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)

The p53 gene has been implicated as a tumor suppressor gene involved in the pathogenesis of lung cancer. Our previous study revealed that the p53 gene is frequently mutated with a distinct nucleotide substitution pattern in small cell lung cancer specimens in Japanese patients. In this study, we examined 30 primary, resected non-small cell lung cancer samples in Japanese patients using complementary DNA-polymerase chain reaction and sequencing. Mutations changing the p53 coding sequence were found in 14 of 30 tumor samples (47%), while G:C to T:A transversions which are uncommon in other cancers such as colon cancer were the most frequently observed mutations, in agreement with an earlier report on non-small cell lung cancer in American patients. Furthermore, the present study shows for the first time that in univariate and multivariate analyses, the presence of p53 mutations is closely associated with lifetime cigarette consumption.
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PMID:p53 mutations in non-small cell lung cancer in Japan: association between mutations and smoking. 131 70

The three ras genes code for proteins with a putative role in cellular signal transduction. They belong to a larger family of small guanosine-triphosphate (GTP)-binding proteins. The ras proteins acquire transforming activity when amino acids are substituted at one of a few specific sites, as a result of a point mutation in the gene. In about one third of adenocarcinomas of the lung, a K-ras mutation is present in codon 12 of the gene. Patients with early stages of K-ras mutation-positive tumors have a very unfavorable prognosis, even if apparently radical resection of the tumor has taken place. K-ras mutations are very rare among nonsmokers, and it is reasonable to assume that carcinogens in tobacco smoke directly cause the mutation. The types of ras mutations found in lung cancer are different from those in gastrointestinal malignancies. Colon cancer is mainly associated with mutations leading to substitution of the normal glycine at amino acid position 12 of K-ras by either valine or aspartic acid, and mutations in N-ras are not exceptional. In contrast, the predominant mutation in lung cancer leads to substitution of cysteine in codon 12. Several other members of the ras gene superfamily are also expressed in human lung cancer, but a possible relationship with lung tumorigenesis remains to be established.
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PMID:The ras gene family in human non-small-cell lung cancer. 132 34

Solitary cerebellar metastatic tumors are rarely reported in the literature. We reviewed 240 posterior fossa tumors treated in the past eight years. There were 11 cases of solitary metastases in the cerebellum. The primary tumor was lung cancer in five cases and breast carcinoma in two cases; the remaining three cases had colon cancer, nasopharyngeal carcinoma (NPC) and Ewing's sarcoma, respectively. All patients underwent craniectomy and gross total excision of the tumor. Seven patients survived less than one year, two cases died in the second year, and one case of NPC survived for more than two years. The only survival is a case of Ewing's sarcoma who underwent surgery 14 months ago. The symptoms and signs of all patients improved satisfactorily after surgery. Four patients received postoperative irradiation to the posterior fossa and two cases of lung cancer had a thoracotomy for the primary lung lesion; however, the survival period was not prolonged. We suggest that a cancer patient or a patient in the fifth to seventh decades of life presenting headache, gait disturbance and vomiting should promptly undergo a computed tomography (CT) scan of the head. In selected cases, surgical intervention for solitary metastatic tumors in the tiny posterior fossa may be the best initial treatment. Adjuvant therapies should then be added according to the type of tumor.
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PMID:Solitary cerebellar metastases: analysis of 11 cases. 136 66

Malignant neoplasms are responsible for more than half a million deaths annually and 22.5% of all deaths in the United States. Cancer is the second leading cause of death overall and the leading cause of death among Americans aged 35-64. Within the next decade it may become the leading cause of death. Cancers of digestive and respiratory organs are responsible for 53% of all cancer deaths. Certain subgroups are at elevated risk for various cancers. For example, sun-sensitive or excessively sun-exposed young white adults, young black women, and elderly patients are at increased risk for cutaneous melanoma, breast cancer, and colon cancer, respectively. Black men have the greatest risk for both lung cancer and cancer of the prostate. Acute lymphoblastic leukemia and solid tumors of the brain and nervous system are the most frequent forms of malignancy occurring among children less than or equal to 14 years. Office screening is the traditional method for identifying cancer victims as early as possible. A suitable screening test should be rapid, simple, inexpensive, and impose minimal discomfort. There must be a window of opportunity available to identify the cancer during a detectable preclinical phase, and therapeutic modalities must be available to alter progression. An office screening test for cancer may have any one of four outcomes, and three of them are bad. False negatives are the worst adverse outcome because cancer remains undetected despite screening. An epidemic of lung cancer, caused by cigarette smoking, is occurring in all race and sex groups. If Americans stopped smoking, 87% of lung cancer deaths could be prevented. Tobacco abuse also is a major risk factor for cancer of the esophagus, larynx, and oral cavity. Cigarette smoking is a contributing factor for cancer of the bladder, kidney, and pancreas, and it has been associated with both cervical cancer and cancer of the stomach. Smoking and smokeless tobacco cessation endorsements, messages, and programs must be part of routine disease prevention and health promotion activities in every primary care practice. More than 1 million Americans became new cancer victims last year, and more than 1 million additional cases will be detected this year. Because of the striking variability in state and regional patterns of various forms of cancer, geographic location of a practice may influence the frequency of cancers seen. Four sites (breast, prostate, lung, colon, and rectum) were responsible for 55% of cancer mortality and 56% of all new cases of cancer detected during 1991.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiology of cancer in the United States. 141 56

A cohort of 11,580 residents of a retirement community initially free from cancer were followed from 1981 to 1989. A total of 1,335 incident cancer cases were diagnosed during the period. Relative risks of cancer were calculated for baseline consumption of vegetables, fruits, beta-carotene, dietary vitamin C, and vitamin supplements. After adjustment for age and smoking, no evidence of a protective effect was found for any of the dietary variables in men. However, an inverse association was observed between vitamin C supplement use and bladder cancer risk. In women, reduced cancer risks of all sites combined and of the colon were noted for combined intake of all vegetables and fruits, fruit intake alone, and dietary vitamin C. Supplemental use of vitamins A and C showed a protective effect on colon cancer risk in women. There was some suggestion that beta-carotene intake and supplemental use of vitamin A, C, and E were associated with reduced risk of lung cancer in women, but none of these results were statistically significant. These inverse associations observed in women seem to warrant further investigation, although there was inconsistency in results between the sexes.
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PMID:Intake of vegetables, fruits, beta-carotene, vitamin C and vitamin supplements and cancer incidence among the elderly: a prospective study. 141 5

Over the past 40 years, the American Cancer Society has led in large-scale, prospective studies of behavioral and environmental risk factors in association with cancer development. Through results of its 1952 study, cigarette smokers were found to have a 10-fold higher risk of lung cancer than nonsmokers. Cancer Prevention Study I (1959-1972) extended these results and also showed the relationship between age smoking began, depth of inhalation, smoking cessation, air pollution, body weight, etc., on all causes of death as well as specific cancer sites. Cancer Prevention Study II began in 1982 and after six years of follow-up has confirmed many earlier findings, and additionally has found: aspirin may be protective against colon cancer; persons reporting themselves to be heavy exercisers had higher standardized mortality ratios (SMR) for lung, colorectal, and pancreas cancer than moderate exercisers; more women who were long-term users of artificial sweeteners reported gaining weight during the past year than nonusers; diesel fume exposure elevated the risk of lung cancer among men ages 40-79; pesticide exposure was associated with an increased risk of multiple myeloma; and based on CPS II mortality rates, an estimated 250 million of the 1.25 billion persons living in developed countries will die because they smoke.
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PMID:Cancer Prevention Study II. The American Cancer Society Prospective Study. 147 48

TNF, a cytokine produced by macrophages, is able either to exert an antitumor activity, or to determine severe clinical complications, such as cachexia and septic shock. Increased blood levels of TNF have been described in cancer patients. The present study was performed to better define TNF secretion in patients with solid tumors. The study included 48 cancer patients (lung cancer: 22; colon cancer: 11; breast cancer: 10; renal cancer: 5), and among them 27 showed distant organ metastases. TNF serum levels were measured by IRMA method. The control group comprised 40 healthy subjects. TNF levels were also evaluated in relation to those of SIL-2R, whose increase seems to be associated with an unfavorable prognosis in cancer. High levels of TNF were seen in 27/48 (56%) patients. Mean levels of TNF were significantly higher in cancer patients than in controls. Moreover, within the cancer group, TNF mean values were significantly higher in metastatic patients than in those without metastases; the highest levels were observed in patients with visceral lesions as dominant metastasis sites. Finally, patients with high TNF concentrations showed significantly higher mean levels of SIL-2R than those with normal values. This study shows that the neoplastic metastatic disease is associated with an exaggerated TNF secretion.
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PMID:Tumor necrosis factor in solid tumors: increased blood levels in the metastatic disease. 149 96

An enzyme-linked immunosorbent assay method for serodiagnosis of cancers was developed by employing histone H2B. This method measures anti-histone H2B antibody levels in sera and includes a device for coating the plastic immunoplate with a mixture of histone H2B and diluted fetal calf serum. The coating of immunoplates with this mixture decreased apparent sensitivity of the assay compared with that in the absence of fetal calf serum, but effective reduction of nonspecific background enabled a specific assay of anti-histone H2B antibody with excellent reproducibility. By this method cancer patients were discriminated from normal healthy subjects at detection rates of 37% for lung cancer, 33% for liver cancer, 50% for pancreatic cancer, 42% for colon cancer, and 78% for cervical cancer. However, stomach and esophagus cancers showed detection rates of less than 17%, which are comparable to the values for benign diseases. It is likely that this assay method detects squamous cell carcinomas at relatively high rates.
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PMID:Serodiagnosis of cancers by ELISA of anti-histone H2B antibody. 154 47

This phase I study investigated flavone acetic acid (FAA) given as a 12-h intravenous infusion every 3 weeks in the absence of urinary alkalinisation. Cohorts of three patients were treated at doses of 7, 10 and 13 g/m2. One subject had colon cancer; 5, renal cancer; and 3, lung cancer. The Eastern Cooperative Oncology Group (ECOG) performance status was 0 in four patients, 1 in two subjects and 2 in three cases. The maximum tolerated dose was 13 g/m2. The dose-limiting toxicities were WHO grade 3 hypotension and grade 3 diarrhoea. Other toxicities included lethargy and dizziness, nausea, temperature fluctuation, myalgia and dry mouth, but no significant myelosuppression was encountered. One patient receiving 10 g/m2 for renal cancer showed a partial response that lasted for 3 months and included the resolution of pulmonary and cutaneous metastases. The pharmacokinetics showed large interpatient variability. At 12-16 h post-infusion, the plasma elimination profile entered a plateau phase, with frequent increases in concentration suggesting enterohepatic recycling. Neither peak FAA levels nor AUC values were dose-dependent at the doses studied. Peak plasma levels were 101-402 micrograms/ml and AUC (0-48 h) values were 75-470 mg ml-1 min. Plasma protein binding varied with total concentration. Two metabolites were detected in the plasma, and both also underwent apparent enterohepatic recycling. Repeat dosing resulted in decreases of up to 48% in peak levels and AUC values for FAA in three of six patients. Of the total FAA dose, 39%-77% was excreted in the urine as FAA or metabolites within 2 days. The dose recommended for further phase II studies is 10 g/m2.
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PMID:A phase I and pharmacokinetic study of 12-h infusion of flavone acetic acid. 155 Nov 73

Plantwide analyses of the mortality experience of 8147 foundrymen revealed excesses for several diseases including lung cancer. Using indirect measures of smoking, it appeared that most, if not all, of the excess of lung cancer deaths could be explained by smoking habits. To explore further the possible association between these mortality excesses and foundry exposures, jobs were grouped into six work areas on the basis of similarities in production processes. The findings of analyses by work areas support the inferences from plantwide observations. No evidence was found of a relationship between lung cancer and foundry exposures. The pattern of mortality from emphysema and cerebrovascular disease in the different work areas paralleled that of lung cancer, suggesting that mortality from these diseases may have been influenced by a common etiologic agent, probably tobacco smoke. The data also reveal possible associations between metal pattern-making and colon cancer, silica or metal dust and stomach cancer, and carbon monoxide and ischemic heart disease.
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PMID:Mortality of iron foundry workers. II. Analysis by work area. 801 21


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