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Biomedical subjects

M J Droller

Publications and source records attributed to M J Droller.

At least 91 records · Page 5Linked to original sources
PubMed1982

Prevention of cyclophosphamide-induced hemorrhagic cystitis.

The occurrence of hemorrhagic cystitis with the use of high-dose cyclophosphamide is thought to be a toxic effect of cyclophosphamide metabolites directly on the bladder mucosa. To decrease both the concentration of metabolites in contact with the bladder mucosa and the time of such contact, a regimen of diuresis and frequent voiding or catheter drainage was instituted in patients at risk for the development of hemorrhage. Prior to institution of this regimen, 8 of 97 patients experienced massive clot-producing hemorrhage, three-quarters of whom died as a direct result of such hemorrhage. Subsequent to use of this regimen, only 1 of 198 patients experienced this degree of hemorrhage. Although this is only a phase II study, the dramatic decrease in the incidence of hemorrhage strongly suggests the efficacy of this regimen in decreasing the potential morbidity associated with cyclophosphamide-induced hemorrhagic cystitis.

Cyclophosphamide↗
PubMed1982

Immunoperoxidase detection of carcinoembryonic antigen and blood group substances in papillary transitional cell carcinoma of the bladder.

Immunoperoxidase localization of A and B blood group substances and carcinoembryonic antigen in papillary transitional cell carcinoma of the bladder demonstrated blood group substances in 22 of 48 carcinomas and trace amounts of carcinoembryonic antigen in 26. All 22 cases of transitional cell carcinoma positive for blood group substances were stage O (noninvasive) and 21 were grade I or II (well differentiated). Of 26 tumors negative for blood group substances 14 were grade III (poorly differentiated). Of 17 patients who had tumors positive for blood group substances at any time no positive tumor was followed by invasive carcinoma. In contrast, of 17 patients who had tumors negative for blood group substances 15 either had invasive carcinoma at the time of diagnosis or later. Carcinoembryonic antigen positivity did not correlate with pathologic stage, histologic grade or clinical course.

ABO Blood-Group System↗
PubMed1982

Expression of the cellular immune response during tumor development in an animal model of bladder cancer.

Papillary and solid transitional cell cancers were induced in the bladders of Fischer rats by ingestion of the carcinogen N-[4-(5-nitro-furyl)-2-thiazolyl] formamide. At sequential regular intervals, purified splenic, peripheral blood, regional lymph node, and thymus lymphocytes were harvested from tumor-bearing and age-matched control animals and tested for cytotoxicity against a variety of cell lines. Lymphocytes were also tested in mixed lymphocyte cultures for blastogenesis. Tumor development was accompanied by decreased lymphocyte cytotoxicity against bladder tumor targets at each interval tested. This decrease was in addition to the age-related decrease in cytotoxicity expressed by lymphocytes from control animals. No corresponding differences were seen in lymphocyte subpopulations as determined by immunofluorescence or in lymphocyte blastogenesis. Suppressor cell activity in tumor-bearing animals could not be demonstrated, and no cause-effect relationship between cytotoxicity depression and tumor development in these experiments was apparent.

Animals↗
PubMed1981

Bladder cancer.

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Humans↗
PubMed1981

Studies of A, B or O (H) surface antigen specificity: carcinoma in situ and non-malignant lesions of the bladder.

A, B or O (H) antigens identical to those that designate blood groups have been shown to be present on normal urothelial cells. Since the loss of these antigens, as measured by the specific red cell adherence test, has been associated with an increased malignant potential of low stage bladder carcinomas it was considered important to examine the specificity of this test by applying it to nonmalignant bladder lesions as well as to specimens of carcinoma in situ in which gross papillary lesions might not be present. Cells lining the lesions of cystitis and cystitis glandularis, appearing to be normal histologically, also were found to be positive for the presence of the A, B or O (H) antigens in all samples. In contrast, 4 specimens of squamous metaplasia, also appearing normal histologically, were negative by the specific red cell adherence testing. Finally, 7 of 8 specimens of carcinoma in situ were antigen-negative, with the remaining lesion showing only minimal adherence of red cells. Further analysis along similar lines is needed to determine the specificity of the specific red cell adherence test to define more clearly its clinical usefulness.

ABO Blood-Group System↗
PubMed1980

Production of prostaglandin E2 by tumor cells in vitro.

Our previous observations on the production of prostaglandin E2 (PGE2) by bladder tumor cell lines in vitro and the enhancement of tumor cell PGE2 production upon exposure to purified peripheral blood lymphocytes from normal human donors prompted us to examine this interaction in an animal model in order to further define conditions that determine the occurrence of this phenomenon. Cell lines derived from carcinogen-induced bladder and mammary tumors and from embryo fibroblasts in Fischer rats were exposed to purified peripheral blood or splenic lymphocytes in the presence or absence of indomethacin (10(-7)M). After varying times at 37 degrees, supernatants were harvested for determination of PGE2 by radioimmunoassay. Time course studies demonstrated rapid PGE2 production with plateau levels appearing at 8 hr. Increased tumor cell PGE2 production occurred in the presence of increased numbers of lymphocytes. Indomethacin partially inhibited PGE2 production. Preincubation studies suggested that the contribution of lymphocytes to overall PGE2 production in the present system was minimal. On the basis of previous observations of PGE2-associated inhibition of lymphocyte cytotoxicity against tumor cells in vitro, the present results suggest that tumor cell PGE2 production may reflect a response of the tumor cells to challenge by effector lymphocytes and may represent a mechanism whereby tumor cells subvert an immune response mounted against them.

Animals↗