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

Topics Community

Article

Mutant p53 stimulates chemoresistance of pancreatic adenocarcinoma cells to gemcitabine.

Biochimica et biophysica acta - 1 Jan 2015

Fiorini Claudia, Cordani Marco, Padroni Chiara, Blandino Giovanni, Di Agostino Silvia, Donadelli Massimo

Abstract excerpt

Pancreatic adenocarcinoma (PDAC) is the fourth leading cause of cancer-related deaths worldwide; PDAC is characterized by poor prognosis, resistance to conventional chemotherapy and high mortality rate. TP53 tumor suppressor gene is frequently mutated in PDAC, resulting in the accumulation of mutated protein with potential gain-of-function (GOF) activities, such as genomic instability, hyperproliferation and...

Topics

Adenocarcinoma
Antimetabolites, Antineoplastic
Apoptosis
Autophagy
Cell Line, Tumor
Cell Proliferation
Deoxycytidine
Drug Resistance, Neoplasm
Humans
Mutation
Pancreatic Neoplasms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Phosphorylation

Pyrimidines

Tumor Suppressor Protein p53

Gemcitabine

Source

Identifiers

PMID: 25311384
DOI: 10.1016/j.bbamcr.2014.10.003

Genes

CCNB1
GEM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 31 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mutant p53 stimulates chemoresistance of pancreatic adenocarcinoma cells to gemcitabine.PMID 25311384Read ↗

Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties.Semantic proximity Read ↗

P53 reactivator PRIMA-1 MET synergizes with 5-Fluorouracil to induce apoptosis in pancreatic tumor cellsSemantic proximity Read ↗

Impact of RUNX2 on drug-resistant human pancreatic cancer cells with p53 mutations.Semantic proximity Read ↗

MicroRNA Profiling Implies New Markers of Gemcitabine Chemoresistance in Mutant p53 Pancreatic Ductal Adenocarcinoma.Semantic proximity Read ↗

Targeting P53 as a Future Strategy to Overcome Gemcitabine Resistance in Biliary Tract CancersSemantic proximity Read ↗

Drug-Induced p53 Activation Limits Pancreatic Cancer InitiationSemantic proximity Read ↗

PRIMA-1, a mutant p53 reactivator, induces apoptosis and enhances chemotherapeutic cytotoxicity in pancreatic cancer cell lines.Semantic proximity Read ↗

Enhancement of gemcitabine-induced apoptosis by restoration of p53 function in human pancreatic tumors.Semantic proximity Read ↗

Overcoming therapeutic resistance in pancreatic cancer: Emerging opportunities by targeting BRCAs and p53Semantic proximity Read ↗

Effects of TP53 Mutations and miRs on Immune Responses in the Tumor Microenvironment Important in Pancreatic Cancer Progression.Semantic proximity Read ↗

Overcoming drug resistance in pancreatic cancer.Semantic proximity Read ↗

Garcinol sensitizes human pancreatic adenocarcinoma cells to gemcitabine in association with microRNA signatures.Semantic proximity Read ↗

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