Advances in therapies for acute promyelocytic leukemia

Tomohiko Kamimura, Toshihiro Miyamoto, Mine Harada, Koichi Akashi

研究成果: ジャーナルへの寄稿評論記事

36 引用 (Scopus)

抄録

Acute promyelocytic leukemia (APL), a distinct subtype of acute myelogenous leukemia (AML), results from the arrest of the maturation of hematopoietic progenitors at the promyelocyte stage. It has been shown that APL is associated with a reciprocal chromosomal translocation, involving chromosomes 15 and 17, which fuses the gene encoding the retinoic acid receptor α (RARα) and the promyelocytic leukemia (PML) gene. The resultant PML-RARα fusion protein plays a critical role in the pathogenesis of APL. Although there are many subtypes of AML, all are typically managed using a standard chemotherapy regimen of an anthracycline plus cytarabine arabinoside (CA). Despite high rates of complete remission following standard chemotherapy, most patients relapse and long-term disease-free survival is only 30-40%. The introduction of drugs such as all-trans retinoic acid (ATRA) that promote progenitor differentiation by directly inhibiting the PML-RARα fusion protein has changed the treatment paradigm for APL and markedly improved patient survival. The purposes of the present review are to provide the latest results and future directions of clinical research into APL and to illustrate how new therapies, such as ATRA plus anthracycline-based induction and consolidation therapy, risk-adapted therapy, salvage therapy containing arsenic trioxide-based regimens, and hematopoietic stem cell transplantation, have improved the treatment outcomes for APL patients.

元の言語英語
ページ(範囲)1929-1937
ページ数9
ジャーナルCancer Science
102
発行部数11
DOI
出版物ステータス出版済み - 11 1 2011

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Acute Promyelocytic Leukemia
Retinoic Acid Receptors
Leukemia
Anthracyclines
Tretinoin
Acute Myeloid Leukemia
Therapeutics
Chromosomes, Human, Pair 15
Drug Therapy
Granulocyte Precursor Cells
Salvage Therapy
Genetic Translocation
Chromosomes, Human, Pair 17
Hematopoietic Stem Cell Transplantation
Cytarabine
Genes
Disease-Free Survival
Proteins
Recurrence
Survival

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

これを引用

Advances in therapies for acute promyelocytic leukemia. / Kamimura, Tomohiko; Miyamoto, Toshihiro; Harada, Mine; Akashi, Koichi.

:: Cancer Science, 巻 102, 番号 11, 01.11.2011, p. 1929-1937.

研究成果: ジャーナルへの寄稿評論記事

Kamimura, Tomohiko ; Miyamoto, Toshihiro ; Harada, Mine ; Akashi, Koichi. / Advances in therapies for acute promyelocytic leukemia. :: Cancer Science. 2011 ; 巻 102, 番号 11. pp. 1929-1937.
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abstract = "Acute promyelocytic leukemia (APL), a distinct subtype of acute myelogenous leukemia (AML), results from the arrest of the maturation of hematopoietic progenitors at the promyelocyte stage. It has been shown that APL is associated with a reciprocal chromosomal translocation, involving chromosomes 15 and 17, which fuses the gene encoding the retinoic acid receptor α (RARα) and the promyelocytic leukemia (PML) gene. The resultant PML-RARα fusion protein plays a critical role in the pathogenesis of APL. Although there are many subtypes of AML, all are typically managed using a standard chemotherapy regimen of an anthracycline plus cytarabine arabinoside (CA). Despite high rates of complete remission following standard chemotherapy, most patients relapse and long-term disease-free survival is only 30-40{\%}. The introduction of drugs such as all-trans retinoic acid (ATRA) that promote progenitor differentiation by directly inhibiting the PML-RARα fusion protein has changed the treatment paradigm for APL and markedly improved patient survival. The purposes of the present review are to provide the latest results and future directions of clinical research into APL and to illustrate how new therapies, such as ATRA plus anthracycline-based induction and consolidation therapy, risk-adapted therapy, salvage therapy containing arsenic trioxide-based regimens, and hematopoietic stem cell transplantation, have improved the treatment outcomes for APL patients.",
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