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Query: UMLS:C0006826 (cancer)
 1,092,456 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum inhibition of autochthonous lymphocyte cytotoxicity for tumour cells has been studied in 112 cases of colonic carcinoma. Addition of patient's serum to the lymphocyte tumour cell reaction mixture resulted in decreased cytotoxic reactivity of lymphocytes from 8 of 39 cytotoxic positive cases. It was also shown that sera could inhibit if separately preincubated with the lymphocytes (4 cases) or the target cells (2 cases). A tumour antigen preparation inhibited only when incubated with the lymphocytes. Inhibition by serum or antigen appeared to be specific for colon carcinoma. Four cases were specially studied to determine the mode of lymphocyte killing of tumour cells: in 3 it was mediated largely if not entirely by T lymphocytes, and in the fourth by both T and non-T cells. The findings support the view that T lymphocytes lose their anti-tumour reactivity in vivo in the presence of circulating antigen or antigen-antibody complexes such as would occur with progressive tumour growth.
Br J Cancer 1975 Jun
PMID:Analysis of inhibition of lymphocyte cytotoxicity in human colon carcinoma. 5 47

Sera from rats bearing primary or grafted colon carcinoma may contain antibodies that can react with antigenic determinants at the surface of cultivated colon cancer cells. Assays with various target cells and absorption experiments suggest that antigens recognized by circulating antibodies are common to independent lines of cultivated colon cancer cells. They are therefore cross-reacting, tumor-type-specific antigens. They could be embryonic or fetal antigens, because some sera from multiparous animals react with colon cancer cells. However, blocking experiments suggest that these antigens differ from the carcinofetal antigen previously demonstrated on the surface of intestinal cancer cells by xenoantiserum.
Cancer Res 1976 Sep
PMID:Circulating antibodies in rats bearing grafted colon carcinoma. 6 8

This study was designed to answer the question, do molecules with carcinoembryonic antigen (CEA) activity from colon, breast, and ovarian cancer differ? Extracts of two breast and three ovarian cancers with CEA activity were compared to three colon cancer CEA preparations and to the related antigen, colon carcinoma antigen-III, in terms of lectin- and antiserum-binding properties. With the use of Farr-type radioimmunoassays with the lectins, concanavalin A and wheat germ agglutinin, the iodinated colon CEA and CEA-like preparations from breast and ovarian cancer all showed distinctly different patterns of binding. Specificity of binding was confirmed by inhibition studies with the relevant monosaccharides. Similarly, with antisera prepared against colon CEA, colon carcinoma antigen-III, or breast CEA, it was shown that, although all preparations shared some antigens, unique antigenic determinants were also present on all preparations. These data are consistent with the concept of a series of closely related CEA and CEA-like molecules with distinct characteristics for each tissue source of CEA.
Cancer Res 1977 Sep
PMID:Evidence for common and distinct determinants of colon carcinoembryonic antigen, colon carcinoma antigen-III, and molecules with carcinoembryonic antigen activity isolated from breast and ovarian cancer. 6 90

Tumor cell fractions isolated from tumor lines SH-3 (breast carcinoma) and RPMI-7932 (malignant melanoma) by differential centrifugations were capable of transforming lymphocytes into cytotoxic effector cells. Lymphocytes cultured alone in human AB plasma did not become cytotoxic to tumor cells. However, when cultured with tumor cell fractions sedimented at 1000 X g(R1), 20,000 X g(R2), and 100,000 X g(R3), these lymphocytes became markedly cytotoxic to specific tumor targets in a 3.5-hr (51)Cr release assay. R2 fractions were significantly more immunogenic than were R3 fractions (p less than 0.05). Although lymphocytes sensitized with SH-3 tumor cell fractions were cytotoxic to SH-3 tumor cells, they were also cytotoxic to cells from RPMI-7932 and RPMI-8322 (malignant melanoma) tumor lines and vice versa. Cells from tumor lines HT-29 (colon carcinoma) and COLO 110 (ovary carcinoma) were significantly less susceptible to lysis by effector cells generated against SH-3. These immune cells, although capable of killing cells from tumor lines, were not able to lyse cells from autochthonous normal lymphoid lines or normal lymphocytes that have been transformed by phytohemagglutinin. Tumor cell fractions were not immunogenic at low (5- to 20-mul/0.75 ml) concentrations; an increase of 4- to 10- fold in their concentrations was usually followed by a decrease in immunization.
Cancer Res 1977 Dec
PMID:In vitro immunization against human tumor cells with tumor cell fractions. 7

The hemocytometer leukocyte adherence inhibition technique was employed in a criss-cross experimental design with two cancer patients (melanoma and colon carcinoma) and the corresponding tumor extracts. These extracts had been repeatedly tested for specific reactivity and lyophilized before transport to the workshop. The patients' leukocytes were mixed singly with each extract in the presence of normal serum, and the adherences of the cells were determined in hemocytometer chambers. Actual cell counts (total cells before washing and adherent cells after washing) are given in detail for the first time. Blood samples and reaction mixtures were coded by an independent observer. Determination of mean % adherence (+/- S.E.) showed that the melanoma patient's leukocytes (original adherence 70.8 +/- 2.8) reached with the melanoma extract (40.7 +/- 2.9; p less than 0.001) but not significantly with the colon carcinoma extract (61.5 +/- 4.1; p greater than 0.05). Similarly, the colon carcinoma patient's leukocytes (original adherence 68.6 +/- 2.7) reacted with the colon carcinoma extract (43.2 +/- 2.3; p less than 0.001) but adherence was not inhibited by the melanoma extract (76.9 +/- 2.6). The cancer patients were thus correctly identified with regard to tumor type in a simple blind trial.
Cancer Res 1979 Feb
PMID:Hemocytometer leukocyte adherence inhibition technique. 8 16

The molecular weight fractions of 10,000-50,000 daltons prepared from "used" medium obtained during cultivation of human colon carcinoma cells (SW-48) in vitro inhibited the proliferation and DNA synthesis of these cells. Fractions exceeding 50,000 daltons were not inhibitory; those less than 10,000 daltons were cytotoxic. The inhibitory fraction did not affect either proliferation of human fibroblasts or transformation of human lymphocytes in vitro. Similar fractions from the colon mucosa of other species inhibited the proliferation of SW-48 cells, whereas extracts of dog jejunum or lung did not. This mitotic inhibition was completely reversible and could be destroyed by preincubation with trypsin. Therefore, colon cells appear to contain a cell- (but not species) specific, endogenous mitotic inhibitor or chalone.
J Natl Cancer Inst 1976 May
PMID:Evidence for a colon chalone. 13 20

Twenty-one patients with disseminated colon carcinoma and clinically significant liver metastases were treated with 5-FUDR via hepatic artery infusion (HAI). All patients had previously received systemic chemotherapy consisting of either 5-fluorouracil aone or in combination with other agents. At the time of the initiation of the HAI, clinical disease in all patients was progressing. A PR of hepatic metastases was noted in eight patients (35%) with a median and mean duration of response of 4.5 and 5.0 months respectively. The median and mean survival from the start of HAI for responders was 8.0 and 9.0 months and for nonresponders was 1.0 and 1.6 months respectively. It appears that a significant response rate can be achieved with HAI of 5-FUDR in spite of previous exposure to fluorinated pyrimidines.
Cancer Treat Rep 1976 Sep
PMID:Hepatic artery infusion of 5-FUDR after prior systemic 5-fluorouracil. 13 80

Cancer-free individuals from family agregates of seemingly hereditary colon carcinoma were studied to determine the nature of their cell-mediated immune capacities in miexed leukocyte culture. Members of families who demonstrated no evidence of a precancerous condition such as polyposis coli did demonstrate substantial cellular immunopathology. Of these, 44% showed a decreased responsiveness of their peripheral mononuclear cells to allogeneic stimuli, and in a number of these individuals this deficiency clearly manifested itself as an inappropriate suppression of potentially normal lymphocyte blastogenic capacities by an adherent population of mononuclear leukocytes. This in vitro defect of recognitive immunity appears to be the same type of defect that has already been described for individuals with established maligancies. The pattern of phenotypic expression of this immunopathology within these families is not inconsistent with an hereditary disorder. Individuals from families with a known hereditary somatic precancerous condition usually did not demonstrate this immunopathology. It is appropriate to speculate that the defect of recognitive immunity in the former families could be contributory to the genesis of the colon carcinoma.
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PMID:Defective recognitive immunity in family aggregates of colon carcinoma. 14 Jan 82

Studies have been initiated to investigate the biochemical basis for selectivity of action of 5-fluorouracil against tumor cells. These studies included the measurement of 5-fluorodeoxyuridine monophosphate pools and the amount of 5-fluorouracil incorporated into RNA at various times following the administration of labeled 5-fluorouracil-6-3H, 5-fluorouridine-6-3H and 5-fluorodeoxyuridine-6-3H to animals bearing sensitive L1210 cells and L1210 resistant to 5-fluorouracil. The data indicate that: 1) in both cell lines the order of drug uptake into cells in vivo was in the order of fluorouride greater than fluorouracil greater then fluorodeoxyuridine; 2) there was no qualitative difference between the two cell lines in term of the extent of drug activation; 3) the data suggest a strong correlation between the amount of 5-fluorodeoxyuridine-monophosphates formed and retained at the target site and responsiveness to these agents. The effects of thymidine administered by continuous infusion and i.v. bolus injection on the antitumor activity of 5-fluorouracil was also investigated in animals bearing the induced colon carcinoma. The data suggest that thymidine, in combination with 5-fluorouracil, improves the therapeutic index of 5-fluorouracil. Initial studies on the metabolism of 5-fluorouracil in patients bearing the colon carcinoma are also reported herein.
Bull Cancer 1979
PMID:Selectivity of action of 5-FU: biochemical basis. 15 52

A Phase I clinical trial of N-(phosphonacetyl)-L-aspartate, an antimetabolite which inhibits a key enzyme in the de novo pathway of pyrimidine biosynthesis, was conducted. N-(Phosphonacetyl)-L-aspartate was given as an i.v. 15-min infusion once daily for five days; cycles of treatment were repeated every three weeks. Thirty-four patients received treatment. Dose-limiting toxicity was observed at 1500 to 2000 mg/sq m/day and was manifested by skin rash, diarrhea, and stomatitis. Rash and diarrhea usually began during the first week of treatment and persisted up to Day 17 of a cycle of therapy. No consistent hematopoietic, hepatic, or renal toxicity was observed. One partial response in a patient with colon carcinoma was seen and continues at more than eight months. Stable disease was observed in three patients with colon carcinoma, two patients with hypernephroma, one patient with pancreatic carcinoma, and one patient with melanoma. The predictability and reversibility of toxicity and the suggestion of antitumor activity in humans are observations which support the further evaluation of N-(phosphonacetyl)-L-aspartate in Phase II studies.
Cancer Res 1979 Oct
PMID:Phase I trial of N-(phosphonacetyl)-L-aspartate. 15 1


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