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)

A prospective ecological evaluation of mortality from common malignancies with dietary risk factors and alcohol consumption was carried out among 10 state capitals of Brazil. Regression analysis was used to examine the association of dietary intake with mortality rates of the most common cancers among adults age 30 years and older. Age-adjusted cancer mortality rates varied 2.4 to 3.3 fold across the state capitals. A positive relationship was observed between energy intake and colon, lung, and esophageal cancer (p</=0.02 for each). Colon cancer mortality was positively associated with consumption of total fat, eggs, alcohol, mate tea, cereals, and vegetables (p</=0.01). Lung cancer was positively associated with mate and cereal intake (p<0.05). Stomach cancer was associated with consumption of eggs (p=0.04); and negatively associated with consumption of high fiber foods, fruits, and vitamin A and C (p</=0.05). Esophageal cancer was positively associated with fat intake, mate and cereals (p</=0.05) and negatively associated with vitamin A (p=0.02); prostate cancer was negatively associated with vitamin C (p=0.007). Breast cancer was not associated with any of the factors studied. The marked variation in cancer mortality rates in Brazil may be partially related to the high variation in dietary components or other diet associated factors.
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PMID:Diet and mortality from common cancers in Brazil: an ecological study. 1090 7

Fas (CD95/APO-1) is a cell surface "death receptor" that mediates apoptosis upon engagement by its ligand, FasL. Fas-mediated apoptosis of lymphocytes normally serves immunoregulatory roles, including tolerance acquisition, immune response termination, and maintenance of immune privilege in certain organs. Colon tumors can exploit this lymphocyte death program by expressing FasL. This may enable colon tumors to mount a "Fas counterattack" against antitumor lymphocytes, impairing antitumor immune responses. FasL-expressing colon tumor-derived cell lines can trigger Fas-mediated apoptosis of cocultured T cells in vitro. FasL expressed in esophageal cancer has been significantly associated with apoptosis and depletion of tumor-infiltrating lymphocytes (TIL) in vivo. FasL may also facilitate metastatic colonization of Fas-sensitive organs such as the liver, by inducing apoptosis of target organ cells. Normal colonic epithelial cells express Fas and are relatively sensitive to Fas-mediated apoptosis. By contrast, colon tumor-derived cell lines are usually resistant to induction of Fas-mediated apoptosis, and colon cancer cells frequently coexpress Fas and FasL. The mechanisms allowing resistance to Fas-mediated apoptosis are complex, and defects have been identified at several levels of Fas signal transduction. The "Bcl-2 rheostat" may be pitched against apoptosis in colon cancer, inasmuch as overexpression of Bcl-2, downregulation of Bak, and mutation of Bax are common defects in colon tumors. Caspase-1 is also downregulated in colon cancer. The high frequency of p53 mutations in late-stage cancers may also inhibit Fas signaling. Fundamental defects in apoptosis signaling may contribute to both immuno- and chemoresistance in colon cancer and allow expression of FasL to counterattack antitumor lymphocytes.
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PMID:Altered mechanisms of apoptosis in colon cancer: Fas resistance and counterattack in the tumor-immune conflict. 1091 13

A phase I study was designed to evaluate the toxicity of escalating doses of gemcitabine along with fixed-dose paclitaxel in patients heavily pretreated with chemotherapy or radiotherapy. All patients had no prior therapy with the study drugs and possessed both adequate performance and end organ function. Eighteen patients were entered in the study. Characteristics included a median age of 66 years (range, 41 to 77) and stage IV disease in all patients; there were six patients with colon cancer, two with bladder cancer, three with non-small-cell lung cancer, two with esophageal cancer, three with pancreatic cancer, and two with cancer of unknown primary. Paclitaxel (150 mg/m2 over 3 hours) was given on day 1 and gemcitabine (800, 900, and 1,000 mg/m2 over 15 minutes) was given in three separate dose-escalating cohorts (1-3) on days 1 and 8. The treatment cycled every 21 days. The dose-limiting toxicity (DLT) proved to be neutropenia. All nonhematologic toxicities were mild and included gastrointestinal (nausea, vomiting, and diarrhea), dermatologic (rash), and neurologic (paresthesias) disturbances along with transient elevations of liver function tests. The combination of gemcitabine and paclitaxel seems to be well tolerated, and the recommended starting dose for a phase II study, in pretreated patients using a day 1/day 8 treatment schedule, should be 900 mg/m2 for gemcitabine (days 1 and 8) along with 150 mg/m2 for paclitaxel (day 1).
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PMID:Phase I study of paclitaxel and day 1/day 8 gemcitabine in patients with solid malignancies. 1095 61

To evaluate the relation between low cholesterol level and mortality, the authors followed 482,472 Korean men aged 30-65 years from 1990 to 1996 after a baseline health examination. The mean cholesterol level of the men was 189.1 mg/100 ml at the baseline measurement. There were 7,894 deaths during the follow-up period. A low cholesterol level (<165 mg/100 ml) was associated with increased risk of total mortality, even after eliminating deaths that occurred in the first 5 years of follow-up. The risk of death from coronary heart disease increased significantly in men with the highest cholesterol level (> or =252 mg/100 ml). There were various relations between cholesterol level and cancer mortality by site. Mortality from liver and colon cancer was significantly associated with a very low cholesterol level (<135 mg/100 ml) without any evidence of a preclinical cholesterol-lowering effect. With lengthening follow-up, the significant relation between a very low cholesterol level (<135 mg/100 ml) and mortality from stomach and esophageal cancer disappeared. The cholesterol level related with the lowest mortality ranged from 211 to 251 mg/100 ml, which was higher than the mean cholesterol level of study subjects.
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PMID:Which cholesterol level is related to the lowest mortality in a population with low mean cholesterol level: a 6.4-year follow-up study of 482,472 Korean men. 1096 71

We examined AIS status in digestive tract cancers and found that all eight esophageal cancer cell lines (100%) showed AIS/TA-AIS gene overexpression, whereas 1 of 12 (8%) gastric cancer and 0 of 14 (0%) colon cancer cell lines showed AIS/TA-AIS gene expression. We then confirmed that the AIS gene, not the TA-AIS gene, was dominantly expressed in esophageal cancers by reverse transcription-PCR. AIS protein was also expressed in AIS gene-positive cell lines. Subsequently, we tested AIS gene expression in paired esophageal normal tissues and cancers. Twenty-five of 39 (64%) primary esophageal cancers demonstrated an obviously higher expression of AIS gene compared to paired normal tissues. Moreover, high AIS gene expression was significantly associated with lymph node metastases in esophageal cancer (P = 0.0271). These results suggested that AIS may be useful as a marker for advanced esophageal cancer.
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PMID:AIS overexpression in advanced esophageal cancer. 1129 35

We previously reported that a novel promoter enhancer element "human tissue inhibitors of metalloproteinases 1 (TIMP-1) enhancer" (HTE) and a novel transacting protein "cysteine rich transcription factor" (CRTF) induced TIMP-1 synthesis in prostate cancer cells 2xN.I.PC-3. In the present study, to clarify the significance of CRTF in gastrointestinal cancers we measured the binding activity of CRTF to HTE using an electrophoretic mobility shift assay (EMSA), and the TIMP-1 concentration by ELISA after various stimulation of six cancer cell lines (KE-3, TE-9, MKN-28, MKN-45, KM12SM, SW620). In three cell lines (KE-3, MKN-45, SW620), both the binding activity of CRTF and TIMP-1 concentration significantly increased after IL-10 stimulation. Fetal bovine serum (FBS) did not affect the binding activity of CRTF, whereas FBS induced TIMP-1 synthesis in all cell lines. In KE-3 esophageal cancer cells and SW620 colon cancer cells, both the binding activity of CRTF and TIMP-1 concentration increased in the presence of a conditioned medium (CM) of fibroblasts which was isolated from human colon cancer tissues, but did not increase in MKN-45 cells. Moreover, in the fibroblasts, both the binding activity of CRTF and the TIMP-1 concentration increased in the presence of CM from KM12SM, SW620, and TE-9 cancer cell lines. These results suggested that IL-I0, and unknown factors in addition to IL-10, induced TIMP-1 synthesis via an increase in the binding activity of CRTF in gastrointestinal cancers, and that interaction between cancer cells and fibroblasts may play an important role in TIMP-1 synthesis through a signal transduction pathway consisting of CRTF phosphorylation and HTE activation.
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PMID:Significance of cysteine rich transcription factor (CRTF) in the synthesis of tissue inhibitor of metalloproteinases 1 (TIMP-1) in gastrointestinal cancers. 1137 Aug 21

The effects of nine new tetramethylpiperidine (TMP)-substituted phenazines on the growth of a human esophageal cancer cell line (WHCO3), two human hepatocellular carcinoma cell lines (PLC and HepG2) and three human colon cancer cell lines (CaCo2, COLO 320DM and HT29) were compared to those of clofazimine, B669 and five standard chemotherapeutic agents. The three most active TMP-substituted phenazines against these cell lines were B3962, B4126 and B4125 with mean IC50 values for all the cancer cell lines tested of 0.36, 0.47 and 0.48 microg/ml respectively. B3962 and B4126, but not B4125 were also the most active against a semi-continuous human fibroblast culture (MRC5). The compound with the highest tumor specificity relative to the fibroblast culture, was B4125. Importantly, there was minimal variation in sensitivity of the different cell lines, including a multidrug resistant cell line (COLO 320DM) expressing high levels of P-glycoprotein, to the TMP-substituted phenazines. This was not the case with the standard chemotherapeutic agents. The efficacy of compounds such as B4125 against a broad spectrum of multidrug resistant cancer cell lines, together with their relatively high tumor specificity, suggests that these agents may be useful in the treatment of intrinsically resistant cancers such as colon and liver cancer.
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PMID:Tetramethylpiperidine-substituted phenazines inhibit the proliferation of intrinsically multidrug resistant carcinoma cell lines. 1156 77

Serological identification of tumor antigens by cDNA expression cloning is a technique used to isolate cDNAs encoding tumor antigens that are recognized by IgG antibodies in sera from cancer patients. It is also useful for the isolation of tumor antigens recognized by T cells. We applied this method to identify melanoma antigens recognized by the serum from a patient with a good prognosis who had T-cell-infiltrated melanoma and vitiligo. By screening a lambda phage cDNA library constructed from a highly pigmented melanoma cell line, SKmel23, with the patient's serum, 50 positive cDNA clones consisting of 26 distinct antigens were isolated. Of these, 20 encoded known proteins, and 6 encoded previously uncharacterized ones. The most frequently isolated clone, which we named KU-MEL-1, was unknown previously but was homologous to partial cDNA sequences registered in the expressed sequence tag database. Reverse transcription-PCR and Northern blot analysis demonstrated that KU-MEL-1 was strongly expressed in most melanoma cell lines, melanoma tissue samples, and cultured melanocytes and weakly expressed in cell lines derived from other types of tumors, as well as in some normal tissues, including testis. Western blot analysis with polyclonal murine antibody generated by immunization with the recombinant KU-MEL-1 protein demonstrated that the KU-MEL-1 protein was preferentially expressed in melanoma cells and melanocytes. IgG antibodies against KU-MEL-1 were detected in the sera from 9 of 26 melanoma patients and from some patients with other cancers, including brain tumor, esophageal cancer, colon cancer, and chronic myelogenous leukemia, but were not detected in sera from 30 healthy individuals. Although the IgG specific for KU-MEL-1 was not detected in sera from 12 vitiligo patients, it was detected in sera from 7 of 11 patients with Vogt-Koyanagi-Harada disease that is thought to be an autoimmune disease against melanocytes. These results suggest that KU-MEL-1 may be a useful target for the development of diagnostic and therapeutic methods for patients with various cancers, particularly with melanoma, as well as patients with autoimmune diseases against melanocytes.
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PMID:Tumor antigens isolated from a patient with vitiligo and T-cell-infiltrated melanoma. 1218 44

Data which have emerged from randomized clinical trials are inconclusive regarding the efficacy of neoadjuvant chemoradiation therapy for patients with esophageal cancer. In 2001, available data appear to support the use of adjuvant chemoradiation therapy following the complete resection of a gastric cancer, adjuvant chemotherapy following the resection of a stage III (and--probably--"high-risk" stage II) colon cancer, and the use of adjuvant (and most likely neoadjuvant) chemoradiation therapy for stages II and III rectal cancer.
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PMID:Efficacy of neo- and adjuvant treatment modalities in gastrointestinal cancer patients. 1177 40

Positron emission tomography (PET) with [18F]-fluorodeoxyglucose (FDG) is a tool for the imaging and evaluation of glucose metabolism. This technique has recently become available in more than thirty hospitals and has been approved under Japan's national health insurance program. FDG uptake correlates with glucose utilization in tissue and is widely used for evaluating malignant tumors as well as brain function and myocardial viability. FDG-PET is useful for the diagnosis of lung cancer, colon cancer, esophageal cancer, malignant lymphoma, malignant melanoma, head and neck cancer, myocardial viability, and epileptic focus. A brief summary of the application and utility of FDG-PET for esophageal carcinoma is described in this article. Because of its limited spatial resolution, FDG-PET is not able to evaluate the invasiveness of primary tumors and small lesions. However, the uptake of FDG correlates with the aggressiveness of the tumor and the prognosis of patients with esophageal carcinoma. The sensitivity, specificity, and accuracy of lymph node staging is higher than that with CT. FDG-PET has the advantage of being able to detect distant metastases on a single occasion. Evaluation of the response to therapy and of recurrence is also possible by means of FDG-PET. There is some normal uptake and physiological distribution of FDG in many organs. Physiological status has an effect on the uptake of FDG in normal organs, and, consequently, on lesion uptake. Understanding of these characteristics makes this procedure a useful diagnostic modality for the management of patients with esophageal carcinoma.
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PMID:[Current status of nuclear medicine. Clinical application of FDG-PET for cancer diagnosis. Esophageal cancer]. 1207 32


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