Infrequent mutation of lysophosphatidic Acid receptor-1 gene in hamster pancreatic duct adenocarcinomas and established cell lines.
ABSTRACT To evaluate the involvement of lysophosphatidic acid receptor-1 (LPA1) gene alteration in pancreatic carcinogenesis, we investigated mutations in the LPA1 gene in hamster pancreatic duct adenocarcinomas (PDAs) and established cell lines. Female Syrian golden hamsters received 30 mg/kg of N-nitrosobis(2-oxopropyl)amine (BOP) followed by repeated exposure to an augmentation pressure regimen consisting of a choline-deficient diet combined with DL-ethionine and then L-methionine and a further administration of 20 mg/kg BOP. A total of 10 PDAs obtained 10 weeks after beginning the experiment and three cell lines established from subcutaneously transplantable PDAs in syngeneic hamsters were examined for mutations using reverse transcription-polymerase chain reaction-single strand conformation polymorphism (RT-PCR-SSCP) analysis. A mutation was detected in only one PDA (1/10, 10%) in the form of a GGA to GTA (Gly to Val) transversion at codon 355, and no mutations were detected in the three cell lines. These results suggest that the LPA1 gene mutation may play roles in a limited fraction of BOP-induced pancreatic duct carcinogenesis in hamsters.
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ABSTRACT: The proliferative potential of six primary ovarian carcinoids with different clinical outcome and histogenetic origin was examined immunohistochemically. The results showed that two cases with extremely high level of proliferative activity were associated with metastatic spread. In the remaining tumors, the examined factor was found to be at low level comparable with excellent prognosis of typical carcinoids in other locations. The preliminary results showed a possibility of a prognosis prediction according to typing of the ovarian carcinoids into two categories, i.e., tumors of low and intermediate malignancy. Topoisomerase II-alpha and Ki-67 are suitable markers giving valuable information about this phenomenon.Gynecological Endocrinology 03/2003; 17(1):1-6. · 1.58 Impact Factor
Article: Annual report to the nation on the status of cancer, 1975-2002, featuring population-based trends in cancer treatment.[show abstract] [hide abstract]
ABSTRACT: The American Cancer Society (ACS), the Centers for Disease Control and Prevention (CDC), the National Cancer Institute (NCI), and the North American Association of Central Cancer Registries (NAACCR) collaborate annually to provide information on cancer rates and trends in the United States. This year's report updates statistics on the 15 most common cancers in the five major racial/ethnic populations in the United States for 1992-2002 and features population-based trends in cancer treatment. The NCI, the CDC, and the NAACCR provided information on cancer cases, and the CDC provided information on cancer deaths. Reported incidence and death rates were age-adjusted to the 2000 U.S. standard population, annual percent change in rates for fixed intervals was estimated by linear regression, and annual percent change in trends was estimated with joinpoint regression analysis. Population-based treatment data were derived from the Surveillance, Epidemiology, and End Results (SEER) Program registries, SEER-Medicare linked databases, and NCI Patterns of Care/Quality of Care studies. Among men, the incidence rates for all cancer sites combined were stable from 1995 through 2002. Among women, the incidence rates increased by 0.3% annually from 1987 through 2002. Death rates in men and women combined decreased by 1.1% annually from 1993 through 2002 for all cancer sites combined and also for many of the 15 most common cancers. Among women, lung cancer death rates increased from 1995 through 2002, but lung cancer incidence rates stabilized from 1998 through 2002. Although results of cancer treatment studies suggest that much of contemporary cancer treatment for selected cancers is consistent with evidence-based guidelines, they also point to geographic, racial, economic, and age-related disparities in cancer treatment. Cancer death rates for all cancer sites combined and for many common cancers have declined at the same time as the dissemination of guideline-based treatment into the community has increased, although this progress is not shared equally across all racial and ethnic populations. Data from population-based cancer registries, supplemented by linkage with administrative databases, are an important resource for monitoring the quality of cancer treatment. Use of this cancer surveillance system, along with new developments in medical informatics and electronic medical records, may facilitate monitoring of the translation of basic science and clinical advances to cancer prevention, detection, and uniformly high quality of care in all areas and populations of the United States.CancerSpectrum Knowledge Environment 11/2005; 97(19):1407-27. · 14.07 Impact Factor
Article: Effects of increasing amounts of dietary cholesterol on postprandial lipemia and lipoproteins in human subjects.[show abstract] [hide abstract]
ABSTRACT: Our aim was to determine the effects of increasing amounts of dietary cholesterol (0-710 mg) on the postprandial plasma lipid responses and lipoprotein changes in normolipidemic human subjects. Ten subjects were fed five different test meals in a random order: one meal did not contain fat or cholesterol while the four others contained a fixed amount of lipids (45 g) and 0, 140, 280, and 710 mg cholesterol, respectively. Fasting and post-meal blood samples were obtained for 7 h. Large and small triglyceride-rich lipoproteins (TRL), low density (LDL), and high density (HDL) lipoproteins were isolated. Compared to the no-fat, no-cholesterol meal, the fat-enriched meals raised (P < 0.05) plasma triglycerides, phospholipids, and free cholesterol and lowered cholesteryl esters postprandially. The meals containing zero or 140 mg cholesterol generally elicited comparable postprandial plasma and lipoprotein lipid responses. The meals providing 280 or 710 mg cholesterol significantly increased postprandial plasma phospholipids and large TRL triglycerides and decreased plasma esterified cholesterol. The lipid composition of the large TRLs and the concentrations of the small TRL lipid components were not altered postprandially by cholesterol intake. On the other hand, LDL free cholesterol increased after 3 h, LDL cholesteryl esters dropped after 3 and 7 h, HDL cholesteryl esters dropped after 3 h, and HDL phospholipids increased 7 h after ingesting meals highly enriched in cholesterol. Blood insulin, apoA-I and apoB were not altered postprandially by cholesterol intake. Thus, the data show that ingesting more than 140 mg cholesterol per meal significantly alters the postprandial lipoprotein response in healthy subjects.The Journal of Lipid Research 12/1994; 35(11):1993-2007. · 5.56 Impact Factor