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Article

CALCRL knockdown suppresses cancer stemness and chemoresistance in acute myeloid leukemia with FLT3-ITD and DNM3TA-R882 double mutations.

Drug development research - 1 Feb 2024

Tang Shanhao, Zhu Huiling, Sheng Lixia, Mu Qitian, Wang Yi, Xu Kaihong, Zhou Miao, Xu Zhijuan, Wu An, Ouyang Guifang

Abstract excerpt

Acute myeloid leukemia (AML) patients with FLT3 internal tandem duplication (FLT3-ITD) and DNA methyltransferase 3A (DNMT3A) R882 double mutations had a worse prognosis compared with AML with FLT3-ITD or DNMT3A R882 single mutation. This study was designed to explore the specific role of Calcitonin Receptor Like (CALCRL) in AML with FLT3-ITD and DNMT3A R882 double mutations. MOLM13 cells were transduced with...

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Share to Cytarabine
Share to Drug Resistance, Neoplasm

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to fms-Like Tyrosine Kinase 3

Share to DNMT3A gene

Share to Leukemia, Myeloid, Acute

Share to Mutation

Share to Receptors, Calcitonin

Share to RNA, Guide, CRISPR-Cas Systems

Source

Identifiers

PMID: 38349260
DOI: 10.1002/ddr.22137

Genes

CALCRL
DNMT3A
FLT3
SOX2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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