ArticleThe Indian journal of medical research2016
Dual transcripts of
Article in The Indian journal of medical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Identification of a novel cryptic variant chromosomal rearrangement involving 9q34, 22q11.2, and 5q22 resulting in ins(9;22) and t(5;22) in chronic myeloid leukemia: a case report.Annals of hematology · 2024Article
- VNTR polymorphism in the breakpoint region of ABL1 and susceptibility to bladder cancer.BMC medical genomics · 2021Article
- Potential Role of Curcumin and Its Nanoformulations to Treat Various Types of Cancers.Biomolecules · 2021Review
- Curcumin as a therapeutic agent in leukemia.Journal of cellular physiology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
objectivesChronic myeloid leukaemia is (CML) characterized by the presence of a hallmark chromosomal translocation, the Philadelphia chromosome. Although there are many reports available regarding the different variants of BCR-ABL in CML, we studied the co-expression of e13a2 and e14a2 transcripts and a few polymorphisms in CML patients.
methodsMolecular genetics approach was adapted to screen for polymorphisms, mutation and translocation in BCR, ABL kinase domain and BCR-ABL breakpoint region in 73 CML patients.
resultsAll eight patients with dual transcripts were found to harbour an exonic polymorphism (c.2700 T>C) and an intronic polymorphism (g.109366A>G) that were earlier reported to be associated with co-expression of both the transcripts. We also observed c.763G>A mutation in ABL kinase domain and two polymorphisms, c.2387 A>G and c.2736A>G in the BCR gene. INTERPRETATION &
conclusionsThough our data support the previous findings that co-expression of BCR-ABL transcripts is due to the occurrence of exonic and intronic polymorphisms in the BCR gene, it also shows that the intronic polymorphism can arise without the linked exonic polymorphism. The occurrence of ABL kinase domain mutation is less frequent in Indian population.
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