Клиническое значение экспрессии гена PRAME при онкогематологических заболеваниях

В.А. Мисюрин

ФГБУ «НМИЦ онкологии им. Н.Н. Блохина» Минздрава России, Москва, Каширское ш., д. 24, 115478

Для переписки: Всеволод Андреевич Мисюрин, канд. биол. наук, Каширское ш., д. 24, Moсква, Российская Федерация, 115478; тел. +7(985)436-30-19; e-mail: vsevolod.misyurin@gmail.com

Для цитирования: Мисюрин В.А. Клиническое значение экспрессии гена PRAME при онкогематологических заболеваниях. Клиническая онкогематология. 2018;11(1):26–33.

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


РЕФЕРАТ

Хотя и активность PRAME была впервые установлена при солидных опухолях, данный ген чрезвычайно часто экспрессируется при онкогематологических заболеваниях. Ген PRAME может быть использован как надежный биомаркер наличия опухолевых клеток. Определение транскриптов PRAME используется при мониторинге минимальной остаточной болезни и диагностике молекулярного рецидива. При проведении экспериментов с PRAME-экспрессирующими линиями лейкозных клеток получены противоречивые результаты. По этой причине объяснить наблюдаемое влияние экспрессии PRAME на прогноз очень сложно. Тем не менее при хронических миелопролиферативных заболеваниях и хроническом миелоидном лейкозе активность PRAME связана с худшим прогнозом, а при острых лейкозах лимфоидной и миелоидной направленности — с лучшим. Несмотря на большой объем клинических наблюдений, при некоторых нозологических формах влияние экспрессии PRAME на прогноз остается неизвестным. В настоящем обзоре литературы широко представлены известные данные об экспрессии гена PRAME при онкогематологических заболеваниях.

Ключевые слова: PRAME, лейкозы, лимфомы, прогноз.

Получено: 14 сентября 2017 г.

Принято в печать: 2 декабря 2017 г.

Читать статью в PDF 

ЛИТЕРАТУРА

  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.

Миелоидные супрессорные клетки при некоторых онкогематологических заболеваниях

А.В. Пономарев

ФГБУ «Российский онкологический научный центр им. Н.Н. Блохина» Минздрава России, Каширское ш., д. 24, Moсква, Российская Федерация, 115478

Для переписки: Александр Васильевич Пономарев, аспирант, Каширское ш., д. 24, Moсква, Российская Федерация, 115478; e-mail: kl8546@yandex.ru

Для цитирования: Пономарев А.В. Миелоидные супрессорные клетки при некоторых онкогематологических заболеваниях. Клиническая онкогематология. 2017;10(1):29–38.

DOI: 10.21320/2500-2139-2017-10-1-29-38


РЕФЕРАТ

Миелоидные супрессорные клетки — это незрелые клетки миелоидного происхождения, обладающие иммуносупрессивными свойствами. В обзоре приведена характеристика миелоидных супрессорных клеток, в т. ч. варианты фенотипа, механизмы супрессивного воздействия на иммунную систему, механизмы рекрутирования опухолью миелоидных супрессоров. Дано краткое описание работ, в которых исследовались миелоидные супрессоры при онкогематологических заболеваниях, включая множественную миелому, лимфомы и лейкозы.

Ключевые слова: миелоидные супрессоры, супрессорные клетки миелоидного происхождения, множественная миелома, лимфомы, лейкозы.

Получено: 8 сентября 2016 г.

Принято в печать: 3 декабря 2016 г.

Читать статью в PDFpdficon


ЛИТЕРАТУРА

  1. Тупицына Д.Н., Ковригина А.М., Тумян Г.С. и др. Клиническое значение внутриопухолевых FOXP3+ Т-регуляторных клеток при солидных опухолях и фолликулярных лимфомах: обзор литературы и собственные данные. Клиническая онкогематология. 2012;(5)3:193–203. [Tupitsyna DN, Kovrigina AM, Tumian GS, et al. Different clinical meaning of intratumoral FOXP3+ T-regulatory cells in solid tumors and follicular lymphomas: literature review and own data. Klinicheskaya onkogematologiya. 2012;(5)3:193–203. (In Russ)]
  2. Кадагидзе З.Г., Черткова А.И., Славина Е.Г. NKT-клетки и противоопухолевый иммунитет. Российский биотерапевтический журнал. 2011;10(3):9–16. [Kadagidze ZG, Chertkova AI, Slavina EG. NKT-cells and antitumor immunity. Rossiiskii bioterapevticheskii zhurnal. 2011;10(3):9–16. (In Russ)]
  3. Gabrilovich DI, Ostrand-Rosenberg S, Bronte V. Coordinated regulation of myeloid cells by tumours. Nat Rev 2012;12(4):253–68. doi: 10.1038/nri3175.
  4. Gabrilovich DI, Bronte V, Chen S-H, et al. The terminology issue for myeloid-derived suppressor cells. Cancer Res. 2007;67(1):425– doi: 10.1158/0008-5472.CAN-06-3037.
  5. Bowen JL, Olson JK. Innate immune CD11b+Gr-1+ cells, suppressor cells, affect the immune response during Theiler’s virus-induced demyelinating disease. J Immunol. 2009;183(11):6971–80. doi: 10.4049/jimmunol.0902193.
  6. Tsiganov EN, Verbina EM, Radaeva TV, et al. Gr-1dim CD11b+ immature myeloid-derived suppressor cells but not neutrophils are markers of lethal tuberculosis infection in mice. J Immunol. 2014;192(10):4718–27. doi: 10.4049/jimmunol.1301365.
  7. Delano MJ, Scumpia PO, Weinstein JS, et al. MyD88-dependent expansion of an immature GR-1(+)CD11b(+) population induces T cell suppression and Th2 polarization in sepsis. J Exp Med. 2007;204(6):1463–74.
  8. Гапонов М.А., Хайдуков С.В., Писарев В.М. и др. Субпопуляционная гетерогенность миелоидных иммуносупрессорных клеток у пациентов с септическими состояниями. Российский иммунологический журнал. 2015;9(18):11–14. [Gaponov MA, Khaidukov SV, Pisarev VM, et al. Subpopulation heterogeneity of immunosuppressive myeloid cells in patients with sepsis. Rossiiskii immunologicheskii zhurnal. 2015;9(18):11–14. (In Russ)]
  9. Makarenkova VP, Bansal V, Matta BM, et al. CD11b+/Gr-1+ myeloid suppressor cells cause T cell dysfunction after traumatic stress. J Immunol. 2006;176(4):2085–94. doi: 10.4049/jimmunol.176.4.2085.
  10. Greten TF, Manns MP, Korangy F. Myeloid derived suppressor cells in human diseases. Int. 2011;11(7):802–7. doi: 10.1016/j.intimp.2011.01.003.
  11. Diaz-Montero CM, Salem ML, Nishimura MI, et al. Increased circulating myeloid-derived suppressor cells correlate with clinical cancer stage, metastatic tumor burden, and doxorubicin–cyclophosphamide chemotherapy. Cancer Immunol Immunother. 2009;58(1):49–59. doi: 10.1007/s00262-008-0523-
  12. Yazdani Y, Mohammadnia-Afrouzi M, Yousefi M, et al. Myeloid-derived suppressor cells in B cell malignancies. Tumour Biol. 2015;36(10):7339–53. doi: 10.1007/s13277-015-4004-z.
  13. Пономарев А.В. Миелоидные супрессорные клетки: общая характеристика. Иммунология. 2016;37(1):47–50. doi: 10.18821/0206-4952-2016-37-1-47-50. [Ponomarev AV. Myeloid suppressor cells: general characteristics. Immunologiya. 2016;37(1):47–50. doi: 10.18821/0206-4952-2016-37-1-47- (In Russ)]
  14. Gabrilovich DI, Nagaraj S. Myeloid-derived-suppressor cells as regulators of the immune system. Nat Rev Immunol. 2009;9(3):162–74. doi: 10.1038/nri2506.
  15. Lechner MG, Megiel C, Russell SM, et al. Functional characterization of human Cd33+ And Cd11b+ myeloid-derived suppressor cell subsets induced from peripheral blood mononuclear cells co-cultured with a diverse set of human tumor cell lines. J Transl 2011;9(1):90. doi: 10.1186/1479-5876-9-90.
  16. Rodriguez PC, Ernstoff MS, Hernandez C, et al. Arginase I–Producing Myeloid-Derived Suppressor Cells in Renal Cell Carcinoma Are a Subpopulation of Activated Granulocytes. Cancer Res. 2009;69(4):1553–60.
  17. Schmielau J, Finn OJ. Activated granulocytes and granulocyte-derived hydrogen peroxide are the underlying mechanism of suppression of T-cell function in advanced cancer patients. Cancer Res. 2001;61(12):4756–60.
  18. Youn J-I, Collazo M, Shalova I, et al. Characterization of the nature of granulocytic myeloid-derived suppressor cells in tumor-bearing mice. J Leuk 2012;91(1):167–81. doi: 10.1189/jlb.0311177.
  19. Youn J-I, Nagaraj S, Collazo M, et al. Subsets of Myeloid-Derived Suppressor Cells in Tumor Bearing Mice. J Immunol. 2008;181(8):5791–802. doi: 10.4049/jimmunol.181.8.5791.
  20. Corzo CA, Condamine T, Lu L, et al. HIF-1alpha regulates function and differentiation of myeloid-derived suppressor cells in the tumor microenvironment. J Exp Med. 2010;207(11):2439–53. doi: 10.1084/jem.20100587.
  21. Yang L, DeBusk LM, Fukuda K, et al. Expansion of myeloid immune suppressor Gr+CD11b+ cells in tumor-bearing host directly promotes tumor angiogenesis. Cancer Cell. 2004;6(4):409–21. doi: 10.1016/j.ccr.2004.08.031.
  22. Zhuang J, Zhang J, Lwin ST, et al. Osteoclasts in multiple myeloma are derived from Gr-1+CD11b+ myeloid-derived suppressor cells. PLoS One. 2012;7(11):e48871. doi: 1371/journal.pone.0048871.
  23. Choi J, Suh B, Ahn YO, et al. CD15+/CD16low human granulocytes from terminal cancer patients: granulocytic myeloid-derived suppressor cells that have suppressive function. Tumour Biol. 2012;33(1):121–9. doi: 10.1007/s13277-011-0254-
  24. Stanojevic I, Miller K, Kandolf-Sekulovic L, et al. A subpopulation that may correspond to granulocytic myeloid-derived suppressor cells reflects the clinical stage and progression of cutaneous melanoma. Int Immunol. 2016;28(2):87–97. doi: 10.1093/intimm/dxv053.
  25. Saiwai H, Kumamaru H, Ohkawa Y, et al. Ly6C+Ly6G– Myeloid-derived suppressor cells play a critical role in the resolution of acute inflammation and the subsequent tissue repair process after spinal cord injury. J Neurochem. 2013;125(1):74–88. doi: 10.1111/jnc.12135.
  26. Rodriguez PC, Augusto CO. Arginine regulation by myeloid derived suppressor cells and tolerance in cancer: mechanisms and therapeutic perspectives. Immunol 2008;222(1):180–91. doi: 10.1111/j.1600-065X.2008.00608.x.
  27. Srivastava MK, Sinha P, Clements VK, et al. Myeloid-derived suppressor cells inhibit T cell activation by depleting cystine and cysteine. Cancer Res. 2010;70(1):68–77. doi: 10.1158/0008-CAN-09-2587.
  28. Chevolet I, Speeckaert R, Schreuer M, et al. Characterization of the in vivo immune network of IDO, tryptophan metabolism, PD-L1, and CTLA-4 in circulating immune cells in melanoma. Oncoimmunology. 2015;4(3):e982382. doi: 10.4161/2162402X.2014.982382.
  29. Jitschin R, Braun M, Buttner M, et al. CLL-cells induce IDOhiCD14+HLA-DRlo myeloid-derived suppressor cells that inhibit T-cell responses and promote Tregs. Blood. 2014;124(5):750–60. doi: 10.1182/blood-2013-12-
  30. Nagaraj S, Gupta K, Pisarev V, et al. Altered recognition of antigen is a mechanism of CD8+ T cell tolerance in cancer. Nat Med. 2007;13(7):828–35. doi: 10.1038/nm1609.
  31. Lu T, Ramakrishnan R, Altiok S, et al. Tumor-infiltrating myeloid cells induce tumor cell resistance to cytotoxic T cells in mice. J Clin 2011;121(10):4015–4029. doi: 10.1172/JCI45862.
  32. Hanson EM, Clements VK, Sinha P, et al. Myeloid-derived suppressor cells down-regulate L-selectin expression on CD4+ and CD8+ T cells. J. Immunol. 2009;183(2):937–44. doi: 10.4049/jimmunol.0804253.
  33. Noman MZ, Desantis G, Janji B, et al. PD-L1 is a novel direct target of HIF-1a, and its blockade under hypoxia enhanced MDSC-mediated T cell activation. J Exp Med. 2014;211(5):781–90. doi: 10.1084/jem.20131916.
  34. Filipazzi P, Valenti R, Huber V, et al. Identification of a new subset of myeloid suppressor cells in peripheral blood of melanoma patients with modulation by a granulocyte-macrophage colony-stimulation factor-based antitumor vaccine. J Clin Oncol. 2007;25(18):2546–53. doi: 10.1200/JCO.2006.08.5829.
  35. Sinha P, Clements VK, Bunt SK, et al. Cross-talk between myeloid-derived suppressor cells and macrophages subverts tumor immunity toward a type 2 response. J Immunol. 2007;179(2):977–83. doi: 10.4049/jimmunol.179.2.977.
  36. Li H, Han Y, Guo Q, et al. Cancer-expanded myeloid-derived suppressor cells induce anergy of NK cells through membrane-bound TGF-beta 1. J Immunol. 2009;182(1):240–9. doi: 10.4049/jimmunol.182.1.240.
  37. Liu C, Yu S, Kappes J, et al. Expansion of spleen myeloid suppressor cells represses NK cell cytotoxicity in tumor-bearing host. Blood. 2007;109(10):4336–42. doi: 10.1182/blood-2006-09-
  38. Elkabets M, Ribeiro VSG, Dinarello CA, et al. IL-1b regulates a novel myeloid-derived suppressor cell subset that impairs NK cell development and function. Eur J Immunol. 2010;40(12):3347–57. doi: 10.1002/eji.201041037.
  39. Hoechst B, Voigtlaender T, Ormandy L, et al. Myeloid derived suppressor cells inhibit natural killer cells in patients with hepatocellular carcinoma via the NKp30 receptor. Hepatology. 2009;50(3):799–807. doi: 10.1002/hep.23054.
  40. Pan PY, Ma G, Weber KJ, et al. Immune stimulatory receptor CD40 is required for T-cell suppression and T regulatory cell activation mediated by myeloid-derived suppressor cells in cancer. Cancer Res. 2010;70(1):99–108. doi: 10.1158/0008-CAN-09-1882.
  41. Hoechst B, Gamrekelashvili J, Manns MP, et al. Plasticity of human Th17 cells and iTregs is orchestrated by different subsets of myeloid cells. Blood. 2011;117(24):6532–41. doi: 10.1182/blood-2010-11-
  42. Shojaei F, Wu X, Malik AK, et al. Tumor refractoriness to anti-VEGF treatment is mediated by CD11b+Gr1+ myeloid cells. Nat Biotechnol. 2007;25(8):911–20. doi: 10.1038/nbt1323.
  43. Connolly MK, Mallen-St Clair J, Bedrosian AS, et al. Distinct populations of metastases-enabling myeloid cells expand in the liver of mice harboring invasive and preinvasive intra-abdominal tumor. J Leuk Biol. 2010;87(4):713–25. doi: 10.1189/jlb.0909607.
  44. Yang L, Huang J, Ren X, et al. Abrogation of TGFb signaling in mammary carcinomas recruits Gr-1+CD11b+ myeloid cells that promote metastasis. Cancer Cell. 2008;13(1):23–35. doi: 10.1016/j.ccr.2007.12.004.
  45. Giles A, Vicioso Y, Kasai M, et al. Bone marrow-derived progenitor cells develop into myeloid-derived suppressor cells at metastatic sites. J Immunother Cancer. 2013;1(Suppl 1):188. doi: 10.1186/2051-1426-1-S1-P188.
  46. Solito S, Falisi E, Diaz-Montero CM, et al. A human promyelocytic-like population is responsible for the immune suppression mediated by myeloid-derived suppressor cells. Blood. 2011;118(8):2254–65. doi: 10.1182/blood-2010-12-
  47. Marigo I, Bosio E, Solito S, et al. Tumor-induced tolerance and immune suppression depend on the C/EBPbeta transcription factor. Immunity. 2010;32(6):790–802. doi: 10.1016/j.immuni.2010.05.010.
  48. Highfill SL, Rodriguez PC, Zhou Q, et al. Bone marrow myeloid-derived suppressor cells (MDSCs) inhibit graft-versus-host disease (GVHD) via an arginase-1-dependent mechanism that is up-regulated by interleukin-13. Blood. 2010;116(25):5738–47. doi: 10.1182/blood-2010-06-
  49. Lechner MG, Liebertz DJ, Epstein AL. Characterization of cytokine-induced myeloid derived suppressor cells from normal human peripheral blood mononuclear cells. J Immunol. 2010;185(4):2273–84. doi: 10.4049/jimmunol.1000901.
  50. Atretkhany KS, Nosenko MA, Gogoleva VS, et al. TNF Neutralization Results in the Delay of Transplantable Tumor Growth and Reduced MDSC Accumulation. Front Immunol. 2016;7:147. doi: 10.3389/fimmu.2016.00147.
  51. De Veirman K, Van Valckenborgh E, Lahmar Q, et al. Myeloid-derived suppressor cells as therapeutic target in hematological malignancies. Front Oncol. 2014;4:349. doi: 10.3389/fonc.2014.00349.
  52. Ramachandran I, Martner A, Pisklakova A, et al. Myeloid-derived suppressor cells regulate growth of multiple myeloma by inhibiting T cells in bone marrow. J Immunol. 2013;190(7):3815–23. doi: 10.4049/jimmunol.1203373.
  53. De Veirman K, Van Ginderachter JA, Lub S, et al. Multiple myeloma induces Mcl-1 expression and survival of myeloid-derived suppressor cells. Oncotarget. 2015;6(12):10532–47. doi: 10.18632/oncotarget.3300.
  54. Brimnes MK, Vangsted AJ, Knudsen LM, et al. Increased level of both CD4+FOXP3+ regulatory T cells and CD14+HLA-DR/low myeloid-derived suppressor cells and decreased level of dendritic cells in patients with multiple myeloma. Scand J Immunol. 2010;72(6):540–7. doi: 10.1111/j.1365-2010.02463.x.
  55. Gorgun GT, Whitehill G, Anderson JL, et al. Tumor-promoting immune-suppressive myeloid-derived suppressor cells in the multiple myeloma microenvironment in humans. Blood. 2013;121(15):2975–87. doi: 10.1182/blood-2012-08-
  56. Gorgun GТ, Samur MK, Cowens KB, et al. Lenalidomide Enhances Immune Checkpoint Blockade-Induced Immune Response in Multiple Myeloma. Clin Cancer Res. 2015;21(20):4607–18. doi: 10.1158/1078-CCR-15-0200.
  57. Busch A, Zeh D, Janzen V, et al. Treatment with lenalidomide induces immuno-activating and counter-regulatory immunosuppressive changes in myeloma patients. Clin Exp Immunol. 2014;177(2):439–53. doi: 10.1111/cei.12343.
  58. Wang Z, Zhang L, Wang H, et al. Tumor-induced CD14+HLA-DR (-/low) myeloid-derived suppressor cells correlate with tumor progression and outcome of therapy in multiple myeloma patients. Cancer Immunol Immunother. 2015;64(3):389–99. doi: 10.1007/s00262-014-1646-
  59. De Keersmaecker B, Fostier K, Corthals J, et al. Immunomodulatory drugs improve the immune environment for dendritic cell-based immunotherapy in multiple myeloma patients after autologous stem cell transplantation. Cancer Immunol Immunother. 2014;63(10):1023–36. doi: 10.1007/s00262-014-1571-
  60. Castella B, Foglietta M, Sciancalepore P, et al. Anergic bone marrow Vg9Vd2 T cells as early and long-lasting markers of PD-1-targetable microenvironment-induced immune suppression in human myeloma. Oncoimmunology. 2015;4(11):e1047580. doi: 10.1080/2162402X.2015.1047580.
  61. Giallongo C, Tibullo D, Parrinello NL, et al. Granulocyte-like myeloid derived suppressor cells (G-MDSC) are increased in multiple myeloma and are driven by dysfunctional mesenchymal stem cells (MSC). Oncotarget. 2016;7(52):85764– doi: 10.18632/oncotarget.7969.
  62. Lee SE, Lim JY, Ryu DB, et al. Circulating immune cell phenotype can predict the outcome of lenalidomide plus low-dose dexamethasone treatment in patients with refractory/relapsed multiple myeloma. Cancer Immunol Immunother. 2016;65(8):983–94. doi: 10.1007/s00262-016-1861-
  63. Favaloro J, Liyadipitiya T, Brown R, et al. Myeloid derived suppressor cells are numerically, functionally and phenotypically different in patients with multiple myeloma. Leuk Lymphoma. 2014;55(12):2893–900. doi: 10.3109/10428194.2014.904511.
  64. Franssen LE, van de Donk NW, Emmelot ME, et al. The impact of circulating suppressor cells in multiple myeloma patients on clinical outcome of DLIs. Bone Marrow Transplant. 2015;50(6):822–8. doi: 10.1038/bmt.2015.48.
  65. Lin Y, Gustafson MP, Bulur PA, et al. Immunosuppressive CD14+HLA-DRlow/– monocytes in B-cell non-Hodgkin lymphoma. Blood. 2011;117(3):872–81. doi: 10.1182/blood-2010-05-
  66. Tadmor T, Fell R, Polliack A, et al. Absolute monocytosis at diagnosis correlates with survival in diffuse large B-cell lymphoma—possible link with monocytic myeloid-derived suppressor cells. Hematol 2013;31(2):65–71. doi: 10.1002/hon.2019.
  67. Gustafson MP, Lin Y, LaPlant B, et al. Immune monitoring using the predictive power of immune profiles. J Immunother Cancer. 2013;1(1):7. doi: 10.1186/2051-1426-1-7.
  68. Wu C, Wu X, Zhang X, et al. Prognostic significance of peripheral monocytic myeloid-derived suppressor cells and monocytes in patients newly diagnosed with diffuse large B-cell lymphoma. Int J Clin Exp Med. 2015;8(9):15173–81.
  69. Sato Y, Shimizu K, Shinga J, et al. Characterization of the myeloid-derived suppressor cell subset regulated by NK cells in malignant lymphoma. Oncoimmunology. 2015;4(3):e995541. doi: 10.1080/2162402X.2014.995541.
  70. Romano A, Parrinello NL, Vetro C, et al. Circulating myeloid-derived suppressor cells correlate with clinical outcome in Hodgkin Lymphoma patients treated up-front with a risk-adapted strategy. Br J Haematol. 2015;168(5):689–700. doi: 10.1111/bjh.13198.
  71. Marini O, Spina C, Mimiola E, et al. Identification of granulocytic myeloid-derived suppressor cells (G-MDSCs) in the peripheral blood of Hodgkin and non-Hodgkin lymphoma patients. Oncotarget. 2016;19(7):27677–88. doi: 10.18632/oncotarget.8507.
  72. Azzaoui I, Uhel F, Rossille D, et al. T-cell defect in diffuse large B-cell lymphomas involves expansion of myeloid derived suppressor cells expressing IL-10, PD-L1 and S100A12. Blood. 2016;128(8):1081–92. doi: 10.1182/blood-2015-08-
  73. Zhang H, Li ZL, Ye SB, et al. Myeloid-derived suppressor cells inhibit T cell proliferation in human extranodal NK/T cell lymphoma: a novel prognostic indicator. Cancer Immunol Immunother. 2015;64(12):1587- doi: 10.1007/s00262-015-1765-6.
  74. Christiansson L, Sоderlund S, Svensson E, et al. Increased Level of Myeloid-Derived Suppressor Cells, Programmed Death Receptor Ligand 1/Programmed Death Receptor 1, and Soluble CD25 in Sokal High Risk Chronic Myeloid Leukemia. PLoS One. 2013;8(1):e55818. doi: 10.1371/journal.pone.0055818.
  75. Giallongo C, Romano A, Parrinello NL, et al. Mesenchymal Stem Cells (MSC) Regulate Activation of Granulocyte-Like Myeloid Derived Suppressor Cells (G-MDSC) in Chronic Myeloid Leukemia Patients. PLoS One. 2016;11(7):e0158392. doi: 10.1371/journal.pone.0158392.
  76. Gustafson МP, Abraham RS, Lin Y, et al. Association of an increased frequency of CD14+HLA-DRlo/neg monocytes with decreased time to progression in chronic lymphocytic leukaemia (CLL). Br J Haematol. 2012;156(5):674–6. doi: 10.1111/j.1365-2011.08902.x.
  77. Liu J, Zhou Y, Huang Q, et al. CD14+HLA-DRlow/– expression: a novel prognostic factor in chronic lymphocytic leukemia. Oncol 2015;9(3):1167–72. doi: 10.3892/ol.2014.2808.
  78. Sun H, Li Y, Zhang ZF, et al. Increase in myeloid-derived suppressor cells (MDSCs) associated with minimal residual disease (MRD) detection in adult acute myeloid leukemia. Int J Hematol. 2015;102(5):579–86. doi: 10.1007/s12185-015-1865-
  79. Gleason MK, Ross JA, Warlick ED, et al. CD16xCD33 bispecific killer cell engager (BiKE) activates NK cells against primary MDS and MDSC CD33+ targets. Blood. 2014;123(19):3016–26. doi: 10.1182/blood-2013-10-
  80. Chen X, Eksioglu EA, Zhou J, et al. Induction of myelodysplasia by myeloid-derived suppressor cells. J Clin Invest. 2013;123(11):4595–611. doi: 10.1172/JCI67580.
  81. Kittang AO, Kordasti S, Sand KE, et al. Expansion of myeloid derived suppressor cells correlates with number of T regulatory cells and disease progression in myelodysplastic syndrome. Oncoimmunology. 2015;5(2):e1062208. doi: 10.1080/2162402X.2015.1062208.
  82. Noonan KA, Ghosh N, Rudraraju L, et al. Targeting immune suppression with PDE5 inhibition in end-stage multiple myeloma. Cancer Immunol Res. 2014;2(8):725–31. doi: 10.1158/2326-CIR-13-0213.

Использование достижений современных геномных технологий при лимфомах

М.В. Немцова1, М.В. Майорова2

1 Российская медицинская академия последипломного образования Минздрава России, ул. Баррикадная, д. 2/1, Москва, Российская Федерация, 125993

2 Московский научно-исследовательский онкологический институт им. П.А. Герцена, 2-й Боткинский пр-д, д. 3, Москва, Российская Федерация, 125284

Для переписки: Марина Вячеславовна Немцова, д-р биол. наук, профессор, ул. Баррикадная, д. 2/1, Москва, Российская Федерация, 125993; тел.: +7(499)252-21-04; e-mail: nemtsova_m_v@mail.ru

Для цитирования: Немцова М.В., Майорова М.В. Использование достижений современных геномных технологий при лимфомах. Клиническая онкогематология. 2016;9(3):265-70.

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


РЕФЕРАТ

Современные достижения в области геномики и биологии рака позволили значительно расширить объем знаний о молекулярном патогенезе лимфом. С использованием полногеномных методов исследования и современных компьютерных технологий удалось доказать, что разнообразные гистологические и иммуноморфологические подтипы лимфом различаются на молекулярном уровне и возникают в результате действия различных онкогенных механизмов. Стало понятно, что в основе вариабельности клинических симптомов, которые наблюдаются у пациентов с лимфомами, лежат как гетерогенность опухолевых клеток, так и особенности молекулярного патогенеза. Основываясь на полученных данных, предложены стратегии для разработки новых препаратов, которые сегодня используются в лечении лимфом. Они включают определение молекулярных этапов патогенеза, оценку значимости каждого этапа для развития опухоли и получение препарата с направленным действием на этот этап. В результате предложено несколько новых классов молекулярных таргетных агентов для лечения лимфом, которые сегодня изучаются в клинических исследованиях. В современную эпоху персонализированной медицины одной из основных задач при лечении пациентов с лимфомами является определение правильной таргетной терапии для каждого типа лимфоидной опухоли, характеризующейся уникальными молекулярными механизмами опухолеобразования.


Ключевые слова: лимфомы, профиль экспрессии генов, микроРНК, сигнальные пути, NF-kB.

Получено: 13 февраля 2016 г.

Принято в печать: 14 марта 2016 г.

Читать статью в PDFpdficon

ЛИТЕРАТУРА

  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.
 

Качество жизни больных лимфомами в различный срок после высокодозной химиотерапии с аутологичной трансплантацией гемопоэтических стволовых клеток

Н.Е. Мочкин1, Д.А. Федоренко1, В.Я. Мельниченко1, Т.И. Ионова2, Т.П. Никитина1,2, К.А. Курбатова2, А.А. Новик1

1 ФГБУ «Национальный медико-хирургический центр им. Н.И. Пирогова» МЗ РФ, ул. Нижняя Первомайская, д. 70, Москва, Российская Федерация, 105203

2 Межнациональный центр исследования качества жизни, ул. Артиллерийская, д. 1, офис 152, Санкт-Петербург, Российская Федерация, 191014

Для переписки: Н.Е. Мочкин, канд. мед. наук, ассистент, ул. Нижняя Первомайская, д. 70, Москва, Российская Федерация, 105203; тел.: +7(495)603-72-17; e-mail: nickmed@yandex.ru

Для цитирования:  Мочкин Н.Е., Федоренко Д.А., Мельниченко В.Я., Ионова Т.И., Никитина Т.П., Курбатова К.А., Новик А.А. Качество жизни больных лимфомами в разные сроки после высокодозной химиотерапии с аутологичной трансплантацией гемопоэтических стволовых клеток. Клин. онкогематол. 2014; 7(4): 577–582.


РЕФЕРАТ

В статье представлены результаты мониторинга показателей качества жизни у 103 больных лимфомами (неходжкинские, n = 36; Ходжкина, n = 67) в разный срок после высокодозной химиотерапии (ВДХТ) с аутологичной трансплантацией гемопоэтических стволовых клеток (аутоТГСК). У большинства пациентов через 1 год после ВДХТ с аутоТГСК зарегистрированы улучшение или стабилизация качества жизни. При этом данные ответа, связанного с качеством жизни, и клинического ответа на лечение совпадали не во всех случаях. Полученные результаты свидетельствуют о важности комплексного подхода к оценке эффективности лечения пациентов и могут быть важным индикатором восстановления функционирования больных в разный срок после трансплантации.


Ключевые слова: качество жизни, лимфомы, высокодозная химиотерапия, аутологичная трансплантация гемопоэтических стволовых клеток.

Принято в печать: 16 сентября 2014 г.

Читать статью в PDF pdficon

 
ЛИТЕРАТУРА
  1. Colpo A., Hochberg E., Chen Y.B. Current status of autologous stem cell transplantation in relapsed and refractory Hodgkin’s lymphoma. Oncologist. 2012; 17: 80–90.
  2. d’Amore F., Relander T., Lauritzen G.F. et al. High-dose chemotherapy and autologous stem cell transplantation in previously untreated peripheral T-cell lymphoma — final analysis of a large prospective multicenter study (NLGT-01). Blood (ASH Annual Meeting Abstracts). 2011; 118: 331.
  3. Damon L.E., Johnson J.L., Neidzwiecki D. et al. Immunochemotherapy and autologous stem-cell transplantation for untreated patients with mantle-cell lymphoma: CALGB 59909. J. Clin. Oncol. 2009; 27: 6101–8.
  4. Freidberg J.W. Relapsed/refractory diffuse large B-cell lymphoma. Hematol. Am. Soc. Hematol. Educ. Program. 2011: 498–501.
  5. Geisler C.H., Polstad A., Laurell A. et al. Long-term progression-free survival of mantle cell lymphoma after intensive front-line immunochemotherapy with in vivo-purged stem cell rescue: a nonrandomized phase 2 multicenter study by the Nordic Lymphoma Group. Blood. 2008; 112: 2687–93.
  6. Hjermstad M.J., Kaasa S. Quality of life in adult cancer patients treated with bone marrow transplantation — a review of the literature. Eur. J. Cancer. 1995; 31A(2): 163–73.
  7. Kiss T.L., Abdolell M., Jamal N. et al. Long-term medical outcomes and quality-of-life assessment of patients with chronic myeloid leukemia followed at least 10 years after allogenic bone marrow transplantation. J. Clin. Oncol. 2002; 20(9); 2334–43.
  8. Anderson K.O., Giralt S.A., Mendoza T.R. et al. Symptom burden in patients undergoing autologous stem-cell transplantation. Bone Marrow Transplant. 2007; 39(12): 759–66.
  9. Grant M., Ferrel B., Schmidt G.M. et al. Measurement of quality of life in bone marrow transplantation survivors. Qual. Life Res. 1992; 1(6): 375–84.
  10. Новик А.А., Ионова Т.И., Афанасьев Б.В. и др. Результаты аутоло- гичной трансплантации костного мозга/стволовых кроветворных клеток у больных гемобластозами: клиническая эффективность и показатели ка- чества жизни. Вестник Межнационального центра исследования качества жизни. 2011; 17–18: 22–32. [Novik A.A., Ionova T.I., Afanas’ev B.V. et al. Results of autologic bone marrow transplantation/hematopoietic stem cells transplantation in patients with hemoblastoses: clinical efficacy and parameters of quality of life. Vestnik Mezhnatsional’nogo tsentra issledovaniya kachestva zhizni. 2011; 17–18: 22–32. (In Russ.)]
  11. Rock E.P., Kennedy D.L., Furness M.H. et al. Patient-reported outcomes supporting anticancer product approvals. J. Clin. Oncol. 2007; 25: 5094–9.
  12. Fairclough D. Patient-reported outcomes as endpoints in medical research. Sta. Meth. Med. Res. 2004; 13: 115–38.
  13. Gondek K., Sagnier P., Gichrist K., Wooley J. Current status of patientreported outcomes in industry-sponsored oncology clinical trials and product labels. J. Clin. Oncol. 2007; 25(32): 5087–93.
  14. Steven B. Patient-reported outcomes assessment in cancer trials: evaluating and enhancing the payoff to decision making. J. Clin. Oncol. 2007; 25(32): 5049–50.
  15. Watkins B. Issues and challenges with integrating patient-reported outcomes in clinical trials supported by the national cancer institute-sponsored clinical trials networks. J. Clin. Oncol. 2007; 25(32): 5051–7.
  16. Molassiotis A., Van der Akker O., Milligan D. et al. Quality of life in longterm survivors of marrow transplantation: Comparison with a matched group receiving maintenance chemotherapy. Bone Marrow Transplant. 1996; 17: 249–58.
  17. Руководство по исследованию качества жизни в медицине, 3-е изд., перераб. и доп. Под ред. Ю.Л. Шевченко. М.: Изд-во РАЕН, 2012. [Shevchenko Yu.L., ed. Rukovodstvo po issledovaniyu kachestva zhizni v meditsine (Guidelines for evaluation of the quality of life in medicine). 3rd revised edition. Moscow: RAEN Publ.; 2012.]
  18. Neitzert C.S., Ritvo P., Dancey J. et al. The psychosocial impact of bone marrow transplantation: A review of the literature. Bone Marrow Transplant. 1998; 22: 409–22.
  19. Wingard J.R. Quality of life following bone marrow transplantation. Curr. Opin. Oncol. 1998; 10: 108–11.
  20. Chao N.J., Tierney D.K., Bloom J.R. et al. Dynamic assessment of quality of life after autologous bone marrow transplantation. Blood. 1992; 80: 825–30.
  21. Cohen M.Z., Mendoza T., Neumann J. et al. Longitudinal assessment of symptoms and quality of life: Differences by ablative and nonablative blood and marrow transplantation. J. Clin. Oncol. 2004; 22(15S): 6630.
  22. Ganz P., Gotay C. Use of Patient-Reported Outcomes in Phase III Cancer Treatment Trials; Lessons Learned and Future Directions. J. Clin. Oncol. 2007; 25(32): 5063–9.
  23. Novik A., Salek S., Ionova T. Patient-reported outcomes in hematology. Guidelines. EHA SWG Quality of Life and Symptoms. Litoprint. Genoa, 2012.
  24. Hays R.D., Sherbourne C.D., Mazel R.M. User’s Manual for Medical Outcomes Study (MOS) Core measures of health-related quality of life. RAND Corporation, MR-162-RC. Available at www.rand.org.
  25. Новик А.А., Ионова Т.И. Исследование качества жизни в медицине: Учебное пособие для вузов. Под ред. Ю.Л. Шевченко. М.: ГЭОТАР-Медиа, 2004. [Novik A.A., Ionova T.I. Issledovanie kachestva zhizni v meditsine (Evaluation of the quality of life in medicine). Textbook for institutes of higher education. Shevchenko Yu.L., ed. Moscow: GEOTAR-Media Publ.; 2004.]
  26. Новик А.А., Ионова Т.И. Интегральный показатель качества жизни — новая категория в концепции исследования качества жизни. Вестник Межнационального центра исследования качества жизни. 2006; 7–8: 7–8. [Novik A.A., Ionova T.I. Integral assessment of quality of life is a new category in the concept of evaluation of quality of life. Vestnik Mezhnatsional’nogo tsentra issledovaniya kachestva zhizni. 2006; 7–8: 7–8. (In Russ.)]

Малоинвазивные хирургические технологии при поражениях позвоночника в онкогематологии

А.К. Валиев, А.В. Соколовский, А.С. Неред, Э.Р. Мусаев

ФГБУ «РОНЦ им. Н.Н. Блохина» РАМН, Москва, Российская Федерация


РЕФЕРАТ

В последние десятилетия отметилась четкая тенденция к росту злокачественных новообразований с поражением костей скелета. Они составляют в среднем 1,5–2 % всех онкологических заболеваний. Наиболее распространены, по данным ряда авторов, множественная миелома (35–50 %), остеосаркома (20–30 %), хондросаркома (10–17 %), саркома Юинга (6–12 %), лимфомы (3–7 %). Соответственно и проблема лечения патологических переломов позвонков у больных с множественной миеломой и лимфомами становится более актуальной. Существующие современные малоинвазивные методы лечения патологических переломов позвонков (чрескожная вертебропластика и кифопластика) у больных множественной миеломой и лимфомами позволяют значительно улучшить качество жизни и в короткий срок начать специальное лечение.


Ключевые слова: позвоночник, вертебропластика, патологические переломы, множественная миелома, лимфомы.

Читать статью в PDF pdficon

ЛИТЕРАТУРА

  1. Malawer M.M. Musculoskeletal Cancer Surgery. In: Treatment of Sarcomas and Allied Diseases. Ed. by M.M. Malawer, P.H. Sugarbaker. Washington: Kluwer Academic Publishers, 2001.
  2. Зацепин С.Т. Костная патология взрослых: Руководство для врачей. М.: Медицина, 2001. [Zatsepin S.T. Kostnaya patologiya vzroslykh: Rukovodstvo dlya vrachey (Bone disorders in adults: manual for medical practitioners). M.: Meditsyna, 2001.]
  3. Алиев М.Д. Злокачественные опухоли костей. M., 2008. [Aliyev M.D. Zlokachestvennyye opukholi kostey (Malignant bone tumors). M., 2008.]
  4. Давыдов М.И., Аксель Е.М. Статистика злокачественных новообразо- ваний в России и странах СНГ в 2009 г. Вестн. онкол. 2011; 22(3 Прил. 1). [Davydov M.I., Aksel E.M. Statistika zlokachestvennykh novoobrazovaniy v Rossii i stranah SNG v 2009 g. (Statistics of malignancies in Russia and CIScountries in 2009). Vestn. onkol. 2011; 22(3 Suppl. 1).]
  5. Kyle R.A., Rajkumar S.V. Multiple myeloma. Blood 2008; 111: 2962–72.
  6. Rehak S., Maisnar V., Malek V. et al. Diagnosis and surgical therapy of plasma cell neoplasia of spine. Neoplasma 2009; 56: 84.
  7. Mendoza S., Urrutia J., Fuentus D. Surgical treatment of solitary plasmocytoma of the spine: case series. Iowa Orthopaed. J. 2004; 24: 86–94.
  8. McDonald R.J., Trout A.T., Gray L.A. et al. Vertebroplasty in Multiple Myeloma: Outcomes in a Large Patient Series. Am. J. Neuroradiol. 2008; 29: 642–8.
  9. Garland P., Gishen P., Rahemtulla A. Percutaneous vertebroplasty to treat painful myelomatous vertebral deposits — long term efficacy outcomes. Ann. Hematol. 2010 Jul 6.
  10. Dimopoulos M.A., Moulopolos L.A., Maniatis A., Alexenian R. Solitary plasmacytoma of bone and asymptomatic multiple myeloma. Blood 2000; 96: 2037–44.
  11. Hu K., Yahalom J. Radiotherapy in the management of plasma cell tumors. Oncology 2000; 14: 101–8.
  12. Maruyama D., Watanabe T., Beppu Y. et al. Primary Bone Lymphoma: A New and Detailed Characterization of 28 Patients in a Single-Institution Study. Hematol. Stem Cell Transplant. Div. 2006; 56–67.
  13. Cortet B., Cotton., Boutry N. et al. Percutaneous vertebroplasty in patients with osteolytic metastases or multiple myeloma [see comments]. Rev. Rheum. Engl. Ed. 1997; 64(3): 177–83.
  14. Durr H.R., Muller P.E., Hiller E. et al. Malignant lymphoma of bone. Arch. Orthopaed. Trauma Surg. 2002; 122: 10–6.
  15. Lecouvet F.E., Van den Berg B.C, Maldague B.E. et al. Vertebral compression fractures in multiple myeloma. Part I. Distribution and appearance at MR imaging. Radiology 1997; 204: 195–9.
  16. Durr H.R., Wegener B., Krodel A. et al. Multiple myeloma: surgery of the spine: retrospective analysis of 27 patients. Spine 2002; 27: 320–6.
  17. Kyle R.A., Gertz M.A., Witzing T.E. et al. Review of 1027 patients with newly diagnosed multiple myeloma. Mayo Clin. Proc. 2003; 78(1): 21–33.
  18. Chahal S., Lagera J.E., Ryder J., Kleinschmidt-DeMasters B.K. Hematological neoplasms with first presentation as spinal cord compression syndromes: a 10-year retrospective series and review of the literature. Clin. Neuropathol. 2003; 22(6): 282–90.
  19. Chiodo A. Spinal cord injury caused by epidural B-cell lymphoma: report of two cases. J. Spinal Cord Med. 2007; 30(1): 70–2.
  20. Rao G., Chul S.H., Chakrabarti I.I. et al. Multiple Myeloma of the cervical spine: treatment strategies for pain and spinal instability. J. Neurosurg. Spine. 2006; 5: 140-145.
  21. Kwon A.-H., Chang U.-K., Gwak H.-S. et al. The Role of Surgery in the Treatment of Spinal Myeloma. J. Korean Neurosurg. Soc. 2005; 37: 187–92.
  22. Masala S., Fiori R., Massari F. et al. Percutaneus kyphoplasty: indications and technique. Tumori 2004; 90: 22–6.
  23. Slatkin N. Cancer-Related Pain and its Pharmacologic Management in the Patients With Bone Metastasis. J. Support Oncol. 2006; 4(Suppl. 1): 015–21.
  24. Алиев М.Д., Долгушин Б.И., Валиев А.К. и др. Чрезкожная вертебро- пластика в онкологии. М.: Издательская группа РОНЦ, 2008: 43–54. [Aliyev M.D., Dolgushin B.I., Valiyev A.K. i dr. Chrezkozhnaya vertebroplastika v onkologii (Transcutaneous vertebroplasty in oncology). M.: Izdatelskaya gruppa RONTS, 2008: 43–54.]
  25. Deramond H., Dion J.E., Chiras J. Complications in vertebroplasty. In: Percutaneous Vertebroplasty. Ed. by J.M. Mathis, H. Deramond, S.M. Belkoff. New York: Springer-Verlag, 2002: 165–73.
  26. Kaemmerlen P., Thiesse P., Jonas P. et al. Percutaneous injection of orthopedic cement in metastatic vertebral lesions [letter]. N. Engl. J. Med. 1989; 321(2): 121.
  27. Komemushi A., Tanigawa N., Kariya S. et al. Percutaneous vertebroplasty for compression fracture: analysis of vertebral body volume by CT volumetry. Acta Radiol. 2005; 46: 276–9.
  28. Валиев А.К., Мусаев Э.Р., Тепляков В.В. и др. Чрезкожная вертебро- пластика в онкологии. М.: ИНФРА-М, 2010: 69. [Valiyev A.K., Musaev E.R., Teplyakov V.V. i dr. Chrezkozhnaya vertebroplastika v onkologii (Transcutaneous vertebroplasty in oncology). M.: INFRA-M, 2010: 69.]
  29. Каллистов В.Е. Метастатические опухоли позвоночника (клиника, диагностика, лечение): Дис. ¼ канд. мед. наук. М., 1999. [Kallistov V.E. Metastaticheskiye opukholi pozvonochnika (klinika, diagnostika, lecheniye): Avtoref. dis. … kand. med. nauk (Metastatic spinal tumors (presentation, diagnosis, management)). Author’s summary of dissertation for the degree of Candidate of medical sciences. M., 1999.]
  30. Wetzel F.T., Maurer P., Thompson K. et al. Minimally Invasive Spine Surgery: A Surgical Manual. Spine 2001; 25: 382–8.
  31. Boriani S., Gasparrini A., Paderni S., Bandiera S., Cappucio M. Terapia chirurgica delle lesioni vertebralinel mieloma. Haematologica 2004; 89: 21–3.
  32. Schiff D. Spinal cord compression. Neurol. Clin. 2003; 21: 67–86.
  33. Walker M.P., Yaszemski M.J., Kim C.W. et al. Metastatic disease of the spine: evaluation and treatment. Clin. Orthop. 2003; 415: S165–75.
  34. Sharma B.S., Gupta S.K., Khosla V.K. et al. Midline and far lateral approaches to foramen magnum lesions. Neurol. India 1999; 47: 268–71.
  35. Chiras J., Deramond H. Complications des vertebroplasties. In: Echecs et Complications de la Chirurgie du Rachis. Chirurgie de Reprise. Ed. by G. Sailant, C. Laville. Paris: Sauramps Medical, 1995: 149–53.
  36. Cyteval C., Sarrabere M.P., Roux J.O. et al. Acute osteoporotic vertebral collapse: open study on percutaneous injection of acrylic surgical cement in 20 patients. Am. J. Roentgenol. 1999; 173(6): 1685–90.
  37. Li K.C., Poon P.Y. Sensitivity and specificity of MRI in detecting malignant spinal cord compression and in distinguishing malignant from benign compression fractures of vertebrae. Magn. Reson. Imaging 1988; 6: 547–56.
  38. Anselmetti G.C., Corgnier A., Debernardi F. et al. Treatment of painful compression vertebral fractures with vertebroplasty: results and complications. Radiol. Med. (Torino) 2005; 110: 262–72.
  39. Grados F., Depriester C., Cayrolle G. et al. Long-term observations of vertebral osteoporotic fractures treated by percutaneous vertebroplasty. Rheumatology (Oxford) 2000, 39: 1410–4.
  40. Uppin A.A., Hirsch J.A., Centenera L.V. et al. Occurrence of new vertebral body fracture after percutaneous vertebroplasty in patients with osteoporosis. Radiology 2003; 226: 119–24.
  41. Harrop J.S., Prpa B., Reinhardt M.K. et al. Primary and Secondary Osteoporosis’ Incidence of Subsequent Vertebral Compression Fractures After Kyphoplasty. Spine 2004; 29: 2120–5.
  42. Синельников Р.Д. Атлас анатомии человека. Т. I. М.: Медицина, 1972. [Synelnikov R.D. Atlas anatomii cheloveka (Atlas of human anatomy). T. I. M.: Meditsyna, 1972.]
  43. O’Brien J.P., Sims J.T., Evans A.J. Vertebroplasty in patients with severe vertebral compression fractures: a technical report. Am. J. Neuroradiol. 2000; 21(8): 1555–8.
  44. Dahl O.E., Garvik L.J., Lyberg T. Toxic effects of methylmetacrylate monomer on leukocytes and endothelial cells in vitro [published erratum appeared in Acta Orthop Scand. 1995; 66(4): 387]. Acta Orthop. Scand. 1994; 65(2): 147–53.
  45. Belkoff S.M., Mathis J.M., Jasper L.E. et al. The biomechanics of vertebroplasty: the effect of cement volume on mechanical behavior. Spine 2001; 26(14): 1537–41.
  46. Barr J.D., Barr M.S., Lemley T.J. et al. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000; 25(8): 923–8.
  47. Heini P.F., Walchli B., Berlemann U. Percutaneous transpedicular vertebroplasty with PMMA: operative technique and early results. A prospective study for the treatment of osteoporotic compression fractures. Eur. Spine J. 2000; 9: 445–50.

Современные аспекты применения позитронно-эмиссионной томографии при лимфомах

Асланиди И.П., Мухортова О.В., Катунина Т.А., Екаева И.В., Шавман М.Г.

ФГБНУ «Научный центр сердечно-сосудистой хирургии им. А.Н. Бакулева», Рублевское ш., д. 135, Москва, Российская Федерация, 121552

Для переписки: Ольга Валентиновна Мухортова, д-р мед. наук, Рублевское ш., д. 135, Москва, Российская Федерация, 121552; тел.: +7(495)414-77-31; e-mail: olgamukhortova@yandex.ru

Для цитирования: Асланиди И.П., Мухортова О.В., Катунина Т.А. и др. Современные аспекты применения позитронно-эмиссионной томографии при лимфомах. Клиническая онкогематология. 2015;8(1):13–25.


РЕФЕРАТ

Цель. Определить наиболее эффективные направления использования позитронно-эмиссионной томографии (ПЭТ) со фтордезоксиглюкозой, меченной 18-фтором (18F-ФДГ), у больных лимфомами.

Методы. Изучено 56 научных источников, опубликованных в 2005–2014 гг., в которых анализируются результаты последних крупных исследований по применению ПЭТ у больных лимфомами.

Результаты. ПЭТ с 18F-ФДГ стала неотъемлемой частью диагностического алгоритма у больных лимфомами, которые характеризуются активным накоплением 18F-ФДГ. Высокая точность ПЭТ у пациентов с некоторыми типами лимфом позволяет эффективно использовать метод в клинической практике для определения стадии заболевания, оценки эффективности лечения, уточнения распространенности рецидива, результатов противорецидивного лечения, а также при подозрении на трансформацию лимфомы. Применение ПЭТ на других этапах лечения больных лимфомами находится в процессе научных разработок. При индолентных лимфомах с известной низкой гликолитической активностью или лимфомах редких гистологических типов ПЭТ для оценки эффективности лечения используется только при наличии исходных (до начала лечения) результатов исследования. Для оценки результатов лечения рекомендуется использовать 5-балльную шкалу Deauville. Соблюдение сроков обследования в процессе противоопухолевой терапии позволяет существенно повысить точность ПЭТ-диагностики. Одиночные очаги, выявленные при ПЭТ и имеющие принципиальное значение для выбора лечения, должны быть верифицированы другими методами диагностики. Выполнение ПЭТ при наблюдении за больными в состоянии ремиссии признается нецелесообразным.

Выводы. ПЭТ является «золотым стандартом» стадирования и оценки эффективности лечения больных лимфомами, которые характеризуются активным накоплением 18F-ФДГ.


Ключевые слова: ПЭТ, лимфомы, международные рекомендации, 5-балльная шкала Deauville.

Получено: 14 ноября 2014 г.

Принято в печать: 18 ноября 2014 г.

Читать статью в PDFpdficon


ЛИТЕРАТУРА

  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.