Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibroblasts underlying human uterine cervical dysplasia, carcinoma in situ, and invasive carcinoma are agglutinable by concanavalin A (Con A) but not by wheat germ agglutinin, except at very high concentration. Studies with low levels of Con A show that maximal agglutination is obtained with fibroblasts from invasive carcinoma, while the fibroblasts underlying dysplasia give minimal agglutination reactions. Fibroblasts underlying carcinoma in situ give agglutination reactions halfway between those obtained with fibroblasts underlying dysplasia and invasive carcinoma. An epithelial-like cell line obtained from a case of dysplasia shows agglutinability by Con A very similar to that obtained with fibroblasts underlying dysplasia. These epithelial-like cells are also not agglutinable by wheat germ agglutinin. Treatment of the cervical cells, both epithelial and fibroblasts, with neuraminidase leads to slight increase in agglutination by both Con A and wheat germ agglutinin. Marked increase in agglutination is not obtained even after treatment with high concentration of neuraminidase (10 units/10(6) cells). Marked agglutinability, however, is observed after trypsin treatment. The results suggest that, while the fibroblasts obtained from normal cervix are not agglutinable by Con A, surface alterations necessary for Con A-specific agglutination exist in fibroblasts during the early stage of development of uterine cervical epithelial neoplasia (dysplasia) and increase with the progression through carcinoma in situ to invasive carcinoma. Loss of cell surface sialic acids may result in a slight increase in agglutinability, but some other mechanism(s) is likely to be involved in alteration of surface properties that lead to marked agglutinability of the human uterine cervical cells obtained from cancer precursor lesions.
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PMID:Different agglutinability of fibroblasts underlying various precursor lesions of human uterine cervical carcinoma. 117 Sep 43

Lymphocyte cytotoxicity, serum cytotoxicity, and the ability of the serum to inhibit lymphocyte cytotoxicity (blocking effect) were studied in a melanoma patient treated with six monthly injections of her own (autologous) tumor cells incubated with neuraminidase to increase their antigenicity. The same tumor cells grown in tissue culture were used as target cells for the cytotoxicity test. Large fluctuations of blocking effect in the serum were found, which correlated with the clinical course of tumor removal, recurrence, and regression. After the fifth injection of autologous tumor cells, the blocking effect disappeared from the serum (unblocking). In general, changes in serum cytotoxicity corresponded with changes in the amount of blocking effect produced by the serum. The results suggest that active immunotherapy may play a role in the prevention of metastases and, that when used within the autologous system, the cytotoxicity test is valuable in studying response to this type of therapy.
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PMID:Cytotoxicity reactions during immunotherapy of melanoma with neuraminidase altered autologous tumor cells. 124 39

A dimethylbenzdithionaphthene (DBDN)-induced fibrosarcoma showed reduced transplantability if previously treated with Vibrio cholerae neuraminidase (VCN). However, the reduced transplantability of VCN-treated tumor cells was not associated with any loss of their viability or tumorigenic capability, but appeared to be due to their increase in immunogenicity. High doses of VCN-treated tumor cells could grow even in normal individuals. Lower doses, which did not induce tumor development in normal individuals, did so if injected into immunosuppressed animals. Although X-irradiation of VCN-treated tumor cells reduced their tumorigenic potential, it did not impair their increased immunogenic properties. Thus a suitable method for the preparation of a "tumor vaccine" was provided. The immunization of animals with the vaccine and a working hypothesis regarding its mechanism of action were described.
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PMID:Antitumor immunity. II. Viability, tumorigenicity, and immunogenicity of neuraminidase-treated tumor cells: effective immunization of animals with a tumor vaccine. 125 53

BCG (Bacillus Calmette-Guerin) vaccine, Tice strain, caused a threefold increase in spleen weight of normal animals and a fourfold increase in spleen weight of sarcoma-bearing mice. In the latter group, the BCG vaccine caused infiltration of the sarcoma cells into the peritoneum and tumor metastasis in the spleen. Spleen lymphocytes from mice immunized with neuraminidase-treated sarcoma or from mice that had overcome an inoculum (100 cells) and a challenge (10(4) cells) of sarcoma P-1798 were cytotoxic against 51 Cr- or 14C-2-thymidine-labeled sarcoma cells. The serum of these mice enhanced the cytotoxic activity and inhibited the migration of the syngeneic lymphocytes. These serums also inhibited the migration of peritoneal macrophages from guinea pigs immunized with the sarcoma cells. BCG vaccine enhanced the development and growth of sarcoma P-1798; i.e., 50-100 viable sarcoma cells produced solid tumors in 8% of the untreated animals but in 100% of the BCG-treated animals. The serum of BCG-treated sarcoma-bearing animals inhibited the spleen lymphocyte-mediated cytotoxic action. The spleen lymphocytes from the BCG-treated sarcoma-bearing animals had no effect against 51Cr- or 14C-2-thymidine-labelled sarcoma cells. The data indicate that the serum from BCG-treated sarcoma-bearing animals blocks the spleen lymphocyte-mediated cytotoxic activities directed against proliferation and growth of the sarcoma.
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PMID:Mechanism of action of BCG vaccine on neoplastic proliferation and host immune responses. 126 78

Cancer-related changes in the serum seromucoid fraction are well known. Last year Woodman published an interesting carbocyanine dye binding method for determination of serum carbohydrate polyanions in sera of normal, traumatized, and tumor-bearing mice. The usefulness of this method for clinical practice has been investigated in this study. Carbocyanine dye-binding polyanion (CPA) and the sialidase-sensitive fraction of this polyanion (SPA) have been determined in sera of 705 human subjects including healthy normal individuals and patients suffering from a broad spectrum of malignant and nonmalignant disease states. Overall, in malignant diseases the CPA and SPA values, in mg pectin equivalents per liter (mean +/-2 S.D.) (292 +/- 111 and 135 +/- 68, respectively) were significantly higher than in the serum from normal controls (166 +/- 33; 74 +/- 18) and patients hospitalized with a variety of nonmalignant disease (195 +/- 56; 92 +/- 36). The highest CPA and SPA values were found in gynecological (331 +/- 117; 149 +/- 69), bronchial (294 +/- 72; 137 +/- 51), and gastrointestinal cancers (316 +/- 111; 154 +/- 69). Elevated CPA values were found in 59.9% and elevated SPA values in 52.8% of patients suffering from malignant diseases. Successfully, radically treated cancer patients with no detectable residues or metastases for at least 1 year had values (186 +/- 39; 76 +/-24) almost within the normal ranges (93 to 250 mg pectin equivalents per liter for CPA and 35 to 120 mg pectin equivalents per liter for SPA).
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PMID:Determination of carbocyanine dye-binding polyanions in malignant and nonmalignant disease states. 127 85

We describe the production, immunochemical and immunohistochemical characterization of monoclonal antibodies (MAbs) raised against the oncofetal small intestinal mucin antigen (SIMA). Four MAbs, reacting with distinct neuraminidase-sensitive SIMA epitopes, were shown to define a novel differentiation-associated relationship of SIMA epitopes within the normal small intestinal villus. Using Swiss rolls of 15 entire colorectal cancer resections, inappropriate expression of SIMA epitopes was detected in all cancers, in adjacent transitional mucosa and remote morphologically normal mucosa, extending as far as resection margins (73%). SIMA expression, whether preexisting or reactive to the tumor, may predispose to malignant change and tumor recurrence.
Tumour Biol 1992
PMID:Expression of a novel family of epitopes on small intestinal mucins in colorectal cancers, adjacent and remote mucosa. 128 25

Loss of O-acetyl substituents from sialic acid expressed in mucin secreted by hyperplastic polyps (21), adenomas (9), a mixed polyp (1) and adenocarcinomas (41) of the colorectum was investigated by mucin histochemistry (diastase PAS and mild PAS) and by lectin histochemistry (Arachis hypogaea or peanut agglutinin) with (nPNA) and without (PNA) prior neuraminidase digestion. Mild PAS and nPNA reactivity were closely correlated, indicating that loss of O-acetyl substituents at C7, C8 and C9 (hence mild PAS positive) and at C4 (hence neuraminidase labile) occur pari passu. These sialic acid alterations were characteristic of mucin secreted by both adenocarcinoma and hyperplastic polyp. The same changes occurred patchily or focally in adenoma. Five "serrated" adenocarcinomas resembled the hyperplastic polyp both morphologically and histochemically. Luminal secretions within cancers were classified as mucin-like (type I) and non-mucin-like (type II). Mild PAS was the most specific technique for mucin-like intraluminal material. However, accumulated luminal secretions (type I or II) and intracytoplasmic lumina were quite specific features of colorectal cancer and could be effectively highlighted by means of dPAS. PNA reactivity without prior neuraminidase digestion showed a distribution unlike nPNA. Whilst PNA expression was more cancer specific than either mPAS or nPNA, it was observed mainly in cancers secreting little or no mucus, thus limiting its value as a tumor marker.
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PMID:Sialic acid and epithelial differentiation in colorectal polyps and cancer--a morphological, mucin and lectin histochemical study. 128 63

The glycoproteins granule membrane protein 140 (GMP140), endothelial-leukocyte adhesion molecule 1 (ELAM-1), and Leu-8 are members of a family of glycoprotein receptors (selectins or LEC-CAMs) that play an important role in adhesive interactions between circulating leukocytes and vascular endothelium. Recently it has been reported that ELAM-1 is able to mediate the binding of the colon carcinoma cell line HT-29 to cytokine-activated vascular endothelium, suggesting that tumor cell adhesion to vascular endothelium, a prerequisite for tumor extravasation and metastasis, is in part the result of adhesive interactions between blood-borne tumor cells and cell surface proteins expressed by vascular endothelium. Here, using an approach in which soluble immunoglobulin chimeras of the GMP140 and ELAM-1 receptors were prepared and used to carry out immunohistological studies, we establish that GMP140 binds to tumor cells in a variety of human carcinoma tissue sections (colon, lung, and breast), whereas ELAM-1 binds exclusively to tumor cells in colon carcinoma tissue sections. In addition, GMP140 was found to bind to the cell surface of a number of cell lines derived from various carcinomas but not from melanomas, whereas ELAM-1 bound only colon carcinoma cell lines. We further investigated the nature of the ligands of GMP140 and ELAM-1 on the surface of the carcinoma cells and found that the GMP140 ligand on the surface of tumor cells appears to be distinct from that expressed on the myeloid cell line HL-60. Neuraminidase treatment of a breast carcinoma cell line does not affect, or in some instances increases, GMP140 binding, whereas it completely abolishes GMP140 binding to HL-60 cells. On the other hand, the ligand of ELAM-1 on both the colon carcinoma and HL-60 cells is neuraminidase sensitive in accord with its identification as sialyl-CD15. Parallel results were obtained with neuraminidase-treated frozen carcinoma tissue sections. The present findings form the basis for investigating the role of GMP140 in tumor invasiveness and metastasis.
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PMID:Granule membrane protein 140 (GMP140) binds to carcinomas and carcinoma-derived cell lines. 137 39

A murine monoclonal antibody designated 4B5 was raised against the high molecular weight fraction of pooled sputum from patients with non-small cell lung cancer (NSCLC). Immunohistochemical staining indicated that 4B5 binds to histologically normal bronchial epithelium distant from tumor in 72% (39 of 54) of patients with NSCLC, but it binds to the primary cancer in only 13% (7 of 54) of the same patients. The antibody reacted less intensely with the bronchial epithelium in 16.6% (3 of 18) of autopsied patients without significant lung disease. The antigen recognized by 4B5 is a high molecular weight glycoprotein of more than 400 kilodaltons, judged by gel filtration and sodium dodecyl sulfate-polyacrylamide gel electrophoresis and western blot analysis. Antigenic activity persisted after heating and resisted treatment with neuraminidase, but it was destroyed using protease and periodate. Multiple epitopes were present on each molecule recognized by 4B5. The determinants recognized by this antibody deserve additional study as possible markers of premalignant change in patients with NSCLC.
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PMID:Detection of a novel marker in the bronchial secretions of patients with non-small cell lung cancer using the 4B5 monoclonal antibody. 137 28

Nd2 was a murine monoclonal antibody produced against a mucin fraction purified from xenografts of the human pancreatic cancer cell line SW1990. The reactivity of Nd2 was reduced by trypsin, but was not influenced by neuraminidase, so the epitope recognized by Nd2 may involve peptide but not sialic acid. The antigen recognized by Nd2 was present in 83% of pancreatic cancer, whereas in tissue of normal pancreas and chronic pancreatitis no reactivity was detected. By biodistribution study, tumor/blood ratio was elevated 8.27 on the 7th day after injection of 125I-labeled Nd2, while tissue/blood ratio in liver was remained 0.53. These results indicate that Nd2 had possibilities in clinical application such as radio-immunodetection and targeting therapy of pancreatic cancer.
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PMID:[Immunohistochemical study and biodistribution of monoclonal antibody (Nd2) against human pancreatic cancer]. 138 Jun 34


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