Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE The Philadelphia chromosome associated with acute lymphoblastic leukemia (ALL) has been linked to a hybrid BCR/ABL protein product that differs from that found in chronic myelogenous leukemia. 2567002 1989
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE The findings suggested two distinct subtypes of ALL: one defined by t(9;22)(q34;q11) and expression of P185BCR-ABL tyrosine kinase and one with variant karyotypes and no P185BCR-ABL expression. 2649173 1989
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE In lymphoblastic leukemias, there are two molecular subtypes of the Ph1 chromosome, one with a rearrangement of the breakpoint cluster region (bcr) of the BCR gene, producing the same 8.5-kilobase BCR-ABL fusion mRNA seen in chronic myelogenous leukemia (CML), and the other, without a bcr rearrangement, producing a 7.0-kilobase BCR-ABL fusion mRNA that is seen only in acute lymphoblastic leukemia (ALL). 2498881 1989
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Detection of BCR/ABL translocation by polymerase chain reaction in leukemic progenitor cells (ALL-CFU) from patients with acute lymphoblastic leukemia (ALL). 1568446 1992
Childhood Acute Lymphoblastic Leukemia
0.400 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
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Diagnosis of the BCR-ABL fusion in ALL is difficult because the molecular findings are more heterogeneous than they are in CML. 1516023 1992
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE The majority of cases (76%) showed the p190 gene subtype similar to pediatric ALL; the BCR-ABL-positive cases displayed a more homogeneous immunophenotype than the BCR-ABL-negative cases and were predominantly CALLA positive (86%) and B-cell surface antigen positive (82%). 1467514 1992
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE The E2A/PBX1 and the BCR/ABL fusion genes result from the t(1;19)(q23;p13) and the t(9;22)(q34;q11), respectively, and encode oncoproteins which are thought to play an important role in the development of acute lymphoblastic leukemia (ALL) subtypes associated with adverse prognosis. 8483319 1993
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE Both retained the Ph1 chromosome and expressed the ALL type bcr/abl chimeric mRNA containing the junction of the first exon of BCR gene (e1) and second exon of c-abl gene (a2). 8428799 1993
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE We have now used the same technique, reverse transcription/polymerase chain reaction amplification of ABL-BCR transcripts, to study nine patients with Philadelphia (Ph) chromosome-positive acute lymphoblastic leukemia (ALL); seven expressed the P190 and two the P210 type of BCR-ABL fusion protein. 8490164 1993
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Finally, the relationship between the two common forms of BCR/ABL, the P190 and P210 configurations, and different disease phenotypes, like CML and Philadelphia (Ph1)-chromosome positive acute lymphoblastic leukemia (ALL), needs to be clarified. 8464245 1993
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE In conclusion, hybridization with D107F9 and cos-abl 8 allows unambiguous diagnosis of BCR-ABL genes and is likely to become an important tool for the monitoring of therapies in patients with CML and ALL. 8142658 1994
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE This observation also confirmed that, as in de novo Ph1-positive ALL, both the P190 and P210 varieties of BCR-ABL mRNA are observed in ALL with late-appearing Ph1. 7564511 1995
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE This genomic structure is of interest because of its analogy to the organization of the ABL gene and because this part of the gene is not affected by the breakpoints occurring in Ph1-positive acute lymphoblastic leukemia (ALL). 8632666 1995
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE In the present study, we analyzed blood or bone marrow smears of 46 patients (34 with chronic myeloid leukemia [CML] and 12 with acute lymphoblastic leukemia [ALL]) for the presence of a BCR-ABL fusion. 8625254 1996
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE The prognosis of BCR-ABL-positive ALL in children is poor, with a probability of event-free survival at 2 years of 8% versus 50% in those without BCR-ABL mRNA or cytogenetic analysis should become part of the routine diagnostic panel for children with newly diagnosed ALL and is fundamental for children presenting with an early bone marrow relapse. 8608244 1996
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE One hundred and forty-three patients with p210 BCR-ABL-positive leukemia were studied for coexpression of p190 BCR-ABL mRNA. p190 mRNA was detected in 14 of 16 (88%) patients with chronic-phase chronic myeloid leukemia (CML) at diagnosis, in 10 of 10 (100%) CML patients in blast crisis, in 75 of 107 (70%) CML patients receiving interferon-alpha (IFN-alpha), and 10 of 10 (100%) patients with p210 BCR-ABL-positive acute lymphoblastic leukemia (ALL). 8652835 1996
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE Immunophenotypic studies at diagnosis in 21 BCR/ABL-positive children identified common ALL in 16 patients (76.2%), pre-B-ALL in four (19.0%), and an early T-lineage ALL in one (4.8%). 8667652 1996
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE The lack of cases with the TEL-AML1 fusion together with the high frequency of BCR-ABL fusion could largely account for the poorer outcome of adult ALL as compared with childhood ALL. 8751462 1996
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE Southern blot analysis revealed no rearrangement in Mbcr1, and direct sequencing of the PCR product confirmed it to be the ALL-type mbcr1 fusion mRNA with the first exon of the BCR gene fused to ABL exon a2. 8756076 1996
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE RT-PCR assays allow rapid identification of patients with MLL-AF4 and BCR-ABL positive ALL. 9250788 1997
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Therefore, CD25 expression may serve as a surrogate marker for BCR/ABL positivity (Philadelphia chromosome), the major poor prognostic parameter in adult ALL. 9369422 1997
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE We sequentially performed cytogenetic analysis and RT-PCR analysis of BCR-ABL transcripts in 17 cases of Ph1-positive ALL who had achieved hematological complete remission (CR) with intensive chemotherapy (CT). 9009095 1997
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE None of the high-risk features predictive of poor treatment outcome in childhood ALL, such as older age, high white blood cell (WBC) count, organomegaly, T-lineage immunophenotype, ability of leukemic cells to cause overt leukemia in severe combined immunodeficient (SCID) mice, presence of MLL-AF4, and BCR-ABL fusion transcripts were associated with high levels of BCL-2 expression. 9160683 1997
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE This la-Ph, expressing an acute lymphoblastic leukemia (ALL)-type BCR/ABL transcript, produces a novel P180BCR/ABL fusion protein reflecting deletion of 174 bases (58 amino acids) encoded by the a2 exon of the ABL gene. 9790503 1998