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)

A characteristic alkaline phosphatase (orthophosphoric monoester hydrolase, alkaline pH optimum, EC 3.1.3.1) was detected in the sera of most patients with infectious mononucleosis, acute and chronic lymphatic leukaemia, non-Hodgkin's lymphoma, Burkitt's lymphoma and nasopharyngeal carcinoma. The enzyme was also present in the sera of nine out of 26 patients with cancer of the cervix. N-APase in these cases counted 30-100% of the total alkaline phosphatase activity. N-APase was absent from the sera of healthy individuals and of patients with acute and chronic granulocytic leukaemia, breast cancer, colon cancer, rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosis, hepatitis and obstructive jaundice. Only three of 22 patients with Hodgkin's disease showed n-apase activity in the serum. In infectious mononucleosis the presence of N-APase activity was well correlated with the clinical course. In 13 cases studied, the clinical improvement was associated with the decrease or disappearance of N-APase activity. N-APase activity could not be detected in white cells of acute myeloid leukaemic patients, nor in the cells of myeloid blastic crisis of chronic granulocytic leukaemia. It was present in the cells of lymphoid blastic crisis of chronic granulocytic leukaemia.
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PMID:N-alkaline phosphatase: a potential disease marker for lymphoproliferative disorders. 43 2

The authors report 8 cases of lympho-reticulosarcoma of the colon and emphasize the rareness of this tumour (10 percent of cases) compared with other localisations in the stomach and small intestine. Whether primary or secondary, lymphosarcoma of the colon has various radiological appearances, depending on the mode of development of the sarcoma in the wall of the colon. Mainly sub-mucosal, it may remain localised or extend to the whole of the colon, predominating in the ileo-coecal and recto-sigmoid regions. Localised tumour forms present either in the form of large polycyclic lacunae, sometimes invaginated or as vast ulcerations with irregular nodular margin, or as due to parietal infiltration and exoluminal development of the tumour mass and neighbouring adenopathy. It is sometimes confused with carcinoma of the colon, e.g. vegetating carcinoma, colloid carcinoma, or peritoneal metastases, or with a regional abscess, e.g. appendix abscess or diverticulosis. The correct diagnosis is made on operation. The extensive colonic forms rarely take on the appearance of lymphoid pseudopolyposis, more often that of a very unusual nodular form formed of hazy lenticular lacunae. It may be confused with nodular colitis, it differs from this, however, by the absence of ulceration, changes in caliber and the persistance of normal haustration, a reticulated appearance of the mucosal outline during evacuation of the barium. In all cases, the discovery of a colonic lympho-reticulosarcoma implies complete digestive radiological investigation in order to seek gastric, duodenal or intestinal localisations, together with a search for other extra-digestive localisations. In fact, the great diffusion of the lesions modifies the prognosis and the therapeutic attitude. These lymphosarcomas and reticulosarcomas of the colon have a similar pathological and radiological appearance but differ by their sensitivity to treatment with cobalt, as reticulosarcomas are more resistant.
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PMID:[Pathological, clinical and radiological study of colonic lympho-reticulosarcoma. Report of 8 cases (author's transl)]. 109 45

Gut-associated lymphoid cells are modulated by several gut hormones. We postulated that lymphokine-associated-killer (LAK) cell cytotoxicity of lymphocytes isolated from the gut mucosa may be increased by substance P (SP). Intestinal lamina propria mononuclear cells (LPMC) and colonic cancer cells were isolated from operative specimens by successive mechanical and enzymatic dissociation methods. Effector LAK cells were induced by culturing LPMC with recombinant interleukin-2 at a concentration of 250 U/ml. Substance P (10(-5) M) was added to the culture medium. Targets consisted of fresh colon cancer cells, HT-29 (cultured human colon cancer cell line), and control cell lines. After 4 days of incubation, cytotoxicity was measured using a 4-h 51Cr release assay. LAK cells alone showed moderate cytotoxicity against HT-29 and none against fresh colon cancer cells. LAK cells generated in the presence of substance P showed moderate cytotoxicity against HT-29 and strong cytotoxicity against fresh colorectal cancer cells. The percentage of cytotoxicity +/- SEM at various effector to target ratios was [(*) denotes P < 0.05 compared with above]: [table: see text] We conclude that substance P significantly increases LAK cell cytotoxicity against fresh colon cancer cells, but not against cultured cells.
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PMID:Substance P increases in vitro lymphokine-activated-killer (LAK) cell cytotoxicity against fresh colorectal cancer cells. 127 74

It was reported that lymphoid infiltration (LI) of colon cancer tended to be found more commonly in patients with colonic cancer in an early stage than in an advanced stage. This time, the correlation among LI of colon cancer, cell-mediated immunity and the cumulative 5-year survival rate was studied in 124 patients with resected colon cancer. The results were as follows: 1) The cumulative 5-year survival rate in patients with positive LI was higher than that in the patients with negative LI. 2) There was correlation between the degree of LI of the cancer and Su-PS skin reaction. 3) Postoperative cell-mediated immunity was reduced in the cases of poor prognosis. Therefore we insist on paying attention to immunochemotherapy for 24 months after surgery.
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PMID:[Lymphoid infiltration of colon cancer and clinical significance of the skin test]. 143 93

The gastrointestinal tract is considered to be a major route of infection for the human immunodeficiency virus (HIV). To understand the interaction of HIV with epithelial cells of the intestinal mucosa, we have studied the infection of a human colon cancer cell clone HT-29-D4. The enterocyte-like differentiation of this clone can be modulated in vitro according to the concentration of glucose. We show that: (i) undifferentiated HT-29-D4 cells can be infected by HIV types 1 and 2 (HIV-1 and HIV-2) strains with no subsequent effect on cell growth; (ii) undifferentiated HT-29-D4 cells express a CD4-related antigen bearing epitopes of the immunoglobulin-like variable (V) region domains V1 and V2 of CD4 but lacking the epitope known to be involved in HIV envelope recognition; (iii) differentiated HT-29-D4 cells can be infected by HIV after an interaction with either the apical brush border membrane (luminal side) or the basolateral side (serosal side); (iv) the CD4-like molecule is restricted to the basolateral domain of differentiated cells; and (v) the infection is not inhibited by anti-CD4 monoclonal antibodies (mAbs) OKT4, OKT4A, Leu-3a, Bl4, 13-B-8-2, S-T4 or S-T40. We conclude that epithelial intestinal cells may represent a major site of entry for HIV. Infection of these epithelial cells may occur via the basolateral membrane by HIV-bearing lymphocytes or macrophages of the lamina propria and via the apical membrane by HIV present in the bowel lumen. This infection may remain silent for up to 9 months, and the virus can be rescued by cocultivation with lymphoid cells. These data may give an explanation for the long latent seronegative state that may occur in a HIV-infected individual.
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PMID:Human immunodeficiency virus can infect the apical and basolateral surfaces of human colonic epithelial cells. 171 4

Laser excitation of hematoporphyrin derivatives (HPD) localizing in tumors of the tracheobronchial tree and bladder is useful in the identification and treatment of those tumors. A comparable utility for HPD in the endoscopic localization of colonic tumors may be possible. In this study the ability of HPD to identify 1,2 dimethylhydrazine (DMH) induced colon cancer in rats is evaluated. A total of 111 rats were studied with HPD. Sixty-nine rats received weekly injections of DMH (20 mg/kg) and 42 received injections of the vehicle alone. Twenty-four hours after the intravenous injection of 5 mg/kg of HPD, 18 DMH-induced tumors were identified by visual fluorescence using excitation by either a blue light (390-436 nm) or an argon laser (488 and 514 nm). This represented 100% of the visually or microscopically detected tumors. Seventy-five fluorescent areas were noted that did not contain evidence of cancer. The majority (63) of false positive areas contained lymphoid follicles. All but 2 false positive areas (73/75, 97%, p less than .001) were seen in DMH-treated animals, suggesting that they were an artifact of DMH treatment. HPD fluorescence did not identify microscopic dysplasia. We conclude that HPD fluorescence is an effective method of identifying early colonic cancer and may have a potential clinical role in patients at high risk for colorectal cancer.
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PMID:Fluorescence localization of early colonic cancer in the rat by hematoporphyrin derivative. 186 65

A total of 72 human leukemia-lymphoma cell lines were studied for reactivity with the monoclonal antibody (MAb) A7, an anti-human colon-cancer-cell-associated antigen reagent, by indirect membrane immunofluorescence. Nine of the 72 cell lines expressed the antigen recognized by A7 MAb. Five of the 34 T-cell lines, 2 of the 21 B-cell lines, and 2 of the 3 non-lymphoid-non-myeloid cell lines were reactive with A7 MAb. By means of SDS-PAGE and immunoblotting, the antigens isolated from both colon cancer cell lines (WiDr, SW1116 and LoVo) and leukemia cell lines (A3/KAWAKAMI, H9, RPMI 8226 and SPI-801) showed an identical MW of 42-43 kDa. The non-glycosylated antigen recognized by A7 MAb, which was expressed on both the colon cancer line (SW1116) and the leukemia line (H9) in the presence of tunicamycin, also showed an identical MW of 36 kDa. However, the quantity of the antigen in the leukemia cells was significantly lower than in the colon cancer cells. Although expression of this colon-cancer-associated antigen in the non-colon cancer cells is real, the significant expression of this antigen in colon-cancer cells makes it useful for clinical monitoring of colon cancer patients.
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PMID:Identification and characterization of a colon-cancer-associated antigen expressed on leukemia-lymphoma cell lines. 199 51

In this report, point mutations of the K-ras gene at codon 146 were analyzed in 25 cases of colon cancer, 4 cases of lung cancer, and 41 cases of lymphoid malignancy. A codon 146 mutation substituting threonine (ACA) for alanine (GCA) was detected in the tumor tissue of a patient with colon cancer and was not detected in the normal tissue of the same patient. Any additional mutations of the ras gene family were not detected in this patient. These results suggest that the codon 146 mutation of the K-ras gene could be involved in the development of naturally occurring human malignancies.
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PMID:A novel point mutation at codon 146 of the K-ras gene in a human colorectal cancer identified by the polymerase chain reaction. 201 78

The antibody-dependent cellular cytotoxicity (ADCC) properties of a murine monoclonal antibody (MAb), designated D612 (IgG2a), which reacts with human colon carcinomas, was studied using normal human peripheral blood lymphocytes (PBMNC). Although the level of ADCC of PBMNC with D612 varied among different donors, it was 20 to 30 times higher than the lytic activity of control cultures containing isotype-matched control MAb. Incubation of PBMNC with recombinant interleukin-2 (IL-2) resulted in a 2- to 5-fold augmentation in the cytotoxicity of effector cells exposed to MAb. This augmentation was apparent after subtracting nonspecific cellular cytotoxicity from the total cytotoxicity mediated by activated effector cells in the presence of D612. Optimal stimulation of specific ADCC with IL-2 appeared after 24 hr of culture in 500 U/ml of IL-2, resulting in a 3.8 +/- 1.7 fold increase in lytic units. However, stimulation of ADCC was also evident at 10 U/ml of IL-2. Furthermore, antibody dose titrations with untreated and IL-2 activated effectors showed that the threshold dose of MAb needed for efficient ADCC was reduced by 200-fold with IL-2. Depletion of FcR gamma III-positive lymphoid cells markedly reduced D612 ADCC, demonstrating the participation of NK/LAK cells in D612-mediated ADCC. Low levels of ADCC activity were found associated with adherent cells, either untreated or following their activation with gamma-interferon, while D612 was most active with non-adherent effectors. The specificity and ADCC properties of the D612 MAb suggest that it should be considered as a candidate for immunotherapy of colon cancer, particularly when used in combination with IL-2 plus LAK cell treatment.
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PMID:Lymphokine-activated killer cell cytotoxicity against human colon carcinomas enhanced by monoclonal antibody D612. 212 77

The correlation among lymphoid cell infiltration (LI), cell-mediated immunity and immunoglobulin-containing cells distribution in the colon cancer was studied in resected materials of 136 patients with colonic cancer. The results were as follows: 1) LI of the colon cancer tended to be found more commonly in patients with colonic cancer in clinical early stage than advanced stage. 2) The cumulative 5-year survival rate in patients with positive LI was longer than that in the patients with negative or normal LI. 3) In colonic cancer patients with the better prognosis, IgA-containing cells were distributed around the tumor tissues more abundantly than that in the poor ones. 4) These results suggest that the IgA system somewhat participates in cancer immunity.
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PMID:[Histology and immunopathology of colonic carcinoma]. 239 58


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