ArticleOncogene2004
The PI 3-kinase/Akt signaling pathway is activated due to aberrant Pten expression and targets transcription factors NF-kappaB and c-Myc in pancreatic cancer cells.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 149 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
149 citing papers in PubMed, 295 citations in OpenAlex.
- A phase I/II, non-randomized, feasibility/safety and efficacy study of the combination of everolimus, cetuximab and capecitabine in patients with advanced pancreatic cancer.Investigational new drugs · 2013Trial
- Inhibition of the mammalian target of rapamycin (mTOR) in advanced pancreatic cancer: results of two phase II studies.BMC cancer · 2010Trial
- Oral mTOR inhibitor everolimus in patients with gemcitabine-refractory metastatic pancreatic cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009Trial
- Oral microbiota member Neisseria elongata exosomes-Cassia fistula association targets PTEN/AKT/IL10/IL1β/BAX/BCL-2 signaling pathway in pancreatic cancer immunotherapy.Antonie van Leeuwenhoek · 2026Article
- PTEN Oxidation Promotes Constitutive PI3K Signaling and Inducible Macropinocytosis in Pancreatic Cancer.Cancer research · 2026Article
- CCR-CCL axes as key upstream influencers of pancreatic ductal adenocarcinoma: CCR2-CCL2, CCR5-CCL5, CCR4-CCL17/22, CCR6-CCL20, CCR7-CCL19/21.Frontiers in immunology · 2026Review
- CX26 promotes pancreatic cancer progression by competitively inhibiting interaction of c-Myc with PSMD2 and enhancing c-Myc stability.Journal of translational medicine · 2025Article
- Muscle fiber Myc is dispensable for muscle growth and its forced expression severely perturbs homeostasis.Nature communications · 2025Article
- Stepwise Stiffening/Softening of and Cell Recovery from Reversibly Formulated Hydrogel Interpenetrating Networks.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- Identified γ-glutamyl cyclotransferase (GGCT) as a novel regulator in the progression and immunotherapy of pancreatic ductal adenocarcinoma through multi-omics analysis and experiments.Journal of cancer research and clinical oncology · 2024Article
- Stepwise Stiffening/Softening of and Cell Recovery from Reversibly Formulated Hydrogel Double Networks.bioRxiv : the preprint server for biology · 2024Article
- Novel PIKfyve/Tubulin Dual-target Inhibitor as a Promising Therapeutic Strategy for B-cell Acute Lymphoblastic Leukemia.Current medical science · 2024Article
- Dynamics simulations of hypoxia inducible factor-1 regulatory network in cancer using formal verification techniques.Frontiers in molecular biosciences · 2024Article
- Role of inositol polyphosphate-4-phosphatase type II in oncogenesis of digestive system tumors.World journal of gastrointestinal oncology · 2023Review
- circACTR2 attenuates gemcitabine chemoresiatance in pancreatic cancer through PTEN mediated PI3K/AKT signaling pathway.Biology direct · 2023Article
- Target-Based Anticancer Indole Derivatives for the Development of Anti-Glioblastoma Agents.Molecules (Basel, Switzerland) · 2023Review
- Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022Article
- Pancreatic Cancer: Beyond Brca Mutations.Journal of personalized medicine · 2022Review
- Mechanistic and functional extrapolation of SET and MYND domain-containing protein 2 to pancreatic cancer.World journal of gastroenterology · 2022Review
- Implications of prognosis-associated genes in pancreatic tumor metastasis: lessons from global studies in bioinformatics.Cancer metastasis reviews · 2021Review
89 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The persistent activation of signaling cascades results in dramatic consequences that include loss of cellular growth control and neoplastic transformation. We show here that phosphoinositide 3-kinase (PI 3-kinase) and its mediator Akt were constitutively activated in pancreatic cancer and that this might be due to the aberrant expression of their natural antagonist MMAC/PTEN. Indeed, our results show that MMAC/PTEN expression was either lost or significantly reduced in five of eight cell lines and in twelve of seventeen tumor specimens examined. That the poor expression of MMAC/PTEN in pancreatic cancer cells could be due to promoter methylation was indicated by methylation-specific PCR analysis. Our studies also indicated that PI 3-kinase targeted two important transcription factors in pancreatic cancer cells. The ability of constitutively activated NF-kappaB to induce gene expression and the stabilization of c-MYC protein by decreased phosphorylation of Thr58 were both dependent on PI 3-kinase activity. When pancreatic cancer cells were treated with a peptide antagonist of NF-kappaB nuclear translocation, or stably transfected with a dominant-negative mutant of MYC, their proliferation was markedly inhibited. Taken together, these data indicate that the aberrant expression of MMAC/PTEN contributes to the activation of the PI 3-kinase/Akt pathway and its transcription factor mediators in pancreatic cancer.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.