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Biomedical subjects

B F Trump

Publications and source records attributed to B F Trump.

402 records · Page 23Linked to original sources
PubMedDate not supplied

The respiratory epithelium. IX. Validity and reproducibility of revised cytologic criteria for human and hamster respiratory tract tumors.

Cytologic criteria, based upon features of differentiation at the cellular level, have been established previously for human and hamster respiratory tract tumors. In order to validate these histogenetic revised criteria and to study their reproducibility, imprint smears of human and hamster tumors, hamster tracheal washing specimens and preoperative human specimens of sputa, bronchial washings and bronchial brushings were coded randomly, followed by blind cytologic study of the tumor cells. The hamster tumors were induced by intratracheal instillation of benzo(a)pyrene-ferric oxide or sequential administration of benzo(a)pyrene-ferric oxide and N-methyl-N-nitrosourea. Greater accuracy and reliability were obtained for the histogenetic cytodiagnosis versus the histogenetic histologic evaluation than were achieved for the conventional cytodiagnosis versus the World Health Organization histologic evaluation of 1967. The histogenetic classification utilizes diagnostic criteria that may be universally applicable by pathologists and cytopathologists. Many poorly to well-differentiated epidermoid carcinomas, poorly to well-differentiated adenocarcinomas, large-cell carcinomas and giant-cell carcinomas, diagnosed as such by conventional cytologic criteria, possessed histogenetic criteria of combined epidermoid and adenocarcinomas. The new data clarify conventional cytodiagnoses of poorly differentiated epidermoid carcinomas and poorly differentiated adenocarcinomas and eliminate vague categories, such as large-cell undifferentiated, giant-cell and small-cell anaplastic carcinomas.

Adenocarcinoma↗
PubMedDate not supplied

Lung cancer, race, and a CYP1A1 genetic polymorphism.

The assessment of human cancer risk using molecular epidemiological techniques involves determining the relative contributions of inherited and acquired genetic predispositions, in the context of environmental exposures. Recently described genetic polymorphisms for CYP1A1, a gene involved in the metabolic activation of polycyclic aromatic hydrocarbons, have been associated with lung cancer risk in a Japanese population. We report herein findings from a United States case-control study of lung cancer (56 cases; 48 controls). The polymerase chain reaction followed by an Msp1 restriction enzyme digestion was used to analyze constitutive DNA but no association between the restriction fragment length polymorphism and lung cancer risk was found (odds ratio, 0.7; 95% confidence interval, = 0.3-1.6). Analysis of genotype by cumulative smoking status did not reveal an elevated risk among lesser or greater smokers. The presence of the CYP1A1 Msp1 site-present allele, which was previously found to be associated with Japanese lung cancer risk, was statistically increased in African compared to Caucasian Americans (odds ratio, 2.9; 95% confidence interval, 1.2-2.7). When stratified by race, however, no association between case status and the polymorphism was observed, but the small number of study subjects within each racial group limited the statistical power. Larger studies are required to evaluate the risk of the CYP1A1 Msp1 polymorphism in African Americans.

Asthma↗
PubMedDate not supplied

Tamoxifen induces deregulation of [Ca2+] in human breast cancer cells.

Tamoxifen is a clinically useful estrogen antagonist at or below 10(-6) M concentration. However, above this concentration tamoxifen exerts non-ER mediated cytotoxicity. Such cytotoxic effects are lethal or sublethal. The lethal effects lead to cell death while the sublethal effects may lead to cellular transformation and response modification participating in the process of tumor resistance or even tumor stimulation. Deregulation of intracellular ionized calcium ([Ca2+]i) could lead to genomic instability and deregulation of oncogene expression which might participate in the process of carcinogenesis and/or tumor promotion. Tamoxifen may cause tumor stimulation due to deregulation of [Ca2+]i or its consequences such as activity of protein kinase C, calmodulin and related protein kinases. Precise understanding of such mechanism is important for avoiding tamoxifen induced tumor resistance or tumor stimulation. The deregulation of [Ca2+]i was studied on fluo-3/AM loaded MCF-7 human breast cancer cells following acute and chronic treatment of tamoxifen and calcium ionophore ionomycin. The elevation of [Ca2+]i preceded the death of MCF-7 cells following treatment with ionomycin as previously reported on other cells. Tamoxifen above 10(-6) M also caused an increase in [Ca2+]i preceding the death of MCF-7 cells. However, below this concentration, tamoxifen caused a decrease in [Ca2+]i without any signs of cytotoxicity. The present data clearly demonstrate a tamoxifen-induced increase in [Ca2+]i and cell death only at the concentration-range in which non-E R mediated cytotoxicity is reported.

Breast Neoplasms↗