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Biomedical subjects

S K Sundar

Publications and source records attributed to S K Sundar.

25 records · Page 2Linked to original sources

Sera from patients with undifferentiated nasopharyngeal carcinoma contain a factor which abrogates specific Epstein-Barr virus antigen-induced lymphocyte response.

A unique association of Epstein-Barr virus (EBV) with the undifferentiated nasopharyngeal carcinoma (NPC) is a well acknowledged phenomenon. We report here the detection of a factor present in the sera of NPC patients which inhibits the blastogenic response of lymphocytes from EBV seropositive individuals to EB virions or soluble antigens. This lymphocyte-stimulation inhibitor (LSI) was found to be associated with the IgA fraction of the serum immunoglobulins. No inhibitory activity was detected in the sera and their immunoglobulin fractions from healthy (both EBV-seropositive and seronegative) individuals and patients with other carcinomas of the head and neck region. Interestingly, the IgA-LSI was absent in the sera of NPC patients who were successfully treated and remained in remission, while it was readily detectable in the sera of NPC patients in relapse, LSI-positive IgA fractions did not inhibit mitogenic response of lymphocytes to phytohemagglutinin. Taken together, the data presented suggest that LSI is a specific inhibitor of the response of sensitized lymphocytes to EBV antigens and that it may indeed represent a marker of great clinical significance regarding undifferentiated nasopharyngeal carcinoma, particularly for its prognosis.

Antigens, Viral↗

Steroids inhibit tumor promoting agent induced Epstein-Barr virus early antigens in Raji cells.

Four steroids and one protease inhibitor were evaluated for their effects on 12-O-tetradecanoyl phorbol 13-acetate (TPA)-induced and Epstein-Barr virus-induced early antigens (EBV-EA) in Raji cells. Continuous treatment with dexamethasone, prednisolone, hydrocortisone and cortisone inhibited TPA-induced EBV-EA to varying degrees, but the protease inhibitor N-alpha-p-tosyl L-lysine chloromethyl ketone-HCl (TLCK) had no significant effect. None of the agents tested inhibited EBV- induced EA. In addition, the effect of the steroids was reversible since the removal of these agents resulted in recovery of the percentage of EBV-EA-positive cells in TPA-treated cultures. These results were in agreement with the in vivo experiments of other investigators, who demonstrated inhibition of tumor promotion with steroids. Since TLCK failed to inhibit TPA-induced EA, it is unlikely that induction of EA by TPA is the result of production of proteases.

Adrenal Cortex Hormones↗

Epstein-Barr virus-induced malignant lymphoma in a white-lipped marmoset.

One of six white-lipped marmosets inoculated with cell-free B95-8 virus developed diffuse malignant lymphoma. Epstein-Barr virus (EBV) DNA was detected in a pathologically enlarged mandibular lymph node by DNA-DNA hybridization. The affected animal at the time of killing had EBV antibody titers of 1:320 for viral capsid antigen (VCA) and 1:20 for early antigen (EA) while all non-diseased animals had less than or equal to 1:80 VCA antibody and no detectable EA antibody. This is the first report of lymphoma development in a white-lipped marmoset following EBV inoculation.

Animals↗

Tumor promoting agent induces lymphocyte mitogenic factor.

Human peripheral mononuclear cells treated with tumor promoting agent, 12-O-tetradecanoyl phorbol 13-acetate (TPA), released a soluble lymphocyte mitogenic factor (MF). The MF was found to be a protein capable of eliciting a proliferative response in normal human lymphocytes within 40-46 hours. The MF was detected in the culture supernatant fluid as early as 12 hours after TPA treatment and reached maximum at 48 hours. The biochemical characterization of MF is under active investigation.

DNA↗

Mitogenic effect of 12-0 tetradecanoyl phorbol 13-acetate on non-human primate mononuclear cells and in vitro interaction with Epstein-Barr virus transformation.

12-0 tetradecanoyl phorbol 13-acetate (TPA), known to promote tumors in mice and also to enhance viral transformation as well as induction of viral antigens, was demonstrated to be mitogenic to peripheral blood mononuclear cells from rhesus monkeys and three species of marmosets. Even though mitogenic responses varied between species and within species, the mitogenic dose response due to TPA was comparable to the response of phytohemagglutinin (PHA-P). A significant synergistic effect of PHA-P and TPA on mononuclear cells from marmosets was evident when they were used together at optimal doses. TPA also increased the efficiency of in vitro transformation of marmoset lymphocytes by Epstein-Barr virus.

Animals↗

Retinoic acid and steroids inhibit Epstein-Barr virus-induced nuclear antigen, DNA synthesis and lymphocyte transformation.

Retinoic acid, dexamethasone and prednisolone were evaluated for their effects on Epstein-Barr virus (EBV)-induced nuclear antigen (EBNA), DNA synthesis and transformation of human thymus-independent, B lymphocytes. It was found that continuous treatment of target cells with these agents completely inhibited EBV-induced transformation events. However, discontinuous treatment of the virus-infected cultures with these agents resulted in the recovery of DNA synthesis, and the appearance of EBNA and transformation. When the cells were treated with these agents 8 days after the virus infection, the inhibitors had no effect. These results show that only continuous treatment with these agents inhibited EBV-mediated transformation; these inhibitors had no effect once the EBNA and EBV-induced DNA synthesis were initiated in target lymphocytes.

Antigens, Viral↗