Вторые первичные опухоли у онкологических больных: лекарственный канцерогенез в онкологии
Аннотация
Цитостатики, используемые в химиотерапии, вызывают образование вторых первичных опухолей у некоторых больных, излеченных от первого новообразования. При этом риск возникновения вторых опухолей после излечения от первых повышается в 4–6 раз по сравнению с общей популяцией. В обзоре приведены современные данные о механизме злокачественной трансформации клеток цитостатиками, группах повышенного риска, связанного с врожденным полиморфизмом систем метаболизма ксенобиотиков и репарацией повреждений ДНК. Наибольший риск лекарственных опухолей отмечен у пациентов с высокой активностью изоформ цитохрома Р450, превращающего транспортные формы цитостатиков в активные электрофильные метаболиты, и с низким уровнем детоксицирующих ферментов. При прочих равных условиях в группу повышенного риска входят больные с низкой активностью ферментов репарации ДНК. Рассматриваются возможности исследования канцерогенного потенциала новых таргетных препаратов в эксперименте в целях минимизации риска возникновения вторых опухолей, обусловленных лечением.
Об авторах
Г. А. Белицкий
Научно-исследовательский институт канцерогенеза ФГБУ «Российский онкологический научный центр им. Н. Н. Блохина» Минздрава России; Россия, 115478, Москва, Каширское шоссе, 24
Россия
Россия
Е. А. Лесовая
Научно-исследовательский институт канцерогенеза ФГБУ «Российский онкологический научный центр им. Н. Н. Блохина» Минздрава России; Россия, 115478, Москва, Каширское шоссе, 24
ФГБОУ ВО «Рязанский государственный медицинский университет им. акад. И.П. Павлова» Минздрава России; Россия, 390026, Рязань, ул. Высоковольтная, 9
Россия
Россия
К. И. Кирсанов
Научно-исследовательский институт канцерогенеза ФГБУ «Российский онкологический научный центр им. Н. Н. Блохина» Минздрава России; Россия, 115478, Москва, Каширское шоссе, 24
Россия
Россия
М. Г. Якубовская
Научно-исследовательский институт канцерогенеза ФГБУ «Российский онкологический научный центр им. Н. Н. Блохина» Минздрава России; Россия, 115478, Москва, Каширское шоссе, 24
Россия
Россия
Список литературы
1. Travis L. B., Demark Wahnefried W., Allan J. M. et al. Aetiology, genetics and prevention of secondary neoplasms in adult cancer survivors. Nat Rev Clin Oncol 2013;10(5):289–301.
2. Friis S., Kesminiene A., Espina C. et al. European Code against Cancer 4th Edn.: Medical exposures, including hormone therapy, and cancer. Cancer Epidemiology 2015;39(Suppl 1):S107–19.
3. Pedersen-Bjergaard J., Pedersen M., Roulston D., Philip P. Different genetic pathways in leukemogenesis for patients presenting with therapy-related myelodysplasia and therapy- related acute myeloid leukemia. Blood 1995;86(9): 3542–52.
4. Савченко В. Г. Паровичникова Е. Н., Афанасьев Б. В. и др. Клинические рекомендации по диагностике и лечению острых миелоидных лейкозов взрослых, 2014. Доступно по: http://blood.ru/documents/clinical%20guidelines/21.%20klinicheskierekomendacii-2014-oml. pdf. [Savchenko V. G. Parovichnikovа Е. N., Аfanas’ev B.V. et al. Clinical recommendations for the diagnostics and treatment of acute myeloid leucosis at adults, 2014. Available at: http://blood.ru/documents/clinical %20guidelines/21. %20klinicheskie-rekomendacii-2014-oml. pdf. (In Russ.)]
5. Jerez A., Sugimoto Y., Makishima H. et al. Loss of heterozygosity in 7q myeloid disorders: clinical associations and genomic pathogenesis. Blood 2012;119(25):6109–17.
6. Yang X. H., Wang B., Cunningham J. M. Identification of epigenetic modifications that contribute to pathogenesis in therapy-related AML: effective integration of genome-wide histone modification with transcriptional profiles. BMC Medical Genomics 2015;8(Suppl 2):1–13.
7. Salas C., Pérez-Vera P., Frías S. Genetic abnormalities in leukemia secondary to treatment in patients with Hodgkin’s disease. Rev Invest Clin 2011;63(1):53–63.
8. Walter M. J., Shen D., Ding L. et al. Clonal architecture of secondary acute myeloid leukemia. N Engl J Med 2012;366(12):1090–8.
9. Волкова М. А. Клиническая онкогематология. M.: Медицина, 2001. [Volkovа М. А. Clinical oncohematology. Moscow: Меditsina, 2001. (In Russ.)].
10. Huitema A. D., Smits K. D., Mathôt R. A. et al. The clinical pharmacology of alkylating agents in high-dose chemotherapy. Anticancer Drugs 2000;11(7):515–33.
11. Johnson L. A., Malayappan B., Tretyakova N. et al. Formation of cyclophosphamide specific DNA adducts in hematological diseases. Pediatr Blood Cancer 2012;58(5):708–14.
12. Allan J. M., Wild C. P., Rollingson S. et al. Polymorphism in glutathione S-transferase P1 is associated with susceptibility to chemotherapy- induced leukemia. Proc Natl Acad Sci USA 2001;98(20):11592–7.
13. Minev B. Cancer management in man: chemotherapy, biological therapy, hyperthermia and supporting measures. New York: Springer, 2011.
14. Mathijssen R. H., van Alphen R. J., Verweij J. et al. Clinical pharmacokinetics and metabolism of irinotecan (CPT-11). Clin Cancer Res 2001;7(8):2182–94.
15. Minami H., Sai K., Saeki M. et al. Irinotecan pharmacokinetics/pharmacodynamics and UGT1A genetic polymorphisms in Japanese: roles of UGT1A1*6 and *28. Pharmacogenet Genomics 2007;17(7):497–504.
16. Toffoli G., Cecchin E., Corona G. et al. The role of UGT1A1*28 polymorphism in the pharmacodynamics and pharmacokinetics of irinotecan in patients with metastatic colorectal cancer. J Clin Oncol 2006;24(19):3061–8.
17. Fujita K., Sparreboom A. Pharmacogenetics of irinotecan disposition and toxicity: a review. Curr Clin Pharmacol 2010;5(3):209–17.
18. Zhuo X., Zheng N., Felix C. A., Blair I. A. Kinetics and regulation of cytochrome P450- mediated etoposide metabolism. Drug Metab Dispos 2004;32(9):993–1000.
19. Kishi S., Yang W., Boureau B. et al. Effects of prednisone and genetic polymorphisms on etoposide disposition in children with acute lymphoblastic leukemia. Blood 2004;103(1):67– 72.
20. Fan Y., Schreiber E. M., Giorgianni A. et al. Myeloperoxidase-catalyzed metabolism of etoposide to its quinone and glutathione adduct forms in HL60 cells. Chem Res Toxicol 2006;19(7):937–43.
21. Lovett B. D., Strumberg D., Blair I. A. et al. Etoposide metabolites enhance DNA topoisomerase II cleavage near leukemiaassociated MLL translocation breakpoints. Biochemistry 2001;40(5):1159–70.
22. Felix C. A., Walker A. H., Lange B. J. et al. Association of CYP3A4 genotype with treatment- related leukemia. Proc Natl Acad Sci USA 1998;95(22):13176–81.
23. Westlind A., Löfberg L., Tindberg N., et al. Interindividual differences in hepatic expression of CYP3A4: relationship to genetic polymorphism in the 5’-upstream regulatory region. Biochem Biophys Res Commun 1999;259(1):201–5.
24. Spurdle A. B., Goodwin B., Hodgson E. et al. The CYP3A4*1B polymorphism has no functional significance and is not associated with risk of breast or ovarian cancer. Pharmacogenetics 2002;12(5):355–66.
25. Collado M., Barragan E., Bolufer P. et al. Lack of association of CYP3A4-V polymorphism with the risk of treatment-related leukemia. Leuk Res 2005;29(5):595–7.
26. Rund D., Krichevsky S., Bar-Cohen S. et al. Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 adult patients. Leukemia 2005;19(11):1919–28.
27. Larson R. A., Wang Y., Banerjee M. et al. Prevalence of the inactivating 609C>T polymorphism in the NAD (P) H: quinone oxidoreductase (NQO1) gene in patients with primary and therapy-related myeloid leukemia. Blood 1999;94:803–7.
28. Mochida Y., Taguchi K., Taniguchi S. et al. The role of P-glycoprotein in intestinal tumorigenesis: disruption of mdr1a suppresses polyp formation in ApcMin/+ mice. Carcinogenesis 2003;24(7):1219–24.
29. Rund D., Krichevsky S., Bar-Cohen S. et al. Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 adult patients. Leukemia 2005;19(11):1919–28.
30. Hitzl M., Drescher S., van der Kuip H. et al. The C3435T mutation in the human MDR1 gene is associated with altered efflux of the P-glycoprotein substrate rhodamine 123 from CD56+ natural killer cells. Pharmacogenetics 2001;11(4):293–8.
31. Sill H., Olipitz W., Zebisch A. et al. Therapy-related myeloid neoplasms: pathobiologyand clinical characteristics. Br J Pharmacol 2011;162(4):792–805.
32. Burden D. A., Osheroff N. Mechanism of action of eukaryotic topoisomerase II and drugs targeted to the enzyme. Biochim Biophys Acta 1998;1400(1–3):139–54.
33. Park S. Y., Lam W., Cheng Y. C. X-ray repair cross-complementing gene I protein plays an important role in camptothecin resistance. Cancer Res 2002;62(2):459–65.
34. Kutschera E., Sauermann-Ruge I. Late results of cataract surgery after oculopression. Klin Monbl Augenheilkd 1975;167(4):550–4.
35. Han J. Y., Lee G. K., Yoo S. Y. et al. Association of SUMO1 and UBC9 genotypes with tumor response in non-small-cell lung cancer treated with irinotecan-based chemotherapy. Pharmacogenomics J 2010;10(2):86–93.
36. Link D. C., Schuettpelz L. G., Shen D. et al. Identification of a novel TP53 cancer susceptibility mutation through wholegenome sequencing of a patient with therapyrelated AML. JAMA 2011;305(15):1568–76.
37. Kleinerman R. A., Tucker M. A., Tarone R. E. et al. Risk of new cancers after radiotherapy in long-term survivors of retinoblastoma: an extended follow-up. J Clin Oncol 2005;23(10):2272–9.
38. Sharif S., Ferner R., Birch J. M. et al. Second primary tumors in neurofibromatosis 1 patients treated for optic glioma: substantial risks after radiotherapy. J Clin Oncol 2006;24(16):2570–5.
39. Goldstein A. M., Yuen J., Tucker M. A. Second cancers after medulloblastoma: population-based results from the United States and Sweden. Cancer Causes Control 1997;8(6):865–71.
40. Breslow N. E., Lange J. M., Friedman D. L. et al. Secondary malignant neoplasms after Wilms tumor: an international collaborative study. Int J Cancer 2010;127(3):657–66.
41. Rai R., Peng G., Li K., Lin S. Y. DNA damage response: the players, the network and the role in tumor suppression. Cancer Genomics Proteomics 2007;4(2):99–106.
42. Berwick M., Begg C. B., Armstrong B. K. et al. Interaction of CDKN2A and sun exposure in the etiology of melanoma in the general population. J Invest Dermatol 2011;131(12):2500–3.
43. Seedhouse C., Faulkner R., Ashraf N. et al. Polymorphisms in genes involved in homologous recombination repair interact to increase the risk of developing acute myeloid leukemia. Clin Cancer Res 2004;10(8):2675–80.
44. Jawad M., Seedhouse C. H., Russell N., Plumb M. Polymorphisms in human homeobox HLX1 and DNA repair RAD51 genes increase the risk of therapy-related acute myeloid leukemia. Blood 2006;108(12):3916–8.
45. Best T., Li D., Skol A. D. et al. Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin’s lymphoma. Nat Med 2011;17(8):941– 3.
46. Allan J. M., Smith A. G., Wheatley K. et al. Genetic variation in XPD predicts treatment outcome and risk of acute myeloid leukemia following chemotherapy. Blood 2004;104(13):3872–7.
47. Ellis N. A., Huo D., Yildiz O. et al. MDM2 SNP309 and TP53 Arg72Pro interact to alter therapy-related acute myeloid leukemia susceptibility. Blood 2008;112(3):741–9.
48. Worrillow L. J., Smith A. G., Scott K. et al. Polymorphic MLH1 and risk of cancer after methylating chemotherapy for Hodgkin lymphoma. J Med Genet 2008;45(3):142–6.
49. Seedhouse C., Bainton R., Lewis M. et al. The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related acute myeloblastic leukemia. Blood 2002;100(10):3761–6.
50. Guillem V. M., Collado M., Terol M. J. et al. Role of MTHFR (677, 1298) haplotype in the risk of developing secondary leukemia after treatment of breast cancer and hematological malignancies. Leukemia 2007;21(7):1413–22.
51. Bhatia S. Genetic variation as a modifier of association between therapeutic exposure and subsequent malignant neoplasms in cancer survivor. Cancer 2015;121(5):648–63.
52. Best T., Li D., Skol A. D. et al. Variants at 6q21 implicate PRDM1 in the etiology of therapy-induced second malignancies after Hodgkin’s lymphoma. Nature Medicine 2011,17(8):941–3.
53. Bernstein J. L., Haile R. W., Stovall M. et al. Radiation exposure, the ATM gene, and contralateral breast cancer in the women’s environmental cancer and radiation epidemiology study. J Natl Cancer Inst 2010;102(7):475–83.
54. Li C. I., Daling J. R., Porter P. L. et al. Adjuvant hormonal therapy for breast cancer and risk of hormone receptor-specific subtypes of contralateral breast cancer. Cancer Res 2009;69(17):6865–70.
55. ARC Monographs series on the evaluation of carcinogenic risks to humans. Some pharmaceutical drugs. Lyon, 1996;66:253–388.
56. Берштейн Л. М. Гормональный канцерогенез. СПб., 2000. [Bersteyn L. М. Hormonal cancerogenesis. Saint Petersburg, 2000. (In Russ.)].
57. Krishnan B., Morgan G. J. Non-Hodgkin lymphoma secondary to cancer chemotherapy. Cancer Epidemiol Biomarkers Prev 2007;16(3):377–80.
58. WHO collaborative study of neoplasia and steroid contraceptives. Depot- medroxyprogesterone acetate(DMPA) and risk of endometrial cancer. Int J Cancer 1991;49(2):186–90.
59. Concannon P. W., Spraker T. R., Casey H. W., Hansel W. Gross and histopathologic effects of medroxyprogesterone acetate and progesterone on the mammary glands of adult beagle bitches. Fertil Steril 1981;36(3):373–87.
60. Kasi P. M., Tawbi H. A., Oddis C. V., Kulkarni H. S. Clinical review: serious adverse events associated with the use of rituximab – a critical care perspective. Critical Care 2012;16(4):231.
61. Yang B., Lu X. C., Yu R. L. et al. Diagnosis and treatment of rituximab-induced acute tumor lysis syndrome in patients with diff use large B-cell lymphoma. Am J Med Sci 2012;343(4):337–41.
62. Tarella C., Passera R., Magni M. et al. Risk factors for the development of secondary malignancy after high-dose chemotherapy and autograft, with or without rituximab: a 20- year retrospective follow-up study in patients with lymphoma. J Clin Oncol 2011;29(7):814– 24.
63. Li Q., Teitz-Tennenbaum S., Donald E. J. et al. In vivo sensitized and in vitro activated B cells mediate tumor regression in cancer adoptive immunotherapy. J Immunol 2009;183(5):3195–203.
64. Baldo B. A. Adverse events to monoclonal antibodies used for cancer therapy: focus on hypersensitivity responses. OncoImmunology 2013;2(10):e26333.
65. Abdulghani J., El-Deiry W. S. TRAIL receptor signaling and therapeutics. Expert Opin Ther Targets 2010;14(10):1091–108.
66. Soria J. C., Smit E., Khayat D. Phase 1b study of dulanermin (recombinant humanApo2L/TRAIL) in combination with paclitaxel, carboplatin, and bevacizumabin patients with advanced non-squamous non-small-cell lung cancer. J Clin Oncol 2010;28(9):1527–33.
67. Miles M. A., Shekhar T. M., Hall N. E., Hawkins C. J. TRAIL causes deletions at the HPRT and TK1 loci of clonogenically competent cells. Mutat Res 2016;787: 15–31.
68. Ko J. C., Hong J. H., Wang L. H. et al. The role of repair protein Rad51 in synergistic cytotoxicity and mutagenicity induced by epidermal growth factor receptor inhibitor (Gefitinib, IressaR) and benzo[a]pyrene in human lung cancer. Exp Cell Res 2008;314(8):1881–91.
69. Baron V., Adamson E. D., Calogero A. et al. The transcription factor Egr1 is a direct regulator of multiple tumor suppressors including TGFbeta1, PTEN, p53, and fibronectin. Cancer Gene Ther 2006;13(2):115–24.
70. Westendorf J. J., Yamamoto C. M., Lenny N. et al. The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation. Mol Cell Biol 1998;18(1):322–33.
71. Castilla L. H., Garrett L., Adya N. et al. The fusion gene Cbfb-MYH11 blocks myeloid differentiation and predisposes mice to acute myelomonocytic leukaemia. Nat Genet 1999;23(2):144–6.
72. Berger M., Habs M., Schmähl D. Noncarcinogenic chemotherapy with combination of vincristine, metotrexate and 5-fluorouracil(VMF) in rats. Int J Cancer 1983;32(2):231–6.
73. Some antineoplstic and immunosuppressive agents. IARC Monogr Eval Carcinog Risk Chem Hum 1981;26:1–411.
74. Schonfeld S. J., Gilbert E. S., Dores G. M. et al. Acute myeloid leukemia following Hodgkin lymphoma: a population-based study of 35,511 patients. J Natl Cancer Inst 2006;98(3):215–8.
Для цитирования:
Белицкий Г.А., Лесовая Е.А., Кирсанов К.И., Якубовская М.Г. Вторые первичные опухоли у онкологических больных: лекарственный канцерогенез в онкологии. Успехи молекулярной онкологии. 2016;3(3):44-55. https://doi.org/10.17650/2313-805X-2016-3-3-44-55
For citation:
Belitskiy G.A., Lesovaya E.A., Kirsanov K.I., Yakubovskaya M.G. Second primary malignancies of cancer patients: treatment-related carcinogenesis. Advances in molecular oncology. 2016;3(3):44-55. (In Russ.) https://doi.org/10.17650/2313-805X-2016-3-3-44-55
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