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Новые возможности в лечении EGFR-позитивных больных немелкоклеточным раком легкого после прогрессирования на ингибиторах тирозинкиназ EGFR I–II поколений
Новые возможности в лечении EGFR-позитивных больных немелкоклеточным раком легкого после прогрессирования на ингибиторах тирозинкиназ EGFR I–II поколений
Лактионов К.К., Реутова Е.В., Нелюбина Л.А. и др. Новые возможности в лечении EGFR-позитивных больных немелкоклеточным раком легкого после прогрессирования на ингибиторах тирозинкиназ EGFR I–II поколений. Современная Онкология. 2018; 20 (2): 50–54. DOI: 10.26442/1815-1434_2018.2.50-54
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Аннотация
Таргетная терапия открыла новую эру в лекарственном лечении больных немелкоклеточным раком легкого с активирующими мутациями в гене рецептора эпидермального фактора роста (EGFR). Однако у большинства пациентов спустя 10–12 мес после начала таргетной терапии наступает прогрессирование болезни. Известны основные механизмы приобретенной резистентности, более чем в половине случаев это вторичная мутация в экзоне 20 гена EGFR. Для ее определения необходимо повторное молекулярно-генетическое тестирование, что в свою очередь требует выполнения ребиопсии. Жидкостная биопсия рассматривается как альтернатива ребиопсии.
Осимертиниб – представитель III поколения ингибиторов тирозинкиназ EGFR, обладает противоопухолевой активностью как в отношении Т790М-позитивных, так и опухолей с активирующими мутациями в экзонах 18, 19 и 21. В рандомизированном исследовании AURA3 применение осимертиниба было эффективно у 71% больных, с медианой времени до прогрессирования 11 мес после прогрессирования на таргетной терапии 1-й линии, что оказалось достоверно выше, чем в случае применения химиотерапии. Больные с метастазами в головной мозг также отвечают на лечение осимертинибом.
В нашем исследовании 29 больных получили осимертиниб после прогрессирования на таргетной терапии ингибиторов тирозинкиназ I–II поколений. Объективный эффект составил 44,8% (полный эффект – 3,4%), стабилизация – 51,7%, прогрессирование – 3,5%. В ближайшем будущем будут представлены данные по времени без прогрессирования. Переносимость лечения хорошая. Осимертиниб зарегистрирован в Российской Федерации для лечения больных с мутацией Т790М после прогрессирования на 1-й линии таргетной терапии, таким образом у нас появились новые возможности для улучшения результатов лечения этой группы пациентов.
Ключевые слова: немелкоклеточный рак легкого, ингибиторы тирозинкиназ EGFR, осимертиниб, приобретенная резистентность, мутация Т790М.
Osimertinib is a third generation EGFR-tyrosine kinase inhibitor, possessing antitumor activity, both, in respect of T790M-positive tumors and of tumors with mutations in exons 18, 19 and 21. In the randomized AURA3 trial, the use of osimertinib was effective in 71% of patients, the median progression free survival was 11 months after the progression on1st-line targeted therapy and was statistically significant than in case of chemotherapy application. Patients with brain metastases also show response to osimertinib treatment.
In our study, 29 patients received osimertinib after the progression on targeted therapy of the 1st and 2nd generation tyrosine kinase inhibitors. Objective response was reported in 44.8% (complete response – 3.4%), stabilization – 51.7% and progression – 3.5%. We will show the results concerning the time without progression in the near future. The tolerance of treatment is good. Osimertinib has been approved for 1st-line targeted therapy treatment of patients with the T790M mutation upon progression in Russian Federation, thus we have new opportunities to improve the results of the treatment in this group of patients.
Key words: non-small-cell lung cancer, EGFR tyrosine kinase inhibitors, osimertinib, acquired resistance, the T790M mutation.
Осимертиниб – представитель III поколения ингибиторов тирозинкиназ EGFR, обладает противоопухолевой активностью как в отношении Т790М-позитивных, так и опухолей с активирующими мутациями в экзонах 18, 19 и 21. В рандомизированном исследовании AURA3 применение осимертиниба было эффективно у 71% больных, с медианой времени до прогрессирования 11 мес после прогрессирования на таргетной терапии 1-й линии, что оказалось достоверно выше, чем в случае применения химиотерапии. Больные с метастазами в головной мозг также отвечают на лечение осимертинибом.
В нашем исследовании 29 больных получили осимертиниб после прогрессирования на таргетной терапии ингибиторов тирозинкиназ I–II поколений. Объективный эффект составил 44,8% (полный эффект – 3,4%), стабилизация – 51,7%, прогрессирование – 3,5%. В ближайшем будущем будут представлены данные по времени без прогрессирования. Переносимость лечения хорошая. Осимертиниб зарегистрирован в Российской Федерации для лечения больных с мутацией Т790М после прогрессирования на 1-й линии таргетной терапии, таким образом у нас появились новые возможности для улучшения результатов лечения этой группы пациентов.
Ключевые слова: немелкоклеточный рак легкого, ингибиторы тирозинкиназ EGFR, осимертиниб, приобретенная резистентность, мутация Т790М.
________________________________________________
Osimertinib is a third generation EGFR-tyrosine kinase inhibitor, possessing antitumor activity, both, in respect of T790M-positive tumors and of tumors with mutations in exons 18, 19 and 21. In the randomized AURA3 trial, the use of osimertinib was effective in 71% of patients, the median progression free survival was 11 months after the progression on1st-line targeted therapy and was statistically significant than in case of chemotherapy application. Patients with brain metastases also show response to osimertinib treatment.
In our study, 29 patients received osimertinib after the progression on targeted therapy of the 1st and 2nd generation tyrosine kinase inhibitors. Objective response was reported in 44.8% (complete response – 3.4%), stabilization – 51.7% and progression – 3.5%. We will show the results concerning the time without progression in the near future. The tolerance of treatment is good. Osimertinib has been approved for 1st-line targeted therapy treatment of patients with the T790M mutation upon progression in Russian Federation, thus we have new opportunities to improve the results of the treatment in this group of patients.
Key words: non-small-cell lung cancer, EGFR tyrosine kinase inhibitors, osimertinib, acquired resistance, the T790M mutation.
Полный текст
Список литературы
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12. Ward RA, Anderton MJ, Ashton S et al. Structure- and Reactivity-Based Development of Covalent Inhibitors of the Activating and Gatekeeper Mutant Forms of the Epidermal Growth Factor Receptor (EGFR). J Med Chem 2013; 56: 7025–48. PubMed: 23930994
13. Chih-Hsin Yang J et al. Osimertinib in Pretreated T790M-Positive Advanced Non–Small-Cell Lung Cancer: AURA Study Phase II Extension Component. J Clin Oncol 2017; 35 (12): 1288-96.
14. Goss G, Tsai CM, Shepherd FA et al. Osimertinib for pretreated EGFR Thr790Met-positive advanced non-small-cell lung cancer (AURA2): a multicentre, open-label, single-arm, phase 2 study. Lancet Oncol 2016; 17 (12): 1643–52. DOI: 10.1016/S1470-2045(16)30508-3. Epub 2016 Oct 14.
15. Mok TS, Yi-Long Wu et al. Osimertinib or Platinum–Pemetrexed in EGFR T790M–Positive Lung Cancer. N Engl J Med 2017; 376: 629–40. DOI: 10.1056/NEJMoa1612674
16. Oxnard GR, Thress KS, Alden RS et al. Association Between Plasma Genotyping and Outcomes of Treatment With Osimertinib (AZD9291) in Advanced Non–Small-Cell Lung Cancer. J Clin Oncol 2016; 34 (jco.ascopubs.org on June 29, 2016)
17. Douillard JY, Ostoros G, Cobo M et al. Gefitinib treatment in EGFR mutated caucasian NSCLC: circulating-free tumor DNA as a surrogate for determination of EGFR status. J Thorac Oncol 2014; 9: 1345–53.
18. Mok T, Wu YL, Lee JS et al. Detection of EGFR-activating mutations from plasma DNA as a potent predictor of survival outcomes in FASTACT 2: a randomized phase III study on intercalated combination of erlotinib (E) and chemotherapy (C). J Thorac Oncol 2013; 31. (Suppl: Abstract 8021).
19. Punnoose EA, Atwal S, Liu W, Raja R et al. Evaluation of circulating tumor cells and circulating tumor DNA in non-small cell lung cancer: association with clinical endpoints in a phase II clinical trialof pertuzumab and erlotinib. Clin Cancer Res 2012; 18: 2391–401.
20. Sun JM, Karlovich C, Wen W et al. Serial monitoring of EGFR mutations in plasma and evaluation of EGFR mutation status in matched tissue and plasma from NSCLC patients treated with CO-1686, Mol. Cancer Ther 2013; 12 (Suppl Abstract B25).
2. Maemondo M, Inoue A, Kobayashi K et al. Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR. N Engl J Med 2010; 362 (25): 2380–88.
3. Rosell R, Carcereny E, Gervais R et al. Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial. Lancet Oncol 2012; 13 (3): 239–46.
4. Miller VA, Hirsh V, Cadranel J et al. Afatinib versus placebo for patients with advanced, metastatic non-small-cell lung cancer after failure of erlotinib, gefitinib, or both, and one or two lines of chemotherapy (LUX- Lung 1): a phase 2B/3 randomised trial. Lancet Oncol 2012; 13 (5): 528–38.
5. Arcila ME, Oxnard GR, Nafa K, Riely GJ et al. Rebiopsy of lung cancer patients with acquired resistance to EGFR inhibitors and enhanced detection of the T790M mutation using a locked nucleic acid- based assay. Clin Cancer Res 2011; 17: 1169–80.
6. Kobayashi S, Boggon TJ, Dayaram T et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med 2005; 352: 786–92.
7. Pao W, Miller VA, Politi KA et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005; 2: e73.
8. Yu HA, Arcila ME, Rekhtman N et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers. Clin Cancer Res 2013; 19: 2240–7.
9. Bean J, Brennan C, Shih JY et al. MET amplifica-tion occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A 2007; 104: 20932.
10. Sequist LV, Waltman BA, Dias-Santagata D et al. Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors. Sci Transl Med 2011; 3, 75ra26.
11. Ross Camidge D, Pao W, Lecia V. Sequist Acquired resistance to TKIs in solid tumours: learning from lung cancer. Nat Rev Clin Oncol 2014; 11: 473–81.
12. Ward RA, Anderton MJ, Ashton S et al. Structure- and Reactivity-Based Development of Covalent Inhibitors of the Activating and Gatekeeper Mutant Forms of the Epidermal Growth Factor Receptor (EGFR). J Med Chem 2013; 56: 7025–48. PubMed: 23930994
13. Chih-Hsin Yang J et al. Osimertinib in Pretreated T790M-Positive Advanced Non–Small-Cell Lung Cancer: AURA Study Phase II Extension Component. J Clin Oncol 2017; 35 (12): 1288-96.
14. Goss G, Tsai CM, Shepherd FA et al. Osimertinib for pretreated EGFR Thr790Met-positive advanced non-small-cell lung cancer (AURA2): a multicentre, open-label, single-arm, phase 2 study. Lancet Oncol 2016; 17 (12): 1643–52. DOI: 10.1016/S1470-2045(16)30508-3. Epub 2016 Oct 14.
15. Mok TS, Yi-Long Wu et al. Osimertinib or Platinum–Pemetrexed in EGFR T790M–Positive Lung Cancer. N Engl J Med 2017; 376: 629–40. DOI: 10.1056/NEJMoa1612674
16. Oxnard GR, Thress KS, Alden RS et al. Association Between Plasma Genotyping and Outcomes of Treatment With Osimertinib (AZD9291) in Advanced Non–Small-Cell Lung Cancer. J Clin Oncol 2016; 34 (jco.ascopubs.org on June 29, 2016)
17. Douillard JY, Ostoros G, Cobo M et al. Gefitinib treatment in EGFR mutated caucasian NSCLC: circulating-free tumor DNA as a surrogate for determination of EGFR status. J Thorac Oncol 2014; 9: 1345–53.
18. Mok T, Wu YL, Lee JS et al. Detection of EGFR-activating mutations from plasma DNA as a potent predictor of survival outcomes in FASTACT 2: a randomized phase III study on intercalated combination of erlotinib (E) and chemotherapy (C). J Thorac Oncol 2013; 31. (Suppl: Abstract 8021).
19. Punnoose EA, Atwal S, Liu W, Raja R et al. Evaluation of circulating tumor cells and circulating tumor DNA in non-small cell lung cancer: association with clinical endpoints in a phase II clinical trialof pertuzumab and erlotinib. Clin Cancer Res 2012; 18: 2391–401.
20. Sun JM, Karlovich C, Wen W et al. Serial monitoring of EGFR mutations in plasma and evaluation of EGFR mutation status in matched tissue and plasma from NSCLC patients treated with CO-1686, Mol. Cancer Ther 2013; 12 (Suppl Abstract B25).
2. Maemondo M, Inoue A, Kobayashi K et al. Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR. N Engl J Med 2010; 362 (25): 2380–88.
3. Rosell R, Carcereny E, Gervais R et al. Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial. Lancet Oncol 2012; 13 (3): 239–46.
4. Miller VA, Hirsh V, Cadranel J et al. Afatinib versus placebo for patients with advanced, metastatic non-small-cell lung cancer after failure of erlotinib, gefitinib, or both, and one or two lines of chemotherapy (LUX- Lung 1): a phase 2B/3 randomised trial. Lancet Oncol 2012; 13 (5): 528–38.
5. Arcila ME, Oxnard GR, Nafa K, Riely GJ et al. Rebiopsy of lung cancer patients with acquired resistance to EGFR inhibitors and enhanced detection of the T790M mutation using a locked nucleic acid- based assay. Clin Cancer Res 2011; 17: 1169–80.
6. Kobayashi S, Boggon TJ, Dayaram T et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med 2005; 352: 786–92.
7. Pao W, Miller VA, Politi KA et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005; 2: e73.
8. Yu HA, Arcila ME, Rekhtman N et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers. Clin Cancer Res 2013; 19: 2240–7.
9. Bean J, Brennan C, Shih JY et al. MET amplifica-tion occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A 2007; 104: 20932.
10. Sequist LV, Waltman BA, Dias-Santagata D et al. Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors. Sci Transl Med 2011; 3, 75ra26.
11. Ross Camidge D, Pao W, Lecia V. Sequist Acquired resistance to TKIs in solid tumours: learning from lung cancer. Nat Rev Clin Oncol 2014; 11: 473–81.
12. Ward RA, Anderton MJ, Ashton S et al. Structure- and Reactivity-Based Development of Covalent Inhibitors of the Activating and Gatekeeper Mutant Forms of the Epidermal Growth Factor Receptor (EGFR). J Med Chem 2013; 56: 7025–48. PubMed: 23930994
13. Chih-Hsin Yang J et al. Osimertinib in Pretreated T790M-Positive Advanced Non–Small-Cell Lung Cancer: AURA Study Phase II Extension Component. J Clin Oncol 2017; 35 (12): 1288-96.
14. Goss G, Tsai CM, Shepherd FA et al. Osimertinib for pretreated EGFR Thr790Met-positive advanced non-small-cell lung cancer (AURA2): a multicentre, open-label, single-arm, phase 2 study. Lancet Oncol 2016; 17 (12): 1643–52. DOI: 10.1016/S1470-2045(16)30508-3. Epub 2016 Oct 14.
15. Mok TS, Yi-Long Wu et al. Osimertinib or Platinum–Pemetrexed in EGFR T790M–Positive Lung Cancer. N Engl J Med 2017; 376: 629–40. DOI: 10.1056/NEJMoa1612674
16. Oxnard GR, Thress KS, Alden RS et al. Association Between Plasma Genotyping and Outcomes of Treatment With Osimertinib (AZD9291) in Advanced Non–Small-Cell Lung Cancer. J Clin Oncol 2016; 34 (jco.ascopubs.org on June 29, 2016)
17. Douillard JY, Ostoros G, Cobo M et al. Gefitinib treatment in EGFR mutated caucasian NSCLC: circulating-free tumor DNA as a surrogate for determination of EGFR status. J Thorac Oncol 2014; 9: 1345–53.
18. Mok T, Wu YL, Lee JS et al. Detection of EGFR-activating mutations from plasma DNA as a potent predictor of survival outcomes in FASTACT 2: a randomized phase III study on intercalated combination of erlotinib (E) and chemotherapy (C). J Thorac Oncol 2013; 31. (Suppl: Abstract 8021).
19. Punnoose EA, Atwal S, Liu W, Raja R et al. Evaluation of circulating tumor cells and circulating tumor DNA in non-small cell lung cancer: association with clinical endpoints in a phase II clinical trialof pertuzumab and erlotinib. Clin Cancer Res 2012; 18: 2391–401.
20. Sun JM, Karlovich C, Wen W et al. Serial monitoring of EGFR mutations in plasma and evaluation of EGFR mutation status in matched tissue and plasma from NSCLC patients treated with CO-1686, Mol. Cancer Ther 2013; 12 (Suppl Abstract B25).
________________________________________________
2. Maemondo M, Inoue A, Kobayashi K et al. Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR. N Engl J Med 2010; 362 (25): 2380–88.
3. Rosell R, Carcereny E, Gervais R et al. Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial. Lancet Oncol 2012; 13 (3): 239–46.
4. Miller VA, Hirsh V, Cadranel J et al. Afatinib versus placebo for patients with advanced, metastatic non-small-cell lung cancer after failure of erlotinib, gefitinib, or both, and one or two lines of chemotherapy (LUX- Lung 1): a phase 2B/3 randomised trial. Lancet Oncol 2012; 13 (5): 528–38.
5. Arcila ME, Oxnard GR, Nafa K, Riely GJ et al. Rebiopsy of lung cancer patients with acquired resistance to EGFR inhibitors and enhanced detection of the T790M mutation using a locked nucleic acid- based assay. Clin Cancer Res 2011; 17: 1169–80.
6. Kobayashi S, Boggon TJ, Dayaram T et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med 2005; 352: 786–92.
7. Pao W, Miller VA, Politi KA et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005; 2: e73.
8. Yu HA, Arcila ME, Rekhtman N et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers. Clin Cancer Res 2013; 19: 2240–7.
9. Bean J, Brennan C, Shih JY et al. MET amplifica-tion occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A 2007; 104: 20932.
10. Sequist LV, Waltman BA, Dias-Santagata D et al. Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors. Sci Transl Med 2011; 3, 75ra26.
11. Ross Camidge D, Pao W, Lecia V. Sequist Acquired resistance to TKIs in solid tumours: learning from lung cancer. Nat Rev Clin Oncol 2014; 11: 473–81.
12. Ward RA, Anderton MJ, Ashton S et al. Structure- and Reactivity-Based Development of Covalent Inhibitors of the Activating and Gatekeeper Mutant Forms of the Epidermal Growth Factor Receptor (EGFR). J Med Chem 2013; 56: 7025–48. PubMed: 23930994
13. Chih-Hsin Yang J et al. Osimertinib in Pretreated T790M-Positive Advanced Non–Small-Cell Lung Cancer: AURA Study Phase II Extension Component. J Clin Oncol 2017; 35 (12): 1288-96.
14. Goss G, Tsai CM, Shepherd FA et al. Osimertinib for pretreated EGFR Thr790Met-positive advanced non-small-cell lung cancer (AURA2): a multicentre, open-label, single-arm, phase 2 study. Lancet Oncol 2016; 17 (12): 1643–52. DOI: 10.1016/S1470-2045(16)30508-3. Epub 2016 Oct 14.
15. Mok TS, Yi-Long Wu et al. Osimertinib or Platinum–Pemetrexed in EGFR T790M–Positive Lung Cancer. N Engl J Med 2017; 376: 629–40. DOI: 10.1056/NEJMoa1612674
16. Oxnard GR, Thress KS, Alden RS et al. Association Between Plasma Genotyping and Outcomes of Treatment With Osimertinib (AZD9291) in Advanced Non–Small-Cell Lung Cancer. J Clin Oncol 2016; 34 (jco.ascopubs.org on June 29, 2016)
17. Douillard JY, Ostoros G, Cobo M et al. Gefitinib treatment in EGFR mutated caucasian NSCLC: circulating-free tumor DNA as a surrogate for determination of EGFR status. J Thorac Oncol 2014; 9: 1345–53.
18. Mok T, Wu YL, Lee JS et al. Detection of EGFR-activating mutations from plasma DNA as a potent predictor of survival outcomes in FASTACT 2: a randomized phase III study on intercalated combination of erlotinib (E) and chemotherapy (C). J Thorac Oncol 2013; 31. (Suppl: Abstract 8021).
19. Punnoose EA, Atwal S, Liu W, Raja R et al. Evaluation of circulating tumor cells and circulating tumor DNA in non-small cell lung cancer: association with clinical endpoints in a phase II clinical trialof pertuzumab and erlotinib. Clin Cancer Res 2012; 18: 2391–401.
20. Sun JM, Karlovich C, Wen W et al. Serial monitoring of EGFR mutations in plasma and evaluation of EGFR mutation status in matched tissue and plasma from NSCLC patients treated with CO-1686, Mol. Cancer Ther 2013; 12 (Suppl Abstract B25).
Авторы
К.К.Лактионов1, Е.В.Реутова*1, Л.А.Нелюбина1, М.Ю.Питкевич1, М.А.Окружнова1, М.С.Ардзинба1, Д.И.Юдин1, И.А.Демидова2, А.Р.Зарецкий3,4
1 ФГБУ «Национальный медицинский исследовательский центр онкологии им. Н.Н.Блохина» Минздрава России. 115478, Россия, Москва, Каширское ш., д. 23;
2 ГБУЗ «Московская городская онкологическая больница №62» Департамента здравоохранения Москвы. 143423, Россия, Московская обл., Красногорский район, пос. Истра, д. 27, стр. 1–26;
3 ФГБУН «Институт биоорганической химии им. акад. М.М.Шемякина и Ю.А.Овчинникова» РАН. 117997, Россия, Москва, ГСП-7, ул. Миклухо-Маклая, д. 16/10;
4 ООО «Евроген Лаб».117997, Россия, Москва, ГСП-7, ул. Миклухо-Маклая, д. 16/10, корп. 15
*marenich.al@yandex.ru
1 N.N.Blokhin National Medical Research Center of Oncology of the Ministry of Health of the Russian Federation. 115478, Russian Federation, Moscow, Kashirskoe sh., d. 23;
2 Moscow City Oncological Hospital No.62. Department of Health of Moscow. 143423, Russian Federation, Moskovskaia obl., Krasnogorskii raion, pos. Istra, d. 27, str. 1–26;
3 Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, RAS. 117997, Russian Federation, Moscow, GSP-7, ul. Miklukho-Maklaia, d.16/10;
4 Eurogen Lab. 117997, Russian Federation, Moscow, GSP-7, ul. Miklukho-Maklaia, d. 16/10, korp. 15;
*marenich.al@yandex.ru
1 ФГБУ «Национальный медицинский исследовательский центр онкологии им. Н.Н.Блохина» Минздрава России. 115478, Россия, Москва, Каширское ш., д. 23;
2 ГБУЗ «Московская городская онкологическая больница №62» Департамента здравоохранения Москвы. 143423, Россия, Московская обл., Красногорский район, пос. Истра, д. 27, стр. 1–26;
3 ФГБУН «Институт биоорганической химии им. акад. М.М.Шемякина и Ю.А.Овчинникова» РАН. 117997, Россия, Москва, ГСП-7, ул. Миклухо-Маклая, д. 16/10;
4 ООО «Евроген Лаб».117997, Россия, Москва, ГСП-7, ул. Миклухо-Маклая, д. 16/10, корп. 15
*marenich.al@yandex.ru
________________________________________________
1 N.N.Blokhin National Medical Research Center of Oncology of the Ministry of Health of the Russian Federation. 115478, Russian Federation, Moscow, Kashirskoe sh., d. 23;
2 Moscow City Oncological Hospital No.62. Department of Health of Moscow. 143423, Russian Federation, Moskovskaia obl., Krasnogorskii raion, pos. Istra, d. 27, str. 1–26;
3 Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, RAS. 117997, Russian Federation, Moscow, GSP-7, ul. Miklukho-Maklaia, d.16/10;
4 Eurogen Lab. 117997, Russian Federation, Moscow, GSP-7, ul. Miklukho-Maklaia, d. 16/10, korp. 15;
*marenich.al@yandex.ru
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