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
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gene which result in constitutive activation of KRas and multiple downstream signaling pathways. It has been difficult to develop specific KRas inhibitors and/or methods that result in recovery of functional TP53 activity. To further elucidate the roles of TP53 in drug-resistance of pancreatic cancer cells, we introduced wild-type (WT) TP53 or a control vector into two different PDAC cell lines. Introduction of WT-TP53 increased the sensitivity of the cells to multiple chemotherapeutic drugs, signal transduction inhibitors, drugs and nutraceuticals and influenced key metabolic properties of the cells. Therefore, TP53 is a key molecule which is critical in drug sensitivity and metabolism of PDAC.
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TP53 mutations occur in late-stage PanINs, indicating p53's role in inhibiting transformation into PDAC.
“Mutations occur in late-stage PanINs, indicating the p53’s role in inhibiting transformation into PDAC.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [29]
The Introduction (‘Genes implicated in PDAC’; page unavailable) identifies TP53 as involved in PDAC progression and describes TP53 properties important for suppressing cell growth. It does not say that TP53 mutations occur in late-stage PanINs or establish p53’s role specifically in preventing their transformation into PDAC. (LLM, conf=0.78)
Experimental — accuracy not yet measuredIn mouse models, intact p53 protects against pancreatic cancer progression, confirming its role in suppressing malignant transformation.
“In mouse models, intact p53 protects against pancreatic cancer progression, confirming its role in suppressing malignant transformation [17,29,36].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [29]
The Abstract (page unavailable) calls TP53 a tumor suppressor gene in pancreatic cancer, supporting the general tumor-suppressor role. But the paper describes experiments in PDAC cell lines, not mouse models, and does not show that intact p53 protects mice against pancreatic cancer progression. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTP53 plays a crucial role in suppressing malignant transformation in pancreatic cancer.
“TP53 plays a crucial role in suppressing malignant transformation in pancreatic cancer.”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [29]
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- Authors
- McCubrey, J. A., Meher, A. K., Akula, S. M., Abrams, S. L., Steelman, L. S., LaHair, M. M., Franklin, R. A., Martelli, A. M., Ratti, S., Cocco, L., Barbaro, F., Duda, P., & Gizak, A.
- Affiliations
- East Carolina University (US)
- University of Bologna (IT)
- University of Parma (IT)
- University of Wrocław (PL)
- Corresponding author
- McCubrey, James A.
- ORCID
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2022-04-27
- Volume
- 14
- Issue
- 8
- Pages
- 3365-3386
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC9085237
- OpenAlex
- W4225092354
- Cited by
- 12
- References
- 103
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 3
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- The Scholarship East Carolina University's Institutional Repository (East Carolina University) (submittedVersion)
- Funders
- East Carolina University (#111110-668715-0000, #111104)
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL146685)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- TP53, pancreatic ductal adenocarcinoma, drug resistance, chemosensitivity, KRAS, nutraceuticals, cancer metabolism
- MeSH terms
- Gain of Function Mutation, Mechanistic Target of Rapamycin Complex 1, Phosphoinositide-3 Kinase Inhibitors, Humans, Mutation, Pancreatic Neoplasms, Tumor Suppressor Protein p53, Proto-Oncogene Proteins p21(ras), Dietary Supplements, Phosphatidylinositol 3-Kinases, Mitogen-Activated Protein Kinase Kinases, Carcinoma, Pancreatic Ductal, Glycogen Synthase Kinase 3, Cell Line, Tumor, Cell Proliferation, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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