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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Cancer Urology</journal-id><journal-title-group><journal-title xml:lang="en">Cancer Urology</journal-title><trans-title-group xml:lang="ru"><trans-title>Онкоурология</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1726-9776</issn><issn publication-format="electronic">1996-1812</issn><publisher><publisher-name xml:lang="en">Publishing House ABV Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">579</article-id><article-id pub-id-type="doi">10.17650/1726-9776-2016-12-2-80-83</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>PROSTATE CANCER</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>РАК ПРЕДСТАТЕЛЬНОЙ ЖЕЛЕЗЫ</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">Gene BRCA1/2 mutation in prostate cancer patients: clinical administration aspects</article-title><trans-title-group xml:lang="ru"><trans-title>Мутации генов BRCA1/2 при раке предстательной железы. Имеются ли перспективы для их клинического применения?</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Koposov</surname><given-names>P. V.</given-names></name><name xml:lang="ru"><surname>Копосов</surname><given-names>П. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>pkoposov@emcmos.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">European Medical Center</institution></aff><aff><institution xml:lang="ru">Европейский медицинский центр</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">35 Shchepkina St., Moscow, 129090, Russia</institution></aff><aff><institution xml:lang="ru">Россия, 129090, Москва, ул. Щепкина, 35</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2016-06-30" publication-format="electronic"><day>30</day><month>06</month><year>2016</year></pub-date><volume>12</volume><issue>2</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>80</fpage><lpage>83</lpage><history><date date-type="received" iso-8601-date="2016-06-24"><day>24</day><month>06</month><year>2016</year></date><date date-type="accepted" iso-8601-date="2016-06-24"><day>24</day><month>06</month><year>2016</year></date></history><permissions><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://oncourology.abvpress.ru/oncur/article/view/579">https://oncourology.abvpress.ru/oncur/article/view/579</self-uri><abstract xml:lang="en"><p>The cases of the uncommon malignant disease state can take place in patients with the prostate cancer. This disease may appear at a young age and the level of the PSA may be normal (to 4 ng / ml), and also the negative clinical prognosis, due to the resistance to standard medical treatment, can take place. In the literature review there is a data on patients’ carrier status of gene BRCA1 / 2 mutation. There are 2 % of such patients and the program of the target screening of the prostate cancer and the special treatment regimen for them should be developed. According to the mechanism of action of the platinum-based drugs and the data from the studies on treatment of the BRCA1 / 2-dependent ovarian cancer in women, where the high sensitivity to the platinum-based drugs in patients with the mutations of the reparation genes of the deoxyribonucleic acid by the homologous recombination was validated, we supposed, that the defects of the deoxyribonucleic acid reparation in patients with the metastatic castration-resistant prostate cancer also might be highly sensitive to the platinum-based drugs.</p></abstract><trans-abstract xml:lang="ru"><p>У пациентов, страдающих раком предстательной железы, выявляют случаи необычного злокачественного течения заболевания. Возникнув в молодом возрасте, это заболевание может сочетаться с нормальными (до 4 нг / мл) значениями простатического специфического антигена, а также иметь плохой клинический прогноз, характеризующийся резистентностью к проводимому стандартному лечению. В обзоре литературы приведены данные по выделению из общей популяции тех пациентов, которые имеют носительство мутаций генов BRCA1 / 2. Доля таких больных составляет 2 %, для них необходимы проведение программ прицельного скрининга рака предстательной железы и разработка специальных схем лечения. Рассматривая механизм действия препаратов платины и данные, полученные из исследований по лечению BRCA1 / 2-зависимого рака яичников у женщин, согласно которым наблюдается высокая чувствительность к препаратам платины у пациенток с мутациями генов репарации дезоксирибонуклеиновой кислоты путем гомологичной рекомбинации, можно предположить, что дефекты репарации дезоксирибонуклеиновой кислоты при метастатическом кастрационно-резистентном раке предстательной железы также могут быть высокочувствительны к препаратам платины.</p></trans-abstract><kwd-group xml:lang="en"><kwd>prostate cancer</kwd><kwd>castration resistance</kwd><kwd>gene BRCA1/2 mutation</kwd><kwd>cisplatin</kwd><kwd>public health organization</kwd><kwd>olaparib</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>рак предстательной железы</kwd><kwd>кастрационная резистентность</kwd><kwd>мутации генов BRCA1 / 2</kwd><kwd>цисплатин</kwd><kwd>организация здравоохранени</kwd><kwd>олапариб</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><citation-alternatives><mixed-citation xml:lang="en">1. Hellerstedt B.A., Pienta K.J. The current state of hormonal therapy for prostate cancer. CA Cancer J Clin 2002;52(3):154–79.</mixed-citation><mixed-citation xml:lang="ru">Hellerstedt B.A., Pienta K.J. The current state of hormonal therapy for prostate cancer. CA Cancer J Clin 2002;52(3):154–79.</mixed-citation></citation-alternatives></ref><ref id="B2"><label>2.</label><citation-alternatives><mixed-citation xml:lang="en">2. Baca S.C., Prandi D., Lawrence M.S. et al. Punctuated evolution of prostate cancer genomes. Cell 2013;153(3):666–77.</mixed-citation><mixed-citation xml:lang="ru">Baca S.C., Prandi D., Lawrence M.S. et al. Punctuated evolution of prostate cancer genomes. Cell 2013;153(3):666–77.</mixed-citation></citation-alternatives></ref><ref id="B3"><label>3.</label><citation-alternatives><mixed-citation xml:lang="en">3. Grasso C.S., Wu Y.M., Robinson D.R. et al. The mutational landscape of lethal castration-resistant prostate cancer. Nature 2012;487(7406):239–43.</mixed-citation><mixed-citation xml:lang="ru">Grasso C.S., Wu Y.M., Robinson D.R. et al. The mutational landscape of lethal castration-resistant prostate cancer. Nature 2012;487(7406):239–43.</mixed-citation></citation-alternatives></ref><ref id="B4"><label>4.</label><citation-alternatives><mixed-citation xml:lang="en">4. de Bono J.S., Ashworth A. Translating cancer research into targeted therapeutics. Nature 2010;467(7315):543–9.</mixed-citation><mixed-citation xml:lang="ru">de Bono J.S., Ashworth A. Translating cancer research into targeted therapeutics. Nature 2010;467(7315):543–9.</mixed-citation></citation-alternatives></ref><ref id="B5"><label>5.</label><citation-alternatives><mixed-citation xml:lang="en">5. Beltran H., Yelensky R., Frampton G.M. et al. Targeted next-generation sequencing of advanced prostate cancer identifies potential therapeutic targets and disease heterogeneity. Eur Urol 2013;63(5): 920–6.</mixed-citation><mixed-citation xml:lang="ru">Beltran H., Yelensky R., Frampton G.M. et al. Targeted next-generation sequencing of advanced prostate cancer identifies potential therapeutic targets and disease heterogeneity. Eur Urol 2013;63(5): 920–6.</mixed-citation></citation-alternatives></ref><ref id="B6"><label>6.</label><citation-alternatives><mixed-citation xml:lang="en">6. Farmer H., McCabe N., Lord C.J. et al. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature 2005;434(7035):917–21.</mixed-citation><mixed-citation xml:lang="ru">Farmer H., McCabe N., Lord C.J. et al. Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy. Nature 2005;434(7035):917–21.</mixed-citation></citation-alternatives></ref><ref id="B7"><label>7.</label><citation-alternatives><mixed-citation xml:lang="en">7. Bryant H.E., Schultz N., Thomas H.D. et al. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADPribose) polymerase. Nature 2005;434(7035):913–7.</mixed-citation><mixed-citation xml:lang="ru">Bryant H.E., Schultz N., Thomas H.D. et al. Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADPribose) polymerase. Nature 2005;434(7035):913–7.</mixed-citation></citation-alternatives></ref><ref id="B8"><label>8.</label><citation-alternatives><mixed-citation xml:lang="en">8. Fong P.C., Boss D.S., Yap T.A. et al. Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. N Engl J Med 2009;361(2):123–34.</mixed-citation><mixed-citation xml:lang="ru">Fong P.C., Boss D.S., Yap T.A. et al. Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. N Engl J Med 2009;361(2):123–34.</mixed-citation></citation-alternatives></ref><ref id="B9"><label>9.</label><citation-alternatives><mixed-citation xml:lang="en">9. Kaufman B., Shapira-Frommer R., Schmutzler R.K. et al. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation.J Clin Oncol 2015;33(3):244–50.</mixed-citation><mixed-citation xml:lang="ru">Kaufman B., Shapira-Frommer R., Schmutzler R.K. et al. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation.J Clin Oncol 2015;33(3):244–50.</mixed-citation></citation-alternatives></ref><ref id="B10"><label>10.</label><citation-alternatives><mixed-citation xml:lang="en">10. Ledermann J., Harter P., Gourley C. et al. Olaparib maintenance therapy in platinumsensitive relapsed ovarian cancer. N Engl J Med 2012;366(15):1382–92.</mixed-citation><mixed-citation xml:lang="ru">Ledermann J., Harter P., Gourley C. et al. Olaparib maintenance therapy in platinumsensitive relapsed ovarian cancer. N Engl J Med 2012;366(15):1382–92.</mixed-citation></citation-alternatives></ref><ref id="B11"><label>11.</label><citation-alternatives><mixed-citation xml:lang="en">11. Ledermann J., Harter P., Gourley C. Olaparib maintenance therapy in patients with platinum-sensitive relapsed serous ovarian cancer: a preplanned retrospective analysis of outcomes by BRCA status in a randomised phase 2 trial. Lancet Oncol 2014;15:856.</mixed-citation><mixed-citation xml:lang="ru">Ledermann J., Harter P., Gourley C. Olaparib maintenance therapy in patients with platinum-sensitive relapsed serous ovarian cancer: a preplanned retrospective analysis of outcomes by BRCA status in a randomised phase 2 trial. Lancet Oncol 2014;15:856.</mixed-citation></citation-alternatives></ref><ref id="B12"><label>12.</label><citation-alternatives><mixed-citation xml:lang="en">12. Mateo J., Carreira S., Sandhu S. et al. DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer. N Engl J Med 2015;373(18):167–708.</mixed-citation><mixed-citation xml:lang="ru">Mateo J., Carreira S., Sandhu S. et al. DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer. N Engl J Med 2015;373(18):167–708.</mixed-citation></citation-alternatives></ref><ref id="B13"><label>13.</label><citation-alternatives><mixed-citation xml:lang="en">13. Castro E., Goh C., Olmos D. et al. Germline BRCA mutations are associated with higher risk of nodal involvement, distant metastasis, and poor survival outcomes in prostate cancer. J Clin Oncol 2013;31(14):1748–57.</mixed-citation><mixed-citation xml:lang="ru">Castro E., Goh C., Olmos D. et al. Germline BRCA mutations are associated with higher risk of nodal involvement, distant metastasis, and poor survival outcomes in prostate cancer. J Clin Oncol 2013;31(14):1748–57.</mixed-citation></citation-alternatives></ref><ref id="B14"><label>14.</label><citation-alternatives><mixed-citation xml:lang="en">14. Castro E., Goh C., Leongamornlert D. et al. Effect of BRCA mutations on metastatic relapse and cause-specific survival after radical treatment for localised prostate cancer. Eur Urol 2015;68(2):186–93.</mixed-citation><mixed-citation xml:lang="ru">Castro E., Goh C., Leongamornlert D. et al. Effect of BRCA mutations on metastatic relapse and cause-specific survival after radical treatment for localised prostate cancer. Eur Urol 2015;68(2):186–93.</mixed-citation></citation-alternatives></ref><ref id="B15"><label>15.</label><citation-alternatives><mixed-citation xml:lang="en">15. Nelson H.D., Pappas M., Zakher B. et al. Risk assessment, genetic counseling, and genetic testing for BRCA-related cancer in women: a systematic review to update the U.S. Preventive Services Task Force recommendation. Ann Intern Med 2014;160(4):255–66.</mixed-citation><mixed-citation xml:lang="ru">Nelson H.D., Pappas M., Zakher B. et al. Risk assessment, genetic counseling, and genetic testing for BRCA-related cancer in women: a systematic review to update the U.S. Preventive Services Task Force recommendation. Ann Intern Med 2014;160(4):255–66.</mixed-citation></citation-alternatives></ref><ref id="B16"><label>16.</label><citation-alternatives><mixed-citation xml:lang="en">16. Alanee S.R., Glogowski E.A., Schrader K.A. et al. Clinical features and management of BRCA1 and BRCA2-associated prostate cancer. Front Biosci (Elite Ed) 2014;6:15–30.</mixed-citation><mixed-citation xml:lang="ru">Alanee S.R., Glogowski E.A., Schrader K.A. et al. Clinical features and management of BRCA1 and BRCA2-associated prostate cancer. Front Biosci (Elite Ed) 2014;6:15–30.</mixed-citation></citation-alternatives></ref><ref id="B17"><label>17.</label><citation-alternatives><mixed-citation xml:lang="en">17. Akbari M.R., Wallis C.J., Toi A. et al. The impact of a BRCA2 mutation on mortality from screen-detected prostate cancer. Br J Cancer 2014;111(6):1238–40.</mixed-citation><mixed-citation xml:lang="ru">Akbari M.R., Wallis C.J., Toi A. et al. The impact of a BRCA2 mutation on mortality from screen-detected prostate cancer. Br J Cancer 2014;111(6):1238–40.</mixed-citation></citation-alternatives></ref><ref id="B18"><label>18.</label><citation-alternatives><mixed-citation xml:lang="en">18. Bancroft E.K., Page E.C., Castro E. et al. Targeted prostate cancer screening in BRCA1 and BRCA2 mutation carriers: results from the initial screening round of the IMPACT study. Eur Urol 2014;66(3):489–99.</mixed-citation><mixed-citation xml:lang="ru">Bancroft E.K., Page E.C., Castro E. et al. Targeted prostate cancer screening in BRCA1 and BRCA2 mutation carriers: results from the initial screening round of the IMPACT study. Eur Urol 2014;66(3):489–99.</mixed-citation></citation-alternatives></ref><ref id="B19"><label>19.</label><citation-alternatives><mixed-citation xml:lang="en">19. Mikropoulos C., Castro E., Bancroft E. et al. Identification of men with a genetic predisposition to prostate cancer: targeted screening in men at higher genetic risk and controls. Program and abstracts of the 2014 Genitourinary Cancers Symposium; January 30 – February 1, 2014; San Francisco, California. Abstr. 8.</mixed-citation><mixed-citation xml:lang="ru">Mikropoulos C., Castro E., Bancroft E. et al. Identification of men with a genetic predisposition to prostate cancer: targeted screening in men at higher genetic risk and controls. Program and abstracts of the 2014 Genitourinary Cancers Symposium; January 30 – February 1, 2014; San Francisco, California. Abstr. 8.</mixed-citation></citation-alternatives></ref><ref id="B20"><label>20.</label><citation-alternatives><mixed-citation xml:lang="en">20. Leongamornlert D., Mahmud N., Tymrakiewicz M. et al. Germline BRCA1 mutations increase prostate cancer risk. Br J Cancer 2012;106(10):1697–701.</mixed-citation><mixed-citation xml:lang="ru">Leongamornlert D., Mahmud N., Tymrakiewicz M. et al. Germline BRCA1 mutations increase prostate cancer risk. Br J Cancer 2012;106(10):1697–701.</mixed-citation></citation-alternatives></ref><ref id="B21"><label>21.</label><citation-alternatives><mixed-citation xml:lang="en">21. Kaufman B., Shapira-Frommer R., Schmutzler R.K. et al. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation. J Clin Oncol 2015;33(3):244–50.</mixed-citation><mixed-citation xml:lang="ru">Kaufman B., Shapira-Frommer R., Schmutzler R.K. et al. Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation. J Clin Oncol 2015;33(3):244–50.</mixed-citation></citation-alternatives></ref><ref id="B22"><label>22.</label><citation-alternatives><mixed-citation xml:lang="en">22. Yang D., Khan S., Sun Y. et al. Association of BRCA1 and BRCA2 mutations with survival, chemotherapy sensitivity, and gene mutator phenotype in patients with ovarian cancer. JAMA 2011;306(14):1557–65.</mixed-citation><mixed-citation xml:lang="ru">Yang D., Khan S., Sun Y. et al. Association of BRCA1 and BRCA2 mutations with survival, chemotherapy sensitivity, and gene mutator phenotype in patients with ovarian cancer. JAMA 2011;306(14):1557–65.</mixed-citation></citation-alternatives></ref><ref id="B23"><label>23.</label><citation-alternatives><mixed-citation xml:lang="en">23. Robinson D., Van Allen E.M., Wu Y.M. et al. Integrative clinical genomics of advanced prostate cancer. Cell 2015;161(5):1215–28.</mixed-citation><mixed-citation xml:lang="ru">Robinson D., Van Allen E.M., Wu Y.M. et al. Integrative clinical genomics of advanced prostate cancer. Cell 2015;161(5):1215–28.</mixed-citation></citation-alternatives></ref><ref id="B24"><label>24.</label><citation-alternatives><mixed-citation xml:lang="en">24. McCabe N., Turner N.C., Lord C.J. et al. Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition. Cancer Res 2006;66(16):8109–15.</mixed-citation><mixed-citation xml:lang="ru">McCabe N., Turner N.C., Lord C.J. et al. Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition. Cancer Res 2006;66(16):8109–15.</mixed-citation></citation-alternatives></ref><ref id="B25"><label>25.</label><citation-alternatives><mixed-citation xml:lang="en">25. Murai J., Huang S.Y., Das B.B. et al. Trapping of PARP1 and PARP2 by clinical PARP inhibitors. Cancer Res 2012;72(2):5588–99.</mixed-citation><mixed-citation xml:lang="ru">Murai J., Huang S.Y., Das B.B. et al. Trapping of PARP1 and PARP2 by clinical PARP inhibitors. Cancer Res 2012;72(2):5588–99.</mixed-citation></citation-alternatives></ref><ref id="B26"><label>26.</label><citation-alternatives><mixed-citation xml:lang="en">26. Miller K.M., Tjeertes J.V., Coates J. et al. Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA nonhomologous end-joining. Nat Struct Mol Biol 2010;17(9):1144–51.</mixed-citation><mixed-citation xml:lang="ru">Miller K.M., Tjeertes J.V., Coates J. et al. Human HDAC1 and HDAC2 function in the DNA-damage response to promote DNA nonhomologous end-joining. Nat Struct Mol Biol 2010;17(9):1144–51.</mixed-citation></citation-alternatives></ref><ref id="B27"><label>27.</label><citation-alternatives><mixed-citation xml:lang="en">27. Chao O.S., Goodman O.B. Jr. Synergistic loss of prostate cancer cell viability by coinhibition of HDAC and PARP. Mol Cancer Res 2014;12(12):1755–66.</mixed-citation><mixed-citation xml:lang="ru">Chao O.S., Goodman O.B. Jr. Synergistic loss of prostate cancer cell viability by coinhibition of HDAC and PARP. Mol Cancer Res 2014;12(12):1755–66.</mixed-citation></citation-alternatives></ref><ref id="B28"><label>28.</label><citation-alternatives><mixed-citation xml:lang="en">28. Sternberg C.N., Petrylak D.P., Sartor O. et al. Multinational, double-blind, phase III study of prednisone and either satraplatin or placebo in patients with castrate refractory prostate cancer progressing after prior chemotherapy: the SPARC trial. J Clin Oncol 2009;27(32):5431–8.</mixed-citation><mixed-citation xml:lang="ru">Sternberg C.N., Petrylak D.P., Sartor O. et al. Multinational, double-blind, phase III study of prednisone and either satraplatin or placebo in patients with castrate refractory prostate cancer progressing after prior chemotherapy: the SPARC trial. J Clin Oncol 2009;27(32):5431–8.</mixed-citation></citation-alternatives></ref><ref id="B29"><label>29.</label><citation-alternatives><mixed-citation xml:lang="en">29. Fong P.C., Yap T.A., Boss D.S. et al. Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval. J Clin Oncol 2010;28(15):2512–9.</mixed-citation><mixed-citation xml:lang="ru">Fong P.C., Yap T.A., Boss D.S. et al. Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval. J Clin Oncol 2010;28(15):2512–9.</mixed-citation></citation-alternatives></ref><ref id="B30"><label>30.</label><citation-alternatives><mixed-citation xml:lang="en">30. Ceccaldi R., O’Connor K.W., Mouw K.W. et al. A unique subset of epithelial ovarian cancers with platinum sensitivity and PARP inhibitor resistance. Cancer Res 2015;75(4):628–34.</mixed-citation><mixed-citation xml:lang="ru">Ceccaldi R., O’Connor K.W., Mouw K.W. et al. A unique subset of epithelial ovarian cancers with platinum sensitivity and PARP inhibitor resistance. Cancer Res 2015;75(4):628–34.</mixed-citation></citation-alternatives></ref></ref-list></back></article>
