Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 GeneticVariation disease BEFREE Imatinib, an ABL tyrosine kinase inhibitor, is dramatically effective in CML patients; however, 30% of CML patients will need further treatment due to progression of CML to blast crisis (BC). 27908728 2017
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE Patients in the chronic phase (CP) of chronic myelogenous leukemia (CML) have been treated successfully following the advent of ABL kinase inhibitors, but once they progress to the blast crisis (BC) phase the prognosis becomes dismal. 24098673 2013
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 AlteredExpression disease BEFREE These results demonstrate that enhanced expression of p210BCR/ABL and deregulated expression of Zfp423/ZNF423 contribute to CML BC. 19234145 2009
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE These results indicate that Bcl11b and H2AX function as tumor suppressor and that haploinsufficiency and acquired loss of these gene products cooperate with p210BCR/ABL to develop CML BC. 19432895 2009
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE Chronic myelogenous leukemia (CML) is a hematopoietic disorder, which begins as indolent chronic phase but inevitably progresses to fatal blast crisis. p210BCR/ABL, a constitutively active tyrosine kinase, is responsible for disease initiation but molecular mechanism(s) underlying disease evolution remains largely unknown. 18193087 2008
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 GeneticVariation disease BEFREE ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia. 15867198 2005
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 GeneticVariation disease BEFREE These findings demonstrate that in late CP or advanced CML, ABL-kinase mutations occur as an intraclonal event in the primitive Ph1+ stem cell compartments with progression of this clone towards IM-resistant blast phase. 15381060 2004
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 GeneticVariation disease BEFREE In conclusion, patients with ABL deletions progress to blast crisis or accelerated phase in a significantly shorter time than do those without such deletions. 12759927 2003
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 GeneticVariation disease BEFREE A point mutation leading to substitution at the ATP binding site of ABL-kinase and insensitivity to imatinib was detected in our patient treated with imatinib, who progressed to blast crisis. 12921956 2003
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 AlteredExpression disease BEFREE The arrest of differentiation is a feature of both chronic myelogenous leukemia cells in myeloid blast crisis and myeloid precursors that ectopically express the p210BCR-ABL oncoprotein; however, its underlying mechanisms remain poorly understood. 11753385 2002
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE The ataxia telangiectasia gene, ATM, is a candidate gene for this transformation because the complex karyotypes associated with BC of CML suggest that DNA double-strand break repair is defective and because the ABL pathway involves the interaction between the Abl and the Atm proteins. 11516106 2001
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 GeneticVariation disease BEFREE We report an at least 15-fold amplification of the ABL oncogene in a 29-year-old male patient with a variant Ph-positive t(19;22)(p13;q11.2) CML who presented in lymphoid blast crisis. 10190307 1999
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 GeneticVariation disease BEFREE Patients with CML in blast crisis, or with Philadelphia positive acute lymphoblastic leukaemia (ALL), can have a smaller BCR-ABL fusion transcript possessing only the first exon of BCR fused to ABL. 9858221 1998
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE In Philadelphia chromosome (Ph1)-positive leukemias such as chronic myelogenous leukemia (CML) and Ph1-positive acute lymphoblastic leukemia (ALL), both of which express bcr-abl fused gene products (P210bcr-abl or P190bcr-abl protein kinase) with augmented tyrosine kinase activities, herbimycin A markedly inhibited the in vitro growth of the Ph1-positive ALL cells and the leukemic cells derived from CML blast crisis. 1515646 1992
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE To investigate the hypothesis that the production of P190 may be associated with the progression from chronic phase to blast crisis in CML, we used polymerase chain reaction to analyze blood from 37 patients with accelerated phase/blast crisis CML for the transcripts coding for the P210BCR-ABL and P190BCR-ABL. 2013978 1991
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 AlteredExpression disease BEFREE In order to better define the relationship between type of genomic rearrangement, variant ABL protein expressed and haematological phenotype, a series of Ph1-positive acute leukaemias, both myeloblastic (AML) and lymphoblastic, and several CML lymphoid blast crises have been analysed at the DNA and protein level. 2223647 1990
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE The data suggest that the phl/abl protein product may influence the timing of the onset of blast crisis and imply a continuing role for this protein during the evolution of the disease. 2683759 1989
CUI: C0005699
Disease: Blast Phase
Blast Phase
0.100 Biomarker disease BEFREE The aberrant abl protein product of a chronic myelogenous leukemia (CML) blast crisis cell line (K562) and of five Philadelphia chromosome-positive CML patients in blast crisis were analyzed by an immune complex kinase assay using two antipeptide sera generated against the hydrophilic domain of v-abl and a region within the third exon of the breakpoint cluster region (bcr) respectively. 2885048 1987