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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cancer stroma is made of cellular and non cellular formations which grow along with cancer cells to build up a tumor. It comes from inflammatory cells and mesenchymal tissue which are mobilized and modified by factors released by cancer cells which bring about inflammatory cell accumulation, angiogenesis, fibroblast mitosis and extracellular matrix production. The extracellular matrix is altogether a barrier against and supporting to cancer cells. The extracellular matrix is also involved in the storage of growth factors which are bound to glycosaminoglycans. Although they are antinomic in vitro, peptidic factors released by tumor cells seem to have an enhancing effect on tumor growth in vivo. The cancer invasion is mediated through diverse enzyme activities, particularly proteases, which degrade the matrix whose degradation products can facilitate the tumor progression. The anti-cancer activity which is exhibited in vitro by macrophages and lymphocytes is expressed at a low level by tumor-macrophages and lymphocytes in vivo. The cancer associated inflammation has no particular feature which could help to screening or to follow up patients. Several elements of the cancer stroma could be selected as targets for investigative cancer therapy.
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PMID:[Cancer stroma]. 176 34

Anti-idiotypic antibodies (Ab2) that functionally mimic epitopes associated with human cancer cells are the most specific cancer vaccines currently available. Ab2 can induce specific humoral anti-tumor immunity in cancer patients. However, the potential of Ab2 for inducing cellular immunity in cancer patients still requires demonstration. Clonotypic antibodies directed against the combining site for tumor Ag on human T-cell clones may provide highly effective reagents for inducing protective T-cell immunity against human cancer. A new generation of cancer vaccines, molecularly cloned tumor-associated antigens (Ag), has recently been developed. Recombinant Ag have been successfully expressed in vectors allowing large scale production of Ag for immunization of cancer patients. Recombinant tumor Ag was shown to induce specific and protective immunity in experimental animals. In contrast to Ab2, which may mimic a single cancer-associated epitope, recombinant Ag express multiple epitopes that are potentially immunogenic. Ag vaccines, therefore, may be more effective in arresting tumor growth than single epitope (Ab2) vaccines because tumor destruction by antibodies is dependent on antibody density on tumor cell surfaces. In light of the important roles that both B and T cells play in the control of tumor growth, the demonstration of induction of specific B and T cell-immunity by recombinant tumor Ag and Ab2 in experimental animals is encouraging. Ultimately, the immunomodulatory role of both types of vaccines has to be compared in cancer patients who are immunologically tolerant to many Ag/epitopes expressed by their growing tumors. The development of both Ab2 and recombinant Ag for single antigenic systems provides the first step towards this goal.
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PMID:Epitope- and antigen-specific cancer vaccines. 177 73

Affinity-purified polyclonal rabbit antibodies prepared against recombinant basic fibroblast growth factor (bFGF) neutralized the ability of bFGF to stimulate plasminogen activator (PA) production and endothelial cell migration in vitro. After iodination and intraperitoneal injection of the antibodies in mice, approximately 76% of the maximum circulating level of 125I-anti-bFGF antibodies (AF) was found as intact IgG after 24 hr. Furthermore, the circulating 125I-AF retained the ability to bind bFGF. Studies were performed to determine whether the growth of three different murine tumors (CT26, EHS, or B16/BL6) could be inhibited with affinity-purified neutralizing antibodies against bFGF. Tumors were injected subcutaneously in syngeneic mice, and neutralizing antibodies against bFGF were injected daily into the peritoneum. All studies, which varied in tumor burden, antibody dose, and study length, indicated that neutralizing antibodies against bFGF had no effect on tumor size, tumor growth, or tumor histology.
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PMID:Studies on the role of basic fibroblast growth factor in vivo: inability of neutralizing antibodies to block tumor growth. 219 45

ATP and AMP exhibit significant anticancer activities against established footpad CT26 colon adenocarcinoma in CB6F1 mice. Adenosine, inorganic phosphate, and inorganic pyrophosphate were without such effects under identical conditions. Daily intraperitoneal injections of adenine nucleotides in large volumes of saline, starting after the tumors became palpable, resulted in inhibition of tumor growth and a few "cures." The treatment was not toxic to the host as determined by changes in body weights. Weight loss observed in animals upon progression of the fast-growing CT26 tumors was slowed markedly in adenine nucleotide-treated mice. The inhibition of weight loss in tumor-bearing mice was shown to be neither the cause nor the effect of the inhibition of tumor growth. Intraperitoneal injections of AMP or ATP but not of adenosine yielded expansions of erythrocyte ATP pools in host animals. The expanded erythrocyte ATP pools are stable over a period of hours, while slowly releasing micromolar amounts of ATP into the blood plasma compartment, leading to several-fold increases in plasma (extracellular) ATP levels. Based on previous studies in which 1-5 microM extracellular ATP effectively inhibited the growth of a variety of tumor cells in several in vitro systems, it is suggested that similar levels of ATP in blood plasma account for the anticancer activities observed in a murine host.
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PMID:Anticancer activities of adenine nucleotides in mice are mediated through expansion of erythrocyte ATP pools. 292 3

Cachectin/tumor necrosis factor (TNF) is a macrophage product which may have a role in cancer cachexia. Recombinant human cachectin/TNF (Cetus Corporation) was administered i.p. twice daily to male F344 rats at varying, nonlethal dosages for either 5 or 10 days, and daily rat food intake and body weight were measured. There was a dose-dependent cachectin/TNF-induced decline in food intake and body weight gain over the treatment period. However, after 1 day rats became tolerant to these effects and increased food intake and gained body weight despite receiving cachectin/TNF. Rats were subsequently inoculated with a transplantable methylcholanthrene-induced sarcoma, and survival was measured. Rats previously treated with high-dose (either 100 or 200 micrograms/kg/day) cachectin/TNF survived significantly longer following tumor inoculation than did control rats given saline or rats given 10 micrograms/kg/day of cachectin/TNF. Analysis of tumor growth curves and tumor weight indicated that high-dose cachectin pretreatment did not retard tumor growth. Analysis of food intake and tumor burden following tumor inoculation indicated that high-dose cachectin pretreatment decreased the reduction in food intake associated with progressive tumor growth and allowed rats to withstand a greater tumor burden at death. Rats immunized with low-dose human cachectin/TNF developed high IgG titers against human TNF, but failed to demonstrate the same protection against a methylcholanthrene-induced tumor challenge as rats made tolerant with repetitive twice daily high-dose cachectin/TNF. The observation of reduced cancer-associated anorexia and increased survival of tumor-bearing rats associated with previous tolerance to exogenous cachectin/TNF strengthens the contention that endogenously produced cachectin may be a factor in the pathogenesis of cancer anorexia in the tumor-bearing rat. The mechanism of this tolerance is unclear but does not appear to be a humoral immune response.
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PMID:Cachectin/tumor necrosis factor: a possible mediator of cancer anorexia in the rat. 316 53

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 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

The antitumor activity of a glycopeptide purified from human malignant effusion, termed cancer-associated galactosyltransferase acceptor (CAGA), was assessed in BALB/c mice bearing primary and metastatic tumors. Initial studies with the fast-growing KA31 and slow-growing KB521 Kirsten sarcoma-transformed mouse fibroblast cell lines confirmed their tumorigenicity and metastatic potential. Inoculation of 1 X 10(5) KA31 cells s.c. resulted in palpable tumor formation in recipient animals within 14 days and death within 42 days from primary tumor growth (mean survival, 26 days; total survival, 0%). Inoculation of the slower-growing KB521 resulted in tumor formation in 85% of recipients, and tumor-bearing animals succumbed within 56 days after primary inoculation (mean survival, 48 days; total survival, 15%). Administration of CAGA by i.p. injection as a single dose or series of five daily doses (each 50 micrograms) inhibited primary tumor growth by 35 to 68% in animals receiving KA31 cells and by 25 to 70% in animals receiving KB521 cells. CAGA increased mean survival 50% from 26 to 38 days and total survival from 0 to 27% in animals bearing KA31-derived primary tumors. In animals bearing KB521-derived tumors, CAGA increased mean survival from 48 to 90 days and total survival from 15 to 50%. Similarly, CAGA was also found to significantly inhibit formation of pulmonary metastases in animals after excision of primary tumors. CAGA administration reduced death from metastatic deposits by 55 to 66% in animals initially inoculated with the KA31 cell line and by 58 to 90% in animals initially bearing primary tumors derived from the KB521 line. There was a corresponding decrease in the number of metastatic deposits per lung after administration of CAGA. Thus, CAGA appears to have potential antitumor activity against tumors with a range of growth rates and appears to inhibit both primary and metastatic tumor growth.
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PMID:Inhibition of primary and metastatic tumor growth in mice by cancer-associated galactosyltransferase acceptor. 640 94

Many studies have suggested that malignant transformation is associated with fundamental changes in the cell surface; similar changes have been described for normal stem cells and cells of embryonic or fetal origin. There is now evidence that the tumor cell secretes or sheds glycoproteins and glycosyltransferases into the surrounding medium and into serum. There are claims that some of these serum glycoproteins and glycosyltransferases are associated with, or specifically related to, the extent of tumor growth and may serve as a cancer marker. A cancer-associated galactosyltransferase isoenzyme (GT-II) has been described and purified. Different isoelectric forms of fucosyltransferase have also been described as indicative of malignancy. The articles to be published in CRC Critical Reviews in Clinical Laboratory Sciences will analyze the evidence for the association of these membrane factors with tumor growth. In order to better understand the possible significance of altered glycoproteins and of increased or different forms of glycosyltransferases during tumor growth, recent data on glycoprotein synthesis will be discussed including the new concepts on the control of glycoprotein synthesis through lipid intermediates. The possible mechanisms whereby malignant transformation could alter glycoprotein synthesis will be discussed with particular emphasis on the significance of these alterations to the biology of the malignant cell. Changes in surface membrane glycoproteins have long been implicated in the ability of a cell to metastasize. Secretion and/or shedding of the cell surface may also be important in the process of metastasis and in altering the host immune response. Detection and the study of these "shed" materials in patients appear to be indicating a new approach to cancer biology detection and therapy.
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PMID:Serum levels of glycosyltransferases and related glycoproteins as indicators of cancer: biological and clinical implications. 645 33

The present study was undertaken to assess the role of tumor-associated urokinase-type plasminogen activator (uPA) and its inhibitor type 1 (PAI-1) as a predictor for early relapse and poor prognosis in patients with stage II cervical cancer of the uterus. We have investigated the localization of uPA and PAI-1 immunohistochemically in formalin-fixed paraffin-embedded tissue sections. uPA and PAI-1 were analyzed antigenically, enzymologically, and zymographically in 28 patients with pelvic lymph node involvement and in 34 cases without nodal spread, as well as in 10 cases with normal cervix. In cancer tissues, strong staining for uPA was found in areas with invasive growth and degradation of surrounding normal tissue, while most tumor nests showed a mild or a moderate, evenly distributed PAI-1 staining. A significantly higher lymph node-positive rate was observed in patients having tumors with strong uPA and/or PAI-1 stainings than in those with tumors with weak stainings. In spite of significantly higher PAI-1 levels in the primary neoplastic tissues, uPA was found to be increased as well, both in antigen level and in activity. Most of PAI-1 obtained from cancer extracts is the latent form. These results suggest that cancer-associated increase in uPA seems not to be affected (or inhibited) by PAI-1 in areas where tumor cells are invading normal tissue. The overall survival and progression-free survival rate was worst in patients with the strong uPA staining confined to the tumor stromas and also with the strong PAI-1 staining at tumor nests, indicating that the greater localization of uPA in stromal cells than in malignant cells is a predictor of early relapse and poor prognosis in patients with cervical cancer of the uterus. Thus, the staining intensities and the localization of uPA and PAI-1 in tissue specimens appear to be predictors of increasing risk for lymph node metastasis, suggesting that some tumor cells recruit stromal cells to produce uPA and that PAI-1 may not act as a defense mechanism for tumor cell invasion and metastasis in the leading edge of tumor growth.
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PMID:Impact of urokinase-type plasminogen activator and its inhibitor type 1 on prognosis in cervical cancer of the uterus. 798 54


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