Loss of p53 and SMAD4 Induces Adenosquamous Subtype Pancreatic Cancer in the Absence of an Oncogenic KRAS Mutation

Authors

Daowei Yang
Xinlei Sun
Rohan Moniruzzaman
Hua Wang
Citu Citu
Zhongming Zhao
Ignacio I Wistuba
Huamin Wang
Anirban Maitra
Yang Chen

Publication Date

9-17-2024

Journal

Cell Reports Medicine

DOI

10.1016/j.xcrm.2024.101711

PMID

39232498

PMCID

PMC11525027

PubMedCentral® Posted Date

September 2024

PubMedCentral® Full Text Version

Post-print

Abstract

Pancreatic cancer is associated with an oncogenic KRAS mutation in approximately 90% of cases. However, a non-negligible proportion of pancreatic cancer cases harbor wild-type KRAS (KRAS-WT). This study establishes genetically engineered mouse models that develop spontaneous pancreatic cancer in the context of KRAS-WT. The Trp53

Keywords

Smad4 Protein, Animals, Pancreatic Neoplasms, Tumor Suppressor Protein p53, Proto-Oncogene Proteins p21(ras), Mutation, Mice, Humans, Carcinoma, Adenosquamous, Disease Models, Animal, Receptor, Transforming Growth Factor-beta Type II, pancreatic ductal adenocarcinoma, pancreatic adenosquamous carcinoma, single-cell RNA-sequencing analysis, genetically engineered mouse models, tumor microenvironment

Published Open-Access

yes

Recommended Citation

Yang, Daowei; Sun, Xinlei; Moniruzzaman, Rohan; et al., "Loss of p53 and SMAD4 Induces Adenosquamous Subtype Pancreatic Cancer in the Absence of an Oncogenic KRAS Mutation" (2024). Faculty, Staff and Student Publications. 2304.
https://digitalcommons.library.tmc.edu/uthgsbs_docs/2304