References

ateroskleroz

Атеросклероз

Ateroscleroz

2078-256X2949-3633

НИИТПМ-филиал ИЦиГ СО РАН

ateroskleroz-9

Research Article

ОБЗОРЫ

REVIEWS

КАРДИОМЕТАБОЛИЧЕСКИЕ ФАКТОРЫ И КОЛОРЕКТАЛЬНЫЙ РАК

CARDIOMETABOLIC FACTORS AND COLORECTAL CANCER

Кручинина

М. В.

Kruchinina

M. V.

kruchmargo@yandex.ru

Курилович

С. А.

Kurilovich

S. A.

kurilovich@yandex.ru

Громов

А. А.

Gromov

A. A.

gromovcenter@rambler.ru

Шварц

Я. Ш.

Schwartz

Ya. Sh.

yshschwartz@mail.ru

Кручинин

В. Н.

Kruchinin

V. N.

noemail@neicon.ru

Рыхлицкий

С. В.

Ryhlitsky

S. V.

rhl@isp.nsc.ru

Володин

В. А.

Volodin

A. A.

volodin@isp.nsc.ru

Федеральное государственное бюджетное научное учреждение «Научно-исследовательский институт терапии и профилактической медицины»Federal State Budgetary of Scientific Institution "Institution of Internal and Preventive Medicine"

Федеральное государственное бюджетное учреждение науки Институт физики полупроводников им. А. В. Ржанова Сибирского отделения Российской академии наукInstitute of Semiconductor Physics, Siberian Branch of the Russian Academy of Sciences Russia

Федеральное государственное бюджетное учреждение науки Институт физики полупроводников им. А. В. Ржанова Сибирского отделения Российской академии наук; Новосибирский государственный университетInstitute of Semiconductor Physics, Siberian Branch of the Russian Academy of Sciences Russia; Novosibirsk State University

2016

27092019

1214660

2019

Кручинина М.В., Курилович С.А., Громов А.А., Шварц Я.Ш., Кручинин В.Н., Рыхлицкий С.В., Володин В.А.

Kruchinina M.V., Kurilovich S.A., Gromov A.A., Schwartz Y.S., Kruchinin V.N., Ryhlitsky S.V., Volodin A.A.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://ateroskleroz.elpub.ru/jour/article/view/9

Отмечается нарастание распространенности метаболического синдрома и висцерального ожирения в общей популяции. Фактическая распространенность метаболического синдрома среди населения составляет 24 % в США, от 24,6 % до 30,9 % в Европе. Как показали многие клинические испытания (NAHANES III, INTERHART), метаболический синдром связан с повышенным риском диабета и сердечно-сосудистых заболеваний. Кроме того, отдельные компоненты метаболического синдрома связаны с развитием рака, в частности, колоректального, эта ассоциация подтверждается многими эпидемиологическими исследованиями. Колоректальный рак является важной проблемой общественного здравоохранения: в 2000 году в общей сложности в мире было диагностировано 944717 случаев заболевания колоректальным раком. Последние отчеты показывают, что лица с метаболическим индромом имеют более высокий риск развития рака толстой или прямой кишки. Кроме того, кластеры компонентов метаболического синдрома повышают риск, связанный с развитием рака. Механизм, который патофизиологически связывает метаболический синдром и колоректальный рак, в основном связан с абдоминальным ожирением и резистентностью к инсулину. Популяционные и кспериментальные исследования показали, что гиперинсулинемия, повышенное содержание С-пептида, повышенный индекс массы тела, высокие уровни фактора роста инсулина-1, низкие уровни фактора роста инсулин-связывающего белка-3, высокий уровень лептина и низкий уровень адипонектина - все эти факторы вовлечены в канцерогенез. Понимание патологических механизмов, которые связывают метаболический синдром и его компоненты с канцерогенезом, имеет большое клиническое значение и перспективы для улучшения здоровья населения при целом ряде заболеваний, включая рак, который представляется одной из основных причин смертности в обществе.

The metabolic syndrome and visceral obesity have an increasing prevalence and incidence in the generalpopulation. The actual prevalence of the metabolic syndrome is 24% in US population and between 24,6% and 30,9% in Europe. As demonstrated by many clinical trials (NAHANES III, INTERHART) the metabolic syndrome is associated with an increased risk of both diabetes and cardiovascular disease. In addition to cardiovascular disease, individual components of the metabolic syndrome have been linked to the development of cancer, particularly to colorectal cancer. Colorectal cancer is an important public health problem; in the year 2000 there was an estimated total of 944717 incident cases of colorectal cancer diagnosed world-wide. This association is sustained by many epidemiological studies. Recent reports suggest that individuals with metabolic syndrome have a higher risk of colon or rectal cancer. Moreover, the clusters of metabolic syndrome components increase the risk of associated cancer. The physiopathological mechanism that links metabolic syndrome and colorectal cancer is mostly related to abdominal obesity and insulin resistance. Population and experimental studies demon trated that hyperinsulinemia, elevated C-peptide, elevated body mass index, high levels of insulin growth factor-1, low levels of insulin growth factor binding protein-3, high leptin levels and low adiponectin levels are all involved in carcinogenesis. Understanding the pathological mechanism that links metabolic syndrome and its components to carcinogenesis has a major clinical significance and may have profound health benefits on a number of diseases including cancer, which represents a major cause of mortality and morbidity in our societies.

метаболический синдромколоректальный ракинсулинорезистентностьожирениеадипокинывоспалительные цитокины

metabolic syndromecolorectal cancerinsulin resistanceexpected renieadipokinesinflammatory cytokines

References1

Zimmet P., Magliano D., Matsuzawa Y., Alberti G., Shaw J. The metabolic syndrome: a global public health problem and a new definition // J. Atheroscler. Thromb. 2005. Vol. 12. P. 295-00.

Vague J. La differenciation sexuelle, facteur determinant des formes de l≫obesite //Presse Med. 1947. Vol. 55. P. 339.

Grundy S. M., Cleeman J. I., Daniels S. R., Donato K. A., Eckel R. H., Franklin B. A., Gordon D. J., Krauss R. M., Savage P. J., Smith S. C. Jr, Spertus А. A., Costa F. Diagnosis and management of the metabolic syndrome: an American Heart Association/ National Heart, Lung, and Blood Institute Scientific Statement // Circulation. 2005. Vol. 112. P. 2735- 2752.

Kahn R., Buse J., Ferrannini E., Stern M. The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes // Diabetes Care. 2005. Vol. 28. P. 2289-304.

Flegal K. M., Carroll M. D., Ogden C. L., Johnson C. L. Prevalence and trends in obesity among US adults, 1999-000 // JAMA. 2002. Vol. 288. P. 1723- 1727.

Martínez M. A., Puig J. G., Mora M., Aragón R., ODogherty P., Antón J. L., Sánchez-Villares T., Rubio J. M., Rosado J., Torres R., Marcos J., Pallardo L. F., Banegas J. R. Metabolic syndrome: prevalence, associated factors, and C-reactive protein: the MADRIC Study // Metabolism. 2008. Vol. 57. P. 1232-240.

Hildrum B., Mykletun A., Hole T., Midthjell K., Dahl A. A. Age-specific prevalence of the metabolic syndrome defined by the International Diabetes Federation and the National Cholesterol Education Program: the Norwegian HUNT 2 study // BMC Public Health. 2007. Vol. 7. P. 220-27.

Cameron A. J., Shaw J. E., Zimmet P. Z. The metabolic syndrome: prevalence in worldwide populations //Endocrinol.Metab.Clin. North Am. 2004. Vol. 33. P. 351-75.

Кайдашев И. П. Эволюция понятия "метаболический синдром" и его современное значение // Укр. Мед. Часопис. 2012. T. 2.№ 88. C. 157-60.

Рекомендации экспертов Всероссийского научного общества кардиологов по диагностике и лечению метаболического синдрома. Второй пересмотр // Кардиоваскулярная терапия и профилактика. 2009. № 6. С. 1-9.

Ninomiya J. K., L»Italien G., Criqui M. H., Whyte J. L., Gamst A., Chen R. S. Association of the metabolic syndrome with history of myocardial infarction and stroke in the Third National Health and Nutrition Examination Survey // Circulation. 2004. Vol. 109. P. 42-6.

Eckel R. H., Grundy S. M., Zimmet P. Z. The metabolic syndrome // Lancet. 2005. Vol. 365. P. 1415- 1428.

Yusuf S., Hawken S., Ounpuu S., Dans T., Avezum A., Lanas F., McQueen M., Budaj A., Pais P., Varigos J., Lisheng L. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): casecontrol study // Lancet. 2004. Vol. 364. P. 937-52.

Kreger B. E., Splansky G. L., Schatzkin A. The cancer experience in the Framingham Heart Study cohort // Cancer. 1991. Vol. 67. P. 1

Boyle P., Leon M. E. Epidemiology of colorectal cancer // Br. Med. Bull. 2002. Vol. 64. P. 1-5.

Cancer Incidence in Five Continents. Vol. IX //Ed. Curado M. P., Edwards B., Ferlay J., Heanue M., Boyle P.:IARC Scientific Publications. 2007.895 p.

GLOBOCAN 2012: Estimated Cancer Incidence, Mortality and Prevalence Worldwide in 2012 // World health organization, International agency for research on cancer //http://globocan.iarc.fr/

Давыдов М И, Аксель Е М Заболеваемость злокачественными новообразованиями населения России и стран СНГ в 2008 г. // Вестник РОНЦ им. Н. Н. Блохина РАМН. 2011. Т. 22. № 3. С. 54-7.

Garow D. Metabolic syndrome is a risk factor for colorectal cancer in the United States // American College of Gastroenterology 2008 Annual Scientific Meeting. 2008. October 6.

Aleksandrova K., Boeing H., Jenab M., Bas Bueno-de-Mesquita H., Jansen E., et al. Metabolic Syndrome and Risk of Colon and Rectal Cancer: The European Prospective Investigation into Cancer and Nutrition Study // Cancer Prev. Res. 2011. Vol. 4. P. 1873-883.

Calle E. E., Rodriguez C., Walker-Thurmond K., Thun M. J. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U. S. adults // N. Engl. J. Med. 2003. Vol. 348. P. 1625-638.

Calle E. E., Kaaks R. Overweight, Obesity and Cancer: Epidemiological Evidence and Prop Mechanisms // NatureReviewsCancer. 2004. Vol. 4. No. 8. P. 579- 591.

Parkin D. M., Boyd L. Cancers attributable to overweight and obesity in the UK in 2011 // BritishJournalofCancer. 2011. Vol. 105. P. 34-7.

Luo W., Cao Y., Liao C., Gao F. Diabetes mellitus and the incidence and mortality of colorectal cancer: A meta-analysis of twenty four cohort studies // Colorectal Disease. 2012. Vol. 14. No. 11. P. 1307- 1312.

Parkin D. M., Boyd L., Walker L. C. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. Summary and conclusions. // Br. J. Cancer. 2011. Vol.105. P. 77-1.

Cao H., Jin C., Huang D. Changes in serum IGF-1 level and tumor VEGF expression in mice with colorectal cancer under hyperglycemic conditions // MolecularmedicineReports. 2013. Vol. 7. No. 4. P. 1361-365.

Ahmed R. L., Schmitz K. H., Anderson K. E., Rosamond W. D., Folsom A. R. The metabolic syndrome and risk of incident colorectal cancer // Cancer. 2006. Vol. 107. P. 28-6.

Trevisan M., Liu J., Muti P., Misciagna G., Menotti A., Fucci F. Markers of insulin resistance and colorectal cancer mortality // Cancer Epidemiol. Biomarkers Prev. 2001. Vol. 10. P. 937-41.

Khaw K. T., Wareham N., Bingham S., Luben R., Welch A., Day N. Preliminary communication: glycated hemoglobin, diabetes, and incident colorectal cancer in men and women: a prospective analysis from the European prospective investigation into cancer-Norfolk study // Cancer Epidemiol. Biomarkers Prev. 2004. Vol. 13. P. 915-19.

Saydah S. H., Platz E. A., Rifai N., Pollak M. N., Brancati F. L., Helzlsouer K. J. Association of markers of insulin and glucose control with subsequent colorectal cancer risk // Cancer Epidemiol. Biomarkers Prev. 2003. Vol. 12. P. 412-18.

Stocks T., Lukanova A., Johansson M., Rinaldi S., Palmqvist R., Hallmans G., Kaaks R., Stattin P. Components of the metabolic syndrome and colorectal А те ро ск ле ро з. 2016. T. 12, №1 58 cancer risk; a prospective study // Int. J. Obes. (Lond.) 2008. Vol. 32. P. 304-14.

Pischon T., Lahmann P. H., Boeing H., Friedenreich C., Norat T., et al. Body size and risk of colon and rectal cancer in the European Prospective Investigation Into Cancer and Nutrition (EPIC) // J. Natl. Cancer Inst. 2006. Vol. 98. P. 920-31.

Moon-Chan Kim, Chang-Sup Kim, Tae-Heum Chung, Hyoung-Ouk Park, Cheol-In Yoo Metabolic syndrome, lifestyle risk factors, and distal colon adenoma: A retrospective cohort study // World J. Gastroenterol. 2011. Vol. 17. No. 35. P. 4031-037.

Moore L. L., Bradlee M. L., Singer M. R., Splansky G. L., Proctor M. H., Ellison R. C., Kreger B. E. BMI and waist circumference as predictors of lifetime colon cancer risk in Framingham Study adults // Int. J. Obes. Relat. Metab. Disord. 2004. Vol. 28. P. 559-67.

Otake S., Takeda H., Suzuki Y., Fukui T., Watanabe S., Ishihama K., Saito T., Togashi H., Nakamura T., Matsuzawa Y., Kawata S. Association of visceral fat accumulation and plasma adiponectin with colorectal adenoma: evidence for participation of insulin resistance //Clin. Cancer Res. 2005. Vol. 11. P. 3642-646.

Hamoudi W. T. Y., Dumitrascu D. L. Is there an association between coronary heart disease and colorectal carcinoma? Results from a pilot study // Rom J. Gastroenterol. 1997. Vol. 6. P. 13-6.

Byung Chang Kim, Aesun Shin, Chang Won Hong, Dae Kyung Sohn, Kyung Su Han, KumHeiRyu, Bum Joon Park, Ji Hyung Nam, Ji Won Park, Hee Jin Chang, HyoSeong Choi, Jeongseon Kim, Jae Hwan Oh Association of colorectal adenoma with components of metabolic syndrome // Cancer Causes Control. 2012. Vol. 23. P. 727-35.

Colangelo L. A., Gapstur S. M., Gann P. H., Dyer A. R., Liu K. Colorectal cancer mortality and factors related to the insulin resistance syndrome // Cancer Epidemiol. Biomarkers Prev. 2002. Vol. 11. P. 385-91.

Schoen R. E., Tangen C. M., Kuller L. H., Burke G. L., Cushman M., Tracy R. P., Dobs A., Savage P. J. Increased blood glucose and insulin, body size, and incident colorectal cancer // J. Natl. Cancer Inst. 1999. Vol. 91. P. 1147-154.

Ma J., Giovannucci E., Pollak M., Leavitt A., Tao Y., Gaziano J. M., Stampfer M. J. A prospective study of plasma C-peptide and colorectal cancer risk in men // J. Natl. Cancer Inst. 2004. Vol. 96. P. 546-53.

Wei E. K., Ma J., Pollak M. N., Rifai N., Fuchs C. S., Hankinson S. E., Giovannucci E. C-peptide, insulinlike growth factor binding protein-1, glycosylated hemoglobin, and the risk of distal colorectal adenoma in women // Cancer Epidemiol. Biomarkers Prev. 2006. Vol. 15. P. 750-55.

Jie You, Wen-Yue Liu, Gui-Qi Zhu, Ou-Chen Wang, Rui-Min Ma, Gui-Qian Huang, Ke-Qing Shi, GuiLong Guo, Martin Braddock, Ming-HuaZheng Metabolic syndrome contributes to an increased recurrence risk of non-metastatic colorectal cancer // Oncotarget. 2015. Vol. 6. No. 23. P. 19880-9890.

Shaposhnikov A. V., Riadinskaya L. A. Comorbidity among patients with colorectal cancer // ASCO Annual Meeting Proccedings. 2014. ID: e 14651.

Sandhu M. S., Dunger D. B., Giovannucci E. L. Insulin, insulinlike growth factor-I (IGF-I), IGF binding proteins, their biologic interactions, and colorectal cancer // J. Natl. Cancer Inst. 2002. Vol. 94. P. 972- 980.

Grimberg A., Cohen P. Role of insulin-like growth factors and their binding proteins in growth control and carcinogenesis // J. Cell Physiol. 2000. Vol. 183. P. 1-.

Warren R. S., Yuan H., Matli M. R., Ferrara N., Donner D. B. Induction of vascular endothelial growth factor by insulinlike growth factor 1 in colorectal carcinoma // J. Biol. Chem. 1996. Vol. 271. P. 29483- 29488.

Gionleme O., Diamantidis M. D., Katsaros M. G. Is diabetes a causal agent for colorectal cancer? Pathophysiological and molecular mechanisms // W. J. G. 2011. Vol. 17. No. 4. P. 444-48.

Pais R., Silaghi H., Silaghi A. C., Rusu M. L., Dumitrascu D. L. Metabolic syndrome and risk of subsequent colorectal cancer // W. J. G. 2009. Vol. 15. No. 41. P. 5141-148.

Jenkins P. J. Acromegaly and cancer // Horm. Res. 2004. Vol. 62. No. 1. P. 108-15.

Giovannucci E., Pollak M. N., Platz E. A., Willett W C., Stampfer M. J., Majeed N., Colditz G. A., Speizer F. E., Hankinson S. E. A prospective study of plasma insulinlike growth factor-1 and binding protein-3 and risk of colorectal neoplasia in women // Cancer Epidemiol. Biomarkers Prev. 2000. Vol. 9. P. 345-49.

Ma J., Pollak M. N., Giovannucci E., Chan J. M., Tao Y., Hennekens C. H., Stampfer M. J. Prospective study of colorectal cancer risk in men and plasma levels of insulinlike growth factor (IGF) -I and IGF-binding protein3 // J. Natl. Cancer Inst. 1999. Vol. 91. P. 620-25.

Williams A. C., Collard T. J. Increased p53-ependent apoptosis by the insulin-like growth factor binding protein IGFBP-3 in human colonic adenoma-derived cells // Cancer Res. 2000. Vol. 60. P. 22-7.

Barnard J. A., Beauchamp R. D., Coffey R. J., Moses H. L. Regulation of intestinal epithelial cell growth by transforming growth factor type beta // Proc. Natl. Acad. Sci. USA. 1989. Vol. 86. P. 1578-582.

Giovannucci E., Ascherio A., Rimm E. B., Colditz G. A., Stampfer M. J., Willett W. C. Physical activity, obesity, and risk for colon cancer and adenoma in men // Ann. Intern. Med. 1995. Vol. 122. P. 327-34.

Kaaks R., Toniolo P., Akhmedkhanov A., Lukanova A., Biessy C., Dechaud H., Rinaldi S., Zeleniuch-Jacquotte A., Shore R. E., Riboli E. Serum C-peptide, insulinlike growth factor (IGF) -I, IGF-binding proteins, and colorectal cancer risk in women // J. Natl. Cancer Inst. 2000. Vol. 92. P. 1592-600.

Cowey S., Hardy R. W. The metabolic syndrome: A high-risk state for cancer? // Am. J. Pathol. 2006. Vol. 169. P. 1505-522.

Calle E. E., Kaaks R. Overweight, Obesity and Cancer: Epidemiological Evidence and Prop Mechanisms // Nature Reviews Cancer. 2004. Vol. 4. No. 8. P. 579-91.

Rob C. M., van Kruijsdijk, van der Wall E., Visseren F. L. Obesity and Cancer: The Role of Dysfunctional Adipose Tissue // Cancer Epidemiol. Biomarkers Prev. 2009. Vol. 18. P. 2569-578.

Vona-Davis L., Howard-McNatt M., Rose D. P. Adiposity, type 2 diabetes and the metabolic syndrome in breast cancer // Obes. Rev. 2007. Vol. 8. P. 395-08.

Barb D., Williams C. J., Neuwirth A. K., Mantzoros C. S. Adiponectin in relation to malignancies: a review of existing basic research and clinical evidence // Am. J. Clin. Nutr. 2007. Vol. 86. P. S858-866.

Rose D. P., Komninou D., Stephenson G. D. Obesity, adipocytokines, and insulin resistance in breast cancer // Obes. Rev. 2004. Vol. 5. P. 153-65.

Wang Y., Lam K. S., Xu J. Y., Lu G., Xu L. Y., Cooper G. J., Xu A. Adiponectin inhibits cell proliferation by interacting with several growth factors in an oligomerizationdependent manner // J. Biol. Chem. 2005. Vol. 280. P. 18341-8347.

Goldstein B. J., Scalia R. Adiponectin: A novel adipokine linking adipocytes and vascular function // J. Clin. Endocrinol. Metab. 2004. Vol. 89. P. 2563- 2568.

Brakenhielm E., Veitonmaki N., Cao R., Kihara S., Matsuzawa Y., Zhivotovsky B., Funahashi T., Cao Y. Adiponectin-induced antiangiogenesis and antitumor activity involve caspasemediated endothelial cell apoptosis // Proc. Natl. Acad. Sci. USA. 2004. Vol. 101. P. 2476-481.

Ferroni P., Palmirotta R., Spila A., Martini F., Raparelli V., Fossile E., Mariotti S., Del Monte G., Buonomo O., Roselli M., Guadagni F. Prognostic significance of adiponectin levels in non-metastatic colorectal cancer // Anticancer Res. 2007. Vol. 27. P. 483-89.

Wei E. K., Giovannucci E., Fuchs C. S., Willett W. C., Mantzoros C. S. Low plasma adiponectin levels and risk of colorectal cancer in men: a prospective study // J. Natl. Cancer Inst. 2005. Vol. 97. P. 1688-694.

Kelesidis I., Kelesidis T., Mantzoros C. S. Adiponectin and Cancer: a systematic review // British Journal of Cancer. 2006. Vol. 94. P. 1221-225.

Slattery M. L., Wolff R. K., Herrick J., Caan B. J., Potter J. D. Leptin and leptin receptor genotypes and colon cancer: gene-gene and gene-lifestyle interactions // Int. J. Cancer. 2008. Vol. 122. P. 1611-617.

Stattin P., Lukanova A., Biessy C., Soderberg S., Palmqvist R., Kaaks R., Olsson T., Jellum E. Obesity and colon cancer: does leptin provide a link? // Int. J. Cancer. 2004. Vol. 109. P. 149-52.

Chia V. M., Newcomb P. A., Lampe J. W., White E., Mandelson M. T., McTiernan A., Potter J. D. Leptin concentrations, leptin receptor polymorphisms, and colorectal adenoma risk // Cancer Epidemiol. Biomarkers Prev. 2007. Vol. 16. P. 2697-703.

Tamakoshi K., Toyoshima H., Wakai K., Kojima M., Suzuki K. et al. Leptin is associated with an increased female colorectal cancer risk: a nested case-control study in Japan // Oncology. 2005. Vol. 68. P. 454-61.

Park J. H. Y., Kang Y.-., Sung M. K., Kwon D. Y., Yang Y. Diet-Indused Obesity, Inflammation and Cancer // J. Food Drug Analysis. 2012. Vol. 20. No. 1. P. 237-40.

Cowey S., Hardy R. W. The metabolic syndrome. A high-risk state for cancer? // Am. J. Pathol. 2006. V. 169. No. 5. P. 1505-522.

Chung Y. C., Chang Y. F. Serum interleukin-6 levels reflect the disease status of colorectal cancer // J. Surg. Oncol. 2003. Vol. 83. P. 222-26.

Sonnenberg G. E, Krakower G. R., Kissebah A. H. A novel тpathway to the manifestations of metabolic syndrome // Obes. Res. 2004. Vol. 12. P. 180-86.

Valko M., Izakovic M., Mazur M., Rhodes C. J., Telser J. Role of oxygen radicals in DNA damage and cancer incidence // Mol. Cell Biochem. 2004. Vol. 266. P. 37-6.

Nikiteas N. I., Tzanakis N., Gazouli M., Rallis G., Daniilidis K., Theodoropoulos G., Kostakis A., Peros G. Serum IL-6, TNFalpha and CRP levels in Greek colorectal cancer patients: prognostic implications // World J. Gastroenterol. 2005. Vol. 11. P. 1639-643.

Fajas L., Debril M. B., Auwerx J. Peroxisome proliferatoractivated receptor-gamma: from adipogenesis to carcinogenesis // J. Mol. Endocrinol. 2001. Vol. 27. P. 1-.

Theocharis S., Giaginis C., Parasi A., Margeli A., Kakisis J., Agapitos E., Kouraklis G. Expression of peroxisome proliferator-activated receptor-gamma in colon cancer: correlation with histopathological parameters, cell cyclerelated molecules, and patients survival // Dig. Dis. Sci. 2007. Vol. 52. P. 2305-311.

Shen D., Deng C., Zhang M. Peroxisome proliferatoractivated receptor gamma agonists inhibit the proliferation and invasion of human colon cancer cells // Postgrad Med. J. 2007. Vol. 83. P. 414-19.

Arcidiacono B. et al. Insulin Resistance and Cancer Risk: An Overview of the Pathogenic Mechanisms // ExperimentalDiabetesResearch. 2012. ID 789174.

The authors declare that there are no conflicts of interest present.