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)

Records were reviewed of 396 men less than 75 years old with a history of transurethral prostatectomies, known smoking habits, height, weight and no prostate malignancy more advanced than stage A. The 51 men with stage A cancer included more current smokers than the 345 without malignancy (45.1% versus 22.3%, odds ratio 2.9, confidence interval 1.6 to 4.5, p < 0.001). Prostatectomy specimens from smokers were smaller than those from nonsmokers (21.4 versus 26.9 gm., p < 0.005) and those from cancer patients were smaller than those from men without cancer. Small adenomas included more cancers per kilogram than large adenomas in smokers and nonsmokers. Men with a history of prostatectomy were less often current smokers than 128 men with newly diagnosed colon cancer (22.3% versus 42.2%, odds ratio 0.49, confidence interval 0.27 to 0.77), and less often ever smokers than 325 men from a general internist's office (46.5% versus 55.4%, odds ratio 0.70, confidence interval 0.52 to 0.94). These data suggest smoking as a risk factor for stage A prostatic cancer and confirm smoking abstinence as a risk factor for prostatic hypertrophy requiring surgery.
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PMID:More stage A prostatic cancers, less surgery for benign hypertrophy in smokers. 767 42

To determine the relative expression of distinct mucin genes in normal and neoplastic tissue, antibodies and cDNA probes that recognize the core tandem repeat sequences of membrane-bound (MUC1) and secreted (MUC2 and MUC3) mucins were used for immunohistochemical and RNA Northern and slot-blot analysis. MUC1 mRNA was detected in all epithelial tissues tested. MUC1 core peptide, recognized by monoclonal antibodies 139H2 and DF3, was highly expressed on apical membranes of bronchus, breast, salivary gland, pancreas, prostate, and uterus, and was sparsely expressed in gastric surface cells, gallbladder, small intestine, and colonic epithelium. In contrast, MUC2 and MUC3 gene expression was primarily restricted to the intestinal tract. MUC2 mRNA was highly expressed in normal jejunum, ileum, and colon, compared with very low levels in normal bronchus and gallbladder. MUC3 mRNA was highly expressed in normal jejunum, ileum, colon, and gallbladder. Immunohistochemical studies using antibodies against synthetic MUC2 (anti-MRP) and MUC3 (anti-M3P) peptides indicate that MUC2- and MUC3-producing cells in the gastrointestinal tract are distinct. Goblet cells of the small intestine and colon reacted strongly with anti-MRP, whereas M3P reactivity was restricted to columnar cells of small intestinal villi, surface colonic epithelium, and gallbladder. Mucin protein epitopes and mRNA levels were frequently altered in adenocarcinomas compared to corresponding normal tissues. Alterations included increased expression, aberrant expression, and, less frequently, loss of expression. Increased MUC1 immunoreactivity was observed in most adenocarcinomas of the breast, lung, stomach, pancreas, prostate, and ovary. In addition, with the exception of prostate cancer, focal aberrant expression of MUC2 and MUC3 epitopes was frequently observed. Increased MUC1, MUC2, and MUC3 epitopes were present in colon adenocarcinomas of all histological subtypes, with the greatest increase of MUC2 epitopes observed in colloid (mucinous) colon cancers. MUC2 or MUC3 mRNA levels were increased in colloid colon cancer compared with normal colon, however in well- and moderately well-differentiated colon cancers MUC1, 2 and 3 mRNA levels were decreased. Compared with corresponding normal tissue, MUC1 mRNA levels were increased in breast cancer and well-differentiated lung cancers, and MUC3 mRNA was increased in gastric adenocarcinomas. Normal stomach lacked both MUC2 and MUC3 immunoreactivity and mRNA, however, MUC2 and MUC3 proteins and mRNA were highly expressed in gastric intestinal metaplasia. In conclusion, mucin genes are independently regulated and their expression is organ- and cell type-specific. Furthermore, neoplastic transformation is associated with dys-regulated expression of both membrane-bound and secreted mucin core protein epitopes and may be due to altered mucin mRNA levels and/or altered mucin glycosylation.
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PMID:Heterogeneity of mucin gene expression in normal and neoplastic tissues. 767 77

The angiogenesis inhibitor O-(chloroacetyl-carbamoyl)fumagillol (TNP-470) showed antitumor activity in three human cancer xenograft systems. TNP-470 potently inhibited the tumor growth of hormone-independent prostate cancer PC-3 cells and breast cancer MDA-MB-231 cells dose dependently at weekly s.c. doses of 50-200 mg/kg with maximum inhibition of 96 and 88% (tumor growth, 4 and 12% of that in the respective control). In experiments of combination therapy with chemotherapeutic agents, the combination of TNP-470 (100 mg/kg) and cisplatin (5 mg/kg) showed an additive antitumor effect (from treated versus control, 38 and 22% to 5%) against PC-3 carcinoma. 5-Fluorouracil and Adriamycin alone did not significantly inhibit MDA-MB-231 tumor growth (treated versus control, 131 and 64%, respectively). TNP-470 also inhibited tumor growth of WiDr colon cancer; although the inhibition was less marked (treated versus control, 39%) than that observed with the hormone-independent cancers used in this study. In an in vitro study, all the cell lines tested were considerably insensitive to TNP-470 in monolayer cultures (50% inhibitory concentration, approximately 5 micrograms/ml), whereas TNP-470 inhibited the anchorage-independent growth of PC-3 and MDA-MB-231 cells (50% inhibitory concentration, 0.05 and 470 ng/ml, respectively). The inhibitory activity of TNP-470 against anchorage-independent growth correlated well with the in vivo antitumor activity among the cell lines tested. Thus, this inhibitory action may partly contribute to the potent antitumor activity of the angiogenesis inhibitor TNP-470, at least in the case of PC-3 and MDA-MB-231. These results suggest that hormone-independent prostate and breast cancers may be appropriate target diseases for TNP-470 clinical trials.
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PMID:Angiogenesis inhibitor TNP-470 (AGM-1470) potently inhibits the tumor growth of hormone-independent human breast and prostate carcinoma cell lines. 769 35

We examined the human anti-mouse antibody (HAMA) response in 61 cancer patients following a single, diagnostic injection of any one of ten 111In conjugated murine monoclonal antibodies. Between 1 and 22 mg of antibody containing 1-5 mCi 111In was administered. The populations studied included 30 patients with colorectal carcinoma (four different antibodies), 22 with malignant melanoma (four antibodies), and nine with prostate cancer (two antibodies). Forty-one percent of the patients developed HAMA within 14 days. Three patients (5%) developed an IgM response, five patients (8%) developed an IgG response, and 17 patients (28%) developed both IgM and IgG. Only 27% of the patients with colon cancer developed HAMA, compared to 55% of the melanoma patients and 56% of the prostate cancer patients. There were no correlations among injected dose, various clinical parameters, and HAMA response. There were variations in the HAMA response to different monoclonal antibodies, but population samples were too small to infer significance. Most of the HAMA responses had a significant proportion of idiotypic or isotypic specificity. Only 1/6 patients who were HAMA negative after the first infusion developed HAMA following subsequent infusions of the same monoclonal antibody. Our data demonstrate that a significant percent of cancer patients develop HAMA following a single, low-dose injection of a radiolabeled monoclonal antibody for diagnostic purposes. This may have important implications for the future therapeutic use of monoclonal antibodies in such patients.
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PMID:Human anti-mouse antibody response in cancer patients following single low-dose injections of radiolabeled murine monoclonal antibodies. 781 54

Germline mutations in a gene on chromosome 17q known as BRCA1 are responsible for a large proportion of inherited predispositions to breast and ovarian cancer. In 33 families with evidence of linkage to BRCA1, we estimated the risks of breast and ovarian cancer from the occurrence of second cancers in individuals with breast cancer, and examined the risks of other cancers in BRCA1 carriers. 26 contralateral primary breast cancers occurring more than 3 years after a first breast cancer were observed before age 70, giving an estimated cumulative risk of breast cancer in gene carriers of 87% by age 70.23 primary ovarian cancers occurred in women with a previous breast cancer, resulting in an estimated cumulative risk of ovarian cancer of 44% by age 70.87 cancers other than breast or ovarian cancer were observed in individuals with breast or ovarian cancer and their first-degree relatives compared with 69.3 expected, based on national incidence rates. Significant excesses were observed for colon cancer (estimated relative risk [RR] to gene carriers 4.11 [95% CI 2.36-7.15]) and prostate cancer (3.33 [1.78-6.20]). No significant excesses (or deficits) were noted for cancers of other sites. Our study provides estimates of breast and ovarian cancer risks which are useful for counselling BRCA1-mutation carriers. It also shows that carriers are at increased risk of colon and prostate cancer, which may be of clinical significance in certain families if the risks are associated with specific mutations.
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PMID:Risks of cancer in BRCA1-mutation carriers. Breast Cancer Linkage Consortium. 790 78

In a cross-sectional study design, a disease free sample of 57 lung, 117 colon, and 104 prostate cancer survivors who represented short, intermediate and long-term survivors completed a detailed assessment of quality of life (QOL) and rehabilitation needs using the CAncer Rehabilitation Evaluation System (CARES). Demographic and medical data, social support, and a global QOL rating were also assessed. Lung cancer patients showed no differences in QOL with respect to their period of survival. QOL improved for survivors of colon cancer as they lived for longer periods, but declined with time for survivors of prostate cancer. The best predictor of QOL for all groups was KPS, although other variables such as type of hospital, gender, and work status were predictive for survivors of colon cancer. For survivors of prostate cancer comorbidity with other medical illnesses, time since diagnosis and comorbidity due to psychiatric difficulties were predictive of QOL. All groups had significant rehabilitation problems in the domains of physical, psychosocial, sexual, medical interaction, and marital relationships. Lung cancer survivors had more problems than the other cancer survivors. We conclude that patients who survive cancer do not return to a state of normal health. They demonstrate a variety of difficulties with which they must cope as they continue to survive. Greater efforts need to be made early in diagnosis and treatment to understand rehabilitation problems and target interventions in the hope of reducing later sequelae.
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PMID:Quality of life in adult survivors of lung, colon and prostate cancer. 804 58

The relationship between a family history of cancer and the risk of breast cancer was investigated in a study of 495 breast cancer cases and 785 controls aged 20 to 56 years. A positive association was found between the occurrence of breast cancer and a history of breast cancer in families. This relationship increased linearly with both the number of the affected relatives and with the degree of kinship between the affected relative and the case. The highest risk was observed when a sister was affected by breast cancer. This could be explained by longer common environmental exposures between sisters than between mother and daughter. This could also be explained by a genetic factor segregating under a recessive model. The risk of breast cancer associated with colon, uterus, ovary, and prostate cancer in the family was not significantly different from one. However, the estimated odds ratios associated with a family history of colon cancer increased with the degree of kinship between the affected relative and the case in a similar manner to those of breast cancer. A relationship between the risk of breast cancer and a family history of colon cancer would support the existence of a common familial factor (be it genetic or not) for these cancers. Further genetic epidemiological studies might help to define the mode of inheritance of the same susceptibility to cancer at different sites.
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PMID:Familial risk of breast cancer in a French case-control study. 807 78

In order to determine if exposure to carcinogens in fire smoke increases the risk of cancer, we examined the incidence of cancer in a cohort of 2,447 male firefighters in Seattle and Tacoma, (Washington, USA). The study population was followed for 16 years (1974-89) and the incidence of cancer, ascertained using a population-based tumor registry, was compared with local rates and with the incidence among 1,878 policemen from the same cities. The risk of cancer among firefighters was found to be similar to both the police and the general male population for most common sites. An elevated risk of prostate cancer was observed relative to the general population (standardized incidence ratio [SIR] = 1.4, 95 percent confidence interval [CI] = 1.1-1.7) but was less elevated compared with rates in policemen (incidence density ratio [IDR] = 1.1, CI = 0.7-1.8) and was not related to duration of exposure. The risk of colon cancer, although only slightly elevated relative to the general population (SIR = 1.1, CI = 0.7-1.6) and the police (IDR = 1.3, CI = 0.6-3.0), appeared to increase with duration of employment. Although the relationship between firefighting and colon cancer is consistent with some previous studies, it is based on small numbers and may be due to chance. While this study did not find strong evidence for an excess risk of cancer, the presence of carcinogens in the firefighting environment warrants periodic re-evaluation of cancer incidence in this population and the continued use of protective equipment.
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PMID:Cancer incidence among firefighters in Seattle and Tacoma, Washington (United States). 816 59

The association of weight, body mass index and other anthropometric measurements with cancer was investigated in a cohort of 7,840 men, examined and interviewed from 1965-1968 in Hawaii. After 23 years of follow-up, histologically confirmed incident cases of prostate (n = 306), colon (n = 289), lung (n = 236), stomach (n = 229) and rectal (n = 108) cancer were identified. Body weight was positively associated with prostate cancer. This direct association was stronger for cases diagnosed 11 or more years after examination than for those diagnosed earlier. A similar pattern was also present for the risk of colon cancer in association with weight and body mass index. For lung cancer, increased subscapular and triceps skinfold thickness were each associated with decreased risk with adjustment for cigarette smoking, but the inverse association did not persist as the time interval from exam to cancer diagnosis lengthened. There was no significant association between anthropometric measurements and stomach or rectal cancer.
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PMID:A prospective study of weight, body mass index and other anthropometric measurements in relation to site-specific cancers. 816 89

In this review we have examined epidemiological data from a variety of sources to assess the relation between vitamin A intake and cancer risk. The potential for recall bias in case-control studies makes their interpretation difficult, particularly if we are searching for modest associations. Prospective data are preferable, but sparse. Studies of blood levels of carotenoids may be informative if the blood is stored at ultra-low temperatures; however, studies of blood retinol levels are largely uninformative as an index of dietary intake because blood retinol is not well correlated with intake except in vitamin A-deficient populations. We have also reviewed the evidence for an influence of vitamin A intake on the incidence of cancer at the three major cancer sites accounting for a substantial portion of cancers in developed countries. The available data are compatible with a modest inverse association between intake of vitamin A and breast cancer, although it is not clear whether this effect may be due to preformed vitamin A, carotenoids, or both. The evidence that vitamin A protects against colon cancer is unconvincing. In the case of prostate cancer, early suggestions that vitamin A may increase incidence have not been confirmed by subsequent studies. Fortunately, prospective data from a number of large ongoing cohort studies in the United States and Europe should be available within the next 5 years or so. These data will permit further assessment of potential correlations between vitamin A and cancer at various sites by analysis of much larger numbers of cases than are presently available.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamin A and cancers of the breast, large bowel, and prostate: epidemiologic evidence. 820 83


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