|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We therefore sought evidence for analogous point mutations in the ABL gene in patients with Ph-negative, BCR-negative CML (n = 25), Ph-negative ALL (n = 18) and in Ph-positive CML in transformation (n = 28).
|
1353550 |
1992 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Approximately five percent of pediatric acute lymphoblastic leukemias (ALL) contain a translocation (9;22)(q34;q11) which results in rearrangement of the bcr and abl genes.
|
1493473 |
1992 |
|
Acute lymphocytic leukemia
|
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 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The ABL oncogene is consistently rearranged and activated as a consequence of the translocation t(9;22) that gives rise to the Philadelphia chromosome in chronic myeloid leukemia and in some cases of acute lymphoblastic leukemia.
|
2334939 |
1990 |
|
Acute lymphocytic leukemia
|
0.100 |
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 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, the order of loci on chromosome 22 is centromere----BCR2, BCR4, and IGL----BCR1----BCR3----SIS, possibly eliminating BCR2 and BCR4 loci as candidate targets for juxtaposition to the ABL gene in the acute lymphoblastic leukemia Ph1 chromosome.
|
3118359 |
1987 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The role of ABL on the Philadelphia chromosome in acute lymphoblastic leukemia is only now beginning to be understood, but is likely to be similar, and a new ABL species has already been identified by several groups.
|
3289649 |
1988 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Analysis of the functions of these new molecules may provide insight into mechanisms by which oncogenic abl proteins participate in the etiology of CML and ALL.
|
7769362 |
1995 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Alternative chimeric proteins, p210BCR-ABL and p190BCR-ABL, are produced that are characteristic of chronic myelogenous leukemia and acute lymphoblastic leukemia, respectively.
|
7777499 |
1995 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The fusion of TEL and ABL in human acute lymphoblastic leukaemia is a rare event.
|
7786792 |
1995 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the present study, three chronic myelogenous leukemia (CML) patients with variant Philadelphia (Ph) chromosomes (complex types), two CML patients with a masked Ph, one case with Ph positive acute lymphocytic leukemia (ALL), and one with Ph positive acute myelocytic leukemia (AML) were analyzed by standard cytogenetic techniques (G-banding), Southern blot studies, and fluorescence in situ hybridization (FISH) procedures using probes from portions of the bcr and abl genes.
|
8242587 |
1993 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Two-thirds of patients with Philadelphia (Ph) chromosome-positive acute lymphoblastic leukaemia (ALL) have a breakpoint in the minor breakpoint cluster region (m-bcr) of the BCR gene, which results in an e1a2 transcript and a P190BCR-ABL fusion protein.
|
8289491 |
1994 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
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 |
|
Acute lymphocytic leukemia
|
0.100 |
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 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
BCR rearrangement without juxtaposition of ABL in pre-T acute lymphoblastic leukaemia.
|
8639438 |
1996 |
|
Acute lymphocytic leukemia
|
0.100 |
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 |
|
Acute lymphocytic leukemia
|
0.100 |
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 |
|
Acute lymphocytic leukemia
|
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 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We used alpha-IFN to treat 10 adult P190BCR-ABL+ ALL patients (eight newly diagnosed; two in first relapse).
|
10637472 |
2000 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Complex chromosome 9, 20, and 22 rearrangements in acute lymphoblastic leukemia with duplication of BCR and ABL sequences.
|
10640143 |
2000 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Molecular therapeutic approaches, for example, those directed against the fusion protein BCR-ABL with ABL-tyrosine kinase inhibitor, are on the way to creating a new avenue for the treatment of ALL.
|
11049022 |
2000 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
BCR/ABL fluorescent in situ hybridization study of chronic myeloid leukemia (CML) and Philadelphia(+) (Ph(+)) acute lymphoid leukemia (ALL) indicated that approximately 9% of patients exhibited an atypical hybridization pattern consistent with a submicroscopic deletion of the 5' region of ABL and the 3' region of the BCR genes on the 9q(+) chromosome.
|
11369654 |
2001 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
However, we detected two ALL cases with ABL deletion but without BCR/ABL rearrangement among 49 Ph(-) ALL and 66 Ph(-) AML patients.
|
12759927 |
2003 |
|
Acute lymphocytic leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In a 25-month follow-up, the transcriptional levels of WT-1, Bcr-Abl, and Abl gene, were quantitatively measured in bone marrow cells from 25 CML or acute lymphoblastic leukemia (ALL) patients with the Ph chromosome.
|
15265366 |
2004 |
|
Acute lymphocytic leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Deletions from the derivative chromosome 9, der(9), of the translocation, t(9;22)(q34;q11), at the site of the ABL/BCR fusion gene, have been demonstrated by fluorescence in situ hybridisation (FISH), in both Philadelphia chromosome (Ph)-positive chronic myeloid leukaemia (CML) and acute lymphoblastic leukaemia (ALL).
|
15716990 |
2005 |