Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancer bearing is frequently accompanied by weight loss, yet the factors causing cancer cachexia remain unclear. This study compares how tumor type and tumor burden affect host carcass fat depletion. Nude mice were inoculated with human malignant melanoma, human colon adenocarcinoma, or murine sarcoma cells, or were noninjected controls. Body weights, tumor burdens, and carcass lipid contents were measured. Carcass weights of melanoma-bearing mice were significantly lower than those of sarcoma-bearing mice, mice exposed to colon cancer antigens but without tumor growth, or control mice (all p less than 0.02). The degree of carcass lipid loss in melanoma-bearing mice (mean tumor burden 3.5% of total body weight [TBW]) was almost three times that of sarcoma-bearing mice (p less than 0.05), which had more than twice the tumor burden (mean tumor burden 7.8% TBW). Exposure to colon cancer antigens without tumor growth resulted in essentially no carcass lipid depletion compared with control mice. These findings argue against a mass effect of tumor as being solely responsible for host fat mobilization and suggest that carcass lipid depletion in tumor-bearing nude mice is more a function of tumor type than of tumor burden.
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PMID:Effects of tumor type and burden on carcass lipid depletion in mice. 373 56

The chemosensitivity of human tumor xenografts to mitozolomide, 8-carbamoyl-3-(2-chloroethyl)imidazo[5-1-d]-1,2,3,5-tetrazin-4(3H) -one, was studied in 3 different assay systems. In concentrations of 1 to 500 micrograms/ml, mitozolomide completely inhibited the colony-forming ability in soft agar of cell suspensions from sarcomas, melanomas, lung and colon cancers, and a mammary carcinoma. When a panel of tumors of the different histological types was tested for its sensitivity to mitozolomide in vitro, in the 6-day subrenal capsule assay in conventional mice, and, in some cases, as s.c. growing tumors in nude mice, good agreement between the different assay systems was seen. In most cases, a very pronounced antitumor effect was observed. The efficacy of mitozolomide was as good or better than that of the drugs clinically used against the tumor types tested. Tumor size measurements and histological examinations indicated that nude mice carrying a melanoma, a small cell lung cancer, and an osteosarcoma were cured of their tumors. The approach here used for evaluating the effect of a new drug on human cancers may be useful for selecting the tumor types which primarily should be studied in clinical trials. The results indicate that clinical responses to mitozolomide may be anticipated in sarcoma, melanoma, small cell lung cancer, and possibly in colon cancer.
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PMID:Activity of mitozolomide (NSC 353451), a new imidazotetrazine, against xenografts from human melanomas, sarcomas, and lung and colon carcinomas. 397 40

The human colon carcinoma cell line HT-29 was adapted to grow in chemically defined medium (CDM). The spent CDM (S-CDM) was concentrated by Amicon filtration and the crude HT-29 S-CDM purified by 40% saturated (NH4)2 SO4 precipitation. The purified antigen was tested by a microcomplement fixation (MCF) assay against the sera of cancer patients of various histologic types and against the sera of normal donors. Fifteen of 20 (75%) colon cancer, 16/20 (80%) breast cancer sera, 14/19 (74%) lung cancer sera, and 13/20 (65%) miscellaneous carcinoma sera were positive in the MCF. By contrast, 2/21 (10%) melanoma sera, 7/20 (35%) sarcoma sera, and 2/19 (11%) normal sera were positive. These data suggest the presence of a carcinoma-associated antigen in the spent CDM of the HT-29 colon carcinoma cell line adapted to grow in CDM.
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PMID:Presence of a carcinoma-associated antigen(s) in the spent chemically defined medium of a human colon carcinoma cell line. 615 28

A method for measuring DNA in tissue cells by flow cytometry utilizing a one step combination nuclear isolation-DNA fluorochrome staining procedure is described. A variety of cells and tissues, both in vivo and in vitro, was used to illustrate the universal nature of this technique. These included murine bone marrow, liver testicle, sarcoma brain tumor, rat pancreatic islets, human peripheral blood, colon mucosa, colon cancer, sarcoma and brain tumor tissues. A special nuclear isolation medium, which contained either of the DNA fluorochromes, 4',6-diamidino-2 phenylindole-2 HCl or propidium iodide, was utilized successfully to isolate single suspensions of DNA fluorochrome stained nuclei in a rapid (5-10 min), consistent manner from a variety of tissues and cells. Multiple sampling of the same tissue or comparison between whole tissues and their single cell isolates showed that a representative sample was being obtained.
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PMID:Preparation of tissues for DNA flow cytometric analysis. 616 10

Soft tissue sarcoma and malignant lymphoma have been related to exposure to chlorinated phenoxy acids or chlorophenols as well as exposure to organic solvents and malignant lymphoma. However, colon cancer studied by the same case-referent design did not show any such associations, which helps to rule out alleged systematical bias of the study approach. Further considerations about exposure routes for phenoxy acids and chlorophenols suggested that nasal and nasopharyngeal cancers should be studied. Forty-four cases with nasal cancer and 27 cases with nasopharyngeal cancer were eligible for study during 1970-1979 together with 541 referents, as utilized also in the aforementioned studies. Exposure to phenoxy acids gave formally a doubled but insignificant risk for the studied cancer types. Exposure to chlorophenols, as present particularly in woodwork, was related to an about sevenfold and significant increase in the risk for both cancer types. In woodworkers without exposure to chlorophenols there was an approximate normal risk, but cabinet makers, even without exposure to chlorophenols, had nearly doubled (but insignificant) risk of nasal cancer.
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PMID:Epidemiological study of nasal and nasopharyngeal cancer and their relation to phenoxy acid or chlorophenol exposure. 630 19

Lethal effects of mitomycin C (MMC), 4-nitroquinoline 1-oxide (4NQO) and ultraviolet light (UV) on fibroblast cell lines derived from a colon cancer-prone substrain of Wistar-Furth rats (WF/OSAKA rats) were measured in terms of the cellular colony-forming ability, and compared with the sensitivity to these agents of human fibroblasts from patients with adenomatosis coli and rectum (ACR). All 6 fibroblast strains from the cancer-prone WF/OSAKA rats were significantly more sensitive (though to various extents) to MMC as well as 4NQO than normal rat fibroblasts derived from the parental WF Hiroshima rats. These WF/OSAKA cell strains were slightly more sensitive to UV than normal rat cell strains. Similarly, 5 out of 6 fibroblast strains derived from ACR patients were hypersensitive to both MMC and 4NQO. Further, the WF/OSAKA cell strains were more susceptible to morphological transformation induced by Kirsten murine sarcoma virus than normal rat strains. The observed higher sensitivity to chemical agents and to viral transformation suggests a close similarity in cellular terms between the colon cancer-prone WF/OSAKA rats and human individuals affected with ACR.
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PMID:Increased sensitivity of cultured fibroblasts from colon cancer-prone rats to cytotoxicity of carcinogens and to viral transformation: a comparison with fibroblasts from patients with adenomatosis coli. 642 45

A human tumor cloning system was utilized to screen for in vitro antitumor effects of the investigational anticancer agent Echinomycin. Tumors from 562 patients (24 different histological tumor types) were placed in culture. Two hundred fifty-five specimens were evaluable for drug sensitivity information (i.e., greater than or equal to 20 colonies in control plates). The overall in vitro response rates (defined as less than 50% survival of tumor colony-forming units) at three different doses of Echinomycin (0.001, 0.01, and 0.1 micrograms/ml) were between 16% and 19%. Echinomycin showed minor in vitro cytotoxic activity in breast and colon cancer, and in sarcoma. A comparison of these in vitro results with the results of phase-II clinical trials, as they become available, will help to evaluate the utility of the human tumor cloning system for predicting clinical antitumor activity of new antineoplastics.
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PMID:Cytotoxic activity of echinomycin in a human tumor cloning system. 654 21

Primary gastrointestinal tumors were induced in male WF rats by 16 weekly sc injections of 1,2-dimethylhydrazine [(DMH) CAS: 540-73-8; 20 mg/kg/wk]. Twenty-four to 28 weeks after the start of DMH injections, all rats were surgically explored and gastrointestinal tumors were resected. Rats with no remaining microscopic disease after operation were immunized with one of four tumor isografts. The first isograft, DMH-W163, is a poorly differentiated mucinous adenocarcinoma explanted from a colon cancer in a DMH-treated animal. It has been shown to possess antigens that cross-react with other DMH-induced bowel adenocarcinoma isografts. The second isograft, DMH-W49, is a carcinosarcoma explanted from a DMH-treated primary colon cancer. It has intermediate antigenic cross-reactivity with other colon adenocarcinoma isografts in the WF model. The third isograft, DMH-W15, is a sarcoma explanted from a DMH-induced colon cancer that does not possess antigens cross-reactive with other DMH-induced colon adenocarcinomas. The fourth isograft, SPK, is a spontaneous (non-DMH-induced) renal cell carcinoma that is immunogenic but should not contain tissue-type-specific antigens cross-reacting with the bowel cancers. Immunized rats received three sc weekly injections of 1 X 10(3) irradiated cells. Concomitant control rats received no immunization after resection of the primary tumor. Within 24 weeks of primary tumor resection, 12 of 16 (75%) rats not immunized had tumor recurrence. Only 8 of 24 (34%) rats immunized with DMH-W163 had tumor recurrence (P less than .025 compared to controls). Fifty percent of animals (10/20) immunized with the carcinosarcoma DMH-W49 had a recurrence. Animals immunized with the non-cross-reacting DMH-W15 sarcoma isograft had a recurrence rate similar to that of controls (16/20, 75%). The rats immunized with SPK were not protected from recurrence. Twelve of 19 (63%) had a recurrence at or near the suture line within 24 weeks following primary tumor resection. These results confirm that adjuvant immunotherapy can decrease the rate of recurrence following primary tumor resection in this model. In addition, immunogens that possessed tissue-type-specific antigens were more effective in preventing tumor recurrence than those that did not.
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PMID:Effects of specific active immunization on tumor recurrence following primary tumor resection in WF rats with 1,2-dimethylhydrazine-induced bowel cancer. 659 Sep 17

A Phase I trial of tricyclic nucleoside phosphate (1,4,5,6,8-pentaazaacenaphthylene-3-amino-1, 5-dihydro-5-methyl-1-beta-D-ribofuranosyl 5'-phosphate ester; NSC 280594) was conducted using a 5-day continuous infusion schedule. Thirty-seven patients with advanced cancer were entered on the study, of whom 33 patients were evaluable for response and toxicity. Dose levels ranged from 10 mg/sq m/day X 5 days to 40 mg/sq m/day X 5 days. Initially, courses were repeated every 3 to 4 weeks. As cumulative toxicity became manifested, the interval between courses was changed to every 6 weeks. Major toxicities included hyperglycemia, hepatotoxicity, and thrombocytopenia. Patients with a prior history of diabetes mellitus, extensive radiation therapy, or significant liver metastases were prone to severe toxicity. Other toxicities noted were nausea and vomiting, abdominal discomfort, anemia, and reduction in serum calcium, phosphorus, and albumin levels. Rare side effects included hypertriglyceridemia, hyperamylasemia, diarrhea, and stomatitis. Antitumor activity observed include improvement in s.c. metastases in a patient with papillary thyroid carcinoma, stabilization of disease in a patient with mesothelioma, and mixed responses in three patients (colon cancer, sarcoma, and tonsillar squamous cell cancer). Recommended schedule for Phase II studies is 20 mg/sq m/day for 5 days every 6 weeks.
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PMID:Phase I study of tricyclic nucleoside phosphate using a five-day continuous infusion schedule. 674 83

Human tumor stem cell assay is an in vitro colony-forming technique. Double soft agar layers are used for culture tumor cells and cell lethality is judged by the numbers of colony formation in this assay. Single-cell suspension made from various malignant materials in cancer patients is placed in culture after exposing to various anticancer agents for one hour and incubated for two weeks. Antitumor effects of various anticancer agents against individual patients are evaluated by % inhibition of colony formation. Of 57 tumor specimens 42 (74%) formed at least five colonies per plate (per 0.5 x 10(6) cells). The colony-forming rates of various malignancies are as follows: breast cancer 14/15 (93%), ovarian cancer 8/10 (80%), stomach cancer 5/13 (38%), sarcoma 4/5 (80%), lung cancer 1/4 (25%), colon cancer 3/3, each of pancreas cancer, leukemia and primary unknown adenocarcinoma 2/2, malignant lymphoma 1/1. The median plating efficiency (number of colonies/number of nucleated cells plated) is 0.02% (range: 0.001-0.3%). High correlation between human tumor stem cell assay results and response of an individual patient's tumor to chemotherapy is reported by Salmon and Von Hoff. Human tumor stem cell assay is useful tool for the high prediction of chemosensitivity response.
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PMID:[Human tumor stem cell assay]. 718 17


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