Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aprotinin, a wide range proteinase inhibitor, was given alone to tumor-bearing mice and life span and several tumor growth parameters were recordered. Aprotinin showed anti-tumor effects in Hepatoma 22 and Lewis lung carcinoma, remaining ineffective in Sarcoma 37, Leukemia L1210 and Ehrlich ascitic carcinoma.
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PMID:Effect of proteinase inhibitor in experimental tumors. 20 10

When given by direct s.c. injection into the Ehrlich solid carcinoma 1 week after s.c. tumor transfer, viable crude spores of Clostridium perfringens type A (attenuated mutant strain LNG11 ATCC 29348) inhibited tumor growth and significantly prolonged the life span of male outbred Swiss mice. Under these conditions a concentrated sterile supernatant of a C. perfringens culture proved to be slightly more effective than were viable crude spores. In contrast viable crude spores were ineffective in the treatment of female Swiss mice, but the sterile supernatant retained significant activity. When given at the time and site of s.c. grafting of Ehrlich tumor cells, a concentrated sterile supernatant of a C. perfringens culture prevented tumor growth in 80% of male outbred Swiss mice. Under these conditions viable crude spores prevented tumor growth in 70% of mice and significantly prolonged the life span in the other 30%. When given by i.p. injection and before i.p. grafting of tumor cells, viable crude spores of C. perfringens prevented Ehrlich ascites tumor in 5 of 12 Swiss mice and prolonged life span in the other 7. In contrast concentrated sterile supernatant and viable purified spores were ineffective in the prevention or delay of the growth of Ehrlich ascites tumor. These data indicate that C. perfringens can be a potent antitumor agent without producing the harmful anaerobic infection of solid tumors (clostridial oncolysis.
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PMID:Growth retardation and prevention of Ehrlich solid tumor by Clostridium perfringens type A spores and culture supernatant. 20 66

Carcinoma of the bronchus can produce several polypeptide hormones and therefore has the capacity to cause most syndromes of endocrine hyperfunction. All pituitary hormones can be synthesized ectopically; furthermore, the production of hormones from the hypothalamus (CRF), the placenta (HCG, HPL) and the C-cells of the thyroid (calcitonin), as well as parathormone and prostaglandins has been described. The paraneoplastic syndrome may often be more dangerous for the patient than the tumor growth itself, and can lead to early death. On the other hand, it may allow the early detection of an unsuspected tumor. The ectopic hormones and other nonendocrine proteins and peptides can be used as tumor markers, and can demonstrate the effect of treatment and early recurrence or metastases. An ideal tumor marker should have the following characteristics: 1. production exclusively by neoplastic tissue, 2. direct correlation with tumor size, 3. substances common to all tumor types ("large spectrum tumor marker") although specific tumor markers for special tumors should be available, 4. the assays must be easy and automation should be possible. At present no tumor marker satisfies all these conditions. The measurement of several tumor markers and the use of discriminant analysis may extend their diagnostic value and open the way for biochemical detection of cancer in the future.
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PMID:[Ectopic hormone formation and tumor markers in bronchial neoplasms]. 22 36

We have tested the hypothesis proposed by Costa, Lyles, and Ullrich. (Effect of Human and Experimental Cancer on the Conversion of 14C Tripalmitin to 14CO2. Cancer (Phila.), 38:1259-1265, 1976) that the transport and/or oxidation of triglyceride fatty acids is markedly impaired in rodents bearing a growing s.c. carcinoma. Specifically, we have tested whether oxidation of triglyceride fatty acids is depressed in cancer-bearing animals. Mice inoculated s.c. with Ehrlich carcinoma cells were given injections (i.v. and i.p.) of 14C-labeled triglyceride fatty acids prepared as very-low-density lipoproteins by physiological methods or (i.p.) with [-14C]tripalmitin dissolved in peanut oil during both early (3 to 4 days) and advanced (7 to 8 weeks) stages of tumor growth. Specific activity of the expired 14CO2 was measured for periods ranging from 1 to 7 hr following injections. Because cancer-bearing mice can become severely hypertriglyceridemic, plasma triglyceride pool sizes were also measured during each experiment to account for the effects of possible differential dilution of the tracers. At no instance did we find any significant differences between specific activities of expired 14CO2 or plasma triglyceride pool sizes of the cancer-bearing animals and controls. Thus, a cancer-induced impairment of triglyceride fatty acid transport and metabolism to CO2, such as reported by Costa et al., does not seem to be a universal phenomenon in rodents.
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PMID:Evaluation of impaired triglyceride fatty acid transport and oxidation for the detection of cancer in mice. 22 96

Transplantable Brown-Pearce carcinoma was adapted successfully in the rabbit anterior chamber. Regression of tumor growth was attained on tri-weekly perfusion of the AC with 10 micromolar of methotrexate. Tumor cyclic nucleotide phosphodiesterase (PDE) and protein activator were found to be markedly depressed during the course of chemotherapy and the PDE cAMP/cGMP ratio was similarly altered. Corroborative light and electron-microscopic studies showed specific alterations of intracellular organelles in relation to MTX and tumor cell death. These findings suggest that metabolic pathways of cyclic nucleotides are important biochemical modulators of neoplastic cells. The method of intraocular perfusion precludes systemic toxic effects and avoids compromising the animals' immunocompetence.
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PMID:Experimental intraocular malignancy: the effect of intracameral perfusion. 23 85

Increased glucose levels in blood of diabetic and of normoinsulinemic hyperglycemic CBA/H mice were accompanied by suppressed growth of aplastic carcinoma. Tumors maintained in diabetic mice grew faster after each subsequent transplantation into diabetic mice, but those maintained in hyperglycemic normoinsulinemic mice grew at a constant rate. Evidence revealed that tumor growth was suppressed by hyperglycemia. The observed proliferation enhancement of aplastic carcinoma maintained in diabetic mice was caused by de novo insulin synthesis, probably by the tumor cells themselves.
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PMID:Aplastic carcinoma in diabetic mice: hyperglycemia-suppressed proliferation rate and insulin synthesis by tumor cells. 28 69

Malignant effusions from 150 patients with breast carcinoma were examined to determine whether cytologic features could be related to prognosis. Four features were studied: tumor cellularity and frequency of mitoses in tumor cells as an indication of their proliferative activity, leukocytic (lymphocytic) background as a possible measure of host reaction and tumor cell cluster formation as an indication of the tumor growth pattern. The clinical outlook was poor in all the patients with effusions due to breast cancer, and we found no good relationship between any of these four cytologic features and prognosis.
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PMID:Absence of prognostic features in the cytology of effusions due to mammary cancer. 28 49

A transplantable murine breast carcinoma in mice was associated with marked leukemoid reaction. Within 1 week of subcutaneous implantation of tumor the leukocyte count began to increase and reached average levels of 165,000 leukocytes per cubic millimeter within 18 days. This represented an increase in mature neutrophils primarily, although other blood leukocytes were modestly increased as well. The total number of neutrophils per humerus was increased but no increase was detected in the number of myloblasts, promyelocytes, or myelocytes. The tritiated thymidine-labeling index of the latter three cells was not significantly changed during tumor growth. The number of progenitor cells forming granulocytic and mononuclear cells in vitro was decreased in the marrow during tumor growth. Colony-stimulating activity in plasma was slightly increased during the early phase of tumor growth and decreased during later phases. Emergence time of blood neutrophils was normal, as measured by labeling with tritiated thymidine, but decline in labeled cells was abnormally slow in tumor-bearing mice. There was a shift of erythropoiesis to the spleen, but total erythropoiesis appeared to be normal in most mice. Surgical excision of the tumor resulted in prompt reversal of the leukemoid reaction. In the aggregate these results are consistent with a hypothesis that the leukemoid reaction was the result of increased blood transit time of neutrophils primarily, rather than increased neutrophil production.
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PMID:Kinetic studies of a tumor-induced leukemoid reaction in mice. 29 65

Since the humoral immune response has been shown to be associated with immunological enhancement of tumor growth, the study of surface immunoglobulin-bearing cells and plasma cell antigen (PCA)-bearing cells during neoplastic development may provide new approaches to the study of tumor immunology. Peripheral blood was collected every other day from normal and carcinoma-bearing mice. Lymphocytes obtained by Ficoll-Hypaque density centrifugation were assayed for immunoglobulin-bearing cells and PCA-bearing cells using either fluorescein-conjugated goat anti-mouse immunoglobulin or rabbit anti-mouse plasma cell serum and fluorescein-conjugated goat anti-rabbit immunoglobulin. A marked increase in immunoglobulin-bearing cells from tumor-bearing mice was observed by Day 6 and peaked at Day 10. An increase in PCA-bearing cells followed the immunoglobulin-bearing cells increas by 2 to 4 days. The immunoglobulin-bearing cells declined by Day 12, whereas PCA-bearing cells remained elevated through Day 20. Using rabbit anti-mouse plasma cell serum as an immunosuppressive agent, a 4-day prolongation of the mean survival time was observed in rabbit anti-mouse plasma cell serum-treated tumor-bearing mice. This suggests that tumor growth in this model may be related to an active humoral immune response and that suppression of the plasma cell population may prove to be beneficial in the treatment of certain tumors.
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PMID:Relationship of surface immunoglobulin-bearing cells, plasma cells, and tumor development in anaplastic carcinoma-bearing A/J mice. 30 Feb 78

The effect of BCG vaccine on the growth of imtransplants of Krebs-2 carcinoma in mice was studied. The simultaneous injection of BCG and tumor cells either inhibited tumor growth (BCG given in admixture with tumor cells) or stimulated it (BCG injected contralateral to the tumor transplantation site). The BCG dose was directly related to the effect. Tumor growth was also stimulated by the ip injection of starch or liquid paraffin. In these experiments, the BCG effect was attributed to the redistribution of cells involved in nonspecific and specific tumor resistance. Shortly after BCG prevaccination, particularly when BCG doses were high and mice were susceptible to vaccine infection, BCG was either without effect or stimulated tumor growth; later, however, tumor growth was inhibited regardless of the BCG dose and the injection site of the BCG. The effect of BCG prevaccination was suggested to be due to: 1)the distraction of macrophages and T-lymphocytes to defend the host against the multiplying mycobacteria, and 2)the activation of the pool of these cells that become capable to participate in antitumor resistance after mycobacteria elimination.
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PMID:Inhibition and stimulation of the growth of Krebs-2 carcinoma by BCG vaccine. 32 6


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