 125993; Tel: +7(499)252-21-04; e-mail: nemtsova_m_v@mail.ru

For citation: Nemtsova MV, Maiorova MV. Application of Modern Genome Technologies in Treatment of Lymphomas. Clinical oncohematology. 2016;9(3):265-70 (In Russ).

DOI: 10.21320/2500-2139-2016-9-3-265-270


ABSTRACT

Modern achievements in genomics and cancer biology have provided an unprecedented body of knowledge regarding the molecular pathogenesis of lymphoma. Genome-wide association studies and modern computer technologies demonstrated that various histological and immunomorphological subtypes of lymphomas differ at the molecular level, and result from various oncogenic mechanisms. It is clear that the variability of clinical symptoms presented by patients with lymphomas is based on the heterogeneity of tumor cells and features of the molecular pathogenesis. Based on data obtained, strategies for the development of new drugs for treatment of lymphoma have been proposed, including identification of the molecular pathogenesis, assessment of the significance of each stage for the development of tumors and synthesis of a drug with a targeted effect. As a result, several new classes of molecular targeted agents for treatment of lymphomas have been proposed and are being tested in clinical trials. In the modern era of personalized medicine, correct targeted therapy for each type of lymphoma characterized by a unique molecular mechanism of tumor formation is a major challenge in lymphoma treatment.


Keywords: lymphoma, genes expression profile, microRNA, signaling pathways, NF-kB.

Received: February 13, 2016

Accepted: March 14, 2016

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REFERENCES

  1. Intlekofer AM, Younes A. Precision therapy for lymphoma—current state and future directions. Nat Rev Clin Oncol. 2014;11(10):585–96. doi: 10.1038/nrclinonc.2014.137.
  2. Roschewski M, Staudt LM, Wilson WH. Diffuse large B-cell lymphoma—treatment approaches in the molecular era. Nat Rev Clin Oncol. 2014;11(1):12–23. doi: 10.1038/nrclinonc.2013.197.
  3. Borchmann P, Eichenauer DA, Engert A. State of the art in the treatment of Hodgkin lymphoma. Nat Rev Clin Oncol. 2012;9(8):450–9. doi: 10.1038/nrclinonc.2012.91.
  4. Campo E, Swerdlow SH, Harris NL, et al. The 2008 WHO classification of lymphoid neoplasms and beyond: evolving concepts and practical applications. Blood. 2011;117(19):5019–32. doi: 10.1182/blood-2011-01-293050.
  5. Немцова М.В., Кушлинский Н.Е. Достижения высокотехнологичных геномных методов для практической онкологии. Медицинский алфавит. 2015;1(2):10–3. [Nemtsova MV, Kushlinskii NE. The achievement of high-genomic methods for practical oncology. Meditsinskii alfavit. 2015;1(2):10–3. (In Russ)]
  6. Alizadeh AA, Eisen MB, Davis RE, et al. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling. Nature. 2000;403(6769):503–11. doi: 10.1038/35000501.
  7. Lenz G, Dave SS, Xiao W, et al. Stromal gene signatures in large-B-cell lymphomas. N Engl J Med. 2008;359(22):2313–23. doi: 10.1056/NEJMoa0802885.
  8. Ngo VN, Davis RE, Lamy L, et al. A loss-of-function RNA interference screen for molecular targets in cancer. Nature. 2006;441(7089):106–10. doi: 10.1038/nature04687.
  9. Compagno M, Lim WK, Grunn A, et al. Mutations of multiple genes cause deregulation of NF-kappa B in diffuse large B-cell lymphoma. Nature. 2009;459(7247):717–21. doi: 10.1038/nature07968.
  10. Lenz G, Davis RE, Ngo VN, et al. Oncogenic CARD11 mutations in human diffuse large B cell lymphoma. Science. 2008;319(5870):1676–9. doi: 10.1126/science.1153629.
  11. Wilson WH. The Bruton’s tyrosine kinase (BTK) inhibitor, ibrutinib (PCI-32765), has preferential activity in the ABC subtype of relapsed/refractory de novo diffuse large B-cell lymphoma (DLBCL): interim results of a multicentre, open-label, phase 2 study. Blood. 2012;120: Abstract 686.
  12. Wang ML, Rule S, Martin P, et al. Targeting BTK with ibrutinib in relapsed or refractory mantle-cell lymphoma. N Engl J Med. 2013;369(6):507–16. doi: 10.1056/NEJMoa1306220.
  13. Morin RD, Mendez-Lago M, Mungall AJ, et al. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma. Nature. 2011;476(7360):298–303. doi: 10.1038/nature10351.
  14. Chi P, Allis CD, Wang GG. Covalent histone modifications—miswritten, misinterpreted and mis-erased in human cancers. Nat Rev Cancer. 2010;10(7):457–69. doi: 10.1038/nrc2876.
  15. Pasqualucci L, Dominguez-Sola D, Chiarenza A, et al. Inactivating mutations of acetyltransferase genes in B-cell lymphoma. Nature. 2011;471(7337):189–95. doi: 10.1038/nature09730.
  16. Lane AA, Chabner BA. Histone deacetylase inhibitors in cancer therapy. J Clin Oncol. 2009;27(32):5459–68. doi: 10.1200/jco.2009.22.1291.
  17. Yap DB, Chu J, Berg T, et al. Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. Blood. 2011;117(8):2451–9. doi: 10.1182/blood-2010-11-321208.
  18. Beguelin W, Popovic R, Teater M, et al. EZH2 is required for germinal centre formation and somatic EZH2 mutations promote lymphoid transformation. Cancer Cell. 2013;23(5):677–92. doi: 10.1016/j.ccr.2013.04.011.
  19. Cairns RA, Iqbal J, Lemonnier F, et al. IDH2 mutations are frequent in angioimmunoblastic T-cell lymphoma. Blood. 2012;119(8):1901–3. doi: 10.1182/blood-2011-11-391748.
  20. Wang F, Travins J, DeLaBarre B, et al. Targeted inhibition of mutant IDH2 in leukemia cells induces cellular differentiation. Science. 2013;340(6132):622–6. doi: 10.1126/science.1234769.
  21. Pasqualucci L, Khiabanian H, Fangazio M, et al. Genetics of follicular lymphoma transformation. Cell Rep., 2014;6(1):130–40. doi: 10.1016/j.celrep.2013.12.027.
  22. Schmitz R, Young RM, Ceribelli M, et al. Burkitt lymphoma pathogenesis and therapeutic targets from structural and functional genomics. Nature. 2012;490(7418):116–20. doi: 10.1038/nature11378.
  23. Bea S, Valdes-Mas R, Navarro A, et al. Landscape of somatic mutations and clonal evolution in mantle cell lymphoma. Proc Natl Acad Sci USA. 2013;110(45):18250–5. doi: 10.1073/pnas.1314608110.
  24. Rossi D, Trifonov V, Fangazio M, et al. The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development. J Exp Med. 2012;209(9):1537–51. doi: 10.1084/jem.20120904.
  25. Новикова М.В., Рыбко В.А., Хромова Н.В. и др. Роль белков Notch в процессах канцерогенеза. Успехи молекулярной онкологии. 2015;2(3):30–42. doi: 10.17650/2313-805X-2015-2-3-30-42. [Novikova MV, Rybko VA, Khromova NV, et al. The role of Notch pathway in carcinogenesis. Advances in molecular oncology. 2015;2(3):30–42. doi: 10.17650/2313-805X-2015-2-3-30-42. (In Russ)]
  26. Zhang J, Grubor V, Love CL, et al. Genetic heterogeneity of diffuse large B-cell lymphoma. Proc Natl Acad Sci USA. 2013;110(4):1398–403. doi: 10.1073/pnas.1205299110.
  27. Rahal R, Frick M, Romero R, et al. Pharmacological and genomic profiling identifies NF-kappaB-targeted treatment strategies for mantle cell lymphoma. Nat Med. 2014;20(1):87–92. doi: 10.1038/nm.3435.
  28. Anderson K, Lutz C, van Delft FW, et al. Genetic variegation of clonal architecture and propagating cells in leukaemia. Nature. 2011;469(7330):356–61. doi: 10.1038/nature09650.
  29. Ding L, Ley TJ, Larson DE, et al. Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing. Nature. 2012;481(7382):506–10. doi: 10.1038/nature10738.
  30. Arcaini L, Rossi D. Nuclear Factor-kB Dysregulation In Splenic Marginal Zone Lymphoma: New Therapeutic Opportunities. Haematologica. 2012;97(5):638–40. doi: 10.3324/haematol.2011.058362.
 

Video-Assisted Thoracoscopic Surgery in Diagnosing Lymphomas

IG Komarov1,2, SYu Sletina1, MI Komarov2, АА Sukhov1

1 N.N. Blokhin Russian Cancer Research Center, 24 Kashirskoye sh., Moscow, Russian Federation, 115478

2 Russian Medical Academy of Postgraduate Education, 23 Kashirskoye sh., Moscow, Russian Federation, 115478

For correspondence: Igor’ Gennad’evich Komarov, DSci, Professor, 24 Kashirskoye sh., Moscow, Russian Federation, 115478; Tel.: +7(499)324-12-70; e-mail: komarovig@mail.ru

For citation: Komarov IG, Sletina SYu, Komarov MI, Sukhov AA. Video-Assisted Thoracoscopic Surgery in Diagnosing Lymphomas. Clinical oncohematology. 2016;9(1):30–41 (In Russ).

DOI: 10.21320/2500-2139-2016-9-1-30-41


ABSTRACT

This article continues a series of papers dwelling on endo-surgery techniques in diagnosing lymphomas. It describes the history of the thoracoscopic surgery and its potential and current use when malignant lymphoproliferative diseases with involvement of chest organs and tissues. It provides brief description of basic instruments, equipment and technique of surgical interventions via the thoracic access. It lists indications and contraindications for the thoracoscopic surgery. In addition, the paper presents analysis of video-assisted thoracoscopic surgeries in 178 patients with suspected malignant lymphoproliferative diseases. During these surgeries, samples for further morphological assessment were obtained from all patients. Lymphomas were confirmed in 120 patients. The article contains two case reports on the video-assisted thoracoscopic interventions performed.


Keywords: lymphoma, diagnostics, video-assisted surgery, thoracoscopy.

Received: November 6, 2015

Accepted: December 24, 2015

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REFERENCES

  1. Jacobeus HC. The practical importance of thoracoscopy in surgery of the chest. Surg Gynecol Obstet. 1921;4:289–96. doi: 10.1007/978-3-662-01566-7_7.
  2. Кобаладзе М.Г. История развития эндоскопии. История науки и техники. 2004;5:18–23. [Kobaladze MG. History of endoscopy. Istoriya nauki i tekhniki. 2004;5:18–23. (In Russ)]
  3. Roviaro G, Rebuffat C, Varoli F, et al. Videoendoscopic pulmonary lobectomy for cancer. Surg Laparosc Endosc. 1992;2(3):244–7.
  4. Сигал Е.И. Первый опыт торакоскопических операций. Казанский медицинский журнал. 1994;6:74–81. [Sigal EI. The first experience of thorascopic surgeries. Kazanskii meditsinskii zhurnal. 1994;6:74–81. (In Russ)]
  5. Комаров И.Г., Степаненкова С.С., Комаров М.И. Видеолапароскопические операции в диагностике лимфом. Клиническая онкогематология. 2014;7(4):540–50. [Komarov IG, Stepanenkova SS, Komarov MI. Video-Assisted Laparoscopic Surgeries in Diagnosing Lymphomas. Klinicheskaya onkogematologiya. 2014;7(4):540–50. (In Russ)]

Secondary Hemophagocytic Syndrome in the Adult Patients. Literature Review and Authors’ Experience

VG Potapenko1,2, NA Potikhonova4, VV Baikov2, MB Belogurova1, IA Lisukov3, AV Klimovich1, SV Lapin2, MO Ivanova2, VM Kravtsova2, EI Podol’tseva1, NV Medvedeva1, BV Afanas’ev2

1 Municipal Clinical Hospital No. 31, 3 Dinamo pr-t, Saint Petersburg, Russian Federation, 197110

2 R.M. Gorbacheva Scientific Research Institute of Pediatric Hematology and Transplantation; Academician I.P. Pavlov First St. Petersburg State Medical University, 12 Rentgena str., Saint Petersburg, Russian Federation, 197022

3 I.I. Mechnikov North-Western State Medical University, 41 Kirochnaya str., Saint Petersburg, Russian Federation, 197022

4 Russian Scientific Research Institute of Hematology and Transfusiology under the Federal Medico-Biological Agency, 16 2-ya Sovetskaya str., Saint Petersburg, Russian Federation, 191024

For correspondence: Vsevolod Gennad’evich Potapenko, Municipal Clinical Hospital No. 31, 3 Dinamo pr-t, Saint Petersburg, Russian Federation, 197110; Tel.: +7(812)230-19-33; e-mail: potapenko.vsevolod@mail.ru

For citation: Potapenko V.G., Potikhonova N.A., Baikov V.V., Belogurova M.B., Lisukov I.A., Klimovich A.V., Lapin S.V., Ivanova M.O., Kravtsova V.M., Podol’tseva E.I., Medvedeva N.V., Afanas’ev B.V. Secondary Hemophagocytic Syndrome in the Adult Patients. Literature Review and Authors’ Experience. Klin. Onkogematol. 2015;8(2):169–84. (In Russ.).


ABSTRACT

Background & Aims. The hemophagocytic syndrome is a dangerous hyperinflammatory syndrome usually caused by an infection. It is a result of excessive cell activation in the mononuclear phagocyte system which is manifested itself through cytopenia, systemic inflammatory reaction, liver and spleen impairment. Since the disease is rare and its diagnosing is very complicated, this syndrome has not been studied thoroughly and is overlooked very often. The aim of this work is to describe authors’ experience in dealing with the secondary hemophagocytic syndrome (HPS) and to present a literature review.

Methods. Clinical and laboratory data of 15 patients aged 16 to 64 (median age 48 years) with secondary HPS observed over the period from 2009 till 2013 were analyzed. Secondary HPS was diagnosed in patients with malignant lymphoproliferative and infectious diseases. HPS signs were found in lymphoproliferative disorders (n = 5), chronic active EBV-infection (n = 3), allogeneic hematopoietic stem cell transplantation (n = 3), acute leukemia (n = 1), multiple myeloma (n = 1), pneumonia (n = 1), and glomerulonephritis (n = 1). 8 patients underwent treatment for HPS: etoposide (n = 1), glucocorticoids (n = 1), intravenous immunoglobulin (n = 2), combination of rituximab + glucocorticoids (n = 2), etoposide + cyclosporine A (n = 1), as well as combined HLH-2004 chemotherapy (n = 1). The median observation period was 42 months.

Results. Among 15 adult patients enrolled into the retrospective analysis, malignant lymphoproliferative disorders and chronic EBV-infection were most common underlying disorders in case of secondary HPS. Early diagnosing is very complicated, because diagnostic criteria accepted at present are typical for the late-phase HPS. The above factors require development of more sensitive and universal diagnostic criteria.

Conclusion. In oncohematological practice, the secondary HPS is a severe complication requiring differential diagnosing with other critical conditions and intensive care. In case of HPS associated with oncohematological disorders, patients require close monitoring throughout the antitumor treatment period and after it.


Keywords: secondary hemophagocytic syndrome, lymphoma, Epstein-Barr virus, etoposide, hematopoietic stem cells transplantation.

Received: December 9, 2014

Accepted: February 7, 2015

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REFERENCES

  1. Carroll WL, Finlay JL, Sudbury MA. Cancer in children and adolescents. Jones & Bartlett; 2010. pp. 254–6.
  2. Chu T, D’Angio GJ, Favara B, et al. Histiocytosis syndromes in children. The Lancet. 1987;329(8526):208–9. doi: 10.1016/s0140-6736(87)90016-x.
  3. Favara BE, Feller AC, Pauli M, et al. Contemporary classification of histiocytic disorders. The WHO Committee On Histiocytic/Reticulum Cell Proliferations. Reclassification Working Group of the Histiocyte Society. Med Pediatr Oncol. 1997;29(3):157–66. doi: 10.1002/(sici)1096-911x(199709)29:3<157::aid-mpo1>3.0.co;2-c.
  4. Swerdlow SH, Campo E, Harris NL, et al, eds. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. 4th edition. Lyon: IARC Press; 2008.
  5. Jordan MB, Allen CE, Weitzman S, et al. How I treat hemophagocytic lymphohistiocytosis. Blood. 2011;118(15):4041–52. doi: 10.1182/blood-2011-03-278127.
  6. Janka GE. Hemophagocytic syndromes. Blood Rev. 2007;21(5):245–53. doi: 10.1016/j.blre.2007.05.001.
  7. Gotze KS, Hoffmann D, Schatzl HM, et al. Fatal Epstein-Barr virus-associated lymphoproliferative disorder following treatment with a novel mTOR inhibitor for relapsed chronic lymphocytic leukemia leukemia cells. Haematologica. 2007;92(9):1282–3. doi: 10.3324/haematol.11155.
  8. Emmenegger U, Schaer DJ, Larroche C, et al. Haemophagocytic syndromes in adults: current concepts and challenges ahead. Swiss Med Wkly. 2005;135(21-22):299–314.
  9. Arico M, Danesino C, Pende D, Moretta L. Pathogenesis of hemophagocytic lymphohistiocytosis. Br J Haematol. 2001;114(4):761–9. doi: 10.1046/j.1365-2141.2001.02936.x.
  10. Henter JI, Horne A, Arico M, et al. HLH-2004: diagnostic and therapeutic guidelines for hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer. 2007;48(2):124–31. doi: 10.1002/pbc.21039.
  11. Filipovich AH. Hemophagocytic lymphohistiocytosis (HLH) and related disorders. Hematology. 2009;2009(1):127–31. doi: 10.1182/asheducation-2009.1.127.
  12. Trottestam H, Horne A, Arico M, et al. Chemoimmunotherapy for hemophagocytic lymphohistiocytosis: long-term results of the HLH-94 treatment protocol. Blood. 2011;118(17):4577–84. doi: 10.1182/blood-2011-06-356261.
  13. Охотникова Е.Н., Меллина К.В., Усова Е.И. и др. Гемофагоцитарный синдром в педиатрической практике. Клиническая иммунология, аллергология, инфектология. 2008;2(13):61–70. [Okhotnikova EN, Mellina KV, Usova EI, et al. Hematophagocytic syndrome in pediatric practice. Klinicheskaya immunologiya, allergologiya, infektologiya. 2008;2(13):61–70. (In Russ)]
  14. Diaz-Guzman E, Dong B, Hobbs SB, et al. Hemophagocytic lymphohistiocytosis after lung transplant: report of 2 cases and a literature review. Exp Clin Transplant. 2011;9(3):217–22.
  15. Охотникова Е.Н., Меллина К.В., Усова Е.И. и др. Гемофагоцитарный синдром в педиатрической практике (Обзор литературы). Здоровье ребенка. 2008;4(13):131–8. [Okhotnikova EN, Mellina KV, Usova EI, et al. Hematophagocytic syndrome in pediatric practice (literature review). Zdorov’e rebenka. 2008;4(13):131–8. (In Russ)]
  16. Karapinar B, Yilmaz D, Balkan C, et al. An unusual cause of multiple organ dysfunction syndrome in the pediatric intensive care unit: hemophagocytic lymphohistiocytosis. Pediatr Crit Care Med. 2009;10(3):285–90. doi: 10.1097/pcc.0b013e318198868b.
  17. Schaer DJ, Schaer CA, Schoedon G, et al. Hemophagocytic macrophages constitute a major compartment of heme oxygenase expression in sepsis. Eur J Haematol. 2006;77(5):432–6. doi: 10.1111/j.1600-0609.2006.00730.x.
  18. Besset S, Schnell D, Azoulay E. Hemophagocytic lymphohistiocytosis mimicking septic shock. Chest. 2012;141(3):835; author reply 836. doi: 10.1378/chest.11-2717.
  19. Raschke RA, Garcia-Orr R. Hemophagocytic lymphohistiocytosis: a potentially underrecognized association with systemic inflammatory response syndrome, severe sepsis, and septic shock in adults. Chest. 2011;140(4):933–8. doi: 10.1378/chest.11-0619.
  20. Gupta A, Tyrrell P, Valani R, et al. The role of the initial bone marrow aspirate in the diagnosis of hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer. 2008;51(3):402–4. doi: 10.1002/pbc.21564.
  21. Wang Z, Chen X, Wu L, et al. Significance of hemophagocytosis in diagnosis of hemophagocytic lymphohistiocytosis. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2009;17(4):1064–6.
  22. Favara BE. Histopathology of the liver in histiocytosis syndromes. Pediatr Pathol Lab Med. 1996;16(3):413–33. doi: 10.3109/15513819609168681.
  23. Wang Z, Wang YN, Feng CC, et al. Diagnostic significance of NK cell activity and soluble CD25 level in serum from patients with secondary hemophagocytic lymphohistiocytosis. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2008;16(5):1154–7.
  24. Wang LL, Hu YX, Chen WF, et al. Significance of soluble interleukin-2 receptor and NK cell activity in patients with hemophagocytic lymphohistiocytosis. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2012;20(2):401–4.
  25. Wang Z, Wang YN, Feng CC, et al. The early diagnosis and clinical analysis of 57 cases of acquired hemophagocytic lymphohistiocytosis. Zhonghua Nei Ke Za Zhi. 2009;48(4):312–5.
  26. Gotoh Y, Okamoto Y, Uemura O, et al. Determination of age-related changes in human soluble interleukin 2 receptor in body fluids of normal subjects as a control value against disease states. Clin Chim Acta. 1999;289(1–2):89–97. doi: 10.1016/s0009-8981(99)00161-8.
  27. Rothkrantz-Kos S, Drent M, Schmitz MP, et al. Biochemical parameters in monitoring severity of sarcoidosis. Chapter 4: Analytical evaluation and determination of reference values of soluble interleukin-2-receptor and serum amyloid-A. 2004.
  28. Janka G. Hemophagocytic lymphohistiocytosis: when the immune system runs amok. Klin Padiatr. 2009;221(5):278–85. doi: 10.1055/s-0029-1237386.
  29. Crook MA. Hyperferritinaemia; laboratory implications. Ann Clin Biochem. 2012;49(Pt 3):211–3. doi: 10.1258/acb.2012.012059.
  30. Park HS, Kim DY, Lee JH, et al. Clinical features of adult patients with secondary hemophagocytic lymphohistiocytosis from causes other than lymphoma: an analysis of treatment outcome and prognostic factors. Ann Hematol. 2012;91(6):897–904. doi: 10.1007/s00277-011-1380-3.
  31. Dhote R, Simon J, Papo T, et al. Reactive hemophagocytic syndrome in adult systemic disease: report of twenty-six cases and literature review. Arthritis Rheum. 2003;49(5):633–9. doi: 10.1002/art.11368.
  32. Mayordomo-Colunga J, Rey C, Gonzalez S, Concha A. Multiorgan failure due to hemophagocytic syndrome: A case report. Cases J. 2008;1(1):209. doi: 10.1186/1757-1626-1-209.
  33. Karras A, Thervet E, Legendre C. Hemophagocytic syndrome in renal transplant recipients: report of 17 cases and review of literature. Transplantation. 2004;77(2):238–43. doi: 10.1097/01.tp.0000107285.86939.37.
  34. Han AR, Lee HR, Park BB, et al. Lymphoma-associated hemophagocytic syndrome: clinical features and treatment outcome. Ann Hematol. 2007;86(7):493–8. doi: 10.1007/s00277-007-0278-6.
  35. Wijsman CA, Roeters van Lennep JE, von dem Borne PA, Fogteloo AJ. A diagnostic difficulty: two cases of haemophagocytic syndrome in adults. Neth J Med. 2009;67(1):29–31.
  36. Machaczka M. Hemophagocytic lymphohistiocytosis–a contemporary medical problem. Pol Merkur Lekarski. 2012;32(187):59–63.
  37. Allen CE, Yu X, Kozinetz CA, McClain KL. Highly elevated ferritin levels and the diagnosis of hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer. 2008;50(6):1227–35. doi: 10.1002/pbc.21423.
  38. Henter JI, Samuelsson-Horne A, Arico M, et al. Treatment of hemophagocytic lymphohistiocytosis with HLH-94 immunochemotherapy and bone marrow transplantation. Blood. 2002;100(7):2367–73. doi: 10.1182/blood-2002-01-0172.
  39. Shin HJ, Chung JS, Lee JJ, et al. Treatment Outcomes with CHOP Chemotherapy in Adult Patients with Hemophagocytic Lymphohistiocytosis. J Korean Med Sci. 2008;23(3):439–44. doi: 10.3346/jkms.2008.23.3.439.
  40. Goede JS, Peghini PE, Fehr J. Oral Low Dose Etoposide in the Treatment of Macrophage Activation Syndrome. Blood (ASH Annual Meeting Abstracts). 2004;104:3817.
  41. Bhattacharyya M, Ghosh MK. Hemophagoctic lymphohistiocytosis–recent concept. J Assoc Physicians India. 2008;56:453–7.
  42. Imashuku S, Hibi S, Kuriyama K, et al. Management of severe neutropenia with cyclosporin during initial treatment of Epstein-Barr virus-related hemophagocytic lymphohistiocytosis. Leuk Lymphoma. 2000;36(3–4):339–46. doi: 10.3109/10428190009148855.
  43. Ishii E, Ohga S, Imashuku S, et al. Review of hemophagocytic lymphohistiocytosis (HLH) in children with focus on Japanese experiences. Crit Rev Oncol Hematol. 2005;53(3):209–23. doi: 10.1016/j.critrevonc.2004.11.002.
  44. Emmenegger U, Reimers A, Frey U, et al. Reactive macrophage activation syndrome: a simple screening strategy and its potential in early treatment initiation. Swiss Med Wkly. 2002;132(17–18):230–6.
  45. Imashuku S, Kuriyama K, Teramura T, et al. Requirement for etoposide in the treatment of Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis. J Clin Oncol. 2001;19(10):2665–73.
  46. Imashuku S, Kuriyama K, Sakai R, et al. Treatment of Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) in young adults: A report from the HLH study center. Med Pediatr Oncol. 2003;41(2):103–9. doi: 10.1002/mpo.10314.
  47. Bosman G, Langemeijer SM, Hebeda KM, et al. The role of rituximab in a case of EBV–related lymphoproliferative disease presenting with haemophagocytosis. Neth J Med. 2009;67(8):364–5.
  48. Kimura H. Pathogenesis of chronic active Epstein-Barr virus infection: is this an infectious disease, lymphoproliferative disorder, or immunodeficiency? Rev Med Virol. 2006;16(4):251–61. doi: 10.1002/rmv.505.
  49. Imashuku S, Teramura T, Tauchi H, et al. Longitudinal follow-up of patients with Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis. Haematologica. 2004;89(2):183–8.
  50. Balamuth NJ, Nichols KE, Paessler M, Teachey DT. Use of rituximab in conjunction with immunosuppressive chemotherapy as a novel therapy for Epstein Barr virus-associated hemophagocytic lymphohistiocytosis. J Pediatr Hematol Oncol. 2007;29(8):569–73. doi: 10.1097/mph.0b013e3180f61be3.
  51. Bosman G, Langemeijer SM, Hebeda KM, et al. The role of rituximab in a case of EBV-related lymphoproliferative disease presenting with haemophagocytosis. Neth J Med. 2009;67(8):364–5.
  52. So MW, Koo BS, Kim YJ, et al. Successful rituximab treatment of refractory hemophagocytic lymphohistiocytosis and autoimmune hemolytic anemia associated with systemic lupus erythematosus. Mod Rheumatol. 2013 Feb 7 (abstract). doi: 10.1007/s10165-013-0838-7.
  53. Stebbing J, Ngan S, Ibrahim H, et al. The successful treatment of haemophagocytic syndrome in patients with humanimmunodeficiency virus-associated multi-centric Castleman’s disease. Clin Exp Immunol. 2008;154(3):399–405. doi: 10.1111/j.1365-2249.2008.03786.x.
  54. Масчан М. Молекулярно-генетическая диагностика и дифференциальная терапия гистиоцитарных пролиферативных заболеваний у детей: Автореф. ¼ д-ра мед. наук. М., 2011. [Maschan M. Molekulyarno-geneticheskaya diagnostika i differentsial’naya terapiya gistiotsitarnykh proliferativnykh zabolevanii u detei. (Molecular genetic diagnosis and differentiated therapy of histiocytic proliferative diseases in children.) [dissertation] Moscow; 2011. (In Russ)]
  55. Filipovich A, McClain K, Grom A. Histiocytic disorders: recent insights into pathophysiology and practical guidelines. Biol Blood Marrow Transplant. 2010;16(1 Suppl):S82–9. doi: 10.1016/j.bbmt.2009.11.014.
  56. Shabbir M, Lucas J, Lazarchick J, Shirai K. Secondary hemophagocytic syndrome in adults: a case series of 18 patients in a single institution and a review of literature. Hematol Oncol. 2011;29(2):100–6. doi: 10.1002/hon.960.
  57. Ramanan AV, Schneider R. Macrophage activation syndrome–what’s in a name! Rheumatol. 2003;30(12):2513–6.
  58. Weitzman S. Approach to hemophagocytic syndromes. Hematology Am Soc Hematol Educ Program. 2011;2011(1):178–83.
  59. Sada E, Shiratsuchi M, Kiyasu J, et al. Primary mediastinal non-seminomatous germ cell tumor associated with hemophagocytic syndrome. J Clin Exp Hematol. 2009;49(2):117–20. doi: 10.3960/jslrt.49.117.
  60. Chaudary IU, Bojal SA, Attia A, et al. Mediastinal endodermal sinus tumor associated with fatal hemophagocytic syndrome. Hematol Oncol Stem Cell Ther. 2011;4(3):138–41. doi: 10.5144/1658-3876.2011.138.
  61. Kounami S, Nakayama K, Yoshiyama M, et al. Early-onset hemophagocytic lymphohistiocytosis after the start of chemotherapy for advanced neuroblastoma. Pediatr Hematol Oncol. 2012;29(1):99–103. doi: 10.3109/08880018.2011.643529.
  62. Karapinar B, Yilmaz D, Balkan C, et al. An unusual cause of multiple organ dysfunction syndrome in the pediatric intensive care unit: hemophagocytic lymphohistiocytosis. Pediatr Crit Care Med. 2009;10(3):285–90. doi: 10.1097/pcc.0b013e318198868b.
  63. Takahashi N. Lymphoma-associated hemophagocytic syndrome (LAHS). Nihon Rinsho. 2000;58(3):665–8 (abstract).
  64. Chang CS, Wang CH, Su IJ, et al. Hematophagic histiocytosis: a clinicopathologic analysis of 23 cases with special reference to the association with peripheral T-cell lymphoma. J Formos Med Assoc. 1994;93:421–8.
  65. Miyahara M, Sano M, Shibata K, et al. B-cell lymphoma-associated hemophagocytic syndrome: clinicopathological characteristics. Ann Hematol. 2000;79(7):378–88. doi: 10.1007/s002770000155.
  66. Takahashi N, Miura I, Chubachi A, et al. A clinicopathological study of 20 patients with T/natural killer (NK)-cell lymphoma-associated hemophagocytic syndrome with special reference to nasal and nasal-type NK/T-cell lymphoma. Int J Hematol. 2001;74(3):303–8. doi: 10.1007/bf02982065.
  67. Abe Y, Hara K, Shiratsuchi M, et al. Two cases of B cell lymphoma associated with hemophagocytic syndrome. Rinsho Ketsueki. 2001;42(1):35–40.
  68. Shimazaki C, Inaba T, Okano A, et al. Clinical characteristics of B-cell lymphoma-associated hemophagocytic syndrome (B-LAHS): comparison of CD5+ with CD5- B-LAHS. Intern Med. 2001;40(9):878–82. doi: 10.2169/internalmedicine.40.878.
  69. Janka G, Imashuku S, Elinder G, et al. Infection- and malignancy-associated hemophagocytic syndromes. Secondary hemophagocytic lymphohistiocytosis. Hematol Oncol Clin North Am. 1998;12(2):435–44. doi: 10.1016/s0889-8588(05)70521-9.
  70. Matzner Y, Behar A, Beeri E, et al. Systemic leishmaniasis mimicking malignant histiocytosis. Cancer. 1979;43(1):398–402. doi: 10.1002/1097-0142(197901)43:1<398::aid-cncr2820430156>3.0.co;2-3.
  71. Castillo L, Carcillo J. Secondary hemophagocytic lymphohistiocytosis and severe sepsis/systemic inflammatory response syndrome/multiorgan dysfunction syndrome/macrophage activation syndrome share common intermediate phenotypes on a spectrum of inflammation. Pediatr Crit Care Med. 2009;10(3):387–92. doi: 10.1097/pcc.0b013e3181a1ae08.
  72. Karapinar B, Yilmaz D, Balkan C, et al. An unusual cause of multiple organ dysfunction syndrome in the pediatric intensive care unit: hemophagocytic lymphohistiocytosis. Pediatr Crit Care Med. 2009;10(3):285–90. doi: 10.1097/pcc.0b013e318198868b.
  73. Buyse S, Teixeira L, Galicier L, et al. Critical care management of patients with hemophagocytic lymphohistiocytosis. Intens Care Med. 2010;36(10):1695–702. doi: 10.1007/s00134-010-1936-z.
  74. Takahashi N, Chubachi A, Kume M, et al. A clinical analysis of 52 adult patients with hemophagocytic syndrome: the prognostic significance of the underlying diseases. Int J Hematol. 2001;74(2):209–13. doi: 10.1007/bf02982007.
  75. Cohen JI, Jaffe ES, Dale JK, et al. Characterization and treatment of chronic active Epstein-Barr virus disease: a 28-year experience in the United States. Blood. 2011;117(22):5835–49. doi: 10.1182/blood-2010-11-316745.
  76. Ishii E, Ohga S, Imashuku S, et al. Nationwide survey of hemophagocytic lymphohistiocytosis in Japan. Int J Hematol. 2007;86(1):58–65. doi: 10.1532/ijh97.07012.
  77. Xiao L, Xian Y, Dai BT, et al. Clinical features and outcome analysis of 83 childhood Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis with HLH-2004 protocol. Zhonghua Xue Ye Xue Za Zhi. 2011;32(10):668–72.
  78. Maia DM, Peace-Brewer AL. Chronic, active Epstein-Barr virus infection. Curr Opin Hematol. 2000;7(1):59–63. doi: 10.1097/00062752-200001000-00011.
  79. Kunitomi A, Kimura H, Ito Y, et al. Unrelated bone marrow transplantation induced long-term remission in a patient with life-threatening Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis. J Clin Exp Hematol. 2011;51(1):57–61. doi: 10.3960/jslrt.51.57.
  80. Ohshima K, Suzumiya J, Sugihara M, et al. Clinicopathological study of severe chronic active Epstein-Barr virus infection that developed in association with lymphoproliferative disorder and/or hemophagocytic syndrome. Pathol Int. 1998;48(12):934–43. doi: 10.1111/j.1440-1827.1998.tb03864.x.
  81. Katano H, Ali MA, Patera AC, et al. Chronic active Epstein-Barr virus infection associated with mutations in perforin that impair its maturation. Blood. 2004;103(4):1244–52. doi: 10.1182/blood-2003-06-2171.
  82. Kasahara Y, Yachie A, Takei K, et al. Differential cellular targets of Epstein-Barr virus (EBV) infection between acute EBV-associated hemophagocytic lymphohistiocytosis and chronic active EBV infection. Blood. 2001;98(6):1882–8. doi: 10.1182/blood.v98.6.1882.
  83. Taniai N, Akimaru K, Kawano Y, et al. Hemophagocytic syndrome after living-donor liver transplantation for fulminant liver failure: a case report. Hepatogastroenterology. 2005;52(63):923–6.
  84. Yoshizumi T, Taketomi A, Kayashima H, et al. Successful treatment for a patient with hemophagocytic syndrome after a small-for-size graft liver transplantation. Hepatogastroenterology. 2008;55(82–83):359–62.
  85. Soyama A, Eguchi S, Takatsuki M, et al. Hemophagocytic syndrome after liver transplantation: report of two cases. Surg Today. 2011;41(11):1524–30. doi: 10.1007/s00595-010-4512-9.
  86. Fukunaga A, Nakamura F, Yoshinaga N, et al. Successful treatment with combined chemotherapy of two adult cases of hemophagocytic lymphohistiocytosis in recipients of umbilical cord blood cell transplantation. Int J Hematol. 2011;93(4):551–4. doi: 10.1007/s12185-011-0792-0.
  87. Asano T, Kogawa K, Morimoto A, et al. Hemophagocytic lymphohistiocytosis after hematopoietic stem cell transplantation in children: a nationwide survey in Japan. Pediatr Blood Cancer. 2012;59(1):110–4. doi: 10.1002/pbc.23384.
  88. Abdelkefi A, Ben Jamil W, Torjman L, et al. Hemophagocytic syndrome after hematopoietic stem cell transplantation: a prospective observational study. Int J Hematol. 2009;89(3):368–73. doi: 10.1007/s12185-009-0261-1.
  89. Okano M, Kawa K, Kimura H, et al. Proposed Guidelines for Diagnosing Chronic Active Epstein-Barr Virus Infection. Am J Hematol. 2005;80(1):64–9. doi: 10.1002/ajh.20398.
  90. Horne A, Trottestam H, Arico M, et al. Frequency and spectrum of central nervous system involvement in 193 children with haemophagocytic lymphohistiocytosis. Br J Haematol. 2008;140(3):327–35. doi: 10.1111/j.1365-2141.2007.06922.x.
  91. Gupta S, Weitzman S. Primary and secondary hemophagocytic lymphohistiocytosis: clinical features, pathogenesis and therapy. Exp Rev Clin Immunol. 2010;6(1):137–54. doi: 10.1586/eci.09.58.

Modern Aspects of Diagnosis and Treatment of Complicated Forms of Non-Hodgkin’s Lymphomas of Small and Large Intestine

OA Malikhova, AO Tumanyan, VA Shalenkov, AG Malikhov, YuP Kuvshinov, GV Ungiadze

N.N. Blokhin Russian Cancer Research Center, 24 Kashirskoye sh., Moscow, Russian Federation, 115478

For correspondence: Ol’ga Aleksandrovna Malikhova, PhD, 24 Kashirskoye sh., Moscow, Russian Federation, 115478; Tel.: +7(499)324-43-27; e-mail: malikhova@inbox.ru

For citation: Malikhova OA, Tumanyan AO, Shalenkov VA, et al. Modern Aspects of Diagnosis and Treatment of Complicated Forms of Non-Hodgkin’s Lymphomas of Small and Large Intestine. Clinical oncohematology. 2015;8(2):129–35 (In Russ).

ABSTRACT

Background & Aims. Lymphomas constitute 5 to 10 % of gastrointestinal tumors and most of them are non-Hodgkin’s lymphomas (NHLs). They constitute 30–45 % of all extranodal NHLs. Primary involvement of the gastrointestinal tract is observed in 2/3 of patients. The objective of this study is to determine clinical and morphological features and treatment outcomes of complicated forms of NHLs of the small and large intestine.

Methods. NHLs of the small and large intestine were studied in 189 patients treated in the N.N. Blokhin Russian Cancer Research Center within the period of 1985–2010. Large intestine involvement was observed in 64 patients and small intestine involvement in 125 patients.

Results. Surgical interventions for ileus, bleeding or perforation of a hollow organ were performed in 92 patients with primary or secondary involvement of the small and large intestine (48.7 %). The intestine involvement was primary in 58.9 % of cases and secondary in 41.0 % of cases.

Conclusion. Complications of gastrointestinal NHLs deteriorate the overall survival rate. Patients with small or large intestine involvement require a special approach to diagnosis and treatment because of a high risk of surgical complications.


Keywords: lymphoma, small intestine, large intestine, oncohematology, non-Hodgkin’s lymphomas.

Received: January 30, 2014

Accepted: February 12, 2015

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REFERENCES

  1. Thorling MS. Gastrointestinal lymphomas: Clinical features, treatment and prognosis. Acta Radiol Oncol. 1984;23(2–3):193–7. doi: 10.3109/02841868409136011.
  2. Ковынев И.Б., Поспелова Т.И., Агеева Т.А., Лосева М.И. Частота и структура неходжкинских злокачественных лимфом в Новосибирске, НСО и городах Сибирского федерального округа. Бюллетень СО РАМН. 2006;4(122):175–81. [Kovynev IB, Pospelova TI, Ageeva TA, Loseva MI. Incidence and structure of non-Hodgkin’s malignant lymphomas in Novosibirsk, Novosibirsk Oblast, and cities of Siberian Federal Okrug. Byulleten’ SO RAMN. 2006;4(122):175–81. (In Russ)]
  3. Поддубная И.В. Первичные лимфомы желудочно-кишечного тракта. В кн.: Клиническая онкогематология. Под ред. М.А. Волковой. М.: Медицина, 2007. С. 734–70. [Poddubnaya IV. Primary lymphomas of the gastrointestinal tract. In: Volkova MA, ed. Klinicheskaya onkogematologiya. (Clinical oncohematology.) Moscow: Meditsina Publ.; 2007. pp. 734–70. (In Russ)]
  4. Mihaljevic B. Primary Extranodal Lymphomas of Gastrointestinal Localization: A Single Institution 5-yr Experience. Med. Oncol. 2006;23(2):225–7. doi: 10.1385/mo:23:2:225.
  5. Bilsel Y, Balik E, Yamaner S, Bugra D. Clinical and therapeutic considerations of rectal lymphoma: A case report and literature review. World J Gastroenterol. 2005;11(3):460–1. doi: 10.3748/wjg.v11.i3.460.
  6. Feller AJ. Histopathology of nodal and extra nodal non-Hodgkin’s lymphomas. 3rd edition. Berlin: Springer-Verlag; 2004. doi: 10.1007/978-3-642-18653-0.
  7. Ferreri AJ. Summary statement on primary central nervous system lymphomas from the Eighth International Conference on Malignant Lymphoma, Lugano, Switzerland, June 12–15, 2002. J Clin Oncol. 2003;21(12):2407–14. doi: 10.1200/jco.2003.01.135.
  8. Rosas ME, Frisnacho VO, Yabar BA. Malignant duodenal neoplasia: clinical-pathologic profile. Rev Gastroenterol Peru. 2003;23(2):99–106.
  9. Ghimire P, Wu GY, Zhu L. Primary gastrointestinal lymphomas. World J Gastroenterol. 2011;17(6):697–707. doi: 10.3748/wjg.v17.i6.697.
  10. Balfe P, O’Brian S, Daly P, et al. Management of gastric lymphoma. Surgeon. 2008;6(5):262–5. doi: 10.1016/s1479-666x(08)80048-0.
  11. Contreary K, Nance FC, Becker WF. Primary lymphoma of gastrointestinal tract. Ann Surg. 1980;191(5):593–8. doi: 10.1097/00000658-198005000-00011.
  12. Dar AM. Isolated primary esophageal lymphoma – a rare case report. Indian J Thorac Cardiovasc Surg. 2011;27(1):53–5. doi: 10.1007/s12055-010-0069-x.
  13. Al-Saleem T. Immunoproliferative small intestinal disease (IPSID): a model for mature B-cell neoplasms. Blood. 2005;105(6):2274–80. doi: 0.1182/blood-2004-07-2755.
  14. Cavalli F, Isaacson PG, Gascoyne RD, Zucca E. MALT Lymphomas. Hematology Am Soc Hematol Educ Program. 2001:241–58.
  15. Azarm T. Primary Gastrointestinal lymphoma, Clinicopathologic Study of 49 Small Intestinal Lymphoma Cases and the Treatment Option of Choice. Intern J Hematol Oncol Stem Cell Res. 2009;3(4):21–3.
  16. Bairey O, Shpilberg O. Non-Hodgkin’s Lymphomas of the Colon. Israel Med Assoc J. 2006;8(12):832–5.
  17. Berthold D, Ghielmini M. Treatment of malignant lymphomas. Swiss Med Wkly. 2004;134(33–34):472–80.
  18. Dughayli MS, Baidoun F, Lupovitch A. Synchronous perforation of Non-Hodgkin’s Lymphoma of the small intestine and colon: a case report. J Med Case Rep. 2011;5:57. doi: 10.1186/1752-1947-5-57.
  19. Cappell MS. Acute Nonvariceal Upper Gastrointestinal Bleeding: Endoscopic Diagnosis and Therapy. Med Clin. 2008;92(3):511–50. doi: 10.1016/j.mcna.2008.01.001.
  20. Неред С.Н., Стилиди И.С., Поддубная И.В., Шаленков В.А. Хирургическое лечение осложненных форм первичных неходжкинских лимфом желудка. Вестник РОНЦ им. Н.Н. Блохина. 2011;1:66–74. [Nered SN, Stilidi IS, Poddubnaya IV, Shalenkov VA. Surgical treatment of complicated forms of gastric non-Hodgkin’s lymphomas. Vestnik RONTs im. N.N. Blokhina. 2011;1:66–74. (In Russ)]
  21. Pennazio M. Small-intestinal pathology on capsule endoscopy: spectrum of vascular lesions. Endoscopy. 2005;37(9):864–9. doi: 10.1055/s-2005-870212.
  22. Khan SH, Ahmaf M, Wani NA, Khardi MY. Primary Ileocaecal Lymphoma: Clinico-Pathological Features and Results of Treatment. JK Science. 2000;2(2):232.
  23. Shum JB, Croome K. Upper gastrointestinal and intra-abdominal hemorrhage secondary to diffuse large B-cell gastric lymphoma. Can J Surg. 2008;51(3):E56–7.
  24. Урядов С.Е., Шапкин Ю.Г., Капралов С.В. Эндоскопический гемостаз при толстокишечных кровотечениях. Саратовский научно-медицинский журнал. 2010;6(3):719–22. [Uryadov SE, Shapkin YuG, Kapralov SV. Endoscopic hemostasis in bleeding from large intestine. Saratovskii nauchno-meditsinskii zhurnal. 2010;6(3):719–22. (In Russ)]
  25. Толпинский А.П., Токарев Б.В., Бахлаев И.Е. Осложнения рака желудка: методические указания к практическим занятиям по онкологии. Петрозаводск: ПетрГУ, 1995. C. 25. [Tolpinskii AP, Tokarev BV, Bakhlaev IE. Oslozhneniya raka zheludka: metodicheskie ukazaniya k prakticheskim zanyatiyam po onkologii. (Complications of gastric cancer: guidelines for practical training in oncology.) Petrozavodsk: PetrGU Publ.; 1995. pр. 25. (In Russ)]
  26. Vadala G, Salice M, L’Anfusa G, et al. Complication of ileal lymphoma. Minerva Chir. 1995;50(11):963–6.
  27. Varghese C, Jose CC, Subhashii J, et al. Primary Small Intestinal Lymphoma. Oncology. 1992;49(5):340–2. doi: 10.1159/000227069.

Positron Emission Tomography in Modern Management of Lymphomas

IP Aslanidi, OV Mukhortova, TA Katunina, IV Ekaeva, MG Shavman

A.N. Bakulev Scientific Center of Cardiovascular Surgery, 135 Rublevskoe sh., Moscow, Russian Federation, 121552

For correspondence: Ol’ga Valentinovna Mukhortova, DSci, 135 Rublevskoe sh., Moscow, Russian Federation, 121552; Tel.: +7(495)414-77-31; e-mail: olgamukhortova@yandex.ru

For citation: Aslanidi IP, Mukhortova OV, Katunina TA, et al. Positron Emission Tomography in Modern Management of Lymphomas. Clinical oncohematology. 2015;8(1):13–25 (In Russ).


ABSTRACT

Objective. The objective is to determine areas of effective application of positron emission tomography (PET) with fluorodeoxyglucose labeled with 18-fluorine (18F-FDG) in patients with lymphomas.

Methods. 56 scientific papers published in 2005–2014 were examined. They analyzed results of recent large studies of PET in patients with lymphomas.

Results. 18F-FDG PET has become an essential part of a diagnostic algorithm for patients with lymphomas which are characterized by active accumulation of 18F-FDG. High precision of PET in patients with some types of lymphomas permit to use this method effectively in clinical practice for staging of the disease, assessment of the treatment efficacy, more precise diagnosis of the relapse prevalence, assessment of results of the anti-relapse therapy, as well as in case of suspected lymphoma transformation. The use of PET at other stages of treatment of lymphoma patients is still pending further scientific research. In case of indolent lymphomas with known low glycolytic activity or lymphomas of rare histological types, PET is used for assessment of the treatment efficacy only if baseline study results (before initiation of treatment) are available. The Deauville five-score scale criteria should be used for assessment of the treatment efficacy. Timely examination during antitumor treatment permits to increase the precision of the PET diagnosing significantly. Solitary foci found by PET are crucial for the choice of treatment and they should be verified by other diagnostic techniques. It is considered unreasonable to use PET for follow-up observation over patients in remission.

Conclusions. PET is a gold standard for staging and assessing the treatment efficacy of lymphomas characterized by active accumulation of 18F-FDG.


Keywords: PET, lymphoma, international guidelines, Deauville five-score scale.

Received: November 14, 2014

Accepted: November 18, 2014

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REFERENCES

  1. Wood KA, Hoskin PJ, Saunders MI. Positron Emission Tomography in Oncology: A Review. Clin Oncol. 2007;19(4):237–55. doi: 10.1016/j.clon.2007.02.001.
  2. Cheson BD. Role of functional imaging in the management of lymphoma. J Clin Oncol. 2011;29(14):1844–54. doi: 10.1200/jco.2010.32.5225.
  3. Collins CD. PET in lymphoma. Cancer Imaging. 2006;6:S63–S70. doi: 10.1102/1470-7330.2006.9013.
  4. Boellaard R, O’Doherty MJ, Weber WA, et al. FDG PET and PET/CT: EANM procedure guidelines for tumor PET imaging: version 1.0. Eur J Nucl Med Mol Imaging. 2010;37(7):181–200. doi: 10.1007/s00259-010-1459-4.
  5. Weiler-Sagie M, Bushelev O, Epelbaum R, et al. (18)F-FDG avidity in lymphoma readdressed: A study of 766 patients. J Nucl Med. 2010;51(1):25–30. doi: 10.2967/jnumed.109.067892.
  6. Kostakoglu L, Cheson D. State-of-the-art research on Lymphomas: role of molecular imaging for staging, prognostic evaluation, and treatment response. Front Oncol. 2013;3:212. doi: 10.3389/fonc.2013.00212.
  7. Cheson BD, Fisher RI, Barrington SF, et al. Recommendations for Initial Evaluation, Staging, and Response Assessment of Hodgkin and Non-Hodgkin Lymphoma: The Lugano Classification. J Clin Oncol. 2014;32(27):3059–67. doi: 10.1200/jco.2013.54.8800.
  8. Barrington SF, Mikhaeel NG, Kostakoglu L, et al. Role of Imaging in the Staging and Response Assessment of Lymphoma: Consensus of the International Conference on Malignant Lymphomas Imaging Working Group. J Clin Oncol. 2014;32(27):3048–58. doi: 10.1200/jco.2013.53.5229.
  9. Engert A, Haverkamp H, Kobe C, et al. Reduced-intensity chemotherapy and PET-guided radiotherapy in patients with advanced stage Hodgkin’s lymphoma (HD15 trial): A randomised, open-label, phase 3 non-inferiority trial. The Lancet. 2012;379(9828):1791–9. doi: 10.1016/s0140-6736(11)61940-5.
  10. Thomson KJ, Kayani I, Ardeshna K, et al. A response-adjusted PET-based transplantation strategy in primary resistant and relapsed Hodgkin lymphoma. Leukemia. 2013;27(6):1419–22. doi: 10.1038/leu.2012.318.
  11. Hutchings M. FDG-PET response-adapted therapy: is 18F-fluorodeoxyglucose positron emission tomography a safe predictor for a change of therapy? Hematol Oncol Clin North Am. 2014;28(1):87–103. doi: 10.1016/j.hoc.2013.10.008.
  12. Radford J, Barrington S, Counsell N, et al. Involved field radiotherapy vs no further treatment in patients with clinical stages IA and IIA Hodgkin lymphoma and a ‘negative’ PET scan after 3 cycles ABVD: results of the UK NCRI RAPID trial. Blood. 2012;120(21):547.
  13. Barrington SF, Mikhaeel NG. When should FDG-PET be used in the modern management of lymphoma? Br J Haematol. 2014;164(3):315–28. doi: 10.1111/bjh.12601.
  14. Omur O, Baran Y, Oral A, et al. Fluorine-18 fluorodeoxyglucose PET-CT for extranodal staging of non-Hodgkin and Hodgkin lymphoma. Diagn Interv Radiol. 2014;20(2):185–92. doi: 10.5152/dir.2013.13174.
  15. Luminari S, Biasoli I, Arcaini L, et al. The use of FDG-PET in the initial staging of 142 patients with follicular lymphoma: A retrospective study from the FOLL05 randomized trial of the Fondazione Italiana Linfomi. Ann Oncol. 2013;24(8):2108–12. doi: 10.1093/annonc/mdt137.
  16. Pelosi E, Pregno P, Penna D, et al. Role of whole-body [18F] fluorodeoxyglucose positron emission tomography/computed tomography (FDGPET/CT) and conventional techniques in the staging of patients with Hodgkin and aggressive non Hodgkin lymphoma. Radiol Med. 2008;113(4):578–90. doi: 10.1007/s11547-008-0264-7.
  17. Casulo C, Schoder H, Feeney J, et al. FDG PET in the staging and prognosis of T cell lymphoma. Leuk Lymphoma. 2013;54(10):2163–7. doi: 10.3109/10428194.2013.767901.
  18. Scott AM, Gunawardana DH, Wong J, et al. Positron emission tomography changes management, improves prognostic stratification and is superior to gallium scintigraphy in patients with low-grade lymphoma: results of a multicentre prospective study. Eur J Nucl Med Mol Imaging. 2009;36(3):347–53. doi: 10.1007/s00259-008-0958-z.
  19. Cortes-Romera M, Sabate-Llobera A, Mercadal-Vilchez S, et al. Bone marrow evaluation in initial staging of lymphoma: 18F-FDG PET/CT versus bone marrow biopsy. Clin Nucl Med. 2014;39(1):e46–52. doi: 10.1097/rlu.0b013e31828e9504.
  20. Adams HJ, Kwee TC, Vermoolen MA, et al. Whole-body MRI for the detection of bone marrow involvement in lymphoma: prospective study in 116 patients and comparison with FDG-PET. Eur Radiol. 2013;23(8):2271–8. doi: 10.1007/s00330-013-2835-9.
  21. Castellucci P, Nanni C, Farsad M, et al. Potential pitfalls of 18F-FDG PET in a large series of patients treated for malignant lymphoma: prevalence and scan interpretation. Nucl Med Comm. 2005;26(8):689–94. doi: 10.1097/01.mnm.0000171781.11027.bb.
  22. Storto G, Di Giorgio E, De Renzo A, et al. Assessment of metabolic activity by PET-CT with F-18-FDG in patients with T-cell lymphoma. Br J Haematol. 2010;151(2):195–7. doi: 10.1111/j.1365-2141.2010.08335.x.
  23. Ansell SM, Armitage JO. Positron Emission Tomographic Scans in Lymphoma: Convention and Controversy. Mayo Clin Proc. 2012;87(6):571–80. doi: 10.1016/j.mayocp.2012.03.006.
  24. Araf S, Montoto S. The use of interim 18F-fluorodeoxyglucose PET to guide therapy in lymphoma. Fut Oncol. 2013;9(6):807–15. doi: 10.2217/fon.13.55.
  25. Zinzani PL, Rigacci L, Stefoni V, et al. Early interim 18F-FDG PET in Hodgkin’s lymphoma: Evaluation on 304 patients. Eur J Nucl Med Mol Imaging. 2012;39(1):4–12. doi: 10.1007/s00259-011-1916-8.
  26. Moulin-Romsee G, Hindie E, Cuenca X, et al. (18) F-FDG PET/CT bone/bone marrow findings in Hodgkin’s lymphoma may circumvent the use of bone marrow trephine biopsy at diagnosis staging. Eur J Nucl Med Mol Imaging. 2010;37(6):1095–105. doi: 10.1007/s00259-009-1377-5.
  27. Hamilton R, Andrews I, McKay P, et al. Loss of utility of bone marrow biopsy as a staging evaluation for Hodgkin lymphoma in the positron emission tomography-computed tomography era: a West of Scotland study. Leuk Lymphoma. 2014;55(5):1049–52. doi: 10.3109/10428194.2013.821201.
  28. Berthet L, Cochet A, Kanoun S, et al. In newly diagnosed diffuse large B-cell lymphoma, determination of bone marrow involvement with 18F-FDG PET/CT provides better diagnostic performance and prognostic stratification than does biopsy. J Nucl Med. 2013;54(8):1244–50. doi: 10.2967/jnumed.112.114710.
  29. El-Galaly TC, d’Amore F, Mylam KJ, et al. Routine bone marrow biopsy has little or no therapeutic consequence for positron emission tomography/computed tomography-staged treatment-naive patients with Hodgkin lymphoma. J Clin Oncol. 2012;30(36):4508–14. doi: 10.1200/jco.2012.42.4036.
  30. El-Galaly TC, Hutchings M, Mylam KJ, et al. Impact of 18F-FDG PET/CT Staging in Newly Diagnosed Classical Hodgkin Lymphoma: Less Cases with Stage I Disease and More with Skeletal Involvement. Leuk Lymphoma. 2014;55(10):2349–55. doi: 10.3109/10428194.2013.875169.
  31. Cheng G, Alavi A. Value of 18F-FDG PET versus iliac biopsy in the initial evaluation of bone marrow infiltration in the case of Hodgkin’s disease: a meta-analysis. Nucl Med Commun. 2013;34(1):25–31. doi: 10.1097/mnm.0b013e32835afc19.
  32. Chen YK, Yeh CL, Tsui CC, et al. F-18 FDG PET for evaluation of bone marrow involvement in non-Hodgkin lymphoma: A meta-analysis. Clin Nucl Med. 2011;36(7):553–9. doi: 10.1097/rlu.0b013e318217aeff.
  33. Мухортова О.В., Асланиди И.П., Шурупова И.В. и др. Применение позитронно-эмиссионной томографии для оценки поражения костного мозга у больных злокачественными лимфомами. Медицинская радиология и радиационная безопасность. 2010;2:43–52. [Mukhortova OV, Aslanidi IP, Shurupova IV, et al. Use of positron emission tomography for assessment of bone marrow damage in patients with malignant lymphomas. Meditsinskaya radiologiya i radiatsionnaya bezopasnost’. 2010;2:43–52. (In Russ)]
  34. Kashyap R, Lau E, George A, et al. High FDG activity in focal fat necrosis: a pitfall in interpretation of posttreatment PET/CT in patients with non-Hodgkin lymphoma. Eur J Nucl Med Mol Imaging. 2013;40(9):1330–6. doi: 10.1007/s00259-013-2429-4.
  35. Hutchings M, Barrington SF. PET/CT for Therapy Response Assessment in Lymphoma. J Nucl Med. 2009;50(Suppl 1):21S–30S. doi: 10.2967/jnumed.108.05719.
  36. Dabaja BS, Phan J, Mawlawi O, et al. Clinical implications of positron emission tomography – negative residual computed tomography masses after chemotherapy for diffuse large B-cell lymphoma. Leuk Lymphoma. 2013;54(12):2631–8. doi: 10.3109/10428194.2013.784967.
  37. Gallamini A, Barringtom S, Biggi A, et al. The predictive role of interim positron emission tomography for Hodgkin lymphoma treatment outcome is confirmed using the interpretation criteria of the Deauville five-point scale. Haematologica. 2014;99(6):1107–13. doi: 10.3324/haematol.2013.103218.
  38. Fuertes S, Setoain X, Lopez-Guillermo A, et al. Interim FDG PET/CT as a prognostic factor in diffuse large B-cell lymphoma. Eur J Nucl Med Mol Imaging. 2013;40(4):496–504. doi: 10.1007/s00259-012-2320-8.
  39. Bodet-Milin C, Touzeau C, Leux C, et al. Prognostic impact of 18F-fluorodeoxyglucose positron emission tomography in untreated mantle cell lymphoma: a retrospective study from the GOELAMS group. Eur J Nucl Med Mol Imaging. 2010;37(9):1633–42. doi: 10.1007/s00259-010-1469-2.
  40. Cahu X, Bodet-Milin C, Brissot E, et al. 18F-fluorodeoxyglucose-positron emission tomography before, during and after treatment in mature T/NK lymphomas: a study from the GOELAMS group. Ann Oncol. 2011;22(3):705–11. doi: 10.1093/annonc/mdq415.
  41. Lee H, Kim SK, Kim YI, et al. Early Determination of Prognosis by Interim 3¢-Deoxy-3¢-18F-Fluorothymidine PET in Patients with Non-Hodgkin Lymphoma. J Nucl Med. 2014;55(2):216–22. doi: 10.2967/jnumed.113.124172.
  42. Le Dortz L, De Guibert S, Bayat S, et al. Diagnostic and prognostic impact of 18F-FDG PET/CT in follicular lymphoma. Eur J Nucl Med Mol Imaging. 2010;37(12):2307–14. doi: 10.1007/s00259-010-1539-5.
  43. Lopci E, Zanoni L, Chiti A, et al. FDG PET/CT predictive role in follicular lymphoma. Eur J Nucl Med Mol Imaging. 2012;39(5):864–71. doi: 10.1007/s00259-012-2079-y.
  44. Oki Y, Chuang H, Chasen B, et al. The prognostic value of interim positron emission tomography scan in patients with classical Hodgkin lymphoma. Br J Haematol. 2014;165(1):112–6. doi: 10.1111/bjh.12715.
  45. Bodet-Milin C, Eugene T, Gastinne T. FDG-PET in Follicular Lymphoma Management. J Oncol. 2012:370272. doi: 10.1155/2012/370272.
  46. Sucak GT, Ozkurt ZN, Suyani E, et al. Early post-transplantation positron emission tomography in patients with Hodgkin lymphoma is an independent prognostic factor with an impact on overall survival. Ann Hematol. 2011;90(11):1329–36. doi: 10.1007/s00277-011-1209-0.
  47. Biggi A, Gallamini A, Chauvie S, et al. International validation study for interim PET in ABVD-treated, advanced-stage Hodgkin lymphoma: Interpretation criteria and concordance rate among reviewers. J Nucl Med. 2013;54(5):683–90. doi: 10.2967/jnumed.112.110890.
  48. Nols N, Mounier N, Bouazza S, et al. Quantitative and qualitative analysis of metabolic response at interim PET-scan combined with IPI is highly predictive of outcome in diffuse large B-cell lymphoma. Leuk Lymphoma. 2014;55(4):773–80. doi: 10.3109/10428194.2013.831848.
  49. Gallamini A, Kostakoglu L. Positron emission tomography/computed tomography surveillance in patients with lymphoma: a fox hunt? Haematologica. 2012;97(6):797–9. doi: 10.3324/haematol.2012.063909.
  50. Yoo C, Lee DH, Kim JE, et al. Limited role of interim PET/CT in patients with diffuse large B-cell lymphoma treated with R-CHOP. Ann Hematol. 2011;90(7):797–802. doi: 10.1007/s00277-010-1135-6.
  51. Pregno P, Chiappella A, Bello M, et al. Interim 18-FDG-PET/CT failed to predict the outcome in diffuse large B-cell lymphoma patients treated at the diagnosis with rituximab-CHOP. Blood. 2012;119(9):2066–73. doi: 10.1182/blood-2011-06-359943.
  52. Safar V, Dupuis J, Itti E, et al. Interim [18F]fluorodeoxyglucose positron emission tomography scan in diffuse large B-cell lymphoma treated with anthracycline-based chemotherapy plus rituximab. J Clin Oncol. 2012;30(2):184–90. doi: 10.1200/JCO.2011.38.2648.
  53. Terasawa T, Dahabreh IJ, Nihashi T. Fluorine-18-Fluorodeoxyglucose positron emission tomography in response assessment before high-dose chemotherapy for lymphoma: a systematic review and meta-analysis. The Oncologist. 2010;15(7):750–9. doi: 10.1634/theoncologist.2010-0054.
  54. Sucak GT, Ozkurt ZN, Suyani E, et al. Early post-transplantation positron emission tomography in patients with Hodgkin lymphoma is an independent prognostic factor with an impact on overall survival. Ann Hematol. 2011;90(11):1329–36. doi: 10.1007/s00277-011-1209-0.
  55. Von Tresckow B, Engert A. The emerging role of PET in Hodgkin lymphoma patients receiving autologous stem cell transplant. Expert Rev Hematol. 2012;5(5):483–6. doi: 10.1586/ehm.12.41.
  56. Bodet-Milin C, Kraeber-Bodere F, Moreau P, et al. Investigation of FDG-PET/CT imaging to guide biopsies in the detection of histological transformation of indolent lymphoma. Haematologica. 2008;93(3):471–2. doi: 10.3324/haematol.12013.

Video-Assisted Laparoscopic Surgeries in Lymphomas Diagnostics

I.G. Komarov1,2, S.S. Stepanenkova3, M.I. Komarov2

1 Surgical Unit No. 2, N.N. Blokhin Russian Cancer Research Center, 24 Kashirskoye sh., Moscow, Russian Federation, 115478

2 Subdepartment of Oncology, Russian Medical Academy of Postgraduate Education, 24 Kashirskoye sh., Moscow, Russian Federation, 115478

3 Subdepartment of Oncology, A.I. Evdokimov Moscow State University of Medicine and Dentistry, 24 Kashirskoye sh., Moscow, Russian Federation, 115478

For correspondence: I.G. Komarov, DSci, Professor, N.N. Blokhin Russian Cancer Research Center, 24 Kashirskoye sh., Moscow, Russian Federation, 115478; Tel: +7(499)324-12-70; e-mail: komarovig@mail.ru

For citation: Komarov I.G., Stepanenkova S.S., Komarov M.I. Video-Assisted Laparoscopic Surgeries in Lymphomas Diagnostics. Klin. Onkogematol. 2014; 7(4): 540–550 (In Russ.).


ABSTRACT

The article describes application of modern minimally invasive surgical technologies in oncohematology. The history of the video-assisted surgery is presented. Modern opportunities of the video-assisted laparoscopic surgery in diagnosing of malignant lymphoproliferative disorders were described. The main tools and the equipment, stages of intervention and technique used in video-assisted surgery are briefly described. Indications and contraindications for laparoscopic interventions are presented.


Keywords: lymphoma, diagnosis, video-assisted surgery, laparoscopy.

Accepted: September 17, 2014

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REFERENCES

  1. Hatzinger M., Fesenko A., Sohn M. The first human laparoscopy and NOTES operation: Dimitrij Oscarovic Ott (1855–1929). Urol. Int. 2014; 92(4): 387–91.
  2. Hatzinger M., Kwon S.T., Langbein S. et al. Hans Christian Jacobaeus: Inventor of human laparoscopy and thoracoscopy. J. Endourol. 2006; 20(11): 848–50.
  3. Radojcic B., Jokic R., Grebeldinger S., Meljnikov I., Radojic N. History of minimally invasive surgery. Med. Pregl. 2009; 62(11–12): 597–602.
  4. Балалыкин А.С., Брискин Б.С. История эндоскопической хирургии. Хирургия. 2005; 5: 9–11. [Balalykin A.S., Briskin B.S. History of endoscopic surgery. Khirurgiya. 2005; 5: 9–11. (In Russ.)]
  5. Boyle G., Smith W. Operative gynecologic endoscopy. New York: Springer Verlag, 2003.
  6. Spaner S.J., Warnock G.L. A brief history of endoscopy, laparoscopy, and laparoscopic surgery. J. Laparoendosc. Adv. Surg. Tech. A. 1997; 7(6): 369–73.
  7. Чернеховская Н.Е. Современное состояние и перспективы развития эндоскопии. Лечащий врач. 2004; 4: 29. [Chernekhovskaya N.E. Present state and perspectives of development of endoscopy. Lechashchii vrach. 2004; 4: 29. (In Russ.)]
  8. Vacchio R., MacFayden B.V., Palazzo F. History of laparoscopic surgery. Panminerva Med. 2000; 42(1): 87–90.
  9. Кобаладзе М.Г. История развития эндоскопии. История науки и техники. 2004; 5: 18–23. [Kobaladze M.G. History of endoscopic surgery. Istoriya nauki i tekhniki. 2004; 5: 18–23. (In Russ.)]
  10. Himal H.S. Minimal invasive (laparoscopic) surgery. Surg. Endosc. 2002; 16(12): 1647–52.
  11. Mettler L. From air insufflation to robotic endoscopic surgery: a rocky road. J. Minim. Invasive Gynecol. 2011; 18(3): 275–83.
  12. Комаров И.Г. Оснащение лапароскопической операционной. В кн.: Лапароскопическая хирургия в онкоурологии. Под ред. В.Б. Матвеева, Б.Я. Алексеева. М.: АБВ-пресс, 2007: 25–37. [Komarov I.G. Equipment in the laparoscopic operating room. In: Matveeva V.B., Alekseeva B.Ya., eds. Laparoskopicheskaya khirurgiya v onkourologii. (Laparoscopic surgery in oncology.) Moscow: ABV-press Publ.; 2007. pр. 25–37. (In Russ.)]

Extensive Combined Surgeries in Patients with Blood Diseases and Gastric Cancer

S.R. Karagyulyan, K.I. Danishyan, A.V. Grzhimolovskii, V.S. Shavlokhov, S.A. Shutov, M.A. Silaev, L.G. Kovaleva, O.M. Sorkina, A.Yu. Bulanov

Hematology Research Center of RF MH, Moscow, Russian Federation

For citation: Karagyulyan S.R., Danishyan K.I., Grzhimolovskii A.V., Shavlokhov V.S., Shutov S.A., Silaev M.A., Kovalyova L.G., Sorkina O.M., Bulanov A.Yu. Extensive Combined Surgeries in Patients with Blood Diseases and Gastric Cancer. Klin. onkogematol. 2014; 7(3): 335–42 (In Russ.).

ABSTRACT

The second tumor in patients with myelo- or lymphproliferative diseases is not rare. However, the state of patients’ hemostasis and severely enlarged spleen can become a contraindication for a surgical intervention in a general surgery unit. Four cases of a successful gastrectomy with expanded lymphodissection are presented in a 53 year old woman with subleukemic myelosis (primary myelofibrosis according to WHO classification) and giant splenomegaly (38 ´ 21 ´ 13 cm, spleen weight: 4500 g) and in a 68 year old man with diffuse large В-cell lymphoma and massive splenomegaly (22 ´ 12 ´ 8 cm, spleen weight: 2850 g). Intraoperative compensated blood loss in both cases was 3800 ml and 3740 ml, respectively. Two patients had mild hemophilia A. Specially designed transfusional and anaesthetic strategy was required in all cases because of hemostatic disorders.


Keywords: stomach cancer, surgical treatment, hemophilia, myelofibrosis, lymphoma.

Address correspondence to: max-blood@mail.ru

Accepted: May 28, 2014

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REFERENCES

  1. Климанский В.А., Бекназаров Я.Б. Опасности и осложнения спле- нэктомии у больных с заболеваниями системы крови. Хирургия 1986; 1: 88–92. [Klimanskii V.A., Beknazarov Ya.B. Hazards and complications of splenectomy in patients with blood diseases. Khirurgiya 1986; 1: 88–92. (In Russ.)].
  2. Климанский В.А. Хирургические аспекты лечения заболевания си- стемы крови. Клин. мед. 1989; 8: 3–8.  [Klimanskii V.A. Surgical aspects of treatment of blood diseases. Klin. med. 1989; 8: 3–8. (In Russ.)].
  3. Arnoletti J.P., Karam J., Brodsky J. Early Postoperative Complications of Splenectomy for Hematologic Disease. Am. J. Clin. Oncol. 1999; 22(2): 114–8.
  4. Nicholson I.A., Falk G.L., Mulligan S.C. Laparoscopically assisted massive splenectomy. A preliminary report of the technique of early hilar devascularization. Surg. Endoscopy 1998; 12: 73–5.
  5. Petroianu A. Subtotal splenectomy for the treatment of chronic lymphocytic leukemia. Ann. Hematol. 2003; 82(11): 708–9. Epub 2003 Aug 2.
  6. Smith L., Luna G., Merg A.R. et al. Laparoscopic splenectomy for treatment of splenomegaly. Am. J. Surg. 2004; 187(5): 618–20.
  7. Мещерякова Л.М., Ковалева Л.Г., Карагюлян С.Р. Патофизиологиче- ские основы лечения сублейкемического миелоза. В кн.: Патофизиология крови. Экстремальные состояния (сборник работ). Под ред. А.И. Воро- бьева, Н.А. Горбуновой. М., 2004: 122–34. [Meshcheryakova L.M., Kovaleva L.G., Karagyulyan S.R. Pathophysiological principles of treatment of subleukemic myelosis. In: Vorob’ev A.I., Gorbunova N.A., eds. Patofiziologiya krovi. Ekstremal’nye sostoyaniya (sbornik rabot). (Blood pathophysiology. Urgent conditions (collection of papers)). Moscow, 2004. pp. 122–34].
  8. Ковалева Л.Г., Карагюлян С.Р., Колосова Л.Ю. и др. Спленэктомия при сублейкемическом миелозе. Гематол. и трансфузиол. 2004; 49(5): 14–21. [Kovaleva L.G., Karagyulyan S.R., Kolosova L.Yu. et al. Splenectomy in subleukemic myelosis. Gematol. i transfuziol. 2004; 49(5): 14–21. (In Russ.)].
  9. Демидова А.В., Хорошко Н.Д. Сублейкемический миелоз. В кн.: Руко- водство по гематологии. Под ред. А.И. Воробьева. М.: Ньюдиамед, 2003; 2: 16–20. [Demidova A.V., Khoroshko N.D. Subleukemic myelosis. In: Vorob’ev A.I., ed. Rukovodstvo po gematologii. (Handbook in hematology). Moscow: N’yudiamed Publ., 2003. Т. 2. рр. 16–20.].
  10. Ковалева Л.Г., Карагюлян С.Р., Колосова Л.Ю. и др. Спленэктомия при сублейкемическом миелозе. Гематол. и трансфузиол. 2004; 5: 14–21. [Kovaleva L.G., Karagyulyan S.R., Kolosova L.Yu. et al. Splenectomy in subleukemic myelosis. Gematol. i transfuziol. 2004; 5: 14–21. (In Russ.)].
  11. Вуд М.Э., Бан П.А. Секреты гематологии и онкологии: Пер. с англ. Под ред. Ю.Н. Токарева, А.Е. Бухны. М.: Бином, 1997. [Wood M.E., Bun P.A. Hematology/Oncology Secrets (Russ. Ed. Yu.N. Tokarev, A.E. Bukhny, eds. Wood M.E., Bun P.A. Sekrety gematologii i onkologii. Moscow: Binom Publ., 1997].
  12. Давыдов М.И., Тер-Ованесов М.Д., Полоцкий Б.Е., Туркин И.Н. Рак желудка. В кн.: Энциклопедия клинической онкологии. Под ред. М.И. Давыдова. М.: РЛС, 2004: 223–7. [Davydov M.I., Ter-Ovanesov M.D., Polotskii B.E., Turkin I.N. Gastric cancer. In: Davydov M.I. Entsiklopediya klinicheskoi onkologii. (Encyclopedia of clinical oncology). Moscow: RLS Publ., 2004. рр. 223–7.]. Горобец Е.С. Принципы анестезии при абдоминальных онкологиче- ских операциях. Регион. анест. и леч. боли 2009; 3(2): 32. [Gorobets E.S. Principles of anesthesia in abdominal oncological surgeries. Region. anest. i lech. boli 2009; 3(2): 32. (In Russ.)].
  13. Щербакова О.В., Шулутко Е.М., Буланов А.Ю. и др. Лапароскопи- ческая спленэктомия в условиях эндотрахеальной анестезии: динамика показателей гемостаза. Эндоскоп. хир. 2004; 1: 192–3. [Shcherbakova O.V., Shulutko E.M., Bulanov A.Yu. et al. Laparoscopic splenectomy with endotracheal anesthesia: changes in hemostatic parameters. Endoskop. khir. 2004; 1: 192–3. (In Russ.)].
  14. Chappell D., Heindl B., Jacob M. et al. Sevoflurane reduces leukocyte and platelet adhesion after ischemia-reperfusion by protecting the endothelial glycocalyx. Anesthesiology 2011; 115(3): 483–91.
  15. Буланов А.Ю., Городецкий В.М., Щербакова О.В. и др. Тромбо- эластографическая оценка системы гемостаза и эффективность ее коррекции перед оперативными вмешательствами у больных с заболеваниями системы крови. Гематол. и трансфузиол. 2012; 57(5): 36–42. [Bulanov A.Yu., Gorodetskii V.M., Shcherbakova O.V. et al. Thromboelastographic evaluation of the hemostatic system and the efficacy of its correction before surgical intervention in patients with blood diseases. Gematol. i transfuziol. 2012; 57(5): 36–42. (In Russ.)].
  16. Буланов А.Ю., Аграчева Н.С., Шулутко Е.М. и др. Т-клеточная лим- фома и рак желудка у пожилого пациента. Трансфузионная терапия при хирургическом вмешательстве. Клин. геронтол. 2009; 15(3): 47–50. [Bulanov A.Yu., Agracheva N.S., Shulutko E.M. et al. T-cell lymphoma and gastric in an elderly patient. Transfusion therapy in surgical intervention. Klin. gerontol. 2009; 15(3): 47–50. (In Russ).]
  17. Mendez D., De La Cruz, Arrebola M.M. et al. The effect of propofol on interaction of platelets with leukocytes and erythrocytes in surgical patients. Anesth. Analg. 2003; 96: 713–9.