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Pancreatic Neoplasms: HELP
Articles by Ajay Rana
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Ajay Rana wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article p110γ deficiency protects against pancreatic carcinogenesis yet predisposes to diet-induced hepatotoxicity. 2019

Torres, Carolina / Mancinelli, Georgina / Cordoba-Chacon, Jose / Viswakarma, Navin / Castellanos, Karla / Grimaldo, Sam / Kumar, Sandeep / Principe, Daniel / Dorman, Matthew J / McKinney, Ronald / Hirsch, Emilio / Dawson, David / Munshi, Hidayatullah G / Rana, Ajay / Grippo, Paul J. ·Department of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL 60612; ctp@ugr.es pgrippo@uic.edu. · Department of Medicine, Division of Gastroenterology and Hepatology, University of Illinois at Chicago, Chicago, IL 60612. · Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, IL 60612. · Research, Jesse Brown VA Medical Center, Chicago, IL 60612. · Department of Surgery, Division of Surgical Oncology, University of Illinois at Chicago, Chicago, IL 60612. · Molecular Biotechnology Center, Department of Molecular Biotechnology and Health Sciences, University of Turin, 10126 Turin, Italy. · Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095. · Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095. · Department of Medicine, Northwestern University, Chicago, IL 60611. ·Proc Natl Acad Sci U S A · Pubmed #31266893.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is notorious for its poor survival and resistance to conventional therapies. PI3K signaling is implicated in both disease initiation and progression, and specific inhibitors of selected PI3K p110 isoforms for managing solid tumors are emerging. We demonstrate that increased activation of PI3K signals cooperates with oncogenic Kras to promote aggressive PDAC in vivo. The p110γ isoform is overexpressed in tumor tissue and promotes carcinogenesis via canonical AKT signaling. Its selective blockade sensitizes tumor cells to gemcitabine in vitro, and genetic ablation of p110γ protects against Kras-induced tumorigenesis. Diet/obesity was identified as a crucial means of p110 subunit up-regulation, and in the setting of a high-fat diet, p110γ ablation failed to protect against tumor development, showing increased activation of pAKT and hepatic damage. These observations suggest that a careful and judicious approach should be considered when targeting p110γ for therapy, particularly in obese patients.

2 Article TGFβ Blockade Augments PD-1 Inhibition to Promote T-Cell-Mediated Regression of Pancreatic Cancer. 2019

Principe, Daniel R / Park, Alex / Dorman, Matthew J / Kumar, Sandeep / Viswakarma, Navin / Rubin, Jonathan / Torres, Carolina / McKinney, Ronald / Munshi, Hidayatullah G / Grippo, Paul J / Rana, Ajay. ·Medical Scientist Training Program, University of Illinois College of Medicine, Chicago, Illinois. Principe@illinois.edu. · University of Illinois College of Medicine, Chicago, Illinois. · Department of Surgery, University of Illinois at Chicago, Chicago, Illinois. · Department of Medicine, University of Illinois at Chicago, Chicago, Illinois. · Department of Medicine, Northwestern University, Chicago, Illinois. ·Mol Cancer Ther · Pubmed #30587556.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) remains remarkably lethal with a 5-year survival rate of 8%. This is mainly attributed to the late stage of presentation, as well as widespread resistance to conventional therapy. In addition, PDAC tumors are largely nonimmunogenic, and most patients have displayed incomplete responses to cancer immunotherapies. Our group has previously identified TGFβ as a crucial repressor of antitumor immune function in PDAC, particularly with respect to cytotoxic T lymphocytes. However, pharmacologic inhibition of TGFβ signaling has had limited efficacy in clinical trials, failing to promote a significant antitumor immune response. Hence, in this work, we extend our analysis to identify and circumvent the mechanisms of resistance to TGFβ signal inhibition in PDAC. Consistent with our previous observations, adoptive transfer of TGFβ-insensitive CD8

3 Article KRAS 2018

Principe, Daniel R / Overgaard, Nana Haahr / Park, Alex J / Diaz, Andrew M / Torres, Carolina / McKinney, Ronald / Dorman, Matthew J / Castellanos, Karla / Schwind, Regina / Dawson, David W / Rana, Ajay / Maker, Ajay / Munshi, Hidayatullah G / Rund, Lauretta A / Grippo, Paul J / Schook, Lawrence B. ·Medical Scientist Training Program, University of Illinois College of Medicine, Chicago, IL, USA. · Department of Immunology and Vaccinology, National Veterinary Institute, Technical University of Denmark Copenhagen, Copenhagen, Denmark. · University of Illinois Department of Animal Sciences, Urbana-Champaign, IL, USA. · Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA. · Department of Radiology, University of Illinois at Chicago, Chicago, IL, USA. · Department of Pathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, Los Angeles, California, USA. · Department of Surgery, University of Illinois at Chicago, Chicago, IL, USA. · Department of Medicine, Northwestern University, Chicago, IL, USA. · Institute for Genomic Biology, University of Illinois, Urbana-Champaign, IL, USA. · Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA. pgrippo@uic.edu. · University of Illinois Department of Animal Sciences, Urbana-Champaign, IL, USA. schook@illinois.edu. · Department of Radiology, University of Illinois at Chicago, Chicago, IL, USA. schook@illinois.edu. ·Sci Rep · Pubmed #30135483.

ABSTRACT: Although survival has improved in recent years, the prognosis of patients with advanced pancreatic ductal adenocarcinoma (PDAC) remains poor. Despite substantial differences in anatomy, physiology, genetics, and metabolism, the overwhelming majority of preclinical testing relies on transgenic mice. Hence, while mice have allowed for tremendous advances in cancer biology, they have been a poor predictor of drug performance/toxicity in the clinic. Given the greater similarity of sus scrofa pigs to humans, we engineered transgenic sus scrofa expressing a LSL-KRAS