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Petr Protiva

Bio: Petr Protiva is an academic researcher from Yale University. The author has contributed to research in topics: Medicine & Adenocarcinoma. The author has an hindex of 20, co-authored 26 publications receiving 1328 citations. Previous affiliations of Petr Protiva include Columbia University & University of Connecticut Health Center.

Papers
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TL;DR: HEV infection contributes to a small but important proportion of cases of acute liver injury that are suspected to be drug induced, andSerologic testing for HEV infection should be performed, particularly if clinical features are compatible with acute viral hepatitis.

295 citations

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TL;DR: The mediocre reliability of the R UCAM is problematic for future studies of drug‐induced liver injury and alternative methods, including modifying the RUCAM, developing drug‐specific instruments, or causality assessment based on expert opinion, may be more appropriate.

162 citations

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TL;DR: Patients with BBPS scores of 2 or 3 for all colon segments have adequate bowel preparation for the detection of adenomas larger than 5 mm and should return for screening or surveillance colonoscopy at standard guideline-recommended intervals.

132 citations

Journal ArticleDOI
TL;DR: The data suggest that smoking at least 20 pack-years is strongly associated with any and large SSAs and diabetes mellitus and obesity seem to be associated with SSAs as well, which has implications for CRC screening.
Abstract: Background Although sessile serrated adenomas (SSAs) may represent a separate and important pathway for colorectal cancer (CRC), little is known about the risk factors for these lesions. Molecular abnormalities such as BRAF have been observed in SSA and smokers. Our hypothesis is that smoking may be associated with these lesions. Methods All patients diagnosed with an SSA from January 2007 to September 2010 were identified retrospectively based on a pathology database query. There were 2 sets of controls. One group had no adenomas, whereas another group had tubular adenomas. These groups were randomly identified from 2007 to 2010. Data collected included age, sex, ethnicity, height, weight, family history of CRC, diabetes mellitus, use of aspirin, statins, and calcium, and serum trigylcerides and cholesterol. We defined smokers as those patients who smoked at least 20 pack-years. Results We identified 90 patients with an SSA of any size, 90 patients with tubular adenomas, and 200 controls with no adenomas. Of the 90 SSAs, 42 were 6 mm or larger and 19 of them were ≥1 cm. Most of the SSAs was flat (76/90; 84.4%). After multivariate analyses, smokers with at least 20 pack-year exposure were found to have an increased risk [adjusted odds ratio (OR)=7.31; 95% confidence interval (CI), 3.92-13.63] of having any SSAs, SSAs ≥6 mm (adjusted OR=7.77; 95% CI, 3.48-17.35), and large SSAs (adjusted OR=10.20; 95% CI, 3.31-31.41) compared with nonsmokers. We also observed this relationship when comparing patients with SSAs to those with tubular adenomas. Conclusions Our data suggest that smoking at least 20 pack-years is strongly associated with any and large SSAs. In addition, diabetes mellitus and obesity seem to be associated with SSAs as well. Our data has implications for CRC screening.

104 citations

Journal ArticleDOI
TL;DR: The data suggest that lovastatin induces morphologic changes and apoptosis by inhibiting geranylgeranylation of small GTPases of the rho family and thereby inactivating them.
Abstract: We earlier showed that lovastatin potentiated the chemopreventive effects of sulindac against colon neoplasia in a rodent model and augments apoptosis induced by 5-FU and cisplatin in human colon cancer cells. In the present study, we investigated effects of lovastatin in spontaneously immortalized rat intestinal epithelial cells, IEC-18 and their K-ras transformed clones. Lovastatin induced morphologic changes (cell rounding and detachment) and apoptosis that were not influenced by K-ras mutations, but were prevented by geranylgeranyl-pyrophosphate or by mevalonate. Clostridium difficile toxin B, which directly inactivates rho, induced similar morphologic changes and apoptosis. Cycloheximide prevented these effects of lovastatin, but not C. difficile toxin B. Lovastatin decreased the amounts of membrane bound rhoA and rhoB. Cycloheximide and geranylgeranyl-pyrophosphate prevented lovastatin induced morphologic changes and apoptosis but did not inhibit lovastatin-induced changes in membrane translocation of rho. Our data suggest that lovastatin induces morphologic changes and apoptosis by inhibiting geranylgeranylation of small GTPases of the rho family and thereby inactivating them. Restoration of membrane translocation of rho is not necessary for preventing lovastatin-induced morphologic changes or apoptosis.

88 citations


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Journal ArticleDOI
TL;DR: Developing new therapies that can improve HBsAg clearance and virological cure is warranted because long-term antiviral treatment can reverse cirrhosis and reduce hepatocellular carcinoma.

1,137 citations

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TL;DR: Understanding the complex cellular effects and underlying molecular mechanisms of statins will advance the development of molecularly targeted agents for preventing cancer, and might also help theDevelopment of drugs for other ageing-related diseases with interrelated molecular pathways.
Abstract: Randomized controlled trials for preventing cardiovascular disease indicated that statins had provocative and unexpected benefits for reducing colorectal cancer and melanoma. These findings have led to the intensive study of statins in cancer prevention, including recent, large population-based studies showing statin-associated reductions in overall, colorectal and prostate cancer. Understanding the complex cellular effects (for example, on angiogenesis and inflammation) and the underlying molecular mechanisms of statins (for example, 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase-dependent processes that involve geranylgeranylation of Rho proteins, and HMG-CoA-independent processes that involve lymphocyte-function-associated antigen 1) will advance the development of molecularly targeted agents for preventing cancer. This understanding might also help the development of drugs for other ageing-related diseases with interrelated molecular pathways.

753 citations

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TL;DR: This review will focus on the multiple functions of p21 in cell cycle regulation, apoptosis and gene transcription after DNA damage and briefly discuss the pathways and factors that have critical roles in p21 expression and activity.

711 citations

Journal ArticleDOI
TL;DR: This ACG Clinical Guideline is presented an evidence-based approach to diagnosis and management of DILI with special emphasis on DILi due to herbal and dietary supplements and DilI occurring in individuals with underlying liver disease.

630 citations