Varaico: Literature-Extracted Genetic Variants

Gene:ABL1
Variant:p.M388L
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ABL1

NM_005157.6:p.M388L

Associated Papers

A Retrospective Analysis of BCR-ABL1 Kinase Domain Mutations in the Frontline Drug Intolerant or Resistant Chronic Myeloid Leukemia Patients: An Indian Experience from a High-End Referral Laboratory.

Majumdar A et al.

South Asian Journal of Cancer, 2024

Detection of kinase domain mutations in BCR::ABL1 leukemia by ultra-deep sequencing of genomic DNA.

Sánchez R et al.

Scientific Reports, 2022

35906470 (PubMed )
Supplement: 41598_2022_17271_MOESM2_ESM.pdf

The Immunogenic Potential of Recurrent Cancer Drug Resistance Mutations: An In Silico Study.

Punta M et al.

Frontiers in Immunology, 2020

33133066 (PubMed )
Supplement: Table_1.xlsx › Resistance-ABL1

Comparison of Frequency and Sensitivity of BCR-ABL1 Kinase Domain Mutations in Asian and White Patients With Imatinib-resistant Chronic-Phase Chronic Myeloid Leukemia.

Kim H et al.

Clinical Lymphoma, Myeloma & Leukemia, 2018

The use of Imatinib resistance mutation analysis to direct therapy in Philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukaemia patients failing Imatinib treatment, in Patan Hospital, Nepal.

Kayastha GK et al.

British Journal of Haematology, 2017

BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.

Zabriskie MS et al.

Cancer Cell, 2014

Implications of BCR-ABL1 kinase domain-mediated resistance in chronic myeloid leukemia.

Soverini S et al.

Leukemia Research, 2014

BCR-ABL kinase domain mutations in tyrosine kinase inhibitors-naïve and -exposed Southeast Asian chronic myeloid leukemia patients.

Wongboonma W et al.

Experimental and Molecular Pathology, 2012

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Regarding the variants extracted from papers and shown text snippets from research papers, the following holds: "Some rights reserved. This work permits non-commercial use, distribution and reproduction in any medium, provided the original author and source are credited."