Cited by 488Autophagy in Disease and TherapyPancreatic and Hepatic Oncology ResearchCalcium signaling and nucleotide metabolism

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Autophagy Is Critical for Pancreatic Tumor Growth and Progression in Tumors with p53 Alterations

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Yang, Annan, Rajeshkumar, N.V., Wang, Xiaoxu, Yabuuchi, Shinichi, Alexander, Brian M., Chu, Gerald C., Von Hoff, Daniel D., Maitra, Anirban, Kimmelman, Alec C.·2014·Cancer Discovery

DOI 10.1158/2159-8290.cd-14-0362PMC PMC4125497

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Abstract

Pancreatic ductal adenocarcinoma is refractory to available therapies. We have previously shown that these tumors have elevated autophagy and that inhibition of autophagy leads to decreased tumor growth. Using an autochthonous model of pancreatic cancer driven by oncogenic Kras and the stochastic LOH of Trp53, we demonstrate that although genetic ablation of autophagy in the pancreas leads to increased tumor initiation, these premalignant lesions are impaired in their ability to progress to invasive cancer, leading to prolonged survival. In addition, mouse pancreatic cancer cell lines with differing p53 status are all sensitive to pharmacologic and genetic inhibition of autophagy. Finally, a mouse preclinical trial using cohorts of genetically characterized patient-derived xenografts treated with hydroxychloroquine showed responses across the collection of tumors. Together, our data support the critical role of autophagy in pancreatic cancer and show that inhibition of autophagy may have clinical utility in the treatment of these cancers, independent of p53 status. Significance: Recently, a mouse model with embryonic homozygous Trp53 deletion showed paradoxical effects of autophagy inhibition. We used a mouse model with Trp53 LOH (similar to human tumors), tumor cell lines, and patient-derived xenografts to show that p53 status does not affect response to autophagy inhibition. These findings have important implications on ongoing clinical trials. Cancer Discov; 4(8); 905–13. ©2014 AACR. See related commentary by Amaravadi and Debnath, p. 873 This article is highlighted in the In This Issue feature, p. 855

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Authors: Yang, A., Rajeshkumar, N. V., Wang, X., Yabuuchi, S., Alexander, B. M., Chu, G. C., Von Hoff, D. D., Maitra, A., & Kimmelman, A. C.
Affiliations: Dana-Farber Cancer Institute (US)
Johns Hopkins University (US)
Brigham and Women's Hospital (US)
4Translational Genomics Research Institute, Phoenix, Arizona; Departments of
The University of Texas MD Anderson Cancer Center (US)
Corresponding author: Kimmelman, Alec C.
ORCID: Yang, Annan
Wang, Xiaoxu
Alexander, Brian M.
Maitra, Anirban
Kimmelman, Alec C.
Venue: Cancer Discovery
Publisher: American Association for Cancer Research (AACR)
Published: 2014-08-01
Volume: 4
Issue: 8
Pages: 905-913
ISSN: 2159-8274 (ISSN-L)
2159-8290
DOI: 10.1158/2159-8290.cd-14-0362
PMC: PMC4125497
OpenAlex: W2148330792
Cited by: 486
References: 33
Citations by year: 2026: 16 · 2025: 32 · 2024: 28 · 2023: 34 · 2022: 47 · 2021: 61 · 2020: 44 · 2019: 43 · 2018: 41 · 2017: 45 · 2016: 37 · 2015: 43 · 2014: 15
FWCI: 35.35
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Cancer Discovery (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (P50CA127003, R01CA157490, P30CA016672)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
Keywords: autophagy, pancreatic ductal adenocarcinoma, p53 status, autophagy inhibition, hydroxychloroquine, KRAS-driven tumors, premalignant pancreatic lesions, tumor progression, patient-derived xenografts
MeSH terms: Animals, Autophagy, Cell Transformation, Neoplastic, Disease Models, Animal, Humans, Pancreatic Neoplasms, Tumor Suppressor Protein p53, Loss of Heterozygosity, Xenograft Model Antitumor Assays, Mice

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Autophagy Is Critical for Pancreatic Tumor Growth and Progression in Tumors with p53 Alterations

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