Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.

By C. Guerra, A. J. Schuhmacher, M. Cañamero, P. Grippo, Lena Verdaguer, L. Pérez-Gallego, P. Dubus, E. Sandgren, M. Barbacid. Cancer Cell, 2007

1,218 citations recorded by the source corpus.

Subfields: Epidemiology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/cfe46b52bfed8a464ab0c1e4922e0a60ced97da9

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In Epidemiology

1. F. Balkwill
2. Orian Shirihai
3. A. Sica
4. A. Mantovani
5. Ergun Sahin
6. M. Liesa
7. Alec C. Kimmelman
8. M. Haigis

In Oncology

1. A. Mantovani
2. A. Sica
3. P. Allavena
4. F. Balkwill
5. M. Karin
6. Shizuo Akira
7. K. Frese
8. Alec C. Kimmelman

In Surgery

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2. A. Mantovani
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4. J. Erler
5. Shizuo Akira

Citations in the corpus

• EMT subtype influences epithelial plasticity and mode of cell migration (2018, background): “Several studies have suggested that acinar cells constitute the major cellular source of PDAC as the result of an acinar-to-ductal metaplasia (ADM) → pancreatic intraepithelial neoplasia (PanIN) → carcinoma sequence (De La et al., 2008; Guerra et al., 2007; Habbe et al., 2008; Kopp et al., 2011).”
• Stromal biology and therapy in pancreatic cancer (2010, background): “Further important work was done by the Barbacid group providing striking evidence that temporal expression of endogenous Kras in acinar cells of adult mice results in PanINs and invasive PDA only in the context of caerulein-induced pancreatitis.(72) Thus, GEMMs (in contrast to xenograft models) are ”
• Inactivating mutations of RNF43 confer Wnt dependency in pancreatic ductal adenocarcinoma (2013, background): “Like KRAS mutations, RNF43 mutations are found at a high frequency in pancreatic cancer precursor lesions IPMNs and MCNs (16), suggesting that RNF43 mutations may contribute to the initiation of PDAC.”
• Pancreatic cancers require autophagy for tumor growth. (2011, positive): “As inflammation and ROS are associated with both Ras transformation and the initiation of PDAC (Irani et al. 1997; Chu et al. 2007; Guerra et al. 2007), it is possible that the elevated basal autophagy in PDAC may also serve as an adaptation to prevent the accumulation of cytotoxic levels of ROS,…”
• Cancer-related inflammation (2008, background): “Members of the RAS family are the most frequently mutated dominant oncogenes in human cancer, and activated oncogenic components of the RAS–RAF signalling pathway, in turn, induce the production of tumour-promoting inflammatory chemokines and cytokine”
• Targeting the LOX/hypoxia axis reverses many of the features that make pancreatic cancer deadly: inhibition of LOX abrogates metastasis and enhances drug efficacy (2015, positive): “Pancreatitis leads to increased risk of PDAC, while cerulein promotes acinar-to-ductal metaplasia and disease progression (Guerra et al , 2007; Rhim et al , 2012).”
• Immunity, Inflammation, and Cancer (2010, neutral): “Even dominant oncogenes such as v-Src or K-Ras are unable to induce cancer in adult animals unless accompanied by injury and subsequent tissue regeneration (Guerra et al., 2007; Sieweke et al., 1990).”
• EMT and dissemination precede pancreatic tumor formation (2012, background): “, 2008), and in both mice and humans, chronic pancreatic inflammation is strongly associated with pancreatic cancer (Grover and Syngal, 2010; Guerra et al., 2007).”
• Stat3/Socs3 activation by IL-6 transsignaling promotes progression of pancreatic intraepithelial neoplasia and development of pancreatic cancer. (2011, background): “In addition to its function as an important regulator of proinflammatory chemokines and cytokines, NF-kBmight therefore be implicated in establishing IL-6 transsginaling during pancreatic oncogenesis (Algul et al., 2007c; Guerra et al., 2007).”