The molecular biology of chronic myeloid leukemia

Blood

Volumn 96, Issue 10, 2000, Pages 3343-3356

  Deininger, M W N ^a   Goldman, J M ^a   Melo, J V ^a  

^a UNIVERSITY OF LEIPZIG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

2 PHENYLAMINOPYRIMIDINE; ANTIBIOTIC AGENT; BCR ABL PROTEIN; CGP 57418B; GENISTEIN; HERBIMYCIN A; IMATINIB; ISOFLAVONOID; MITOGEN ACTIVATED PROTEIN KINASE; MYC PROTEIN; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN INHIBITOR; PROTEIN TYROSINE KINASE; PROTEIN TYROSINE KINASE INHIBITOR; RAS PROTEIN; RIBONUCLEASE P; STAT PROTEIN; UNCLASSIFIED DRUG;

APOPTOSIS; BLAST CELL CRISIS; CANCER IMMUNOTHERAPY; CELL ADHESION; CHRONIC MYELOID LEUKEMIA; GENE THERAPY; GENE TRANSLOCATION; HUMAN; LEUKEMOGENESIS; MALIGNANT TRANSFORMATION; MITOGENESIS; MOLECULAR BIOLOGY; NONHUMAN; ONCOGENE; PHILADELPHIA 1 CHROMOSOME; PRIORITY JOURNAL; PROTEIN STRUCTURE; REVIEW; SIGNAL TRANSDUCTION;

EID: 0034670036     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood.v96.10.3343     Document Type: Review

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4. Philadelphia chromosomal breakpoints are clustered within a limited region, bcr, on chromosome 22
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15. Cell cycle-regulated binding of c-Abl tyrosine kinase to DNA
16. An actin-binding function contributes to transformation by the Bcr-Abl oncoprotein of Philadelphia chromosome-positive human leukemias
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44. The novel activation of ABL by fusion to an ets-related gene, TEL
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46. The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity
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49. Chronic myelogenous leukemia and exposure to ionizing radiation - A retrospective study of 443 patients
50. Selective induction of leukemia-associated fusion genes by high-dose ionizing radiation
51. Distribution of ABL and BCR genes in cell nuclei of normal and irradiated lymphocytes
52. The nuclear topography of ABL, BCR, PML, and RARα genes: Evidence for gene proximity in specific phases of the cell cycle and stages of hematopoietic differentiation
53. The presence of BCR-ABL fusion genes in leukocytes of normal individuals: Implications for the assessment of minimal residual disease
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56. Evidence for a multistep pathogenesis of chronic myelogenous leukemia
57. BCR-ABL-induced oncogenesis is mediated by direct interaction with the SH2 domain of the GRB-2 adaptor protein
58. BCR sequences essential for transformation by the BCR-ABL oncogene bind to the ABL SH2 regulatory domain in a non-phosphotyrosine-dependent manner
59. Differential complementation of Bcr-Abl point mutants with c-Myc
60. The SH2 domain of P210BCR/ABL is not required for the transformation of hematopoietic factor-dependent cells
61. Mutagenic analysis of the roles of SH2 and SH3 domains in regulation of the Abl tyrosine kinase
62. Jak-STAT signaling induced by the v-abl oncogene
63. Abl-interactor-1, a novel SH3 protein binding to the carboxy-terminal portion of the Abl protein, suppresses v-abl transforming activity
64. Abi-2, a novel SH3-containing protein interacts with the c-Abl tyrosine kinase and modulates c-Abl transforming activity
65. Identification of a protein that binds to the SH3 region of Abl and is similar to Bcr and GAP-rho
66. Oncogenic Abl and Src tyrosine kinases elicit the ubiquitin-dependent degradation of target proteins through a Ras-independent pathway
67. The PAG gene product, a stress-induced protein with antioxidant proper ties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity
68. Oncogenic activation of c-ABL by mutation within its last exon
69. Mutation of a phenylalanine conserved in SH3-containing tyrosine kinases activates the transforming ability of c-Abl
70. The fusion of TEL and ABL in human acute lymphoblastic leukaemia is a rare event
71. Consistent fusion of ZNF198 to the fibroblast growth factor receptor-1 in the 1(8;13)(p11;q12) myeloproliferative syndrome
72. Fusion of PDGF receptor beta to a novel ets-Iike gene, tel, in chronic myelomonocytic leukemia with t(5;12) chromosomal translocation
73. Crkl is the major tyrosine-phosphorylated protein in neutrophils from patients with chronic myelogenous leukemia
74. p62(dok): A constitutively tyrosine-phosphorylated, GAP-associated protein in chronic myelogenous leukemia progenitor cells
75. Shc phosphorylation in myeloid cells is regulated by granulocyte macrophage colony-stimulating factor, interleukin-3, and steel factor and is constitutively increased by p210BCR/ABL
76. Increased tyrosine phosphorylation of focal adhesion proteins in myeloid cell lines expressing p210BCR/ ABL
77. Molecular cloning of human paxillin, a focal adhesion protein phosphorylated by P210BCR/ABL
78. Tyrosine phosphorylation and activation of focal adhesion kinase (p125FAK) by BCR-ABL oncoprotein
79. p210Bcr/Abl and p160v-Abl induce an increase in the tyrosine phosphorylation of p93c-Fes
80. Potential molecules implicated in downstream signaling pathways of p185BCR-ABL in Ph-positive ALL involve GTPase-activating protein, phospholipase C-gamma 1, and phosphatidylinositol 3'-kinase
81. Tumour induction by activated abl involves tyrosine phosphorylation of the product of the cbl oncogene
82. Tyrosine phosphorylation of p95Vav in myeloid cells is regulated by GM-CSF, IL-3 and steel factor and is constitutively increased by p210BCR/ABL
83. SH2-containing phosphotyrosine phosphatase Syp is a target of p210 bcr-abl tyrosine kinase
84. Protein tyrosine phosphatase 1B antagonizes signaling by oncoprotein tyrosine kinase p210 bcr-abl in vivo
85. Protein tyrosine phosphatase PTP1B suppresses p210 bcr-abl-induced transformation of rat-1 fibroblasts and promotes differentiation of K562 cells
86. BCR-ABL tyrosine kinase activity regulates the expression of multiple genes implicated in the pathogenesis of chronic myeloid leukemia
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88. Bcr-Abl oncoproteins bind directly to activators of the Ras signalling pathway
89. Inhibition of apoptosis by BCR-ABL in chronic myeloid leukemia
90. Integrin-mediated regulation of hematopoiesis: Do BCR/ABL-induced defects in integrin function underlie the abnormal circulation and proliferation of CML progenitors?
91. Interferon-alpha restores normal adhesion of chronic myelogenous leukemia hematopoietic progenitors to bone marrow stroma by correcting impaired beta 1 integrin receptor function
92. Presence of the adhesion inhibitory β1B integrin isoform on CML but not normal progenitors is at least in part responsible for the decreased CML progenitor adhesion
93. Integrin regulation of c-Abl tyrosine kinase activity and cytoplasmic-nuclear transport
94. The adapter protein Crkl links Cbl to C3G after integrin ligation and enhances cell migration
95. The protooncogene product p120CBL and the adaptor proteins CRKL and c-CRK link c-ABL, p190BCR/ABL and p210BCR/ABL to the phosphatidylinositol-3' kinase pathway
96. p130CAS forms a signaling complex with the adapter protein CRKL in hematopoietic cells transformed by the BCR/ABL oncogene
97. Differential signaling after β1 integrin ligation is mediated through binding of CRKL to p120(CBL) and p110(HEF1)
98. Bcr/Abl expression stimulates integrin function in hematopoietic cell lines
99. Constitutive phosphorylation of Shc proteins in human tumors
100. The CRKL adaptor protein transforms fibroblasts and functions in transformation by the BCR-ABL oncogene
101. Direct binding of CRKL to BCR-ABL is not required for BCR-ABL transformation
102. Absence of N-ras mutations in myeloid and lymphoid blast crisis of chronic myeloid leukemia
103. Ras recruits Raf-1 to the plasma membrane for activa- tion by tyrosine phosphorylation
104. Signalling pathways: Jack of all cascades
105. A temperature sensitive p210 BCR-ABL mutant defines the primary consequences of BCR-ABL tyrosine kinase expression in growth factor dependent cells
106. The BCR-ABL tyrosine kinase activates mitotic signaling pathways and stimulates G1-to-S phase transition in hematopoietic cells
107. The Bcr-Abl leukemia oncogene activates Jun kinase and requires Jun for transformation
108. BCR/ ABL-mediated leukemogenesis requires the activity of the small GTP-binding protein Rac
109. GCKR links the BCR-ABL oncogene and RAS to the stress-activated protein kinase pathway
110. P210 Bcr-Abl interacts with the interleukin 3 receptor beta(c) subunit and constitutively induces its tyrosine phosphorylation
111. Interaction of the receptor tyrosine kinase p145c-kit with the p210bcr/abl kinase in myeloid cells
112. c-kit ligand stimulates tyrosine phosphorylation of a similar pattern of phosphotyrosyl proteins in primary primitive normal hematopoietic progenitors that are constitutively phosphorylated in comparable primitive progenitors in chronic phase chronic myelogenous leukemia
113. Molecular cloning and characterization of p56dok-2 defines a new family of RasGAP-binding proteins
114. Interactions of p62(dok) with p210(bcr-abl) and Bcr-Abl-associated proteins
115. P210 and P190(BCR/ ABL) induce the tyrosine phosphorylation and DNA binding activity of multiple specific STAT family members
116. Constitutive activation of JAKs and STATs in BCR-Abl-expressing cell lines and peripheral blood cells derived from leukemic patients
117. STAT5 activation by BCR-Abl contributes to transformation of K562 leukemia cells
118. STAT5 as a molecular regulator of proliferation, differentiation and apoptosis in hematopaietic cells
119. Blockade of the Bcr-Abl kinase activity induces apoptosis of chronic myelogenous leukemia cells by suppressing signal transducer and activator of transcription 5-dependent expression of Bcl-xL
120. STAT5 activation contributes to growth and viability in Bcr/Abl-transformed cells
121. Transformation of an interteukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210bcr/abl protein
122. Expression of bcr-abl abrogates factor-dependent growth of human hematopoietic M07E cells by an autocrine mechanism
123. Autocrine production and action of IL-3 and granulocyte colony-stimulating factor in chronic myeloid leukemia
124. Apoptosis in chronic myeloid leukaemia: Normal responses by progenitor cells to growth factor deprivation, X-irradiation and glucocorticoids
125. Bcr-Abl kinase promotes cell cycle entry of primary myeloid CML cells in the absence of growth factors
126. p210 Bcr-Abl expression in a primitive multipotent haematopoietic cell line models the development of chronic myeloid leukaemia
127. Phosphatidylinositol-3 kinase activity is regulated by BCR/ABL and is required for the growth of Philadelphia chromosome-positive cells
128. Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway
129. PI3K: Downstream AKTion blocks apoptosis
130. Interleukin-3-induced phosphorylation of bad through the protein kinase akt
131. p150Ship, a signal transduction molecule with inositol polyphosphate-5-phosphatase activity
132. A novel SH2-containing phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase (SHIP2) is constitutively tyrosine phosphorylated and associated with src homologous and collagen gene (SHC) in chronic myelogenous leukemia progenitor cells
133. Dominant negative MYC blocks transformation by ABL oncogenes
134. Induction of c-myc transcription by the v-Abl tyrosine kinase requires Ras, Raf1, and cyclin-dependent kinases
135. Role for E2F1 in p210 BCR-ABL downstream regulation of c-myc transcription initiation: Studies in murine myeloid cells
136. Apoptotic cell death induced by c-myc is inhibited by bcl-2
137. Induction of apoptosis in fibroblasts by c-myc protein
138. Transformation of an interleukin 3-dependent hematopoietic cell line by the chronic myelogenous leukemia-specific P210(bcr/abl) protein
139. Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis
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141. BCR-ABL delays apoptosis upstream of procaspase-3 activation
142. Bcr-Abl exerts its antiapoptotic effect against diverse apoptotic stimuli through blockage of mitochondrial release of cytochrome C and activation of caspase-3
143. Regulation of Bcl-2 gene expression by BCR-ABL is mediated by Ras
144. Bcl-2 targets the protein kinase Raf-1 to mitochondria
145. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L)
146. The survival function of the Bcr-Abl oncogene is mediated by Bad-dependent and -independent pathways: Roles for phosphatidylinositol 3-kinase and Raf
147. Activation of mitochondrial Raf-1 is involved in the antiapoptotic effects of Akt
148. Regulation of apoptosis in myeloid cells by interferon consensus sequence-binding protein
149. Expression of interferon consensus sequence binding protein (ICSBP) is downregulated in Bcr-Abl-induced murine chronic myelogenous leukemia-like disease, and forced coexpression of ICSBP inhibits Bcr-Abl-induced myeloproliferative disorder
150. Immunodeficiency and chronic myelogenous leukemia-like syndrome in mice with a targeted mutation of the ICSBP gene
151. Altered development and cytokine responses of myeloid progenitors in the absence of transcription factor, interferon consensus sequence binding protein
152. Apoptosis and the cell cycle
153. Expression of p210 bcr/abl increases hematopoieric progenitor cell radiosensitivity
154. Primary proliferating immature myeloid cells from CML patients are not resistant to induction of apoptosis by DNA damage and growth factor withdrawal
155. Regulation of the Fas apoptotic cell death pathway by Abl
156. Fas-mediated modulation of Bcr/Abl in chronic myelogenous leukemia results in differential effects on apoptosis
157. The susceptibility of Philadelpha chromosome-positive cells to FAS-mediated apoptosis is not linked to the tyrosine kinase activity of BCR-ABL
158. BCR-ABL accelerates C2-ceramide-induced apoptosis
159. BCR-ABL does not prevent apoptotic death induced by human natural killer or lymphokine-activated killer cells
160. An assay for cellular transformation by SV40
161. The BCR-ABL oncogene transforms Rat-1 cells and cooperates with v-myc
162. The CML-specific P210 bcr/abl protein, unlike v-abl, does not transform NIH/3T3 fibroblasts
163. Oncogenic v-Abl tyrosine kinase can inhibit or stimulate growth, depending on the cell context
164. Leukemia cell lines: In vitro models for the study of Philadelphia chromosome-positive leukemia
165. BCR-ABL-positive lymphoblastoid cells display limited proliferative capacity under in vitro culture conditions
166. The TEL/platelet-derived growth factor beta receptor (PDGF beta R) fusion in chronic myelomonocytic leukemia is a transforming protein that self-associates and activates PDGF beta R kinase-dependent signaling pathways
167. Secondary mutation maintains the transformed state in BaF3 cells with inducible BCR/ABL expression
168. Growth factor independence and BCR/ABL transformation: Promise and pitfalls of murine model systems and assays
169. Regulated expression of P210 Bcr-Abl during embryonic stem cell differentiation stimulates muitipotential progenitor expansion and myeloid cell fate
170. Generation of an embryonic stem cell (ES) model of chronic myelogenous leukemia (CML)
171. Generation of a hematopoietic stem cell line from ES cells using the oncogene BCR/ABL
172. Ex vivo expansion and characterisation of CD34+ cells derived from chronic myeloid leukaemia bone marrow and peripheral blood, and from normal bone marrow and mobilised peripheral blood
173. Tyrosine phosphorylation of p62dok by p210bcr-abl inhibits RasGAP activity
174. Role of B7-1 in mediating an immune response to myeloid leukemia cells
175. Propagation of human blastic myeloid leukemias in the SCID mouse
176. Normal and leukemic SCID-repopulating cells (SRC) coexist in the bone marrow and peripheral blood from CML patients in chronic phase, whereas leukemic SRC are detected in blast crisis
177. Long-term marrow culture reveals chromosomally normal hematopoietic progenitor cells in patients with Philadelphia chromosome-positive chronic myelogenous leukemia
178. The kinetics and extent of engraftment of chronic myelogenous leukemia cells in non-obese diabetic/severe combined immunodeficiency mice reflect the phase of the donor's disease: An in vivo model of chronic myelogenous leukemia biology
179. A bcr-v-abl oncogene induces lymphomas in transgenic mice
180. Human bcr-abl gene has a lethal effect on embryogenesis
181. The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products
182. Reversibility of acute B-cell leukaemia induced by BCR-ABL1
183. Acute leukaemia in bcr/abl transgenic mice
184. BCR/ABL P210 and P190 cause distinct leukemia in transgenic mice
185. Development of acute lymphoblastic leukemia and myeloproliferative disorder in transgenic mice expressing p210 bcr/abl: A novel transgenic model for human Ph1-positive leukemias
186. bcr-abl, the hallmark of chronic myeloid leukaemia in man, induces multiple haemopoietic neoplasms in mice
187. Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL
188. Hematologic disease induced in BALB/c mice by a bcr-abl retrovirus is influenced by the infection conditions
189. Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow
190. Bcr-Abl efficiently induces a myeloproliferative disease and production of excess interleukin-3 and granulocyte-macrophage colony-stimulating factor in mice: A novel model for chronic myelogenous leukemia
191. Homozygous deletions of the p16 tumor-suppressor gene are associated with lymphoid transformation of chronic myeloid leukemia
192. p53 in chronic myelogenous leukemia in acute phase
193. Absence of the human retinoblastoma gene product in the megakaryoblastic crisis of chronic myelogenous leukemia
194. Abnormal expression of Evi-1 gene in human leukemias
195. Mutator phenotype of BCR-ABL transfected Ba/F3 cell lines and its association with enhanced expression of DNA polymerase beta
196. The BCR-ABL oncoprotein potentially interacts with the xero-derma pigmentosum group B protein
197. Acquired loss of p53 induces blastic transformation in p210(bcr/abl)-expressing hematopoietic cells: A transgenic study for blast crisis of human CML
198. BCR-ABL as a target for antisense intervention
199. Nucleic acid therapeutics: State of the art and future prospects
200. The therapeutic potential of ribozymes
201. In vivo inhibition by a site-specific catalytic RNA subunit of RNase P designed against the BCR-ABL oncogenic products: A novel approach for cancer treatment
202. Donor lymphocyte infusions for relapse of chronic myeloid leukemia after allogeneic stem cell transplant: Where we now stand
203. Vaccination of patients with chronic myelogenous leukemia with bcr-abl oncogene breakpoint fusion peptides generates specific immune responses
204. Tyrosine protein kinase inhibition and cancer
205. Tyrosine kinase inhibition: An approach to drug development
206. Selective inhibition of the platelet-derived growth factor signal transduction pathway by a protein-tyrosine kinase inhibitor of the 2-phenylaminopyrimidine class
207. In vivo eradication of human BCR/ABL-positive leukemia cells with an ABL kinase inhibitor
208. Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: Diverse mechanisms of resistance
209. Mutant forms of growth factor-binding protein-2 reverse BCR-ABL-induced transformation
210. RAS endoprotease inhibitors are potent cytotoxic agents against acute lymphoblastic leukemia
211. Inhibition of juvenile myelomonocytic leukemia cell growth in vitro by farnesyl transferase inhibitors
212. Abl kinase but not PI3-kinase links to the cytoskeletal defects in Bcr-Abl transformed cells
213. The Src family kinase Hck interacts with Bcr-Abl by a kinase-independent mechanism and phosphorylates the Grb2-binding site of Bcr
214. Tyrosine phosphorylation of rasGAP and associated proteins in chronic myelogenous leukemia cell lines