Liver failure in an antimitochondrial antibody-positive patient with sarcoidosis: primary biliary cirrhosis or hepatic sarcoidosis?
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Autoantibodies↗
Biomedical subjects
Cynthia F Caracta
Publications and source records attributed to Cynthia F Caracta.
Patterns of allelic loss differ in lung adenocarcinomas of smokers and nonsmokers.
Cigarette smoking is the most important cause of lung cancer, however approximately 10% of patients with lung cancer have no history of smoking. While the molecular pathogenesis of smoking associated lung carcinogenesis is becoming well characterized, the pathogenesis of lung cancer in nonsmokers is not. We designed a study to examine the pathogenesis of adenocarcinoma in nonsmokers by determining if loss of heterozygosity (LOH) in tumors of nonsmokers differs from those of smokers. We evaluated six cases of primary adenocarcinoma in never smokers and six selected cases in smokers, matched by clinical and histological criteria. LOH in tumor DNA relative to nonmalignant lung DNA was determined at 52 microsatellites located on ten chromosomal loci. The extent of allelic loss in smokers, as measured by fractional allelic loss (FAL), was compared with nonsmokers. LOH was more frequent in the tumors of nonsmokers than of smokers with mean FAL of 46% in nonsmokers and 28% in smokers (P<0.05). Increased LOH in nonsmokers was most pronounced at chromosomes: 3p, 8p, 9p, 10p, and 18q. Since this study compared allelic loss between lung and tumor-bearing lung, less frequent LOH in smokers' tumors can be interpreted to suggest LOH was already present in the nonmalignant lung of smokers and fewer additional instances of allelic loss were present in the tumors of smokers. Our results suggest that the early steps of lung carcinogenesis differ in nonsmokers compared with smokers. In addition, the chromosomal sites of LOH may identify genes important for lung carcinogenesis in nonsmokers.
Adenocarcinoma↗
Gender differences in pulmonary disease.
Epidemiologic evidence points to gender-based differences in incidence, risk, histology, and pathogenesis of certain lung diseases in women as compared with men. Gender influences not only physiological differences, but also the social, economic, and cultural context in which men and women coexist. Central to these differences is the role of sex hormones, which may contribute to the pathogenesis of disease or serve as protective factors. This paper seeks to review the role of gender in major areas of pulmonary disease and explore the mechanisms that may underlie gender differences in asthma, chronic obstructive pulmonary disease and mycobacterial disease (tuberculosis and Mycobacterium avium intracellulare infection), on lung cancer.
Culture↗