Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.
Carmen Guerra,Alberto J. Schuhmacher,Marta Cañamero,Paul J. Grippo,Lena Verdaguer,Lucía Pérez-Gallego,Pierre Dubus,Eric P. Sandgren,Mariano Barbacid +8 more
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TLDR
It is reported that selective expression of an endogenous K-Ras(G12V) oncogene in embryonic cells of acinar/centroacinar lineage results in pancreatic intraepithelial neoplasias (PanINs) and invasive PDA, suggesting that PDA originates by differentiation of acINs or their precursors into ductal-like cells.About:
This article is published in Cancer Cell.The article was published on 2007-03-13 and is currently open access. It has received 1074 citations till now. The article focuses on the topics: Pancreatic Intraepithelial Neoplasia.read more
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Cancer-related inflammation.
TL;DR: The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.
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Immunity, Inflammation, and Cancer
TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
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EMT and Dissemination Precede Pancreatic Tumor Formation
Andrew D. Rhim,Emily T. Mirek,Nicole M. Aiello,Anirban Maitra,Jennifer M. Bailey,Florencia McAllister,Maximilian Reichert,Gregory L. Beatty,Anil K. Rustgi,Robert H. Vonderheide,Steven D. Leach,Ben Z. Stanger +11 more
TL;DR: It is suggested that inflammation enhances cancer progression in part by facilitating EMT and entry into the circulation and tagged cells invaded and entered the bloodstream unexpectedly early, before frank malignancy could be detected by rigorous histologic analysis.
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Pancreatic cancers require autophagy for tumor growth
Shenghong Yang,Xiaoxu Wang,Gianmarco Contino,Marc Liesa,Ergun Sahin,Haoqiang Ying,Alexandra S. Bause,Ying-Hua Li,Jayne M. Stommel,Giacomo Dell'Antonio,Josef Mautner,Giovanni Tonon,Marcia C. Haigis,Orian S. Shirihai,Claudio Doglioni,Nabeel Bardeesy,Alec C. Kimmelman +16 more
TL;DR: Inhibition of autophagy by genetic means or chloroquine treatment leads to robust tumor regression and prolonged survival in pancreatic cancer xenografts and genetic mouse models, and drugs that inactivate this process may have a unique clinical utility in treating pancreatic cancers and other malignancies with a similar dependence on Autophagy.
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Genetics and biology of pancreatic ductal adenocarcinoma
Haoqiang Ying,Prasenjit Dey,Wantong Yao,Alec C. Kimmelman,Giulio Draetta,Anirban Maitra,Ronald A. DePinho +6 more
TL;DR: The path to meaningful clinical progress has never been clearer to improve PDAC patient survival and a deeper understanding of cancer cell biology, particularly altered cancer cell metabolism and impaired DNA repair processes, is providing novel therapeutic strategies that show strong preclinical activity.
References
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Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity.
Michael Karin,Yinon Ben-Neriah +1 more
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Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Lawrence A. Donehower,Michele Harvey,Betty L. Slagle,Mark J. McArthur,Charles A. Montgomery,Janet S. Butel,Allan Bradley +6 more
TL;DR: Observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
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IKKbeta links inflammation and tumorigenesis in a mouse model of colitis-associated cancer.
Florian R. Greten,Lars Eckmann,Tim F. Greten,Jin Mo Park,Zhi-Wei Li,Laurence J. Egan,Laurence J. Egan,Martin F. Kagnoff,Michael Karin +8 more
TL;DR: It is shown that although deletion of IKKbeta in intestinal epithelial cells does not decrease inflammation, it leads to a dramatic decrease in tumor incidence without affecting tumor size, which is linked to increased epithelial apoptosis during tumor promotion.
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