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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A specific collagenase (EC 3.4.24.3) has been found and purified from serum-free culture medium of 11095 epidermoid carcinoma of rat prostate. The molecular weight of this collagenase was estimated at 71 000 and the pH optimum was approx. 7. At 26 degrees C, the collagenase cleaved collagen at a site 3/4 the length from the N-terminus. At 37 degrees C, this collagenase degraded collagen to smaller peptides. The enzyme activity was inhibited by serum, cysteine and EDTA, but not by protease inhibitors. The presence of collagenase in rat tumor tissue suggests that this enzyme might play a significant role in tissue invasion by cancer cells.
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PMID:Collagenase activity in cultures of rat prostate carcinoma. 3 9

A 13-year-old male who had bilateral cryptorchid testes since birth underwent testicular biopsies and subsequent left orchiectomy following a diagnosis of malignant germ cell tumor. No tumor mass was noted although the malignant cells were seen within the seminiferous tubules and the interstitium. Five recorded cases of in-situ or incipient germ cell neoplasms of the testes are reviewed; three were infertile, another had a cryptorchid testis, and the fifth was both infertile and cryptorchid. Two of these patients have developed frank carcinoma, which would suggest that the process represents an early phase of invasive germ cell neoplasia.
Cancer 1979 Oct
PMID:Incipient germ cell tumor in a cryptorchid testis. 4 Jun 86

The effects of dietary-induced acidosis on the growth and rates of complete regression of Sarcoma 180 in mice have been studied. The experiments here reported have demonstrated that mineral acidification of laboratory food produces a late decrease in tumor growth and significantly increases the rates of complete tumor regression. Blood acid-base studies also demonstrate the effects of these diets in altering the acid-base balance, and seemingly, this is independent of starvation and/or ketosis. The relationships of such in vivo acid-base metabolic changes to the control of tumor metabolism are briefly discussed. A therapeutic potential for this preliminary approach is considered.
Cancer Res 1979 Nov
PMID:Effects of systemic acidification of mice with Sarcoma 180. 4 Jun 91

Tissue (extracellular) pH (pHe) and intracellular pH (pHi) were measured together in vivo in the solid Yoshida sarcoma and normal organs (liver, gastrocnemius muscle) of noninbred Wistar rats. pHe was monitored by insertion of a miniature capillary glass electrode, and pHi was measured indirectly by equilibrium partitioning of the weak organic acid 5,5-dimethyloxazolidine-2,4-dione across the cell membrane. Under normal conditions, tumor, liver, and gastrocnemius had a similar pHe of 7.05--7.30; tumor pHi was consistently higher (7.2) than that of the normal tissues (6.8--7.1). Curative hyperthermia (42 degrees C for 1 hr) did not significantly change tumor pHe or pHi. After ip glucose injection [6 g/kg body wt; blood glucose level greater than 400 mg/100 ml (22 mmoles/liter) for 4 hr], tumor pHe decreased markedly to 6.6 within 4 hours and did not return to normal for a further 12--14 hours, whereas tumor pHi was hardly affected. No marked change was noted in pHe or pHi of the normal organs following glucose loading of the host. In tumor slices removed from hyperglycemic hosts, marked reduction of both respiration and glycolysis was observed. Hyperglycemia (4 hr) plus hyperthermia at 40 degrees C (1 hr) had a synergistic inhibitory effect on metabolism that was equivalent to heat alone at 42 degrees C, and respiration and glycolysis almost ceased after 3--4 hours. However, tumor heating at 40 degrees C in hyperglycemic hosts was not equivalent to hyperthermia at 42 degrees C: With the former treatment, tumor regression did not occur, and animal survival did not differ from that of control untreated rats. The data do not support the postulate that the effects of heat on tumor cells are mediated via low pHi or that hyperglycemia leads to a lowered pHi which sensitizes the tumor to destruction at 40 degrees C instead of 42 degrees C.
J Natl Cancer Inst 1979 Dec
PMID:Effects of hyperglycemia and hyperthermia on the pH, glycolysis, and respiration of the Yoshida sarcoma in vivo. 4 58

Tissue analyses and tumour regression studies using the oncolytic antibiotic, adriamycin (14-hydroxydaunomycin), and its DNA complex at adriamycin dosages of 5 mg/kg and 10 mg/kg were made on C3H mice with transplanted mammary adenocarcinoma. Chemical analysis indicated a significantly lower (P < 0.05) uptake of adriamycin into cardiac tissue for the adriamycin-DNA complex. Tumour regression was comparable for both the complex and free adriamycin. Results suggest an advantageous role for the adriamycin DNA complex in the chemotherapy of metastatic breast carcinoma.
Cancer Lett 1977 Mar
PMID:The comparative toxicity and therapeutic efficacy of adriamycin and the adriamycin-DNA complex in the chemotherapy of C3H mice with transplanted mammary adenocarcinoma. 4 24

Phorbolol myristate acetate, a metabolite of the tumor promotor phorbol muristate acetate in mouse skin, has one-fiftieth the potency of the parent molecule for the induction of cell division in stationary cultures of BALB/c-3T3 mouse embryo cells. Similarly, in a mixed cell culture assay devised for detection of tumor-promoting agents, phorbolol myristate acetate exhibited only a small fraction of the activity of unmetabolized phorbol ester. The results indicate that the biological activity of phorbol esters either does not require metabolic conversion or is converted by the cells used in this system and that phorbolol myristate acetate would be a tumor promotor of low potency for mouse skin compared to phorbol myristate acetate.
Cancer Lett 1977 Mar
PMID:Comparison of the biological activity of the tumor promotor phorbol myristate acetate and a metabolite, phorbolol myristate acetate, in the cell culture. 4 32

Areas of hyperplastic livers that acquire hyperbasophilic properties at advanced stages of carcinogenesis apparently represent the sites of neoplastic trasnformation, and hyperstaining of cytoplasmic RNA with basic dyes also characterizes the cancer cells. Estimations of the RNA content of cell fractions from normal rat liver and solid Novikoff hepatoma provided no evidence that the intense staining of cancer cells could be explained on the basis of an increase in cytoplasmic RNA content. The possibility that cytoplasmic fractions of Novikoff hepatoma show greater affinity for basic dyes than corresponding normal fractions has been examined by means of a test-tube toluidine blue-binding assay. The results revealed that the dye-binding capacity of total cytoplasmic fractions from tumors is 75% higher than normal after Carnoy fixation which retains mostly ribosomal RNA. Assays on fresh ribosomes indicated that tumor ribosomes bind 71% more toluidine blue per mg of RNA than the ribosomal preparation from normal liver. This study thus demonstrates a greater affinity of tumor RNA for basic dyes, and a comparison of biochemical and cytophotometric analyses suggests that an increase in basophilia by a factor OF ABOUT 2 WOULD BE DUE TO A qualitative alteration in robosomal RNA molecules and/or ribosome structure in cnacer cells.
Cancer Res 1975 Jan
PMID:Biochemical estimation of the basic dye-binding capacity of RNA from rat hepatoma. 4 92

Nuclear fluorescence metachromasia of heated fixed cells subsequently stained with acridine orange was compared in smears and isolated nuclei of various types of primary tumors and normal cells from the tissues that gave rise to the tumors. The ratios of fluorescence emission at 590 and 530 nm reflect the thermal stability of chromatin in situ. The results show that the mean thermal stability of the chromatin in neoplastic cells was lower than the stability of their normal counterparts in all cases. This was found in both spontaneous and chemically induced tumors as divergent in type as a dog vaginal tumor and murine lymphocytic leukemia. These data, together with our previous observations in other neoplastic systems, indicate that reduced chromatin thermal stability may be a general characteristic of cells that have undergone neoplastic transformation and is not confined to rapidly growing tumors. The present investigation identifies the sources of variability encountered in measuring fluorescence metachromasia in slide preparations, and methods of minimizing this variability for potential cytodiagnostic application are discussed.
Cancer Res 1975 Jan
PMID:Microfluorometric comparisons of heat-induced nuclear acridine orange metachromasia between normal cells and neoplastic cells from primary tumors of diverse origin. 4 93

A correlated morphological study, employing endocrine cell stains, immunofluorescence, and electron microscopy, was performed on biopsy specimens taken from a pancreatic tumor and liver metastases in a woman with hypoglycemic symptoms and high fasting insulin levels. The study revealed the tumor to be composed of two different endocrine cell populations, irrespective of the primary or metastatic growth. The first cell type fulfilled all the morphological characteristics of the islet B cells. The second was argyrophil (with the Grimelius silver method) and showed the morphological pattern of polypeptide-hormone-producing cells. With the lack of a detectable symptomatology, normal blood levels of the hormones other than insulin, and the negative results of a large number of immunofluorescence tests, we were unable to indetify the specific nature of the second type of cells.
Cancer 1975 Feb
PMID:Endocrine tumor of the pancreas composed of argyrophil and B cells. A correlated light, immunofluorescent, and ultrastructural study. 4 81

The serial development of cell-mediated immunity (CMI), cytotoxic antibody activity, serum blocking activity, and virus-neutralizing antibody levels were monitored in vitro for beagle and mongrel puppies inoculated with feline sarcoma virus (FeSV) and were compared to in vivo histologic markers of regression of induced sarcomas. CMI developed rapidly and maintained a high level of in vitro activity throughout the tumor life-span. Cytotoxic antibody levels similarly rose rapidly to peak just before clinically detectable regression and then declined during most of the regression sequence. This suggested antibody fixation at the tumor site, correlating with the histologic finding of focal necrosis and neutrophilic infiltrates. Inactivation of antibody by circulating antigen with subsequent immune complex formation was a possibility. Levels of virus-neutralizing antibody in sera paralleled those of cytotoxic antibody; their relationship in the circulation was not clear, but each related to virus-determined antigenic specificities. Serum blocking activity rose rapidly, leveled off during most of the tumor life-span, and rose slightly during the last stages of regression. This partly explained the lack of in vivo tumor lymphoid infiltrates to correlate with the striking in vitro CMI. Blocking activity was also present, however, when lymphoid infiltrates were seen histologically. Thus in vitro-in vivo correlation was best for cytotoxic antibody, which suggested that antigen-antibody reactions involving neutrophil-mediated regression sequences were important in effecting tumor-cell destruction.
J Natl Cancer Inst 1975 Feb
PMID:Regression of feline sarcoma virus-induced sarcomas in dogs. II. Immunologic investigations. 4 76


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