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)

Several experiments conducted by our group over a period of 6 years have shown that nutritional stress, especially protein and/or calorie deprivation, leads to many, often dramatic, changes in the immune responses of mice, rats, and guinea pigs. Chronic protein deprivation (CPD) has been shown to create an enhancing effect on the cell-mediated immune responses of these animals. Humoral responses under CPD conditions were most often found to be depressed, but sometimes were unaffected, depending on the nature of the antigen employed. Chronic protein deprivation, consistent with the pattern just mentioned, improved tumor immunity by depressing production of B-cell blocking factors, and, in at least one instance, resistance to development of mammary adenocarcinoma in C3H mice was associated with evidence of increased numbers of T suppressor cells. Profound nutritional deficits (less than 5% protein per total daily food intake) depressed both cellular and humoral immunity. Early, though temporary, protein deprivation caused a long-term depression of both cellular and humoral immunity also, with the humoral component being the first to recover. Manipulation of protein and calories was found to have a profound effect on certain autoimmune conditions. Diets high in fat and low in protein favored reproduction but shortened the life of NZB mice, whereas diets high in protein and low in fat inhibited development of autoimmunity and prolonged life. Chronic moderate protein restriction permitted NZB mice to maintain their normally waning immunologic functions much longer than mice fed a normal protein intake. Further, the low-protein diet was associated with a delay in development of manifestations of autoimmunity. Decreasing dietary calories by a reduction of fats, carbohydrates, and proteins more than doubled the average life span of (NZB X NZW)F1 mice, a strain prone to early death from autoimmune disease. Histopathologic studies using immunofluorescent microscopy revealed that the development of the renal lesions caused by the deposition of antigen-antibody complexes, which is so characteristic of these mice, was markedly delayed.
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PMID:Nutritional deficiency, immunologic function, and disease. 0 88

Tumor incidence was studied in 1,2-dimethylhydrazine (DMH) injected male rats assigned at weaning to isoenergetic casein-sucorse deits containing 7.5%, 15%, or 22.5% protein with or without 2.5% urea. Twenty rats fed each diet were given weekly intraperitoneal injections of DMH (15 mg/kg body weight/week) for the first 24 weeks and 20 were given saline. Of 96 DMH-injected rats necropsied after 28 weeks, 88 were necropsied during the 32nd or final week of the experiment. Adenocarcinomas of the small and large intestine were larger and significantly more numberous in rats fed 15% and 22.5% dietary protein. Keratin producing papillomas of the sebaceous glands of the external ear were observed first at 21 weeks in DMH-injected rats fed 22.5% protein. These were subsequently observed in some rats from all DMH-treated groups. As time progressed, the ear tumors increased in size and number in all groups but the greatest incidence was in the group fed 22.5% protein. No tumors were observed in saline-injected rats. Urea feeding did not increase the number of tumors nor cause changes in pH, urease activity or ammonia concentration of contents of the colon or cecum, or blood cholesterol. As dietary protein increased, cecal ammonia concentrations rose while both colon and cecal pH dropped. Portal blood urea and cholesterol reose as dietary protein was increased. DMH-treated rats had significantly higher concentrations of colon and cecal ammonia and lower blood cholesterol. Altough the rats fed 7.5% protein gained significantly less weight during 0 to 6 weeks of feeding, their weight gain was significantly higher during 6 to 26 weeks. No tumors were found in rats necropsied at 16 weeks.
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PMID:Nitrogen intake and tumorigenesis in rats injected with 1,2-dimethylhydrazine. 1 Mar 59

Rabbit antiserum to a tissue extract of human mucinous cystadenocarcinoma of the ovary reacted with tissue extracts of normal ovary and various ovarian malignancies, and ascitic or cystic fluids of ovarian origin by Ouchterlony double gel diffusion and precipitin inhibition techniques. The tumor-associated antigen(s) of mucinous cystadenocarcinoma, which were demonstrated by Ouchterlony double diffusion, were not present in tissue extract of pooled normal ovaries and cystic fluid of benigh tubo-ovarian cyst. An organ-associated tumor antigen as well as the type-specific tumor antigen may exist in mucinous cystadenocarcinoma of the ovary. The mucinous cystadenocarcinoma was not very immunologically different but was distinguishable from serous cystadenocarcinoma and other types of ovarian cancer by double gel diffusion. Precipitin-inhibition reactions demonstated that the adsorbed antiserum to human ovarian mucinous cystadenocarcinoma mixed with tissue extracts of dysgerminoma and serous cystadenocarcinoma, and ascitic fluid of papillary embryonal adenocarcinoma of the ovary could not eliminate the specific precipin line developed with tissue extract of mucinous cystadenocarcinoma.
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PMID:Detection of tumor-specific antigens in human mucinous cystadenocarcinoma of the ovary by immunodiffusion. 1 19

We have used indirect immunofluorescence to study antibody responses directed against membrane antigens expressed on in vitro and in vivo T1699 mammary adenocarcinoma cells. IgG1, IgG2a, IgG2b, IgG3, IgA, and IgM antibodies were present in the serum of DBA/2 mice bearing T1699 tumors; IgG2a and IgG2b antibodies were readily detected on the cells in situ. Lesser amounts of the other classes and subclasses could be detected by indirect immunofluorescence measurements on in vivo tumor cells and with low pH eluates of in vivo cells tested on the in vitro line of T1699. The antigenic determinants on in situ tumor cells are not saturated with antibody as these cells demonstrated enhanced fluorescence of all immunoglobulin classes and subclasses when treated with autologous serum. Experiments with thymus-depleted mice indicated that immunoglobulin production was strongly dependent on thymus-derived cells for all immunoglobulin classes and subclasses except IgG2b. Our studies suggest that IgG2a may be active in the macrophage-mediated cytotoxic reaction and IgG2b in the immediate hypersensitivity reaction to T1699 cells. These results provide further evidence for an active role of tumor-specific antibody in the host defense to the T1699 adenocarcinoma in situ.
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PMID:The antibody response to the T1699 murine adenocarcinoma: antibody class and subclass heterogeneity detected in serum and in situ. 1 30

Living CF1 mouse-transplantable spontaneous mammary adenocarcinoma cells were modified with glutaraldehyde, formalin, 2,4,6-trinitrophenylate, Vibrio cholerae neurominidase, iodoacetate, heparin, histamine and adenosine 3'5'-monophosphate (cAMP), then used to immunize syngeneic CF1 mice. Animals immunized with the fixed (formalinized or glutaraldehyde fixed) neuraminidase-treated cells or the membrane of these cells, rejected two challenging doses of 10(8) viable unmodified adenocarcinoma cells. Animals immunized with adenocarcinoma cells treated with neuraminidase (170 IU/5x10(5) cells) or with the spontaneous adenocarcinoma-cell surface glycoprotein, rejected the first challenging dose but developed tumors and died on the second challenge with the viable untreated adenocarcinoma cells. Animals immunized with the adenocarcinoma cells pretreated with trinitrophenylate, glutaraldehyde or formalin, developed temporary resistance to the spontaneous mammary adenocarcinoma. Adenocarcinoma cells pretreated with NaF, iodoacetate, heparin, EDTA, Colchicine or histamine showed reduced oncogenicity and stronger resistance in mice to the development of a mammary tumor than to a smaller number (10(3) AdCa cells) of untreated viable adenocarcinoma cells. Cells treated with adenosine 3'5'-monophosphate accelerated tumor development.
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PMID:Modification of the immunologic properties of the cell surface. 2 83

We have recently described the presence of a guanylate cyclase [GTP pyrophosphate-lyase (cyclizing), EC 4.6.1.2] inhibitor (GCI) in an aqueous extract of the balsam pear (Momordica charantia abbreviata). Because the guanylate cyclase-cyclic GMP system is though to be involved in cell growth, DNA and RNA synthesis, and possible malignant transformation, we examined the effect of the aqueous extract containing GCI on an undifferentiated adenocarcinoma of the rat prostate and concanavalin-A-stimulated [3H]thymidine incorporation into cultured splenic lymphocytes, a process thought to be mediated by cyclic GMP. The results demonstrate that the extract of the balsam pear blocks both the growth of the rat prostatic adencarcinoma in vitro and [3H]thymidine incorporation into DNA. DNA histograms from flow cytometry indicated that the extract containing GCI inhibited in the G2 + M phase of the cell cycle, a presumed locus of cyclic GMP effects. In addition, guanylate cyclase activity was significantly greater in the tumor than normal prostate tissue and was decreased by the extract containing GCI. Cyclic GMP levels in the tumor in culture wer also decreased by addition of the extract. It remains to be determined whether or not the anti-tumor agent and GCI are the same substance.
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PMID:Inhibition of growth and guanylate cyclase activity of an undifferentiated prostate adenocarcinoma by an extract of the balsam pear (Momordica charantia abbreviata). 2 47

Tissue analyses and tumour regression studies using the oncolytic antibiotic, adriamycin (14-hydroxydaunomycin), and its DNA complex at adriamycin dosages of 5 mg/kg and 10 mg/kg were made on C3H mice with transplanted mammary adenocarcinoma. Chemical analysis indicated a significantly lower (P < 0.05) uptake of adriamycin into cardiac tissue for the adriamycin-DNA complex. Tumour regression was comparable for both the complex and free adriamycin. Results suggest an advantageous role for the adriamycin DNA complex in the chemotherapy of metastatic breast carcinoma.
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PMID:The comparative toxicity and therapeutic efficacy of adriamycin and the adriamycin-DNA complex in the chemotherapy of C3H mice with transplanted mammary adenocarcinoma. 4 24

In an evaluation of indium-111-bleomycin as a tumor-imaging agent, 357 whole-body tumor scans were performed in 293 patients. Of 246 studies performed in patients with a variety of active solid tumors, 218 (89%) were true-positive studies and 28 (11%) were false-negative. Of 69 scans in patients thought to be free of tumor after therapy, 32 (46%) were false-positive studies and 37 (54%) were true-negative. The true-positive rates by major tumor type were: adenocarcinoma of gastrointestinal tract origin (95%), lymphoma (88%), melanoma (87%), sarcomas (82%), lung (77%), breast (77%), childhood tumors (71%), gynecologic tumors (70%), and genitourinary tumors (68%). Soft tissue and lymphatic sites of tumor, both above and below the diaphragm, were easily visualized, whereas hepatic and bone marrow sites of involvement were less easily discerned. False-positive uptake with 111In-bleomycin was noted in lungs (6%), gut (3%), mediastinum (2%), normal breast tissue (0.8%), and in occasional inflammatory lesions. In 19 patients with multiple myeloma or leukemia, a pattern of diminished bone marrow uptake associated with abnormal accumulation of 111In-bleomycin in extramedullary sites of involvement was the rule. In another 23 patients in whom scans were performed because an occult tumor was suspected, scanning did not lead to specific diagnosis of tumor in a single instance. We conclude that 111In-bleomycin is a safe, effective, and useful new tumor-imaging agent in the initial staging and followup of patients with a variety of solid tumors. Significant advantages of this agent over other currently available radiopharmaceuticals include: A) a broader spectrum of tumors taking up the radio-pharmaceutical, and B) generally better delineation of abdominal and pelvic disease due to lack of interference from gut uptake.
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PMID:A clinical evaluation of indium-111 bleomycin as a tumor-imaging agent. 4 76

Specimens from various types of Paget disease, other tumors, and certain normal tissues were examined with a battery of histochemical techniques, including the sodium borohydride-potassium hydroxide-PAS method that specifically stains certain sialomucins that are found in terminal parts of the ileum and of the colon. These sialomucins were present in normal anal ducts but were not present in transitional or anal-covering epithelium. A case of perianal Paget disease showed strongly positive staining, both in the underlying mucinous adenocarcinoma and in Paget cells of the affected anal and perianal skin. In contrast, stains of other forms of Paget disease were totally negative with this technique, as well as malignant melanoma and Bowen disease. These results support the theory that Paget disease represents epidermal invasion by malignant cells from underlying tumor.
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PMID:Perianal Paget disease. Histochemical differentiation utilizing the borohydride-KOH-PAS reaction. 5 63

Twenty-seven unselected patients with limited disease non-oat-cell bronchogenic carcinoma were treated with a chemotherapy- radiotherapy protocol which consisted of bleomycin, vincristine, and methotrexate followed by split-course radiation. There were 15 objective responders with a median survival time in excess of 70+ weeks in contrast to a median survival time of 26 weeks for nonresponders (P less than 0.01). Objective benefit was limited to the epidermoid carcinoma group since none of the adenocarcinoma group achieved a greater than 50% reduction in maximum tumor diameter. The median survival time for the entire groups was 42 weeks in contrast to a recent split-course radiotherapy historical control group whose median survival time was 38 weeks. Toxic effects were predominantly gastrointestinal.
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PMID:Combination chemotherapy with bleomycin (NSC-125066), vincristine (NSC-67574), and methotrexate (NSC-740) plus split-course radiotherapy in the treatment of non-oat-cell bronchogenic carcinoma. 5 Jan 24


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