The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Trp53R172H and KrasG12D cooperate to promote chromosomal instability and widely metastatic pancreatic ductal adenocarcinoma in mice
Open accessAbstract
To define the genetic requirements for pancreatic ductal adenocarcinoma (PDA), we have targeted concomitant endogenous expression of Trp53(R172H) and Kras(G12D) to the mouse pancreas, revealing the cooperative development of invasive and widely metastatic carcinoma that recapitulates the human disease. The primary carcinomas and metastases demonstrate a high degree of genomic instability manifested by nonreciprocal translocations without obvious telomere erosion-hallmarks of human carcinomas not typically observed in mice. No mutations were discovered in other cardinal tumor suppressor gene pathways, which, together with previous results, suggests that there are distinct genetic pathways to PDA with different biological behaviors. These findings have clear implications for understanding mechanisms of disease pathogenesis, and for the development of detection and targeted treatment strategies.
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“which is derived from a liver metastasis of the autochthonous KPC model of pancreatic cancer,73 which recapitulates the low immunogenicity and immunotherapy responsiveness of the human pancreatic cancer.”
From Cystatin C is glucocorticoid responsive, directs recruitment of Trem2+ macrophages, and predicts failure of cancer immunotherapy (2023) · cites this paper as [73]
In the citing paper
“GEMMs with compound mutations that combine Kras mutation with the inactivation of tumor suppressor genes Cdkn2a and Tp53, or with the inactivation of the TGFβ-SMAD4 signaling pathway in the pancreas develop invasive and metastatic PDAC (74–76), thus validating the role of these tumor suppressor pathways in PDAC progression (4).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [75]
In the citing paper
“combined expression of oncogenic Kras coupled with the deletion or loss of function of Trp53, Cdkn2a, or Smad4 in the pancreas of mice readily leads to invasive PDAC29–32.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [30]
In the citing paper
“altered p53 function has a multitude of tumor-promoting effects on neoplastic cells, including increased genomic instability30, reprogrammed cellular metabolism57,58, and enhanced metastatic propensity59.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [30]
Citations
Cites
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Burris, H. A., Moore, M. J., Andersen, J., Green, M. R., Rothenberg, M. L., Modiano, M., Cripps, M. C., Portenoy, R. K., Storniolo, A. M., Tarassoff, P. G., et al. (1997) · Journal of Clinical Oncology · doi:10.1200/jco.1997.15.6.2403 · Cited by 5,895
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
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Genetic instabilities in human cancers
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Participation of p53 protein in the cellular response to DNA damage.
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Crystal Structure of a p53 Tumor Suppressor-DNA Complex: Understanding Tumorigenic Mutations
Cho, Y., Gorina, S., Jeffrey, P. D., & Pavletich, N. P. (1994) · Science · doi:10.1126/science.8023157 · Cited by 2,559 · cited 1×
“The TP53R175H mutation (Trp53R172H in mice) results in a partially denatured structure that impairs DNA binding (Cho et al., 1994).”
BackgroundPreinvasive and invasive ductal pancreatic cancer and its early detection in the mouse
Hingorani, S. R., Petricoin, E. F., Maitra, A., Rajapakse, V., King, C., Jacobetz, M. A., Ross, S., Conrads, T. P., Veenstra, T. D., Hitt, B. A., et al. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00309-x · Cited by 2,471
Self-citationTumor spectrum analysis in p53-mutant mice
Jacks, T., Remington, L., Williams, B. O., Schmitt, E. M., Halachmi, S., Bronson, R. T., & Weinberg, R. A. (1994) · Current Biology · doi:10.1016/s0960-9822(00)00002-6 · Cited by 2,051
Genetic instability in colorectal cancers
Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1997) · Nature · doi:10.1038/386623a0 · Cited by 1,995
Cited by
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Olive, K. P., Jacobetz, M. A., Davidson, C. J., Gopinathan, A., McIntyre, D., Honess, D., Madhu, B., Goldgraben, M. A., Caldwell, M. E., Allard, D., et al. (2009) · Science · doi:10.1126/science.1171362 · Cited by 3,170
Self-citationÖzdemir, B. C., Pentcheva-Hoang, T., Carstens, J. L., Zheng, X., Wu, C.-C., Simpson, T. R., Laklai, H., Sugimoto, H., Kahlert, C., Novitskiy, S. V., et al. (2014) · Cancer Cell · doi:10.1016/j.ccr.2014.04.005 · Cited by 2,681
Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver
Costa-Silva, B., Aiello, N. M., Ocean, A. J., Singh, S., Zhang, H., Thakur, B. K., Becker, A., Hoshino, A., Mark, M. T., Molina, H., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3169 · Cited by 2,692
Distinct populations of inflammatory fibroblasts and myofibroblasts in pancreatic cancer
Öhlund, D., Handly-Santana, A., Biffi, G., Elyada, E., Almeida, A. S., Ponz-Sarvise, M., Corbo, V., Oni, T. E., Hearn, S. A., Lee, E. J., et al. (2017) · Journal of Experimental Medicine · doi:10.1084/jem.20162024 · Cited by 2,590
Self-citationHidalgo, M. (2010) · New England Journal of Medicine · doi:10.1056/nejmra0901557 · Cited by 2,570
Metadata
- Authors
- Hingorani, S. R., Wang, L., Multani, A. S., Combs, C., Deramaudt, T. B., Hruban, R. H., Rustgi, A. K., Chang, S., & Tuveson, D. A.
- Affiliations
- Abramson Cancer Center (US)
- The University of Texas MD Anderson Cancer Center (US)
- Johns Hopkins University (US)
- University of Pennsylvania (US)
- Corresponding author
- Hingorani, Sunil R.
- Tuveson, David A.
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2005-05
- Volume
- 7
- Issue
- 5
- Pages
- 469-483
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W1992995822
- Cited by
- 2,609
- References
- 61
- Citations by year
- 2026: 128 · 2025: 127 · 2024: 208 · 2023: 213 · 2022: 171 · 2021: 217 · 2020: 180 · 2019: 176 · 2018: 164 · 2017: 151 · 2016: 146 · 2015: 128 · 2014: 112 · 2013: 116 · 2012: 77
- FWCI
- 18.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (K08AG001019)
- National Cancer Institute (R25-CA87812, P50CA-62924, U01CA084291, R25CA087812, R01CA101973, P50CA062924)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK60694, R01DK060694)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- pancreatic ductal adenocarcinoma, KRAS G12D, chromosomal instability, non-reciprocal translocation, metastasis, tumor suppressor, oncogene cooperation, mouse model, pancreatic carcinogenesis, genomic instability
- MeSH terms
- Animals, Chromosome Aberrations, Gene Expression Regulation, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Mutant Strains, Mice, Transgenic, Neoplasm Metastasis, Translocation, Genetic, Gene Rearrangement, Trans-Activators, Cadherins, Gene Expression, Survival Analysis, Genes, Tumor Suppressor, Tumor Suppressor Protein p53, Proto-Oncogene Proteins p21(ras), Telomere, Centrosome, Homeodomain Proteins, Disease Progression, ras Proteins, Oncogene Proteins v-erbB, Integrases, Mutation, Missense, Cytogenetic Analysis, Carcinoma, Pancreatic Ductal, Chromosomal Instability, Mice
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