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

TRIP13 protects pancreatic cancer cells against intrinsic and therapy-induced DNA replication stress.

NAR cancer - 1 Mar 2025

Anand Jay R, Droby Gaith N, Joseph Sayali, Patel Urvi, Zhang Xingyuan, Klomp Jeffrey A, Der Channing J, Purvis Jeremy E, Wolff Samuel C, Bowser Jessica L, Vaziri Cyrus

Abstract excerpt

Oncogene activation in normal untransformed cells induces DNA replication stress and creates a dependency on DNA damage response (DDR) mechanisms for cell survival. Different oncogenic stimuli signal via distinct mechanisms in every cancer setting. The DDR is also pathologically reprogrammed and deployed in diverse ways in different cancers. Because mutant KRAS is the driver oncogene in 90% of pancreatic ductal...

Read the complete abstract on PubMed

Topics

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

Share to ATPases Associated with Diverse Cellular Activities
Share to Carcinoma, Pancreatic Ductal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Line, Tumor

Share to Cell Survival

Share to DNA Damage

Share to DNA Replication

Share to Pancreatic Neoplasms

Share to Proto-Oncogene Proteins p21(ras)

Source

Open in PubMed Open full text

Identifiers

PMID: 40115747
DOI: 10.1093/narcan/zcaf009
PMCID: PMC11923746

Genes

TRIP13
KRAS

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

TRIP13 protects pancreatic cancer cells against intrinsic and therapy-induced DNA replication stress.PMID 40115747Read ↗

TRIP13 protects pancreatic cancer cells against intrinsic and therapy-induced DNA replication stressSemantic proximity Read ↗

Targeting DNA Damage Response and Replication Stress in Pancreatic CancerSemantic proximity Read ↗

Targeting DNA Damage Response and Replication Stress in Pancreatic CancerSemantic proximity Read ↗

PCNA Inhibition Enhances the Antitumor Activity of KRAS-Targeted Therapies in Pancreatic CancerSemantic proximity Read ↗

Base-excision repair pathway regulates transcription-replication conflicts in pancreatic ductal adenocarcinomaSemantic proximity Read ↗

Base Excision Repair Pathway Regulates Transcription-Replication Conflicts in Pancreatic Ductal AdenocarcinomaSemantic proximity Read ↗

Cytidine deaminase protects pancreatic cancer cells from replicative stress and drives resistance to DNA-targeting drugsSemantic proximity Read ↗

Therapeutic Targeting of Oncogene-induced Transcription-Replication Conflicts in Pancreatic Ductal AdenocarcinomaSemantic proximity Read ↗

Inhibition of DNA2 nuclease as a therapeutic strategy targeting replication stress in cancer cellsSemantic proximity Read ↗

Combination of PARP and KRASG12D inhibitors enhances therapeutic efficacy by exploiting vulnerabilities in PDAC.Semantic proximity Read ↗

Inhibition of DNA2 nuclease as a therapeutic strategy targeting replication stress in cancer cellsSemantic proximity Read ↗

Changes in the Transcriptome and Synthetic Lethal Dependencies Following <i>KRAS</i> Mutant Expression Reveal Profound Tissue-SpecificitySemantic proximity Read ↗

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