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Biomedical subjects

J Albright

Publications and source records attributed to J Albright.

29 records · Page 2Linked to original sources
PubMed1982

A transplantable anaplastic oral cancer model.

A stable model has been developed for oral mucosal anaplastic epidermoid carcinoma. This model more closely resembles the biologic characteristics of human oral carcinoma than previous models, such as primary epidermoid carcinomas induced in hamster buccal pouches or tongue by chemical carcinogens. This anaplastic oral cancer model was developed by serial abdominal transplantation in neonatal hamsters of original DMBA-induced primary epidermoid carcinomas of hamster buccal pouch. After the second generation, the tumors became stable, maintained an anaplastic appearance histologically, and were biologically aggressive, with rapid growth and metastatic potential. The original DMBA-induced buccal pouch tumors from 42 adult hamsters were transplanted abdominally through five generations in 151 neonatal hamsters. Immunosuppression was crucial in the initial transplantation but became unnecessary in the later serial transplantations. This model can serve as the basis for a variety of future immunologic and biologic studies dealing with oral cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Anaplastic carcinoma in the buccal pouches of hamsters as a model of oral cancer.

An anaplastic model of oral cancer has been developed by abdominal transplantation of carcinomas induced in buccal pouches of hamsters by DMBA. The transplanted tumors were replanted abdominally through five generations. The original carcinomas of the buccal pouch became stable in the abdomen after two generations of such transplantations and could thereafter be retransplanted intraperitoneally with 100% of success, as well as being transferable again to the buccal pouches of hamsters, where they were capable of being maintained as an oral model for anaplastic epidermoid carcinoma.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Transplantation of hamster buccal pouch carcinoma to neonatal hamsters.

Epidermoid carcinomas of oral mucosa were induced with DMBA in the buccal pouches of hamsters. The well-differentiated primary tumors were allografted into the peritoneal cavities of neonatal hamsters that had been treated with antilymphocyte serum. Solid tumors grew rapidly in the peritoneum and were harvested 6 to 31 days postimplantation. Gross and histopathologic specimens revealed infiltrative masses of tumor that had become more anaplastic than the original tumor. This in vivo model has considerable potential as a means of studying the immunology of oral cancers during tumor progression.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1975

Trisomy 8 mosaicism syndrome.

Chromosome 8 is the largest autosome thus far found to be trisomic among liveborn infants. Trisomy 8 "mosaicism" syndrome (T8mS) consists primarily of individuals whose chromosome complement is mosaic for chromosome 8 (T8m), i.e., patients with a chromosomally normal cell line in addition to the trisomic 8 cell line, and a few known individuals with full trisomy 8 (T8), i.e., each cell observed contains an extra chromosome 8. Reported cases of both types share a number of common features and thus have helped to delineate a new syndrome. Common features of T8mS include mild-to-moderate mental retardation, strabismus, osseous and soft tissue abnormalities, lowset and/or malformed ears, broad bulbous nose, palate deformity, various types of congenital cardiovascular disorders, hydronephrosis, cryptorchidism, and characteristic dermatoglyphics. Since chromosomal mosaicism is often present in this syndrome it is not surprising that considerable phenotypic variation exists. The present report of one of the youngest individuals yet described with T8m adds two more physical findings (dense corneal clouding and a heretofore undescribed clavicular deformity) to the constellation of abnormalities associated with T8mS. On the basis of the phenotypic and cytogenetic findings in this and 17 similar patients previously reported it is proposed that T8mS is a distinct clinical entity.

Abnormalities, Multiple↗
PubMedDate not supplied

Maximizing the motivational impact of feedback of lung cancer susceptibility on smokers' desire to quit.

This two-by-two factorially designed study evaluate approaches for communicating feedback of lung cancer susceptibility to smokers as a method for motivating smoking cessation. The study factors were: method of communicating feedback (by mail with telephone follow-up or in-person) and carbon monoxide feedback (yes or no). One-hundred-forty-four smokers were stratified on race and randomized to one of four conditions. Participants were surveyed at baseline and 2-month follow-up. Polymerase chain reaction (PCR) testing for the absence of the glutathione S transferase mu (GSTM1) gene was the susceptibility marker. Regardless of counseling method or carbon monoxide (CO) feedback, the majority (90%) of smokers accurately recalled the test result and 66% accurately interpreted the meaning of the test result. Smokers who received their result in person were significantly less likely to have read the result booklet than those in the telephone counseling group (OR = .28, 95%; CI .12-.62; p < .05). Neither counseling method nor CO feedback increased smokers' perceived risks for lung cancer. However, at the counseling session those who received in-person counseling were significantly less frightened by the test result than those who received telephone counseling (OR = .42, 95%; CI .20-86; p < .05) and at the 2-month follow-up those who received a CO test were significantly less frightened by their susceptibility result (OR = .40, 95%; CI .17-.92; p < .05) than those who did not have a CO test. Evaluation of further refinements in communicating the meaning of susceptibility results to motivate smoking cessation is warranted.

Adult↗