BCR/ABL fusion located on chromosome 9 in chronic myeloid leukemia with a masked Ph chromosome.

Genes Chromosomes Cancer

Department of Pathology, Harper Hospital, Wayne State University, Detroit, Michigan 48201, USA.

Published: June 1995

AI Article Synopsis

Article Abstract

A reciprocal translocation, t(10;22)(q22;q11), resulting in a masked Ph chromosome was identified in a patient diagnosed with chronic myeloid leukemia (CML). Both homologs of chromosome 9 were of the normal pattern. Two signals for the ABL probe, both of them hybridized to chromosome 9, were demonstrated via fluorescence in situ hybridization (FISH). Furthermore, cohybridization with two differently labeled BCR/ABL translocation DNA probes indicated a BCR/ABL fusion apparently located on 9q34. Molecular studies revealed a rearrangement of the BCR region and expression of a chimeric BCR/ABL mRNA of CML configuration. These findings indicate that the BCR/ABL fusion resulted from an unusual relocation of the BCR gene from its normal position on 22q11 to 9q34 adjacent to the ABL gene.

Download full-text PDF

Source
http://dx.doi.org/10.1002/gcc.2870130210DOI Listing

Publication Analysis

Top Keywords

bcr/abl fusion
12
fusion located
8
chronic myeloid
8
myeloid leukemia
8
masked chromosome
8
bcr/abl
5
chromosome
5
located chromosome
4
chromosome chronic
4
leukemia masked
4

Similar Publications

Despite the study of BCR::ABL1-positive and -negative myeloproliferative neoplasms (MPNs) providing seminal insights into cancer biology, tumor evolution and precision oncology over the past half century, significant challenges remain. MPNs are clonal hematopoietic stem cell-derived neoplasms with heterogenous clinical phenotypes and a clonal architecture which impacts the often-complex underlying genetics and microenvironment. The major driving molecular abnormalities have been well characterized, but debate on their role as disease-initiating molecular lesions continues.

View Article and Find Full Text PDF

Vodobatinib is a Bcr-Abl 1 inhibitor, currently entering into Phase 2 clinical trials as a potential drug to treat glioblastoma patients. In the present work, a validated high-performance liquid chromatography (HPLC) detection method for the quantification of vodobatinib in rat plasma was established. Sample preparation involved liquid-liquid extraction method.

View Article and Find Full Text PDF

Overexpression of the myeloid Src-family kinases Fgr and Hck has been linked to the development of acute myeloid leukemia (AML). Here we characterized the contribution of active forms of these kinases to AML cell cytokine dependence, inhibitor sensitivity, and AML cell engraftment in vivo. The human TF-1 erythroleukemia cell line was used as a model system as it does not express endogenous Hck or Fgr.

View Article and Find Full Text PDF

[Acquisition of Primary Ph Bone Marrow Cells and Establishment of Ph B-ALL Mouse Model].

Zhongguo Shi Yan Xue Ye Xue Za Zhi

December 2024

Blood Disease Institute, Xuzhou Medical University,Xuzhou 221000, Jiangsu Province, China.

Article Synopsis
  • The objective of the study was to harvest primary Philadelphia chromosome-positive (Ph) cells from B-acute lymphoblastic leukemia (B-ALL) and create a B-ALL mouse model.
  • Methods included infecting bone marrow cells from C57BL/6J mice with a retrovirus, followed by the transplantation of transfected cells into irradiated mice, resulting in the establishment of multiple generations of Ph cells.
  • The results showed significant health deterioration in the mice post-transplant, with pathological features such as weight loss and leukemic cell infiltration in the liver, confirming the successful creation of a B-ALL mouse model through progressive passages of Ph cells.
View Article and Find Full Text PDF

Identification of novel BCR::ABL1 kinase domain mutation in patients with chronic myeloid leukaemia and imatinib resistance.

Malays J Pathol

December 2024

National Institutes of Health, Institute for Medical Research, Cancer Research Centre, Haematology Unit, 40170 Shah Alam, Selangor, Malaysia.

Introduction: The emergence of mutations in the BCR::ABL1 kinase domain (KD) impairs imatinib mesylate (IM) binding capacity, thus contributing to IM resistance. Identification of these mutations is important for treatment decisions and precision medicine in chronic myeloid leukaemia (CML) patients. Our study aims to determine the frequency of BCR::ABL1 KD mutations in CML patients with IM resistance.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!