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Biomedical subjects

D Dyall-Smith

Publications and source records attributed to D Dyall-Smith.

24 records · Page 2Linked to original sources
PubMed1991

Benign human papillomavirus infection in renal transplant recipients.

Warts and cutaneous squamous cell carcinomas are common complications of immunosuppression. We studied a total of 189 renal transplant recipients clinically for such lesions. The incidence of warts increased steadily after transplant, such that of patients transplanted for more than 5 years, 92% were found to have warts and 65% had more than five warts each. DNA extracted from scrapings of their warts showed they carried the same human papillomavirus types as the general population, and not the unique set found on patients with epidermodysplasia verruciformis (who share with transplant recipients an increased incidence of warts and squamous cell carcinomas).

Adult↗
PubMed1989

Epidermodysplasia verruciformis.

A patient with epidermodysplasia verruciformis was followed over a ten year period. This rare genetic disorder, characterised by papillomavirus-associated skin lesions and squamous cell carcinomas, is difficult to manage and invariably shortens the lifespan due to metastases from skin carcinomas. In our case, we confirmed the diagnosis using nucleic acid hybridisation, at high stringency, to cloned papillomavirus DNA. Relentless progression of disease occurred despite varied and increasingly vigorous treatment modalities.

Adult↗
PubMed1988

Transformation of bone marrow cells from E mu-myc transgenic mice by Abelson murine leukemia virus and Harvey murine sarcoma virus.

Transgenic mice harboring a c-myc gene subjugated to the immunoglobulin heavy chain enhancer offer a unique opportunity to investigate whether deregulated myc expression potentiates the transformation of B lymphoid cells by other oncogenes. By assessing colony formation in semi-solid medium, we have compared the potential of bone marrow cells from E mu-myc mice and their normal littermates for transformation by Harvey murine sarcoma virus and Abelson murine leukemia virus. E mu-myc bone marrow yielded more lymphoid colonies than normal marrow after infection with Harvey virus. The increased transformation frequency may reflect increased clonogenicity due to complementation between myc and ras and/or the increased number of pre-B cells in E mu-myc marrow. Surprisingly, however, the number of lymphoid colonies induced by Abelson virus was not enhanced. Our interpretation of these results is that the primary Abelson target is more primitive than the pre-B cells expressing the E mu-myc transgene and is therefore not present at increased frequency in the E mu-myc marrow. The cells from most virus-infected E mu-myc colonies failed to grow indefinitely when placed in liquid culture in the absence of a feeder layer. Thus expression of a deregulated c-myc gene together with either v-Ha-ras or v-abl does not ensure fully autonomous growth of early B lymphoid cells.

Abelson murine leukemia virus↗