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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrin is trophic for normal gastric and colonic mucosa. We examined the potential trophic effects of chronic gastrin administration on the growth of mouse colon adenocarcinoma (MC-26). Thirty-three mice bearing transplantable MC-26 colon cancers were treated with varying doses (125, 250, or 500 micrograms/kg/day) of pentagastrin. Significant increases in tumor weight and DNA content were observed. Fundic mucosal weight and DNA content in these mice showed a dose-related trophic response. The weight of control fundic mucosa was 10 mg and rose to 20, 45, and 65 mg with increasing doses of gastrin. The DNA content of control fundic mucosa was 155 micrograms and rose to 220, 340, and 480 micrograms as the dose of gastrin was increased. Pentagastrin stimulated growth of the MC-26 colon cancer, but the threshold for gastrin-stimulated tumor growth was different from that of normal mucosal growth. The hyperplastic response of the fundic mucosa was increased by increasing gastrin doses; whereas, colon cancer hyperplasia was maximal at the lowest dose tested (125 micrograms/kg/day) and did not increase further with increasing doses of hormone. Mice bearing gastrin-stimulated tumors died at a significantly greater rate than did mice with untreated tumors (80% of control mice and none of the treated mice were alive at day 55). The effects of gastrin treatment on the growth of MC-26 colon cancer persist after treatment is discontinued; mice with tumors that were treated with gastrin for either 7 or 14 days and in which the treatment was stopped were all dead by 35 or 28 days, respectively, after the end of treatment.
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PMID:Gastrin stimulates growth of colon cancer. 395 54

Serum tissue polypeptide antigen (TPA) levels were measured in 33 patients with esophageal cancer, 39 with stomach cancer and 50 with colon cancer. At the same time five glycoproteins, namely immunosuppressive acidic glycoprotein (IAP), alpha 1-antichymotripsin (alpha 1-ACT), acid soluble glycoproteins (ASP), sialic acid and carcinoembryonic antigen (CEA), were measured for comparison. The mean TPA values were 59.0 +/- 15.4 U/l in 61 normal subjects, 103.6 +/- 104.2 U/l (positive rate, 24.2%) in esophageal cancer patients, 111.9 +/- 49.8 U/l (71.8%) in stomach cancer patients and 124.8 +/- 195.5 U/l (40%) in colon cancer patients. The serum TPA levels in patients with stomach cancer rose with an increased number of involved lymph nodes and with a higher degree of infiltrative growth and increased with the advancement of tumor growth postoperatively. Serum TPA levels correlated well with those of alpha 1-ACT, IAP and ASP in stomach cancer patients and with those of CEA, ASP and sialic acid in colon cancer, but not in esophageal cancer patients. It is suggested that the serum TPA might represent one of the reactant proteins and/or tumor-associated antigens that appear to be dependent upon the cancer status.
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PMID:[Clinical evaluation of tissue polypeptide antigen in patients with esophageal, stomach and colon cancer]. 648 66

A new multihit model of carcinogenesis is developed for use in evaluating age-specific cancer incidence rates in human populations. The model allows for some heterogeneity in both risk (perhaps genetic) and pathway (number of hits). Fitting the model yields estimates of (1) levels of effect of background exposure to environmental agents, (2) tumor growth times after initiation of a malignant cell, and (3) relative sizes of high-risk groups in a human population. Maximum likelihood procedures are used to fit the model to the polyposis coli data of Veale and the colon cancer incidence data from the Third National Cancer Survey. Model estimates may be verified in some cases by review of independent data in the literature and results have both theoretical and practical implications. Findings are generally consistent with the adenoma-carcinoma etiologic sequence postulated by Hill, Morson and Bussey with one exception. A large proportion of the population may be at risk of four-hit colon tumors following a non-adenoma etiologic sequence.
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PMID:The multihit model of carcinogenesis: etiologic implications for colon cancer. 672

A randomized study was performed in advanced cancer to test the effectiveness of total parenteral nutrition (TPN) in maintaining and improving nutrition, to examine the effects of TPN on tumor growth, and to determine if TPN altered chemotherapy response rates, treatment tolerance, and survival. Forty-five patients on identical chemotherapy were randomized to TPN versus ad libitum feeding. TPN was well tolerated. No clinical or tumor marker evidence suggesting neoplastic growth stimulation was obtained. Chemotherapy-related complications and chemotherapy responses did not differ between the two groups. TPN had little effect on performance status. TPN patients gained an average of 2.8 kg before chemotherapy, but triceps skinfold and mid-arm muscle area did not change significantly during TPN. Survival did not improve with TPN. We conclude that current techniques of TPN are of limited benefit in advanced colon cancer. A small subset of patients with short-gut malabsorption may be helped. Further study is needed to determine the mechanisms of cancer undernutrition and to refine nutritional supplementation techniques on the basis of these mechanisms.
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PMID:Total parenteral nutrition as an adjunct to chemotherapy of metastatic colorectal cancer. 680 21

Time trends in serum cholesterol were analyzed in the Framingham Study data to determine whether low serum cholesterol, which appears to be associated with increased cancer risk, can truly be called a precursor to the development of the disease. Serum cholesterol measured at base line was found to be associated with the risk of both fatal cancer and all cancers occurring in the subsequent 18 years in men (P less than 0.05). This inverse association seems particularly strong for colon cancer in men. Analysis of time trends in the Framingham data did not yield consistent results for all ages. Men 50--59 years old had a statistically significant lower serum cholesterol measured 16--18 years before cancer diagnosis. For men 60--65 years old, a statistically significant trend toward lower serum cholesterol was apparent as measurement was made closer to the time fo cancer diagnosis. Although the Framingham data are not conclusive, they do suggest that in some cancer cases where the serum cholesterol level was lower than that expected at as much as 16--18 years before cancer diagnosis, the depressed level was likely to be a precursor to the tumor growth. However, consistent with the metabolic consequences of tumor growth, the data show that in some cancer cases, serum cholesterol had decreased at measurements made close to the time of cancer diagnosis.
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PMID:The serum cholesterol-cancer relationship: an analysis of time trends in the Framingham Study. 695 62

Radiolabeled monoclonal antibodies (MoAbs) have been used for radioimmunotherapy (RIT) of human colon cancer xenografts in an attempt to develop promising clinical approaches to improving therapy success. Several strategies have been investigated to accomplish this task while decreasing toxicity. The CC49 antibody was selected for the present studies because of its relatively high affinity constant (16.2 x 10(9) M-1) for the high molecular weight TAG-72 mucinous antigen secreted by human colon cancer cells. In previous studies, when CC49 was labeled with 131I, it demonstrated a substantial therapeutic advantage over the lower affinity antibody (B72.3) reactive with TAG-72. One of the chief problems in achieving cures with RIT is that hematological toxicity limits the quantity of radionuclide that can be administered. In other studies of dose fractionation using athymic nude mice and 131I-labeled intact MoAbs reactive with human colon cancer xenografts, multiple administrations at approximately 1-week intervals were found to produce more prolonged tumor growth inhibition and less toxicity than single administrations. The purpose of this study was to investigate the therapeutic efficacy and toxicity of 131I-labeled CC49 MoAb administered with short fractionation schedules against human colon cancer xenografts to determine the optimal treatment schedule, with the ultimate aim of applying this approach in clinical trials. The results reported here demonstrate that in an animal colon cancer xenograft model, RIT delivered in a fractionated schedule clearly presents a therapeutic advantage. For example, one administration of 600 microCi 131I-labeled CC49 to LS174T tumor-bearing mice was lethal to approximately 25% of mice but produced no tumor regressions. Fractionation of this dose to two administrations of 300 microCi 131I-labeled CC49 at a 3-day interval resulted in tumor regression in approximately 30% of the animals, accompanied by a similar 25% death rate. The administration of 300 microCi 131I-labeled CC49 at a 7-day interval resulted in 15% animal lethality, but no complete tumor regressions. When three administrations of 300 microCi 131I-labeled CC49 were given over a 1-week period on days 0, 3, and 7, tumor regressions occurred in approximately 40% of the animals, accompanied by a 30% death rate. Moreover, three administrations of 300 microCi 131I-labeled CC49 resulted in 20% tumor recurrence, whereas two administrations of 131I-labeled CC49 resulted in 60% tumor recurrence.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Fractionated radioimmunotherapy of human colon carcinoma xenografts with 131I-labeled monoclonal antibody CC49. 749 64

The mechanisms of immunosuppression induced by colon cancer in rats were investigated at the systemic and tumor levels. During tumor growth (after i.p. injection of rat colon adenocarcinoma cells in syngeneic BD IX rats), Con A-induced proliferation of splenic mononuclear cells decreased and nitric oxide (NO) production by splenic macrophages increased concomitantly. Incubating splenic mononuclear cells with an inhibitor of NO synthase, NG-monomethyl-L-arginine, restored lymphocyte proliferation. A low level of inducible NO synthase mRNA was detectable in tumors by Northern blotting, with a weak increase during tumor growth. The NO concentration measured in the tumor nodules increased weakly parallel to the tumor growth. Five and six weeks after tumor cell injection, tumor-infiltrating lymphocytes from disaggregated tumors did not proliferate in the presence of Con A. Addition of NG-monomethyl-L-arginine inhibited the production of NO in tumor dissociations and enhanced tumor-infiltrating lymphocyte proliferation. Glyceryl trinitrate (a NO-releasing compound) totally inhibited the lymphocyte proliferation in vitro while it slightly reduced the tumor cell proliferation. T lymphocytes were therefore more sensitive to NO than were tumor cells. Culture medium from tumor cells induced NO production by splenic macrophages, although the factor involved has not yet been identified. Furthermore, tumor cells could also play a part in NO production by tumors because the tumor cells were induced to produce NO by IFN-gamma plus IL-1. These results strongly suggest the participation of NO in the tumor-induced immunosuppression in rats.
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PMID:Nitric oxide involvement in tumor-induced immunosuppression. 751 29

In different human tumors, splice variants of the surface glycoprotein CD44 (CD44v) are correlated with advanced stages of tumor growth and metastatic potential. In breast cancer and colon cancer, expression of epitopes encoded by exon v6 on primary tumors is an independent prognostic factor for poor patient survival. Two different screening methods for the detection of CD44 variants in tumors have been applied: immunohistochemistry (IHC) and semi-quantitative reverse transcription PCR (RT-PCR). In this study, we have compared the predictive capacity and the applicability of both approaches, using 31 human breast-tissue specimens (normal and neoplastic). IHC reveals lack of expression of CD44v on normal ductal epithelial cells but strong expression on myoepithelial cells. The majority of tumors express CD44 epitopes encoded by several variant exons. RT-PCR detects splice variants in normal epithelium, probably derived from RNA expressed in the myoepithelium. In tumors, RT-PCR reveals expression of a wide range of splice variants, including new ones that are not detected in normal breast tissue, e.g. ones that contain all variant exons. The conclusion of this comparison is that IHC is the better method for breast-tumor sample screening but that the increased sensitivity of RT-PCR can help to distinguish CD44v-positive from CD44v-negative tumors in cases where only a few tumor cells express variants or where epitopes are masked.
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PMID:Comparison of immunohistochemistry and RT-PCR for detection of CD44v-expression, a new prognostic factor in human breast cancer. 753 Feb 37

Angiogenesis inhibitors have attracted considerable interest. The anti-tumor and anti-metastatic effects of TNP-470, an angiogenesis inhibitor, and mitomycin C (MMC), a representative anti-neoplastic agent, were investigated using a xenotransplanted human colon cancer, TK-4. Suturing of small pieces of TK-4 tumors to the cecal wall in nude mice (orthotopic transplantation) induced liver metastasis. Mice were randomly divided into 3 groups; a control group given saline solution, a group receiving TNP-470 and a group receiving MMC. TNP-470 was given s.c. on alternate days for 5 weeks from day 10 after cecal transplantation and MMC was administered intraperitoneally (i.p.) once a week from day 10 after cecal transplantation. MMC significantly inhibited cecal tumor growth. In the control group, liver metastases developed in 9 out of 10 mice, including 3 with more than 20 metastatic foci. Liver metastasis also developed in 8 out of 10 mice receiving MMC, 2 of which had many metastases. In contrast, liver metastasis developed in only 2 out of 8 mice in the TNP-470 group and neither of these animals had numerous metastases.
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PMID:Comparison of the inhibitory effect of the angiogenesis inhibitor, TNP-470, and mitomycin C on the growth and liver metastasis of human colon cancer. 753 57

PDGF-B released from colon tumor cells regulated tumor growth in athymic mice in a paracrine manner by inducing blood vessel formation. A positive correlation was found between expression of PDGF B-chain in cells grown in vitro and the number of factor VIII-positive blood vessels in tumors induced by three classes of colon carcinoma cell lines. Elevated expression of PDGF-B was also correlated with tumor size. Each cell line had the same mutations in the colon cancer genes APC, DCC, and p53 and had wild type c-K-ras genes (Huang et al. [1994] Oncogene, 9:3701-3706.) eliminating the possibility that any differences in tumor blood vessel formation were due to mutations and/or deletions in these genes. Colon carcinoma cells released biologically active PDGF capable of stimulating the growth of NIH3T3 cells, which was inhibited by neutralizing antisera to PDGF-AB chains. An inverse correlation was found between induction of factor VIII-positive blood vessels and expression of vascular endothelial growth factor (VEGF), while no correlation was seen with expression of either TGF alpha or k-FGF. Basic fibroblast growth factor (FGF) expression was not detected in these tumor cells. TGF beta 1 was capable of inducing PDGF-B expression in the undifferentiated U9 colon carcinoma cell line, but this sensitivity was not seen in differentiated cells. In contrast, TGF beta 1 inhibited VEGF expression in both undifferentiated cells and differentiated colon cancer cells. Thus, TGF beta 1 has two roles in the growth of undifferentiated U9 colon carcinoma cells in vivo: direct stimulation of cell proliferation as we have showed in earlier studies, and an increase in angiogenesis by inducing PDGF-B.
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PMID:Platelet-derived growth factor-B increases colon cancer cell growth in vivo by a paracrine effect. 759 1


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