Bcr-Abl variants:: biological and clinical aspects

被引：86

作者：

Advani, AS

Pendergast, AM

机构：

[1] Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, LSRC, Durham, NC 27710 USA

[2] Duke Univ, Med Ctr, Dept Hematol & Oncol, Durham, NC 27710 USA

来源：

LEUKEMIA RESEARCH | 2002年 / 26卷 / 08期

关键词：

Philadelphia chromosome; Bcr-Abl; acute lymphocytic leukemia; chronic myelogenous leukemia; chronic neutrophilic leukemia;

D O I：

10.1016/S0145-2126(01)00197-7

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Bcr-Abl is an oncogene that arises from fusion of the Bcr gene with the c-Abl proto-oncogene. Three different Bcr-Abl variants can be formed, depending on the amount of Bcr gene included: p185, p210, and p230. The three variants are associated with distinct types of human leukemias. Examination of the signaling pathways differentially regulated by the Bcr-Abl proteins will help us gain better insight into Bcr-Abl mediated leukemogenesis. (C) 2002 Elsevier Science Ltd. All rights reserved.

引用

收藏

页码：713 / 720

页数：8

相关论文

共 148 条

[111] Analysis of the biologic properties of p230 Bcr-Abl reveals unique and overlapping properties with the oncogenic p185 and p210 Bcr-Abl tyrosine kinases [J].

Quackenbush, RC ;

Reuther, GW ;

Miller, JP ;

Courtney, KD ;

Pear, WS ;

Pendergast, AM .

BLOOD, 2000, 95 (09) :2913-2921

[112] POLYMERASE CHAIN-REACTION DETECTION OF THE BCR-ABL FUSION TRANSCRIPT AFTER ALLOGENEIC MARROW TRANSPLANTATION FOR CHRONIC MYELOID-LEUKEMIA - RESULTS AND IMPLICATIONS IN 346 PATIENTS [J].

RADICH, JP ;

GEHLY, G ;

GOOLEY, T ;

BRYANT, E ;

CLIFT, RA ;

COLLINS, S ;

EDMANDS, S ;

KIRK, J ;

LEE, A ;

KESSLER, P ;

SCHOCH, G ;

BUCKNER, CD ;

SULLIVAN, KM ;

APPELBAUM, FR ;

THOMAS, ED .

BLOOD, 1995, 85 (09) :2632-2638

[113]

Raitano A. B., 1997, BIOCHIM BIOPHYS ACTA, V1333, P201, DOI DOI 10.1016/S0304-419X(97)00023-1

[114] THE BCR-ABL LEUKEMIA ONCOGENE ACTIVATES JUN KINASE AND REQUIRES JUN FOR TRANSFORMATION [J].

RAITANO, AB ;

HALPERN, JR ;

HAMBUCH, TM ;

SAWYERS, CL .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (25) :11746-11750

[115]

REARDON DA, 1994, CANCER, V73, P1526, DOI 10.1002/1097-0142(19940301)73:5<1526::AID-CNCR2820730534>3.0.CO

[116]

2-E

[117] A requirement for NF-κB activation in Bcr-Abl-mediated transformation [J].

Reuther, JY ;

Reuther, GW ;

Cortez, D ;

Pendergast, AM ;

Baldwin, AS .

GENES & DEVELOPMENT, 1998, 12 (07) :968-981

[118] THE SMALL GTP-BINDING PROTEIN RHO REGULATES THE ASSEMBLY OF FOCAL ADHESIONS AND ACTIN STRESS FIBERS IN RESPONSE TO GROWTH-FACTORS [J].

RIDLEY, AJ ;

HALL, A .

CELL, 1992, 70 (03) :389-399

[119] The Src homology 2 domain of Bcr/Abl is required for efficient induction of chronic myeloid leukemia-like disease in mice but not for lymphoid leukemogenesis or activation of phosphatidylinositol 3-kinase [J].

Roumiantsev, S ;

de Aos, IE ;

Varticovski, L ;

Ilaria, RL ;

Van Etten, RA .

BLOOD, 2001, 97 (01) :4-13

[120] NEW CONSISTENT CHROMOSOMAL ABNORMALITY IN CHRONIC MYELOGENOUS LEUKEMIA IDENTIFIED BY QUINACRINE FLUORESCENCE AND GIEMSA STAINING [J].

ROWLEY, JD .

NATURE, 1973, 243 (5405) :290-293

← 6 7 8 9 10 11 12 13 14 15 →