Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Biological Features of KLC2 Mutations in Chronic Myeloid Leukemia and Their Contribution to Inducing Drug Resistance.

Oncology research - 1 Jan 2025

Bera Rabindranath, Ochi Yotaro, Huang Ying-Jung, Kuo Ming-Chung, Yoshida Kenichi, Ogawa Seishi, Shih Lee-Yung

Abstract excerpt

Background: Breakpoint Cluster Region-Abelson (BCR::ABL1) fusion protein is essential in the pathogenesis of chronic myeloid leukemia (CML); however, the chronic-to-blast phase transformation remains elusive. We identified novel kinesin light chain 2 (KLC2) mutations in CML-myeloid blast phase patients. We aimed to examine the functional role of KLC2 mutations in leukemogenesis. Methods: To evaluate the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Fusion Proteins, bcr-abl
Share to Imatinib Mesylate

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to K562 Cells

Share to Kinesins

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

Share to Microtubule-Associated Proteins

Share to STAT3 Transcription Factor

Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 41502514
DOI: 10.32604/or.2025.070259
PMCID: PMC12774541

Genes

KLC2
ABL1
BCR
SMAD2
STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Biological Features of KLC2 Mutations in Chronic Myeloid Leukemia and Their Contribution to Inducing Drug Resistance.PMID 41502514Read ↗

Therapeutic targeting of CK2 in acute and chronic leukemiasSemantic proximity Read ↗

A novel mouse model identifies cooperating mutations and therapeutic targets critical for chronic myeloid leukemia progression.Semantic proximity Read ↗

Multi-omics analysis reveals CLEC2A is a leukemia-restricted CART target in KMT2A-rearranged Acute Myeloid LeukemiaSemantic proximity Read ↗

β-Arrestin2 mediates the initiation and progression of myeloid leukemia.Semantic proximity Read ↗

CaMKK2 Identifies Biologically Aggressive Chronic Lymphocytic Leukemia and Regulates Leukemic Survival and Nurse-Like Cell SupportSemantic proximity Read ↗

Disrupting BCR-ABL in combination with secondary leukemia-specific pathways in CML cells leads to enhanced apoptosis and decreased proliferation.Semantic proximity Read ↗

Mutant Cbl proteins as oncogenic drivers in myeloproliferative disordersSemantic proximity Read ↗

E3 ligase-defective Cbl mutants lead to a generalized mastocytosis and myeloproliferative disease.Semantic proximity Read ↗

Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies.Semantic proximity Read ↗

CXCR2 As a Novel Target for Overcoming Resistance to Tyrosine Kinase Inhibitors in Chronic Myelogenous Leukemia CellsSemantic proximity Read ↗

Novel oncogenic mutations of CBL in human acute myeloid leukemia that activate growth and survival pathways depend on increased metabolism.Semantic proximity Read ↗

JAK2 is dispensable for maintenance of JAK2 mutant B-cell acute lymphoblastic leukemias.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.