Bcr-Abl-induced evasion from apoptosis: A mechanism for tumorigenicity

被引：0
|
作者：
Jagani, Z
Ghaffari, S
Song, K
Kitidis, C
Lodish, H
Khosravi-Far, R
机构：
[1] Harvard Univ, Sch Med, BIDMC, Boston, MA USA
[2] Mt Sinai Sch Med, Carl C Icahn Inst Gene Therapy & Mol Med, New York, NY USA
[3] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA
来源：
MOLECULAR BIOLOGY OF THE CELL | 2004年 / 15卷
关键词：
D O I：
暂无
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
2071
引用
收藏
页码：375A / 375A
页数：1
相关论文
共 50 条
  • [21] BCR-ABL-induced senescence-associated autophagy bring about maintenance of CML stemness
    Tanabe, Yamato
    Baba, Tomohisa
    Mukaida, Naofumi
    CANCER SCIENCE, 2021, 112 : 505 - 505
  • [22] The Arf tumor suppressor in acute leukemias:: Insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia
    Williams, Richard T.
    Sherr, Charles J.
    ADVANCES IN MOLECULAR ONCOLOGY, 2007, 604 : 107 - 114
  • [23] DECREASE OF WNT5A EXPRESSION IN THE NICHE PROMOTES ONSET OF BCR-ABL-INDUCED LEUKEMIA
    Eckl, Christina
    Bock, Franziska
    Istvanffy, Rouzanna
    Vilne, Baiba
    Peschel, Christian
    Oostendorp, Robert
    EXPERIMENTAL HEMATOLOGY, 2012, 40 (08) : S88 - S89
  • [24] Chronic myeloid leukaemia: an investigation into the role of Bcr-Abl-induced abnormalities in glucose transport regulation
    Kay Barnes
    Elizabeth McIntosh
    Anthony D Whetton
    George Q Daley
    Johanne Bentley
    Stephen A Baldwin
    Oncogene, 2005, 24 : 3257 - 3267
  • [25] EFFICIENT TRANSPLANTATION OF BCR-ABL-INDUCED CHRONIC MYELOGENOUS LEUKEMIA-LIKE SYNDROME IN MICE
    GISHIZKY, ML
    JOHNSONWHITE, J
    WITTE, ON
    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (08) : 3755 - 3759
  • [26] Chronic myeloid leukaemia: an investigation into the role of Bcr-Abl-induced abnormalities in glucose transport regulation
    Barnes, K
    McIntosh, E
    Whetton, AD
    Daley, GQ
    Bentley, J
    Baldwin, SA
    ONCOGENE, 2005, 24 (20) : 3257 - 3267
  • [27] Nfkb1 Plays a Tumor-Suppressing Role in BCR-ABL-Induced Leukemias
    Sullivan, Con
    Chen, Yaoyu
    Guo, Zhiru
    Shan, Yi
    Peng, Cong
    Zhang, Haojian
    Bubier, Jason
    Sproule, Thomas
    Roopenian, Derry
    Li, Shaoguang
    BLOOD, 2012, 120 (21)
  • [28] Rac guanosine triphosphatases represent integrating molecular therapeutic targets for BCR-ABL-induced myeloproliferative disease
    Thomas, Emily K.
    Cancelas, Jose A.
    Chae, Hee-Don
    Cox, Adrienne D.
    Keller, Patricia J.
    Perrotti, Danilo
    Neviani, Paolo
    Druker, Brian J.
    Setchell, Kenneth D. R.
    Zheng, Yi
    Harris, Chad E.
    Williams, David A.
    CANCER CELL, 2007, 12 (05) : 467 - 478
  • [29] PAK-dependent STAT5 serine phosphorylation is required for BCR-ABL-induced leukemogenesis
    Berger, A.
    Hoelbl-Kovacic, A.
    Bourgeais, J.
    Hoefling, L.
    Warsch, W.
    Grundschober, E.
    Uras, I. Z.
    Menzl, I.
    Putz, E. M.
    Hoermann, G.
    Schuster, C.
    Fajmann, S.
    Leitner, E.
    Kubicek, S.
    Moriggl, R.
    Gouilleux, F.
    Sexl, V.
    LEUKEMIA, 2014, 28 (03) : 629 - 641
  • [30] Rac GTPase activation mediates BCR-ABL-induced B-cell acute lymphoblastic leukemia
    Sanchez-Aguilera, Abel
    Sengupta, Amitava
    Williams, David A.
    Cancelas, Jose A.
    EXPERIMENTAL HEMATOLOGY, 2008, 36 (07) : S3 - S3
12345