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At least 19 recordsLinked to original sources
PubMed2000

Wilms' tumor gene (WT1) expression in lung cancer, colon cancer and glioblastoma cell lines compared to freshly isolated tumor specimens.

The Wilms' tumor gene (WT1) encodes a transcriptional regulator involved in growth and differentiation of various tissue types. A continuous over-expression of WT1 was found in leukemic blasts, thus suggesting an oncogenic function. Solid cancer entities have also been described as expressing WT1. We systematically analyzed WT1 expression in small-cell and non-small-cell lung cancer, colon cancer and glioblastoma patients and in the respective tumor cell lines. Using reverse transcription/polymerase chain reaction, we found WT1 expression in glioblastoma (5 of 8), lung (5 of 11), and colon cancer (5 of 15) cell lines. While WT1 was expressed in only 1 of 12 lung cancer and 1 of 5 glioblastoma specimens, it was not detected in colon cancer or macroscopically tumor-free colon and lung tissue. In addition, HT29 colon cancer cells showed a loss of WT1 expression when grown to confluence or induced to differentiate by sodium butyrate. From this evidence, testing for WT1 expression is not clinically relevant for colon cancer, lung cancer, or glioblastoma patients. WT1 expression in cancer cell lines can probably be attributed to optimized in vitro growth conditions.

Central Nervous System Neoplasms↗
PubMed1999

Microsatellite instability and hMSH2 gene mutation in a triple cancer (colon cancer, endometrial cancer, ovarian cancer) patient in hereditary non-polyposis colorectal cancer (HNPCC) kindred.

A patient who had triple cancer (colon cancer, endometrial cancer, and ovarian cancer) in HNPCC kindred is reported. Her family history revealed the occurrence of colon cancer in her paternal aunt and in two cousins, fulfilling the minimum HNPCC criteria. Microsatellite instability analysis revealed replication error (RER)+ in all cancer lesions at 2 microsatellite loci (D1S191, BAT 40). SSCP analysis suggested germline mutation in exon 2 of the hMSH2 gene. This case showed the importance of complete family-history investigations to identify HNPCC patients. In the near future, definitive diagnosis of HNPCC will be possible on the basis of DNA studies.

Adenocarcinoma↗
PubMed1984

Fecal bile acid excretion in patients with colon cancer, colon polyp and peptic ulcer.

Fecal bile acids were analyzed by gas chromatography in 10 patients with colon cancer, 25 patients with colon polyp and 10 patients with peptic ulcer. On admission total bile acid excretion in patients with colon cancer was significantly higher than in patients with peptic ulcer (P less than 0.01). Also, concentration of cholic acid, chenodeoxycholic acid and primary bile acids in patients with colon cancer were significantly higher than those in patients with peptic ulcer (P less than 0.05, P less than 0.025) and in patients with colon polyp (P less than 0.005). Primary bile acids in patients with colon cancer significantly decreased under ward conditions after admission (P less than 0.05). Total bile acids in patients with colon cancer decreased after admission though there was no significant difference. It is of considerable interest that the fecal bile acid composition of colon cancer patients was different from that of colon polyp and peptic ulcer patients. Fecal bile acids may be involved in the pathogenesis of colon cancer.

Adenoma↗
PubMed2000

The mRNA of L-type calcium channel elevated in colon cancer: protein distribution in normal and cancerous colon.

Previous reports indicate that the mRNA for the cardiac isoform of the voltage-gated L-type calcium channel (alpha(1C)) is elevated in colon cancer. The aim of these experiments was to verify that the mRNA for alpha(1C) was significantly increased in tumors of two separate populations of patients when compared to normal adjacent mucosa. The second aim was to measure the distribution of alpha(1C) using immunocytochemistry in normal human colon and in colon cancer and to determine what might regulate the channel expression. Biopsies were taken from patients with various stages of colon cancer and nearby normal mucosa were used as control. RNA was prepared and mRNA level measured by semiquantitative reverse transcriptase-polymerase chain reaction. The mRNA of the calcium channel was compared with other markers including beta-actin. The mRNA for alpha(1C) was increased significantly in colon cancers compared to nearby adjacent mucosa. Using confocal microscopy alpha(1C) was localized mainly at the apical membrane in the surface epithelium of normal human colon with less distribution on the lateral and basal membranes. The channel was localized on the lateral and basal membranes in crypt cells. Calcium channel localization appeared to be nearer nuclei in colon cancer samples, in part because of the smaller size of the cells. Likewise, cultured Caco-2 and T84 cells showed a membrane distribution. Western blotting indicated that alpha(1C) protein was increased in nonconfluent cultures of colonic carcinoma cells compared to confluent cells and immunocytochemistry confirms that there is more calcium channel protein in cells that are nonconfluent. We conclude that the increase in mRNA of alpha(1) subunit of the cardiac isoform of the L-type calcium channel may be a useful marker of colon cancer compared to other markers because the increase is large and this increase can be documented on small samples using a simple semiquantitative reverse transcriptase-polymerase chain reaction. We found that alpha(1C) protein is increased when colonic cells are nonconfluent or dividing which may account for the increase in cancer.

Blotting, Western↗
PubMed1983

Fibronectin concentration in plasma of patients with breast cancer, colon cancer, and acute leukemia.

Plasma fibronectin was measured in patients with breast cancer, colon cancer, and acute leukemia. In the patients with solid tumors, mean levels were significantly elevated above the mean level of age- and sex-matched normals whether the disease was thought to be metastatic or not (P less than 0.001). It did not make a difference whether the determinations were done prior to or during chemotherapy. Fibronectin was measured serially in eight hospitalized patients with leukemia during intensive induction chemotherapy. Normal concentrations were found prior to therapy. However, fibronectin concentration fell on the day following chemotherapy in nine of 12 episodes (P less than 0.05), and during sepsis in 13 of 13 episodes (P less than 0.001). Thus, the concentration was influenced by at least two factors: recent chemotherapy and sepsis. Because fibronectin concentration is sensitive to clinical events other than the status of the malignancy, it seems unsuitable as a tumor marker, at least as a single isolated measurement.

Adult↗
PubMed2003

Evaluating health utility in patients with melanoma, breast cancer, colon cancer, and lung cancer: a nationwide, population-based assessment.

BACKGROUND: Understanding the quality of life and health utility for cancer survivors is important; however, little data are available-particularly for long-term (>5 year) survivors. Using "health utility" scores as a proxy for quality of life may be advantageous because it is a single value. Utility scores range from 1.0 (perfect health) to 0 (death), and have been shown to be a good numerical summary of overall quality of life. Using a validated instrument for health utility (HALex), we calculated and report the scores of four different surgical cancers at multiple periods of follow-up, ranging from <1 year to >5 years after diagnosis. METHODS: Patients diagnosed with either breast, colon, melanoma, or lung cancer were studied using the 1998 National Health Information Survey. Responses to several validated questions were collected and health utility scores were calculated. Different time periods were measured; acute (<1 year), short term (1-5 years), and long term (>5 years). Once a single health utility score was calculated, multivariate analyses were performed to identify important predictors of better versus worse health utility scores. RESULTS: The total sample size was 692 (breast 377, colon 169, melanoma 92, lung 54). Mean ages at diagnosis for the cancer groups were 56, 61, 52, and 60 years, respectively. The mean health utility scores in the acute period after diagnosis were: breast 0.62, colon 0.67, melanoma 0.73, and lung 0.42. In this acute period, the mean utility score for lung cancer survivors was statistically lower versus the others in the acute period (P < 0.001). Although variable trends were noted in the short-term period, all cancers demonstrated an increase in mean scores in the long-term period; the percent increases were: breast 15% (P = 0.01), colon 12%, melanoma 7%, and lung 47%. Multivariate regression analyses identified important associations of health utility scores. Significant predictors of lower health utility included the presence of pain and the presence of co-existent diseases, most commonly joint problems, cardiovascular disease, and diabetes. CONCLUSIONS: For four surgical cancers in three time periods after diagnosis, health utility scores were lowest immediately after treatment and improved over time. Long-term (>5 year) survivors had the highest scores. Additionally, our analyses show that a part of health utility in this cohort is determined by the presence of pain and co-existent diseases, which are often items that can be improved by quality clinical care.

Aged↗
PubMed1991

The association of oral contraception with kidney cancer, colon cancer, gallbladder cancer (including extrahepatic bile duct cancer) and pituitary tumours.

This paper reviews the evidence for a relationship between oral contraceptive use and certain neoplasms: cancers of the kidney, colon and gallbladder (including the extrahepatic bile ducts) and tumours (benign or malignant) of the pituitary. Special reference is made to controlled epidemiological studies, both case-control and cohort. There is no convincing evidence that oral contraceptive use is causally related, either negatively or positively, to any of the tumours studied.

Bile Duct Neoplasms↗
PubMed2006

A NAD(P)H:quinone oxidoreductase 1 polymorphism is a risk factor for human colon cancer.

Colon cancer is one of the most common cancers in North America and generally develops from colonic epithelial cells following initiation by carcinogens. We have shown that the phase II detoxifying enzyme, NAD(P)H:quinone oxidoreductase 1 (NQO1) contributes to the inhibition of carcinogen-induced colon cancer in rats at both the initiation and postinitiation stages. An inactivating polymorphism at base 609 of the NQO1 gene, (609)C (NQO1 *1) --> (609)T (NQO1 *2), occurs at high frequency in the human population. Thus, we carried out a case-control study to determine if this polymorphism is associated with an increased risk of developing colon cancer. A total of 298 patients with colon cancer and 349 healthy controls matched for age, gender, and ethnic origin were enrolled in the study. There was an increased incidence of the NQO1 *2/*2 genotype in patients with colon cancer, with a gender and age-adjusted odds ratio of 2.68 (95% confidence intervals, 1.14-6.28). However, the incidence of the NQO1 *1/*2 genotype was not increased in patients with colon cancer compared with controls. When the patient and control groups were stratified by tobacco and alcohol use, the incidences of the NQO1 *2/*2 genotype were increased in patients with colon cancer for tobacco and alcohol users and nonusers, suggesting that there is no interaction between the NQO1 base 609 polymorphism and tobacco or alcohol use. These results strongly suggest that NQO1 plays a significant role in preventing the development of colon cancer, and individuals with an NQO1 *2/*2 genotype are at an increased risk of developing this disease.

Adult↗
PubMed2003

Identification of calreticulin as a nuclear matrix protein associated with human colon cancer.

Colon cancer is one of the most common malignancies among populations in the United States and Western Europe, and one of the leading causes of worldwide morbidity and mortality due to cancer. The early detection of colon cancer is central to the effective treatment of this disease and early detection markers are needed. We have demonstrated that high-resolution two-dimensional gel analysis of nuclear matrix proteins (NMPs) demonstrated a specific oncological fingerprint of colon cancer. Utilizing this approach, four proteins specific for colon cancer was identified. Additionally, one protein was expressed much more strongly in colon cancer compared to adjacent and normal donor tissue. The amino acid composition of this protein revealed sequence similarity with calreticulin. The multi-functional protein, calreticulin, is normally found in the lumen of the endoplasmic reticulum although some reports have described a nuclear localization of the protein. The aim of this study was to confirm the identity of the protein as calreticulin as well as to evaluate the localization of calreticulin in the nuclear matrix of colon cancer tissue.

Adenocarcinoma↗
PubMed2005

Epigenetic events in the colorectum and in colon cancer.

Colon cancers arise from benign neoplasms and evolve into adenocarcinomas through a stepwise histological progression sequence, proceeding from either adenomas or hyperplastic polyps/serrated adenomas. Genetic alterations have been associated with specific steps in this polyp-adenocarcinoma sequence and are believed to drive the histological progression of colon cancer. Recently, epigenetic alterations, which include CGI (CpG island) DNA methylation, have been shown to occur in colon polyps and colon cancer. The aberrant methylation of genes appears to co-operate with the genetic alterations to drive the initiation and progression of colon polyps to colon cancer. CGI DNA methylation is an epigenetic mechanism that represses gene transcription in normal cellular processes, but it becomes excessive and aberrant in many neoplasms. The aberrant DNA methylation affects CpG-rich regions, called CGIs, in the 5' region of genes and results in transcriptional silencing through effects on transcription factor binding and associated changes in chromatin structure. These hypermethylated genes are not only probable pathogenic events affecting colon-cancer formation, but also neoplasm-specific molecular events that may be useful as molecular markers for colon tumours. Furthermore, aberrant DNA methylation of tumour-suppressor genes may occur secondary to a genetic predisposition or to a field-cancerization effect in the colon and may be useful as molecular markers for the risk of developing colon cancer.

Colon↗
PubMed1998

Eating patterns and risk of colon cancer.

Colon cancer has been associated with several nutrients and foods. The authors used data from a population-based study conducted in Northern California, Utah, and Minnesota to examine associations between dietary eating patterns and risk of developing colon cancer. Through factor analysis, detailed dietary intake data obtained from 1,993 cases (diagnosed in 1991-1994) and 2,410 controls were grouped into factors that were evaluated for relations with lifestyle characteristics and colon cancer risk. Several dietary patterns emerged. The dietary patterns with the most variation were labeled "Western," "prudent," "high fat/sugar dairy," "substituters," and "drinkers." The "Western" dietary pattern was associated with a higher body mass index and a greater intake of total energy and dietary cholesterol. The "prudent" pattern was associated with higher levels of vigorous leisure time physical activity, smaller body size, and higher intakes of dietary fiber and folate. Persons who had high scores on the "drinker" pattern were also more likely to smoke cigarettes. The "Western" dietary pattern was associated with an increased risk of colon cancer in both men and women. The association was strongest among people diagnosed prior to age 67 years (for men, odds ratio (OR)=1.96, 95% confidence interval (CI) 1.22-3.15; for women, OR=2.02, 95% CI 1.21-3.36) and among men with distal tumors (OR=2.25, 95% CI 1.47-3.46). The "prudent" diet was protective, with the strongest associations being observed among people diagnosed prior to age 67 years (men: OR=0.63, 95% CI 0.43-0.92; women: OR=0.58, 95% CI 0.38-0.87); associations with this dietary pattern were also strong among persons with proximal tumors (men: OR=0.55, 95% CI 0.38-0.80; women: OR=0.64, 95% CI 0.45-0.92). Although "substituters" (people who substituted low fat dairy products for high fat dairy products, margarine for butter, poultry for red meat, and whole grains for refined grains) were at reduced risk of colon cancer, the reduction in risk was not statistically significant. These data support the hypothesis that overall dietary intake pattern is associated with colon cancer, and that the dietary pattern associated with the greatest increase in risk is the one which typifies a Western-style diet.

Adult↗
PubMed2003

Preclinical models for chemoprevention of colon cancer.

Colon cancer is the second leading cause of cancer incidence and death in the USA in 2002. Specific genetic defects have been identified which cause hereditary colon cancers in humans. In addition, a number of intestinal luminal risk factors for colon cancer have been described. This information has been exploited to develop experimental cell and rodent models which recapitulate features of human colon cancer. In this chapter, we will discuss the strengths and limitations of these models to further our understanding of basic mechanisms of colon carcinogenesis and to develop strategies for colon cancer chemoprevention.

Animals↗
PubMed2001

Adjuvant chemotherapy for colon cancer.

Colon cancer remains the third most common cancer, and cause of cancer-related death in the United States. Greater public awareness and acceptance of screening programs have contributed significantly to increasingly earlier detection of colon cancer and decreased mortality. Advances made in the understanding of this disease, both in terms of its clinical behavior and molecular pathogenesis, have translated into major improvements in its therapy. Several large randomized trials during the last two decades have helped the oncology community forge a successful multi-modality treatment strategy against colon cancer. These studies have defined the role of adjuvant therapy for colon cancer after curative surgery. Despite all the advances, a large number of patients continue to succumb to this disease, and the search for better therapies is still necessary. In this article, we discuss the evolution and the current state of adjuvant chemotherapy in colon cancer and briefly review new developments.

Antimetabolites, Antineoplastic↗
PubMed1998

Loss of heterozygosity in the region including the BRCA1 gene on 17q in colon cancer.

Colon cancer has been proved to be an excellent model to identify and to study the different genetic alterations taking part in its development. BRCA1, a susceptibility gene for breast cancer, has been identified. Evidence of a significant risk for colon cancer in BRCA1-linked families has been reported. We undertook the present study to investigate the possible relation of BRCA1 and other genes on chromosome 17q21 to colon cancer. Eighty-five tumors were examined for loss of heterozygosity at seven microsatellite loci spanning the 17q21 region. Loss of heterozygosity was present in 39 (49%) of the 79 informative cases, with at least one marker. Two loci, D17S855 and D17S579, showed higher rates of allelic loss (16% and 22%, respectively) than the remaining markers. Tumors on the right side of the colon exhibited allelic loss more frequently than those on the left side. Our data suggest that BRCA1 and other genes in the 17q21 region may play an important role in the development of colon cancer.

Base Sequence↗
PubMed2006

Genetic testing for colon cancer.

Colon cancer remains the third leading cause of death due to cancer in the US, where it affected more than 145,000 individuals in 2005. Up to 30% of these cases exhibit familial clustering, which means that tens of thousands of individuals have a disease with a potentially definable genetic component. Approximately 3-5% of colon cancers are associated with high-risk, inherited colon cancer syndromes. Identification of the genes that cause these colon cancer syndromes, coupled with additional insights into their clinical course, has led to the development of specific management guidelines--and genetic tests--that can diagnose these familial disorders. These guidelines can be life-saving, not only for the affected patient, but also for their family members.

Adenomatous Polyposis Coli↗
PubMed2000

Selenium from high selenium broccoli protects rats from colon cancer.

Colon cancer is the third most common newly diagnosed cancer in the United States and the third most common cause of cancer-related deaths. Previous supplementation studies have demonstrated the efficacy of selenium (Se) for prevention of colon cancer in humans. The metabolism of Se depends on its chemical form, and studies have shown that the chemical form of Se in broccoli does not accumulate in the body as fast as other forms of Se and may be especially beneficial for prevention of cancer. In the first experiment of the present study, Fisher F-344 rats (n = 45) were allotted randomly to torula yeast-based diets supplemented with the following: 1) no Se; 2) 0.1 microg Se/g diet as selenate; 3) 1.0 microg Se/g diet as selenate; 4) 0.1 microg Se/g diet as selenized broccoli (Se concentration of approximately 500 microg/g); or 5) 1.0 microg Se/g diet as selenized broccoli. In Experiment 2, rats (n = 80) were allotted randomly to the same basal diet supplemented with the following: 1) no added Se; 2) 2.0 microg Se/g diet as selenite; 3) 2. 0 microg Se/g diet as selenite + low Se broccoli; and 4) 2.0 microg Se/g diet as selenized broccoli. Rats were fed the diets for 2 wk and injected with a chemical carcinogen (3,2 dimethyl 4-amino biphenyl or dimethyl-hydrazine in Experiment 1 or dimethyl hydrazine in Experiment 2; 2 rats/treatment were used as vehicle controls). Supranutritional amounts of Se supplied as high Se broccoli significantly decreased (P: < 0.05) the incidence of aberrant crypts (AC) and aberrant crypt foci (ACF; preneoplastic lesions indicative of colon cancer) compared with other dietary treatments. Diets were controlled for the presence or absence of broccoli and for the total amount of Se. The reduction in AC and ACF was a function of Se in high Se broccoli and not a result of broccoli alone or Se alone. Adequate dietary Se supplied as high Se broccoli did not accumulate in tissues or increase glutathione peroxidase activity as well as other forms and amounts of Se. Thus, Se from high Se broccoli may be metabolized in a manner that diverts much of the Se into a pool that provides protection against colon cancer.

Analysis of Variance↗
PubMed2005

Adjuvant treatment strategies for early colon cancer.

Colon cancer remains a major cause of death; however, in the last 3 years a number of trials have been published that have led to changes in the treatment of patients with this disease. Initially, the adjuvant treatment of patients following curative resection was based on their Dukes staging; this is now being refined by consideration of other pathological factors, as well as the investigation of newer prognostic markers such as p53, Ki67 and a number of genes on chromosome 18. Tumours generally develop from the progressive accumulation of genetic events, although some develop through mutation or inactivation of DNA mismatch repair proteins leading to microsatellite instability; this is particularly important in Lynch's syndrome. The loss of gene expression can occur by deletion or mutation of genes or by aberrant methylation of CpG islands. In patients with Dukes C colon cancer the standard of care for adjuvant chemotherapy was previously based on bolus fluorouracil (5-fluorouracil) and folinic acid (leucovorin) administered 5 days per month or weekly for 6 months. Recent studies with a combination of infusional fluorouracil, folinic acid and oxaliplatin have been found to be superior. A further study replacing fluorouracil with oral capecitabine has also demonstrated equivalent disease-free survival. Although some debate remains regarding the benefit of adjuvant treatment for patients with Dukes B colon cancer, the emerging consensus is that, for those patients who are younger and have high-risk features, chemotherapy should be discussed. A number of large vaccine trials have also been conducted in the adjuvant setting and, overall, these have been disappointing. This is a rapidly advancing area of therapy and the results of new trials are awaited to determine whether additional benefits can be achieved with biological therapies such as anti-vascular endothelial growth factor and anti-epithelial growth factor receptor monoclonal antibodies, which have already been shown to be effective in setting of metastatic colon cancer.

Chemotherapy, Adjuvant↗