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)

Platelet-adhesive protein-tumor cell interaction was studied in vitro and in vivo. Monoclonal antibody 10E5, which inhibits binding of fibronectin and von Willebrand factor to the platelet membrane glycoprotein GPIIb-GPIIIa complex, inhibited the binding of mouse CT26 and human HCT8 colon carcinoma cells to platelets by 63-65%, whereas an irrelevant monoclonal antibody, 3B2, had no effect. Monoclonal antibody 6D1, which inhibits binding of von Willebrand factor to GPIb, also had no effect. RGDS, a tetrapeptide that represents the adhesive domain of fibronectin and von Willebrand factor inhibited binding of the tumors to platelets by 64-69%. Monospecific polyclonal antifibronectin antibody inhibited binding by 60-82%; anti-von Willebrand factor antibody inhibited binding by 75-81%. In vivo, polyclonal monospecific anti-mouse von Willebrand factor antibody inhibited pulmonary metastases induced by CT26 tumor cells by 53-64%, B16a amelanotic melanoma cells by 45% and T241 Lewis bladder cells by 46% without induction of thrombocytopenia. Pulmonary metastases with CT26 cells could be inhibited by induction of thrombocytopenia, and reconstituted by infusion of either murine or human platelets. Reconstitution of pulmonary metastases with human platelets could be inhibited 77% by preincubation of human platelets with monoclonal antibody 10E5 before infusion of platelets into mice. Thus, platelets appear to contribute to metastases by their adhesive interaction with tumor cells via the adhesive proteins fibronectin and von Willebrand factor.
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PMID:Role of adhesive proteins in platelet tumor interaction in vitro and metastasis formation in vivo. 328 May 98

Cancer cachexia describes a syndrome of progressive weight loss, anorexia, and persistent erosion of host body cell mass in response to a malignant growth. Although often associated with preterminal patients bearing disseminated disease, cachexia may be present in the early stages of tumor growth before any signs or symptoms of malignancy. A decline in food intake relative to energy expenditure (which may be increased, normal, or decreased) is the fundamental physiologic derangement leading to cancer-associated weight loss. In addition, abnormalities of host carbohydrate, protein, and fat metabolism lead to continued mobilization and ineffective repletion of host tissue, despite adequate nutritional support. Mediators of cancer anorexia and associated abnormalities are unknown. Cachectin/TNF or other host-derived cytokines (produced as a defense against malignancy) have been implicated as signal molecules in cachexia, based upon similar metabolic derangements produced by these cytokines in other chronic wasting illnesses. Nutritional support is effective in maintaining body weight of cachectic cancer patients, but ineffective in maintaining lean body mass. Although in one study parenteral nutritional support has improved operative morbidity and mortality in cancer patients, it has not yet improved response to chemotherapy or radiation therapy. Because of metabolic derangements seen in cancer cachexia, effective nutritional treatment regimens will probably require manipulation of host intermediary metabolism in addition to feeding. Insulin therapy or exercise are two such methods which appear to preserve host composition by preferential feeding of the host at the expense of the tumor. Future studies which more clearly define the role of signal molecules in producing cancer cachexia syndrome may lead to new treatment strategies, possibly involving modulation of the effects of such molecules on host metabolism.
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PMID:Cancer cachexia. 329 98

The advances of both murine and human monoclonal antibody (MoAb) technology have allowed the development of several antibodies against gynecologic tumors. The goals are to produce effective and specific reagents for both immunodiagnosis and therapy. However, despite an extensive research effort, a clear demonstration of specific cancer-associated antigens in gynecologic malignancies, or of specific immune responses to such antigens has been elusive. Currently, most antibodies found are cross reactive with either oncofetal antigens or some normal adult tissues. Clinical usefulness of these MoAbs as a screening test in radioimaging or in immunotherapy remains to be proven. However, the use of MoAb technology in defined antigens/tumor markers such as beta-human chorionic gonadotropin, and alpha fetal proteins has provided convenient, reproducible and highly specific reagents. More recently, promising antibodies have been shown to detect tumor antigens in serum of patients with ovarian cancer.
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PMID:Clinical applications of monoclonal antibodies in gynecologic oncology. 330 66

Twenty-three chemicals evaluated as hepatocarcinogens in B6C3F1 mice by the National Toxicology Program (NTP) and nine showing equivocal liver tumor effects were examined to determine if the occurrence of liver neoplasms was associated with caging, i.e., if there were significant differences in tumor incidence among cages. A total of 79 dosed groups showing increased liver tumor incidence were evaluated. The analysis showed that the number of instances in which liver tumors showed significant cage effects agreed closely with chance expectation. Experimental design protocols now utilized by the NTP (including random assignment of columns of cages to dosed and control groups, periodic rotation of cage location, and individual caging of mice) further reduce the likelihood that factors associated with the housing of the animals could influence tumor incidence.
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PMID:Lack of cage effects on liver tumor incidence in B6C3F1 mice. 335 Feb 26

As previously reported for natural killer (NK) cells of normal individuals, prior incubation of peripheral blood lymphocytes from cancer patients with human normal serum or monomeric immunoglobulin G reduced their subsequent capacity to kill K562 target cells in a 4-h 51Cr release assay. The NK activity of such treated effector cells was significantly inhibited only by 58% of sera from patients with colorectal adenocarcinoma (21 of 36 cases) and by 67% of sera from patients with other lymphoid or nonlymphoid solid tumors (22 of 33 cases). The cytotoxic activity of cells previously incubated with eight noninhibitory sera was even augmented relative to medium-treated peripheral blood lymphocytes (control). The 26 untreated cancer sera which did not inhibit significantly the NK activity (I-) always developed significant inhibitory capacity upon heating at 56 degrees C for 30 min (delta+). An additional seven (21%) patients with colorectal carcinoma and four (27%) patients with other cancers were identified as having type II NK regulation, defined as sera with untreated inhibitory capacity (I+) but with appreciably more inhibition after heating (delta+). The sera of the last group of patients with colorectal adenocarcinoma (14 of 36 cases) defined as having type III NK regulation were not different from control sera isolated from normal individuals (I+ delta-) except that they induced an inhibition greater than that caused by normal sera. The modulatory characteristics of sera from the first two categories of patients appear to be cancer associated, since the patterns I- delta+ or I+ delta+ were observed with sera from only one of 30 patients with benign digestive diseases and two of 100 apparently healthy individuals. Preliminary results of longitudinal investigations of patients with colorectal adenocarcinoma revealed also that these patterns disappeared several months after resection of their tumor in all five tested patients, whereas the type III NK regulation found in patients with poor prognostic factors was unchanged after surgery in the other five of six patients. The three different categories of cancer sera identified by the functional assay of NK regulation indicated differences among our group of patients which were not paralleled by differences in levels of cytotoxic reactivity of their NK cells assayed in vitro in the absence of autologous serum.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modulation of natural killer cell activity by serum from cancer patients: preliminary results of a study of patients with colorectal adenocarcinoma or other types of cancer. 335 20

Previous studies from this laboratory have demonstrated that arylsulfatase B (ASB) is phosphorylated by a protein kinase, which is the first finding of phosphorylation in lysosomal hydrolases. The present study was undertaken to characterize the sites of phosphorylation in ASB from transplanted human lung cancer and from normal human tissues, and to identify type of tumor protein kinase responsible for the phosphorylation of ASB. When ASB purified from liver and placenta was phosphorylated in vitro by a cAMP-dependent protein kinase, it gave a single tryptic phosphopeptide (X) and phosphothreonine. On the other hand, the tumor ASB which had been phosphorylated in vivo demonstrated two phosphopeptides X and Y. Since the tumor ASB had been shown to be phosphorylated both at threonine and serine residues, phosphorylation at threonine residue of peptide X, which is phosphorylated by a cAMP-dependent protein kinase, will be cancer-associated. Through photoaffinity labeling with a labeled cAMP analogue to detect regulatory subunits of cAMP-dependent protein kinase subtypes, it was found that the cAMP-dependent protein kinase in the transplanted lung tumor was largely type II which can be ascribed to the appearance of highly phosphorylated ASB in the tumor.
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PMID:Protein phosphorylation of human lysosomal arylsulfatase B from normal and cancer tissues. 338 98

The nucleotide sequences of partial cDNA clones coding for the core protein of a human polymorphic epithelial mucin were determined, and a large domain was found to consist of a 60-base pair tandem repeat sequence. The cDNA clones were originally selected (Gendler, S. J., Burchell, J. M., Duhig, T., Lamport, D., White, R., Parker, M., and Taylor-Papadimitriou, J. (1987) Proc. Natl. Acad. Sci. U. S. A. 84, 6060-6064) using three monoclonal antibodies which show differential reactivity with the mucin produced by normal and malignant breast. Two of the epitopes are exposed in the normally processed and cancer-associated mucin, while one epitope is unmasked only in the cancer-associated mucin (Burchell, J. M., Durbin, H., and Taylor-Papadimitriou, J. (1983) J. Immunol. 131, 508-513; Burchell, J., Gendler, S., Taylor-Papadimitriou, J., Girling, A., Lewis, A., Millis, R., and Lamport, D. (1987) Cancer Res. 47, 5476-5482). We show here that all three antibodies react with a synthetic peptide with an amino acid sequence corresponding to that predicted by the tandem repeat. Identification of the epitopes preferentially expressed on the cancer-associated mucin should allow a directed approach to the development of tumor-specific antibodies using synthetic peptides as immunogens.
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PMID:A highly immunogenic region of a human polymorphic epithelial mucin expressed by carcinomas is made up of tandem repeats. 341 35

Immense amounts of data about cancer-associated chromosome aberrations have been collected during the last 10 years, and the systematic evaluation of these data has disclosed a number of correlations between chromosome change and neoplastic disease. These results are of practical clinical significance for the evaluation of diagnosis, treatment, and prognosis; they are also of theoretical interest in cancer research and cell biology. This paper reviews the nature, occurrence, and significance of nonrandom and specific chromosome aberrations and discusses briefly the theoretical implications of these changes.
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PMID:Chromosome changes in cancer. 346 Jul 1

The aim of this study was to investigate the effects of a mechanical stressor and individual behavior differences (separately and in combination) on tumor development in the female Syrian hamster. Studies by other investigators have documented the tumor-enhancing effects of such mechanical stressors as rotational stress. Previous studies by our group found that both size of tumor and time to tumor detection were significantly related to a dimension we call "activation." Eighty 100-day old female Syrian hamsters were placed in circular plexiglas environments in groups of 10. Nineteen days after introduction to the cages, a stress condition was imposed on half the animals (four cages). This consisted of shaking each cage of animals three times a week for three 10-minute intervals. Each group's behavior was videotaped in multiple samples to document pre- and poststress behaviors. Twelve days after the stress condition was initiated, each animal was injected subcutaneously midback with one melanoma tumor fraction. Animals were palpated every three days to determine time to detection of tumor. The videotaped behavior samples were coded for behaviors associated with "activation," inactivity, and interaction. Factor analysis resulted in basically the same first factor of activation found in our previous studies. Hamsters in the nonstressed groups had a significantly longer time to tumor development than those in the stressed groups (22.5 days vs. 12.6 days, p less than 0.005). While no prestress behaviors were associated significantly with time to tumor detection, the poststress activation factor was significantly correlated with longer time to tumor development in the stressed group (r = .61, p less than 0.0001). These results suggest that while the stress condition is more powerful than prestress individual behaviors in affecting the outcome variable, stress appears to interact with the individual behaviors related to "activation" to mitigate the negative effects of stress on tumor growth.
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PMID:Stress-behavior interactions in hamster tumor growth. 347 85

Separation of cells within a perfused suspension system is still a problem. We modified the rotating steel wire cage described by other researchers (2) for separation of single cells from suspension. The system was mounted to the stirrer shaft of a circular-loop fermenter. After optimization of fermenter design experimental data showed good separation of cells at useful perfusion rates. Data of a 5 l-prototype show with a mammalian tumor cell line a retention rate of better than 95% at a perfusion rate of D = 0.05. Scaling-up studies show a good scaling-up potential and a wide range of possible applications.
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PMID:Use of a rotating wire cage for retention of animal cells in a perfusion fermentor. 358 56


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