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

Wee1 promotes cell proliferation and imatinib resistance in chronic myeloid leukemia via regulating DNA damage repair dependent on ATM-γH2AX-MDC1

27 Dec 2022

Abstract excerpt

BACKGROUND: The treatment of chronic myeloid leukemia (CML) is facing the dilemma of tyrosine kinase inhibitors (TKIs) resistance and disease recurrence. The dysfunctional DNA damage repair mechanism plays an essential role not only in the initiation and progression of hematological malignancies but also links to the development of TKI resistance. Deciphering the abnormally regulated DNA damage repair and...

Read the complete abstract on PubMed

Topics

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

Share to Chronic Myeloid Leukemia Treatments
Share to DNA Repair Mechanisms
Share to Microtubule and mitosis dynamics

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36575478
DOI: 10.1186/s12964-022-01021-z

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 23 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Wee1 promotes cell proliferation and imatinib resistance in chronic myeloid leukemia via regulating DNA damage repair dependent on ATM-γH2AX-MDC1PMID 36575478Read ↗

A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target.Semantic proximity Read ↗

A Review on the Therapeutic Role of TKIs in Case of CML in Combination With Epigenetic DrugsSemantic proximity Read ↗

CHK1 and WEE1 inhibition combine synergistically to enhance therapeutic efficacy in acute myeloid leukemia ex vivoSemantic proximity Read ↗

Myt1 overexpression mediates resistance to cell cycle and DNA damage checkpoint kinase inhibitorsSemantic proximity Read ↗

Predictive and Prognostic Value of DNA Damage Response Associated Kinases in Solid TumorsSemantic proximity Read ↗

Exploring the Involvement of FoxM1 in CML Cells from DNA Damage Response-Regulatory ProspectiveSemantic proximity Read ↗

Leukemia stem cells: the root of chronic myeloid leukemiaSemantic proximity Read ↗

DNA damage accumulation and repair defects in acute myeloid leukemia: implications for pathogenesis, disease progression, and chemotherapy resistance.Semantic proximity Read ↗

Polo-like Kinase-1, Aurora Kinase A and Wee1 Kinase Are Novel Therapeutic Targets in Chronic Myeloid LeukemiaSemantic proximity Read ↗

Molecular Pathways: Targeting the Protein Kinase Wee1 in CancerSemantic proximity Read ↗

DNA damage response defects in hematologic malignancies: mechanistic insights and therapeutic strategiesSemantic proximity Read ↗

Cancer Vulnerabilities Through Targeting the ATR/Chk1 and ATM/Chk2 Axes in the Context of DNA DamageSemantic proximity Read ↗

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