Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the past ten years numerous studies have been carried out to identify tumour markers able to diagnose cancer of the digestive tract. The paper reports the combined use of some markers (CEA, TPA, GICA, CA 125) in patients with carcinoma of the colon-rectum. The Authors conclude that although these markers are of little use, especially in association, in the early diagnosis of disease, it is very important to utilise these markers to monitor patients following surgical, chemotherapeutic or radiotherapeutic treatment.
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PMID:[Tumor markers in colorectal cancer]. 140 23

To examine whether protein kinase C (PKC) plays a role in mediating growth inhibitory effects of hexamethylene bisacetamide (HMBA) we compared a control H29 colon cancer cell line to a derivative, HT29-PKC7, that overexpresses high levels of PKC beta 1. We found that although HMBA markedly inhibited the growth of the control cells, no inhibition was seen with the HT29-PKC7 cells. On the other hand the tumor promoter 12-0-tetradecanoyl-phorbol-13 acetate inhibited the growth of HT29-PKC7 cells, but no inhibition was seen with the control cells. Maximum inhibition of the growth of both cell lines was obtained by combined treatment with HMBA and TPA. These results may be relevant to the use of HMBA in combination with other agents in the therapy of specific cancers.
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PMID:The modulation of growth by HMBA in PKC overproducing HT29 colon cancer cells. 175 60

Treatment of rodent cells with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate activates protein kinase C, leading to increased expression of several genes, including a gene originally designated TPA-S1 or phorbin (M. D. Johnson, G. M. Housey, P. T. Kirschmeier, and I. B. Weinstein, Mol. Cell Biol., 7: 2821-2829, 1987). Sequence analysis of this cloned gene indicated homology with human erythroid-potentiating activity and tissue inhibitor of metalloproteinase (TIMP-1). Elevated levels of phorbin mRNA have been observed in human colon tumors (J. G. Guillem, M. F. Levey, L. L. Hsieh, M. D. Johnson, P. LoGerfo, K. A. Forde, and I. B. Weinstein, Mol. Carcinogen., 3: 68-74, 1990) and this increase correlated with the extent of invasion. To further investigate this phenomenon at the protein level, monoclonal antibodies were developed against the recombinant form of TIMP-1. A competitive enzyme-linked immunosorbent assay was developed for quantitation of the TIMP-1 protein in tissue extracts. Elevated levels of TIMP-1 protein were found in 31 human colon tumors, compared to paired samples of adjacent normal mucosa. In a subset of samples, previously analyzed for phorbin mRNA levels (n = 25), there was a good correlation between the abundance of TIMP-1 protein and phorbin mRNA. Immunoaffinity column purification of tumor extracts followed by Western blot analysis was used to confirm the enzyme-linked immunosorbent assay data. These results provide evidence that phorbin and TIMP-1 represent the same gene. In addition, the immunoassays we have developed may be useful in further studies on the role of TIMP-1 in human colon cancer.
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PMID:Immunological quantitation of levels of tissue inhibitor of metalloproteinase-1 in human colon cancer. 193 83

In 98 patients affected by colorectal cancer (43 patients with colon cancer, 55 patients with rectosigmoid cancer) the specificity of some tumor markers (CEA, GICA, TPA, alpha-FP, FpA, gamma-GT) has been tested in evidencing the coexistence of liver metastases and the site of the primary tumor, i.e. the rectosigmoid region (rectum + 15 cm of the adjacent sigmoid colon) vs the rest of the colon. Liver metastases, present in 19 patients with colon cancer and in 24 with recto-sigmoid cancer, were previously ascertained by various instrumental investigations. Unlike previous studies which indicated CEA or alpha-FP as the most reliable markers to suggest the coexistence of liver metastases in such patients, the reported results allow the following sequence, in decreasing order of sensitivity, to be proposed: gamma-GT; FpA; CEA and GICA to a similar degree; TPA, which increases only when liver metastases from colon cancer are present; lastly, alpha-FP, which rises only in very few cases of massive hepatic involvement.
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PMID:Specificity of tumor markers (CEA, GICA, TPA, alpha-FP, FpA, gamma-GT) for the diagnosis of hepatic metastases from large bowel cancers. 247 62

Rectal mucosa from normal controls (n = 25) and tumor tissue and rectal mucosa from patients with colorectal cancer (n = 38) and adenoma (n = 35) were biopsied via colonoscopy. Ornithine decarboxylase (ODC) activity was determined in order to study the role of promoters in the process of colorectal carcinogenesis. ODC activity of cancer tissue was significantly higher than that of adenoma tissue. Normal mucosal ODC activity in rectum and sigmoid colon was 2 to 4 times higher than that in the proximal colon. Moreover, rectal mucosal ODC activity was significantly higher in patients with cancer or adenoma than that in normal controls. When ODC activity is regarded as an index of promoter, the possibility is suggested that cancer and adenoma developed in similar mucosa of the large bowel. Furthermore, ODC activity in colon cancer was significantly higher than that in rectal cancer. This suggests the possibility that TPA type promoter assumes a greater role in the process of carcinogenesis of colon cancer than that of rectal cancer.
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PMID:[A study of ornithine decarboxylase activity in tumor tissue and rectal mucosa in patients with colorectal cancer or adenoma]. 279 55

Sixty-four consecutive patients who had undergone curative resection for colorectal carcinoma were studied prospectively to evaluate the roles of sequential CEA determinations and independent instrumental follow-up in the early detection of resectable recurrences. Fifty-two of these patients also were submitted to sequential determinations of other tumor antigens: TPA (tissue polypeptide antigen) and Ca 19-9 (colon cancer antigen detected with a monoclonal antibody), for a retrospective evaluation of their utility as markers of recurrent tumors. Twenty-two recurrences were detected in a period ranging from 12 to 72 months (median, 47 months). CEA was the best predictor of recurrence (sensitivity, 90 percent) when compared with the other two markers (TPA sensitivity, 60 percent; Ca 19-9 sensitivity, 20 percent). When compared with the instrumental or biochemical examinations of the follow-up, CEA was still the most sensitive indicator of relapse although the specificity was quite low (78 percent) if minimal significative increases were considered. History and physical examination were more useful than CEA in detecting local recurrences in rectal cancer where the preoperative CEA level was low. A few second-look explorations based solely on small CEA increases failed to demonstrate recurrence or revealed peritoneal carcinomatosis. Selected second-look surgery based on demonstrated recurrences resulted in a resectability rate of 57 percent. A follow-up program based on frequent CEA assays, history, and physical examinations, including rectal, vaginal, and perineal exploration, is proposed. Extensive instrumental investigations should follow when a minimal significative CEA rise is observed, or when history and physical examinations suggest a possible recurrence. Second-look surgery should be evaluated after confirmed or highly suspected diagnosis of recurrence, on the basis of instrumental or clinical examinations.
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PMID:Follow-up of colorectal cancer resected for cure. An experience with CEA, TPA, Ca 19-9 analysis and second-look surgery. 347 Jan 72

Serum TPA and CEA level were measured in patients with gastric or colon cancer during the course of surgical treatment, and those clinical utility was evaluated. Both markers level were shown to be highest in colon cancer, followed by gastric cancer, benign diseases, and healthy subjects. Late stage patients, especially inoperable patients or patients in recurrence showed significantly high TPA and CEA level compared to early stage patients. Both markers were considered to be useful not only postoperative following up for recurrence but also preoperative evaluation for resectability and prognosis and postoperative evaluation for the treatment itself.
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PMID:[Clinical utility of tumor markers in gastric and colon cancer]. 386 84

We have studied the PKC isoforms present in HT-29 M6 colon cancer cells, the differentiation of which to mucus-secreting cells is blocked by TPA. In addition to a major 72 kDa band, a 77 kDa PKC isoform was recognized by two different antibodies raised against a C-terminus-specific peptide for the TPA-insensitive isoform, PKC zeta. By different criteria (association to the membrane, down-regulation, PKC activity in immunoprecipitates) we conclude that, contrary to the 72 kDa band, the 77 kDa band corresponds to a Ca(2+)- and TPA-sensitive PKC. These results suggest that antipeptide antibodies directed against the C-terminus of PKC zeta react in human cells with a member of the conventional PKC subfamily besides PKC zeta. Therefore, the data indicating that PKC zeta is sensitive to different agents in various cell lines should be carefully re-evaluated.
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PMID:Antipeptide antibodies directed against the C-terminus of protein kinase C zeta (PKC zeta) react with a Ca(2+)- and TPA-sensitive PKC in HT-29 human intestinal epithelial cells. 818 76

At present there is at least one optimal tumor marker and/or optimal marker combination available for the most frequent carcinomas. For colorectal carcinomas (CRC) the general consensus is that CEA is the best single marker, however, other markers, like CA 19/9, TPA and more recently CA 242 were reported to be just as useful. Since CA 242 is a relatively new marker we decided to assess comparatively the value of the four markers in CRCs. Although 308 sera from patients with CRCs, benign digestive diseases (n = 128) and healthy controls (n = 45) were analyzed using commercially available testkits. None of the mean values of the four markers were elevated above their respective cut-off levels in the controls. CEA was the most sensitive marker in early stage cancer, while CA 19/9 was the least sensitive marker, and hence should not be used for the study of this kind of malignancy. However, it remains usefull for carcinomas of the pancreas. As regards specificity, CA 242 was the most specific marker in hepatobiliary diseases. Used concomitantly, CEA and TPA and CEA plus CA 242 augmented the sensitivity markedly, hence these combinations can be recommended. CEA remains the most reliable marker for the follow-up of colon cancer patients, the novel marker CA 242 has a similar performance, the combination of the two markers ameliorates the specificity of CEA used as a single marker.
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PMID:Comparative evaluation of four tumor markers, CA 242, CA 19/9, TPA and CEA in carcinomas of the colon. 869 64

Butyrate is a potentially selective therapeutic agent for many adenocarcinomas. Butyrate causes reversible growth arrest as well as some death of VACO 5 colon cancer cells. Combined treatment with butyrate and the phorbol ester TPA leads instead only to cell death, while TPA causes little death on its own. Cells dying during treatment with TPA and butyrate, as well as those dying in the presence of butyrate alone, exhibit features typical of apoptosis, including detachment, shrinkage and internucleosomal DNA cleavage. Pre-treating VACO 5 cell cultures with TPA for as little as 6 hr prior to butyrate addition led to a markedly diminished enhancement of butyrate-induced apoptosis. Treatment with a distinct PKC activator, bryostatin 1, was ineffective in enhancing butyrate-induced death and, furthermore, counteracted the death-enhancing actions of TPA. Such antagonism was apparent when bryostatin was added after 12 hr of TPA/butyrate treatment but was much less effective thereafter. The duration of TPA/butyrate treatment required for depressing cell survival by >95% was thereby estimated to be 24 hr. Other colon cancer cell lines were examined for the extent of cell death following treatment with TPA/butyrate. In each of these lines, butyrate inhibited cell replication in a reversible manner, similar to that seen in VACO 5. However, the combination of butyrate and TPA led to high levels of cell death in only a subset of these lines. TPA/butyrate-treated cultures of COLO 201 exhibited extensive apoptosis, similar in timing and magnitude to the response by VACO 5, whereas HCT 116 was reversibly growth-arrested. Our findings indicate that the PKC system plays a critical role in maintaining cell survival during butyrate-induced growth arrest.
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PMID:Phorbol ester augments butyrate-induced apoptosis of colon cancer cells. 878 64


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