Targeted therapies in myeloid leukemia

A M John; N S B Thomas; G J Mufti; R A Padua

doi:10.1016/j.semcancer.2003.11.006

Targeted therapies in myeloid leukemia

A M John, N S B Thomas, G J Mufti, R A Padua

Research output: Contribution to journal › Literature review › peer-review

44 Citations (Scopus)

Abstract

Targeted therapies for hematological malignancies have come of age since the advent of all trans retinoic acid (ATRA) for treating APL and STI571/Imatinib Mesylate/Gleevec for CML. There are good molecular targets for other malignancies and several new drugs are in clinical trials. In this review, we will concentrate on individual abnormalities that exist in the myelodysplastic syndromes (MDS) and myeloid leukemias that are targets for small molecule therapies (summarised in Fig. 1). We will cover fusion proteins that are produced as a result of translocations, including BCR-ABL, the FLT3 tyrosine kinase receptor and RAS. Progression of diseases such as MDS to secondary AML occur as a result of changes in the balance between cell proliferation and apoptosis and we will review targets in both these areas, including reversal of epigenetic silencing of genes such as p15(INK4B). (C) 2003 Elsevier Ltd. All rights reserved.

Original language	English
Pages (from-to)	41 - 62
Number of pages	22
Journal	Seminars in Cancer Biology
Volume	14
Issue number	1
DOIs	https://doi.org/10.1016/j.semcancer.2003.11.006
Publication status	Published - Feb 2004

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title = "Targeted therapies in myeloid leukemia",

abstract = "Targeted therapies for hematological malignancies have come of age since the advent of all trans retinoic acid (ATRA) for treating APL and STI571/Imatinib Mesylate/Gleevec for CML. There are good molecular targets for other malignancies and several new drugs are in clinical trials. In this review, we will concentrate on individual abnormalities that exist in the myelodysplastic syndromes (MDS) and myeloid leukemias that are targets for small molecule therapies (summarised in Fig. 1). We will cover fusion proteins that are produced as a result of translocations, including BCR-ABL, the FLT3 tyrosine kinase receptor and RAS. Progression of diseases such as MDS to secondary AML occur as a result of changes in the balance between cell proliferation and apoptosis and we will review targets in both these areas, including reversal of epigenetic silencing of genes such as p15(INK4B). (C) 2003 Elsevier Ltd. All rights reserved.",

author = "John, {A M} and Thomas, {N S B} and Mufti, {G J} and Padua, {R A}",

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T1 - Targeted therapies in myeloid leukemia

AU - John, A M

AU - Thomas, N S B

AU - Mufti, G J

AU - Padua, R A

PY - 2004/2

Y1 - 2004/2

N2 - Targeted therapies for hematological malignancies have come of age since the advent of all trans retinoic acid (ATRA) for treating APL and STI571/Imatinib Mesylate/Gleevec for CML. There are good molecular targets for other malignancies and several new drugs are in clinical trials. In this review, we will concentrate on individual abnormalities that exist in the myelodysplastic syndromes (MDS) and myeloid leukemias that are targets for small molecule therapies (summarised in Fig. 1). We will cover fusion proteins that are produced as a result of translocations, including BCR-ABL, the FLT3 tyrosine kinase receptor and RAS. Progression of diseases such as MDS to secondary AML occur as a result of changes in the balance between cell proliferation and apoptosis and we will review targets in both these areas, including reversal of epigenetic silencing of genes such as p15(INK4B). (C) 2003 Elsevier Ltd. All rights reserved.

AB - Targeted therapies for hematological malignancies have come of age since the advent of all trans retinoic acid (ATRA) for treating APL and STI571/Imatinib Mesylate/Gleevec for CML. There are good molecular targets for other malignancies and several new drugs are in clinical trials. In this review, we will concentrate on individual abnormalities that exist in the myelodysplastic syndromes (MDS) and myeloid leukemias that are targets for small molecule therapies (summarised in Fig. 1). We will cover fusion proteins that are produced as a result of translocations, including BCR-ABL, the FLT3 tyrosine kinase receptor and RAS. Progression of diseases such as MDS to secondary AML occur as a result of changes in the balance between cell proliferation and apoptosis and we will review targets in both these areas, including reversal of epigenetic silencing of genes such as p15(INK4B). (C) 2003 Elsevier Ltd. All rights reserved.

U2 - 10.1016/j.semcancer.2003.11.006

DO - 10.1016/j.semcancer.2003.11.006

M3 - Literature review

VL - 14

SP - 41

EP - 62

JO - Seminars in Cancer Biology

JF - Seminars in Cancer Biology

IS - 1

ER -

Targeted therapies in myeloid leukemia

Abstract

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