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Article

Discovery of a small molecule targeting SET-PP2A interaction to overcome BCR-ABLT315I mutation of chronic myeloid leukemia.

Oncotarget - 20 May 2015

Wang Shuzhen, Xie Weiquan, Wang Duowei, Peng Zhigang, Zheng Yan, Liu Nan, Dai Wen, Wang Yang, Wang Zongqiang, Yang Yong, Chen Yijun

Abstract excerpt

Despite the great success in using tyrosine kinase inhibitors (TKIs) to treat chronic myeloid leukemia (CML), the frequent development of multi-drug resistance, particularly the T315I mutation of BCR-ABL, remains a challenging issue. Enhancement of protein phosphatase 2A (PP2A) activity by dissociating its endogenous inhibitor SET is an effective approach to combat TKI-based resistance. Here, we report the...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Proliferation

Share to Fusion Proteins, bcr-abl

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Share to Mice, Inbred BALB C

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Source

Open in PubMed Open full text

Identifiers

PMID: 25900240
DOI: 10.18632/oncotarget.3665
PMCID: PMC4494927

Genes

SET
BCR

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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