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Biomedical subjects

G M Taylor

Publications and source records attributed to G M Taylor.

138 records · Page 8Linked to original sources
PubMed1975

Evidence of donor suppression of anti-donor PFC responses in mice.

Mice receiving high doses of mitomycin C-treated allogeneic spleen donor cells produced more host anti-donor plaque-forming cells than mice receiving high doses of untreated allogeneic spleen donor cells, showing that immunocompetent donor cells capable of recognizing host H-2 antigens can suppress host anti-donor H-2 primary antibody responses. Responses to semi-allogeneic spleen donor cells were consistently lower than responses to allogeneic cells. Low doses of normal allogeneic spleen donor cells showed stimulation of the host anti-donor PFC response compared with similar doses of mitomycin C-treated allogeneic spleen donor cells.

Animals↗
PubMedDate not supplied

Secondary leukemia in a child with neuroblastoma while on oral etoposide: what is the cause?

To date little has been reported about the risk of therapy-related leukaemia (t-AML) in children receiving oral etoposide therapy. The authors present a case of t-AML that developed in a child with metastatic neuroblastoma 18 months after he received oral etoposide, given for palliation purpose. The leukemic blasts were examined by morphological, immunohistochemical, cytogenetic, and molecular genetic analyses. Although the t-AML developed following oral etoposide therapy, the child had previously received high-dose, multiagent chemotherapy, and rearrangement of the MLL gene was not demonstrated. The use of modern multiagent therapy often makes it difficult to appropriately apportion blame for causation of specific side effects. Moreover, the etiology of t-AML and mechanism of leukemogenesis are likely to be multifactorial and complex. Further studies on the precise association with different therapies are thus needed. Oral etoposide remains an effective palliative agent and its usage should not be excluded without most careful consideration of the risks.

Administration, Oral↗
PubMedDate not supplied

Monoclonal antibodies to CD18 and CD11A (LFA-1) distinguish Down's syndrome (trisomy 21) from normal lymphoblastoid cells.

To evaluate the potential of using fluorescence flow cytometry (FFC) in the diagnosis of Down's syndrome we analysed a series of Trisomy 21 lymphoid cell-lines (LCL) with a panel of monoclonal antibodies (MoAb) to the CD11a and CD18 subunits of lymphocyte function associated antigen 1 (LFA-1). In pairwise analysis of Trisomy 21 (T21) and normal LCL with 6 CD18 and 10 CD11a MoAb we found that T21 LCL could be distinguished from normal LCL with both types of MoAb, even though only the CD18 gene is duplicated in Down's syndrome. Experiments in which CD18 or CD11a were capped showed that the two subunits co-migrate on T21 and normal LCL, probably as heterodimers. This appears to explain the increased expression of CD11a on Trisomy 21 LCL. There was no evidence that T21 LCL express the other two leucocyte integrin subunits CD11b and CD11c, indicating that Trisomy 21 has little affect on tissue specific control of these molecules. In contrast, there appears to be reduced expression of an unrelated adhesion molecule LFA-3 on Trisomy 21 LCL. We discuss the relevance of these results in the diagnosis of Down's syndrome.

Antibodies, Monoclonal↗