急性骨髄性白血病に対する分子標的治療薬
急性骨髄性白血病（acute myeloid leukemia：AML）の分子病態の解明により，種々の新規分子標的薬が開発されている．FLT3阻害薬やIDH1/2阻害薬のように特定のドライバー遺伝子変異に対する標的薬（actionable mutation）と，BCL2阻害薬やSMO阻害薬のように遺伝子変異に依存せず，広くAMLに共有される機能分子に対する阻害薬（broad approach），さらに抗体医薬（CD47抗体，TIM3抗体）も開発されている．詳細なマルチオミクス解析の導入により，新たな治療標的分子の同定と新規薬剤の開発が進められ，従来の予後分類に基づいた画一的な治療からAML個別...
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| Published in | 日本内科学会雑誌 Vol. 111; no. 6; pp. 1186 - 1192 |
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| Main Authors | , |
| Format | Journal Article |
| Language | Japanese |
| Published |
一般社団法人 日本内科学会
10.06.2022
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0021-5384 1883-2083 |
| DOI | 10.2169/naika.111.1186 |
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| Abstract | 急性骨髄性白血病（acute myeloid leukemia：AML）の分子病態の解明により，種々の新規分子標的薬が開発されている．FLT3阻害薬やIDH1/2阻害薬のように特定のドライバー遺伝子変異に対する標的薬（actionable mutation）と，BCL2阻害薬やSMO阻害薬のように遺伝子変異に依存せず，広くAMLに共有される機能分子に対する阻害薬（broad approach），さらに抗体医薬（CD47抗体，TIM3抗体）も開発されている．詳細なマルチオミクス解析の導入により，新たな治療標的分子の同定と新規薬剤の開発が進められ，従来の予後分類に基づいた画一的な治療からAML個別化医療の展開が期待される． |
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| AbstractList | 急性骨髄性白血病（acute myeloid leukemia：AML）の分子病態の解明により，種々の新規分子標的薬が開発されている．FLT3阻害薬やIDH1/2阻害薬のように特定のドライバー遺伝子変異に対する標的薬（actionable mutation）と，BCL2阻害薬やSMO阻害薬のように遺伝子変異に依存せず，広くAMLに共有される機能分子に対する阻害薬（broad approach），さらに抗体医薬（CD47抗体，TIM3抗体）も開発されている．詳細なマルチオミクス解析の導入により，新たな治療標的分子の同定と新規薬剤の開発が進められ，従来の予後分類に基づいた画一的な治療からAML個別化医療の展開が期待される． |
| Author | 宮本, 敏浩 菊繁, 吉謙 |
| Author_xml | – sequence: 1 fullname: 宮本, 敏浩 organization: 金沢大学医薬保健研究域医学系・血液内科学 – sequence: 1 fullname: 菊繁, 吉謙 organization: 九州大学病院・遺伝子・細胞療法部 |
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| Copyright | 2022 一般社団法人 日本内科学会 |
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| References | 12) Wei AH, et al: Venetoclax plus LDAC for newly diagnosed AML ineligible for intensive chemotherapy: a phase 3 randomized placebo-controlled trial. Blood 135 (24): 2137-2145, 2020. 5) Stone RM, et al: Midostaurin plus Chemotherapy for Acute Myeloid Leukemia with a FLT3 Mutation. N Engl J Med 377 (5): 454-464, 2017. 11) Jones CL, et al: Inhibition of Amino Acid Metabolism Selectively Targets Human Leukemia Stem Cells. Cancer Cell 34 (5): 724-740 e4, 2018. 1) Papaemmanuil E, et al: Genomic Classification and Prognosis in Acute Myeloid Leukemia. N Engl J Med 374 (23): 2209-2221, 2016. 3) Assi R, Ravandi F: FLT3 inhibitors in acute myeloid leukemia: Choosing the best when the optimal does not exist. Am J Hematol 93 (4): 553-563, 2018. 10) Wilde L, Kasner M: Whom should we treat with novel agents? Specific indications for specific and challenging populations. Hematology Am Soc Hematol Educ Program 2021 (1): 24-29, 2021. 9) Thol F: What to use to treat AML: the role of emerging therapies. Hematology Am Soc Hematol Educ Program 2021 (1): 16-23, 2021. 8) Cortes JE, et al: Quizartinib versus salvage chemotherapy in relapsed or refractory FLT3-ITD acute myeloid leukaemia (QuANTUM-R): a multicentre, randomised, controlled, open-label, phase 3 trial. Lancet Oncol 20 (7): 984-997, 2019. 2) Jaiswal S, et al: Age-related clonal hematopoiesis associated with adverse outcomes. N Engl J Med 371 (26): 2488-2498, 2014. 6) Pollyea DA, et al: NCCN clinical practice guidelines in oncology, Acute myeloid leukemia, version 1. 2022. 2022: https://www.nccn.org/professionals/physician_gls/pdf/aml.pdf. 4) Kiyoi H, et al: FLT3 mutations in acute myeloid leukemia: Therapeutic paradigm beyond inhibitor development. Cancer Sci 111 (2): 312-322, 2020. 7) Perl AE, et al: Gilteritinib or Chemotherapy for Relapsed or Refractory FLT3-Mutated AML. N Engl J Med 381 (18): 1728-1740, 2019. |
| References_xml | – reference: 9) Thol F: What to use to treat AML: the role of emerging therapies. Hematology Am Soc Hematol Educ Program 2021 (1): 16-23, 2021. – reference: 5) Stone RM, et al: Midostaurin plus Chemotherapy for Acute Myeloid Leukemia with a FLT3 Mutation. N Engl J Med 377 (5): 454-464, 2017. – reference: 11) Jones CL, et al: Inhibition of Amino Acid Metabolism Selectively Targets Human Leukemia Stem Cells. Cancer Cell 34 (5): 724-740 e4, 2018. – reference: 12) Wei AH, et al: Venetoclax plus LDAC for newly diagnosed AML ineligible for intensive chemotherapy: a phase 3 randomized placebo-controlled trial. Blood 135 (24): 2137-2145, 2020. – reference: 2) Jaiswal S, et al: Age-related clonal hematopoiesis associated with adverse outcomes. N Engl J Med 371 (26): 2488-2498, 2014. – reference: 4) Kiyoi H, et al: FLT3 mutations in acute myeloid leukemia: Therapeutic paradigm beyond inhibitor development. Cancer Sci 111 (2): 312-322, 2020. – reference: 6) Pollyea DA, et al: NCCN clinical practice guidelines in oncology, Acute myeloid leukemia, version 1. 2022. 2022: https://www.nccn.org/professionals/physician_gls/pdf/aml.pdf. – reference: 3) Assi R, Ravandi F: FLT3 inhibitors in acute myeloid leukemia: Choosing the best when the optimal does not exist. Am J Hematol 93 (4): 553-563, 2018. – reference: 7) Perl AE, et al: Gilteritinib or Chemotherapy for Relapsed or Refractory FLT3-Mutated AML. N Engl J Med 381 (18): 1728-1740, 2019. – reference: 8) Cortes JE, et al: Quizartinib versus salvage chemotherapy in relapsed or refractory FLT3-ITD acute myeloid leukaemia (QuANTUM-R): a multicentre, randomised, controlled, open-label, phase 3 trial. Lancet Oncol 20 (7): 984-997, 2019. – reference: 1) Papaemmanuil E, et al: Genomic Classification and Prognosis in Acute Myeloid Leukemia. N Engl J Med 374 (23): 2209-2221, 2016. – reference: 10) Wilde L, Kasner M: Whom should we treat with novel agents? Specific indications for specific and challenging populations. Hematology Am Soc Hematol Educ Program 2021 (1): 24-29, 2021. |
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| Snippet | 急性骨髄性白血病（acute myeloid leukemia：AML）の分子病態の解明により，種々の新規分子標的薬が開発されている．FLT3阻害薬やIDH1/2阻害薬のように特定のドライバー遺... |
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| SubjectTerms | 個別化医療 分子標的 急性骨髄性白血病 抗体医薬 |
| Title | 急性骨髄性白血病に対する分子標的治療薬 |
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