Cancer causes & control : CCC · 2008
Past medical conditions and K-ras mutations in pancreatic ductal adenocarcinoma: a hypothesis-generating study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Crous-Bou Marta, Porta Miquel, Morales Eva, López Tomàs, Carrato Alfredo, Puigdomènech Elisa, Real Francisco X, PANKRAS II Study Group
Аннотация
BACKGROUND: In pancreatic ductal adenocarcinoma (PDA) evidence on the etiopathogenic role of past medical conditions in the occurrence and persistence of K-ras mutations is scant.
METHODS: Incident cases of PDA were interviewed face-to-face about past medical history and other factors. Logistic regression was used to compare PDA cases (n = 120) with wild-type and mutated K-ras tumors (case-case study).
RESULTS: Patients with wild-type K-ras tumors were more likely to have a prior diagnosis of pancreatitis (Odds ratio [OR] = 6.11, p = 0.041). Diabetes mellitus (DM) was non-significantly more common among cases with a K-ras wild-type tumor, and the OR for DM of >6 years of duration was 4.54 (p = 0.39). Patients with wild-type K-ras were significantly more likely to have had a surgically treated peptic ulcer (OR = 9.03, p = 0.027). The probability of having a K-ras wild-type tumor increased with the number of medical conditions (p for trend = 0.012); the corresponding OR for two or more medical conditions was 4.46 (95% CI: 1.37-14.50).
CONCLUSIONS: Results raise the hypothesis that pancreatitis and possibly peptic ulcer might influence pancreatic carcinogenesis through pathways independent of K-ras mutation, perhaps related to growth factors or mediators of the inflammatory response. Large unselected studies should be conducted to refute or replicate our findings.
METHODS: Incident cases of PDA were interviewed face-to-face about past medical history and other factors. Logistic regression was used to compare PDA cases (n = 120) with wild-type and mutated K-ras tumors (case-case study).
RESULTS: Patients with wild-type K-ras tumors were more likely to have a prior diagnosis of pancreatitis (Odds ratio [OR] = 6.11, p = 0.041). Diabetes mellitus (DM) was non-significantly more common among cases with a K-ras wild-type tumor, and the OR for DM of >6 years of duration was 4.54 (p = 0.39). Patients with wild-type K-ras were significantly more likely to have had a surgically treated peptic ulcer (OR = 9.03, p = 0.027). The probability of having a K-ras wild-type tumor increased with the number of medical conditions (p for trend = 0.012); the corresponding OR for two or more medical conditions was 4.46 (95% CI: 1.37-14.50).
CONCLUSIONS: Results raise the hypothesis that pancreatitis and possibly peptic ulcer might influence pancreatic carcinogenesis through pathways independent of K-ras mutation, perhaps related to growth factors or mediators of the inflammatory response. Large unselected studies should be conducted to refute or replicate our findings.