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)

Soluble lung tumor activity as determined by LAI2 was enriched by physicochemical methods from chemically - defined spent medium of a lung cancer cell line (NCI-H69). To identify the polypeptide carrying the antigenic determinant, splenic lymphocytes of BALB/c mice were immunized with the enriched isolate and hybridized with mouse plasmacytoma cells. Eight hybrids were cloned successfully and produced MAbs that immunoprecipitated principally a single chain of Mr 40,000 (p40) as well as minor chains of Mr 25,000 (p25) and Mr 13,000 (p13) which were probably degradation products of p40. On 2D gels, p40 was composed of 7 spots with a p1 of 6.3 to 7.6, which was not altered by neuraminidase digestion. Affinity chromatography with MAb anti-p40 absorbed p40 and LAI activity. The bound and recovered fraction was enriched for p40 and LAI activity. Affinity-purified p40 also contained the previously identified p25 and p13 as well as a Mr 32,000 peptide (p32). MAb anti-p40 was directed to a common framework determinant on p40 since MAb anti-p40 bound to cancer cells from other organs. The comparatively lung cancer organ-specific determinant recognized by leukocytes from lung cancer patients was not recognized by the MAb. Affinity-purified p40 triggered LAI for leukocytes from patients with lung cancer but not for leukocytes from control subjects or patients with colon cancer or malignant melanoma in rigorous blind testing. Crossreactivity was observed with leukocytes from patients with breast cancer. LAI activity of affinity-purified p40 seems unlikely to result from an unidentified impurity. Thus a p40 molecule has been purified that is expressed on the membranes of lung cancer cells and triggers immunologically-mediated LAI.
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PMID:Purification from a human lung cancer cell line of a water soluble molecule mediating leukocyte adherence inhibition for patients with lung cancer. 400 98

A novel, substituted 4-quinolinecarboxylic acid (NSC 339768) demonstrated antitumor activity against L1210 leukemia and B16 melanoma in the National Cancer Institute's Developmental Therapeutics Program. An extensive analogue synthesis program was initiated; over 200 derivatives were synthesized and tested for anticancer activity. One of these compounds, 6-fluoro-2-(2'-fluoro-1,1'-biphenyl-4-yl)-3-methyl-4-quinolinecarboxylic acid sodium salt, NSC 368390 (DuP-785), was selected for further investigation because of its efficacy against a spectrum of human solid tumors and its water solubility. In initial studies with L1210 leukemia, the compound caused an increase in life span of greater than 80%. The activity was schedule dependent, and the compound was equally efficacious when administered i.p., i.v., s.c., or p.o. In tests against human tumors xenografted under the renal capsule of nude mice, NSC 368390 when injected i.p. in doses of 20-40 mg/kg daily for 9 days inhibited the growth of the MX-1 breast, LX-1 lung, BL/STX-1 stomach, and CX-1 colon carcinomas by greater than 90%. NSC 368390 also inhibited the growth of three distinct human colon carcinomas, the HCT-15, clone A, and DLD-2 tumors, growing s.c. in nude mice. An i.p. dose of 25 mg/kg given daily for 9 days inhibited the growth of the DLD-2 colon cancer by 98%. 1-beta-D-Arabinofuranosylcytosine and Adriamycin were ineffective, and fluorouracil was only moderately effective against these colon tumors. Because of its good activity against human colon tumors and other human carcinomas and its water solubility, NSC 368390 (DuP-785) is being developed as a Phase 1 anticancer agent.
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PMID:Activity of a novel 4-quinolinecarboxylic acid, NSC 368390 [6-fluoro-2-(2'-fluoro-1,1'-biphenyl-4-yl)-3-methyl-4-quinolinecarb oxylic acid sodium salt], against experimental tumors. 405 30

Among 41,109 women diagnosed with breast cancer between 1935 and 1982 in Connecticut, 3,984 developed a second cancer, whereas 2,426 were expected [relative risk (RR) = 1.64; 95% CI = 1.6-1.7]. This increased risk persisted for 30 years and was highest in women under 55 years of age at the time of breast cancer diagnosis. Second primary breast cancers (RR = 3.0) accounted for almost one-half of all new neoplasms. However, if subsequent breast cancers were excluded, the risk for all other second cancers was only 1.15 (95% CI = 1.10-1.20), and no excess risk was seen among women over age 55 at initial breast cancer. Significant risks were found for cancers of the ovary (RR = 1.7) and uterine corpus (RR = 1.4), possibly linked with shared reproductive factors such as nulliparity or late age at menopause. Malignant melanoma (RR = 1.5), thyroid cancer (RR = 1.6), and colon cancer (RR = 1.2) were also significantly elevated; possible shared risk factors remain to be elucidated. Significant deficits of multiple myeloma and chronic lymphocytic leukemia were noted. Women who received initial radiotherapy compared with those who did not were at slightly higher risk of developing a second cancer, most notably acute nonlymphocytic leukemia, non-Hodgkin's lymphoma, and cancers of the esophagus, kidney, and connective tissue, although the nature of the associations was not always clear. Some of the soft tissue sarcomas were lymphangiosarcomas of the arm, a consequence of the lymphedema that may complicate radical mastectomy (Stewart-Treves syndrome). Women treated with radiation were at higher risk of developing a second breast neoplasm (RR = 3.9) than nonirradiated women (RR = 2.8). Further investigation should focus on the mechanisms underlying the relationships between breast, genital tract, and colon cancers, and on the effects of treatment modalities on the risk of subsequent neoplasms.
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PMID:Second cancer following cancer of the breast in Connecticut, 1935-82. 408 15

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

Pulmonary resection for metastatic disease in 167 patients undergoing 207 thoracotomies resulted in a cumulative survival rate of 29% at five years and 20% at 10 years, with an operative mortality of 0.6%. The most favorable prognosis was associated with testicular and renal cell carcinomas and sarcomas. Less favorable tumors were malignant melanoma, carcinoma of the colon and rectum, and cervix uteri. A significant factor influencing survival was duration of disease-free interval with a 50% five-year survival rate in patients whose primary tumor was treated over five year ago. Patients with multiple pulmonary metastases had a five-year survival rate of 27% vs. 22% of patients with solitary metastases. Of 23 patients with tumor extending to the chest wall, diaphragm, or pleura, only two survived five years. Of 26 patients with mediastinal involvement none survived two years.
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PMID:Surgical resection for metastatic neoplasms of the lung: experience at the University of Minnesota Hospitals. 615 86

A fraction of the alpha-globulins (NHG) from normal human serum was cytotoxic for mouse L-cells in culture and Meth A tumors in mice. NHG inhibited the growth in vitro of human colon cancer (HT-29), melanoma (RPMI 7931) and a neuroblastoma cell line. Survival of HeLa S-3 cell colonies after 24 h exposure to 25, 50, 75 or 100 micrograms NHG/ml medium was 86%, 77%, 40% and 10%, respectively. Whole human serum or purified serum albumin had no anti-HeLa cell activity. These results confirm the presence of a protein in human serum with antitumor activity. An assay for NHG using HeLa S-3 tumor cells is described.
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PMID:A protein fraction (NHG) from serum of normal humans which is cytotoxic for HeLa cells in culture. 617 Apr 26

Double antibody radioimmunoassay (RIA), using radioiodinated melanoma-associated antigens (MAA), rabbit antiserum raised against 3 M KCl extract of human melanoma (AHMS) and goat antirabbit IgG antibody, was employed for the detection of MAA in tumors as well as in sera of melanoma patients. MAA were partially purified from crude KCl extract of melanoma tissue by affinity column chromatography using AHMS and concanavalin A. A high content of MAA was detected in all but one melanoma extract, while normal tissue and nonmelanoma tumor extracts contained MAA to a much lesser extent than did melanoma extracts. MAA were also found in melanoma patients' sera (20/45) but not in sera of normal donors (0/10) and colon cancer patients (0/10). Immunochemical data suggest that AHMS-defined MAA consist of two major glycoproteins with molecular weights of 37K and 31K daltons, which does not cross-react either with carcinoembryonic antigen or beta 2-microglobulin or with BCG.
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PMID:Immunodiagnosis of human melanoma: characterization of human melanoma antigens and their detection in sera of melanoma patients by radioimmunoassay. 617 26

A review of the case histories over the 10-year period 1969 to 1978 revealed 80 patients with cerebral metastases. Group 1 comprised 41 patients (43.9% carcinoma of the breast, 12.2% malignant melanoma, 9.8% hypernephroma, 9.8% carcinoma of the colon) in whom the primary site had been established before the manifestation of neurological deficit. Group 2 comprised 39 patients (56.4% bronchogenic carcinoma, 10.1% hypernephroma, 20.5% primary malignancy not identifiable) in whom the neurological symptoms due to metastasis had been first manifestation of malignancy. The sex distribution, age distribution, site of metastasis, cerebral symptoms and the time-lag before the diagnosis were analysed and compared with the literature. The patients in group 1 had an average survival time of 9 months, as compared with 7 months in group 2, from the time of the initial symptoms of cerebral metastasis. The survival time was not essentially different whether surgical or radiotherapeutic measures were undertaken.
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PMID:[Cerebral metastases as the first clinical manifestation of cancer]. 617 5

A new modification of our detergent technique for the preparation of nuclei for flow cytometric DNA analysis is described. The attainment of low coefficients of variation of the peaks and of quantitative staining of nuclei from different tissues was a problem with the original method. This was solved in the new modification by trypsinization of the unfixed nuclei. The nuclei were stabilized by spermine. A simple procedure for long-term storage of samples at -80 degrees C was integrated into the method. The fluorescence of the nuclei was stable for at least 3 hours after staining. Light exposure protection of the samples was essential. No cell loss was caused by storage or staining. The method was successfully applied on samples including: (a) Normal tissues--human lymphocytes, granulocytes and spleen. Mouse lymphocytes, bone marrow, spleen, liver, kidney and thymus. (b) Human neoplasms--lung cancer, breast cancer, lymphoma, leukemia, bladder cancer and cancer of the oral cavity. (c) Human tumors in nude mice--breast cancer, lung cancer, melanoma and colon cancer. (d) Mouse ascites tumors--JB-1, L 1210, Ehrlich and P 383. It therefore seems well suited as a routine clinical procedure.
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PMID:A detergent-trypsin method for the preparation of nuclei for flow cytometric DNA analysis. 618 86

A mouse monoclonal antibody, WI-MN-1, was raised against G-361 melanoma cell line. Reactivity of this antibody was characterized by indirect immunofluorescence against 22 cell lines and normal and neoplastic human tissues. Positive reactions were seen against three melanoma cell lines (G-361, HT-144, and MeWo). It also reacted against an epidermoid carcinoma cell line (Hep-2) and amnion cells (WISH). The antibody failed to react against cell lines derived from granulocytic leukemias, lymphocytic leukemias, Burkitt's lymphoma, carcinoma of the lung, carcinoma of the cervix, carcinoma of the colon, carcinoma of the breast, astrocytoma, and a human monocytoid cell line. Mouse melanoma and mouse fibroblast cell lines were also nonreactive. Similarly, there was no reaction against human peripheral blood, bone marrow, spleen, lymph node, thymus, breast, lung, stomach, heart, brain, kidney, liver, skin, or testis. The antibody was also tested by indirect immunofluorescence against 17 samples of metastatic malignant melanoma which were removed from 13 patients. WI-MN-1 gave positive reaction against 16 of these specimens, and it reacted with the cryostat section in the immunoperoxidase test, delineating neoplastic melanoma from the normal brain tissue. The antibody precipitated Mr 105,000 and 38,000 antigens from biosynthetically labeled G-361 cells. It was suggested that WI-MN-1 was a useful addition to the panel of monoclonal antibodies against melanoma-associated antigens.
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PMID:Mouse monoclonal antibody (WI-MN-1) against malignant melanoma. 619 9


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