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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Life-long bowel habits of 685 colorectal cancer cases and 723 age/sex frequency matched community controls were investigated as one part of a large, comprehensive, population-based study of colorectal cancer incidence, etiology, and survival, The Melbourne Colorectal Cancer Study. Self-reported chronic constipation was statistically significantly more common in cases than in controls (P = .05). Three or more bowel actions per day were reported by more cases than controls but the total number of respondents in this subset consisted of only ten cases and two controls. Otherwise, the frequency and consistency of bowel motions was similarly distributed among cases and controls. Constipation disappeared as a significant risk when simultaneously adjusted for previously determined dietary risk factors, indicating that it is the diet and not the constipation that is associated with the risk of large-bowel cancer. Additionally, a highly statistically significant association (P = .02) was found with the risk of colorectal cancer in those who reported constipation and also had a high fat intake, a finding consistent with current hypotheses of colorectal carcinogenesis. It is concluded that chronic constipation, diarrhea, and the frequency and consistency of bowel motions, as well as laxative use, are unlikely to be etiologic factors in the development of colorectal cancer. Self-reported chronic constipation is a marginally significant indicator of excess risk of large-bowel cancer and may be used as one of the indices in the screening of individuals for this cancer.
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PMID:The role of chronic constipation, diarrhea, and laxative use in the etiology of large-bowel cancer. Data from the Melbourne Colorectal Cancer Study. 339 Oct 59

Recent advances in molecular biology have revealed that the alteration of multiple genes, eg., APC, K-ras, p53, DCC, are involved in multistep colorectal carcinogenesis. Some of these alterations can be used as molecular markers in genetic diagnosis. Genetic diagnoses for colorectal cancer are classified into three categories, eg., 1. identification of the career in the family of patient with hereditary disease such as FPC (Familial Polyposis Coli) or HNPCC (Hereditary Non-Polyposis Colorectal Cancer), 2. early diagnosis of colorectal cancer by identifying gene mutations in the stool, 3. assist for histopathological diagnosis, or risk assessment of the metastasis, recurrence or secondary cancer by molecular means. However, there are several problems in these genetic diagnoses. These consist of two categories, eg., 1. problems in the method of gene analyses or assay system and 2. problems in performing genetic diagnoses itself. The former includes the problem of contamination of different tissue, false positive or negative result in PCR-based analyses, heterogeneity of gene mutation in tumor tissue, and the latter includes the social, ethical or economical problems mainly related to the genetic diagnosis for hereditary colorectal cancers. In this paper, we describe the possibility of genetic diagnosis for colorectal cancers and the current problems, especially from the molecular pathological aspect, in genetic diagnosis.
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PMID:[Molecular-pathological problems of genetic diagnosis for colorectal cancer]. 910 43

We determined the levels of 15 elements in drinking water from 34 water treatment plants in Aomori Prefecture and studied how element levels relate to colorectal cancer incidence by district. Colorectal cancer incidence was calculated from the data of Aomori Colorectal Cancer Registry. Multiple regression analysis was performed by using age-adjusted incidences of rectal cancer and colon cancer by gender as object variables and each element level as an explanatory variable. The standardized partial regression coefficient was significant in gold (p < 0.01), magnesium (p < 0.01), selenium (p < 0.01) and tin (p < 0.05) for age-adjusted rectal cancer incidence in men as objective variable; in gold (p < 0.05), calcium (p < 0.01) and phosphorus (p < 0.01) with age-adjusted colon cancer incidence in men as the objective variable; and in sodium (p < 0.05), phosphorus (p < 0.05), tin (p < 0.05) and strontium (p < 0.01) with age-adjusted colon cancer incidence in women as the objective variable. These results confirm the need to further study trace elements in drinking water and food, and relationship to colorectal carcinogenesis.
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PMID:Trace element levels in drinking water and the incidence of colorectal cancer. 1058 13

Functional Food Ingredients Against Colorectal Cancer is one of the first European Union funded Research Projects at the cross-road of functional genomics [comprising transcriptomics, the measurement of the expression of all messengers RNA (mRNAs) and proteomics, the measurement of expression/state of all proteins], nutrition and human health. The goal of Functional Food Ingredients Against Colorectal Cancer is to develop a colon epithelial cell line-based screening assay for nutrients with presumed anti-colorectal carcinogenic properties. Genes involved in colon carcinogenesis are identified at the RNA and protein level, using a variety of methods (subtractive hybridisation, DNA microarray, proteomics) in combination with models for colorectal cancer development (human biopsies, rat model for colorectal carcinogenesis, colorectal cancer epithelial cell lines). Secondly, colorectal cancer epithelial cell lines are selected, in terms of their capacity to undergo gene/protein expression changes representing different phases in the colorectal carcinogenesis. Thirdly, these cell lines are used to determine the effects of nutrients with presumed anti-carcinogenic properties (e.g. resveratrol, flavonoids) on functional genomics-derived endpoints. Once validated against the effects of these nutrients in in vivo animal models and classical biomarkers for colorectal carcinogenesis, these cell line models combined with functional genomics represent useful tools to study colorectal carcinogenesis and screen for nutrients with anti-carcinogenic properties.
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PMID:Functional food ingredients against colorectal cancer. An example project integrating functional genomics, nutrition and health. 1189 63

The majority of modern hormone replacement therapy (HRT) regimens contain estrogen and progestogens, given either in a cyclical or continuous manner. About 15% of the endometrial biopsies taken from women on sequential HRT show proliferative activity including atypical endometrial hyperplasia in up to 1% of the cases. The majority of biopsies from women under continuous combined HRT show an endometrial atrophy. About 2-3% of these women will present proliferative activity, usually without atypical hyperplasia. Contrary to breast cancer, an increased risk of endometrial cancer has not been reported in the WHI- and HERS-studies. However, endogenous factors, such as obesity, diabetes mellitus, the distribution of estrogen receptors alpha and beta and genetic polymorphisms for receptors and enzymes might alter the endometrial stimulation under different types of HRT. There should be a liberal indication for endometrial biopsies in Hereditary Non-Polyposis Colorectal Cancer (HNPCC). HNPCC-patients under HRT as well as for ultrasonographic evaluation of the endometrium. The risk of atypical hyperplasias or carcinoma under unopposed estrogen-therapy varies from 2 to 10%. So, this kind of HRT should not be used in non-hysterectomised women. As far as the risk of endometrial cancer under any kind of HRT is concerned, the different molecular pathways of endometrial carcinogenesis (type 1 and 2 cancers) should be taken into account. The use of tibolone leaves the endometrium unaffected.
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PMID:Hormone replacement therapy (HRT) and endometrial morphology under consideration of the different molecular pathways in endometrial carcinogenesis. 1592 47

Colorectal cancer (CRC) is one of the 3 most common types of cancer in women, but CRC during pregnancy is rare, with a reported incidence of approximately 0.002%. Synchronous colon cancer during pregnancy presents a diagnostic and therapeutic challenge for clinicians because there are no generally accepted guidelines regarding diagnosis or treatment. The diagnosis is challenging because the presenting signs/symptoms of CRC are often attributed to the usual complications of pregnancy, which could delay the diagnosis and allow the cancer to progress to an advanced stage. Carcinogenesis of colon cancer in pregnancy is not clear, but a few studies suggest that the increased levels of estrogen and progesterone related to pregnancy stimulate the growth of CRC with their receptors. The aim of treatment is to start therapy for the mother as early as possible and to simultaneously deliver the baby at the earliest time allowable. The management mandates a multidisciplinary approach involving experts in obstetrics, neonatology, gastrointestinal surgery, and medical oncology. The medical community should be able to diagnose colon cancer earlier in pregnancy in order to improve prognosis. The primary care physician or obstetrician should refer the pregnant patient with significant gastrointestinal symptoms to the gastroenterologist for evaluation. Likewise, the gastroenterologist should be prepared to perform sigmoidoscopy (preferably without endoscopic medications) for significant lower gastrointestinal symptoms such as persistent rectal bleeding. Herein, the author reviews the literature concerning the diagnosis and treatment of CRC in pregnancy and discusses the role of newer agents approved for the treatment of CRC.
Clin Colorectal Cancer 2005 Nov
PMID:Management of colorectal cancer in pregnancy: a multimodality approach. 1637 42

Cyclooxygenase (COX)-2 enzyme catalyzes the rate-limiting step of prostaglandin formation in pathogenic states, and overexpression of COX-2 occurs at multiple stages of colon carcinogenesis, allowing elevated prostaglandin synthesis to occur in the tumor microenvironment. In normal cells, COX-2 expression levels are potently regulated at the posttranscriptional level through various RNA sequence elements present within the mRNA 3' untranslated region (3'UTR). A conserved AU-rich element functions to target COX-2 mRNA for rapid decay and translational inhibition through association with various RNA-binding proteins to influence the fate of COX-2 mRNA. The 3'UTR contains alternative polyadenylation signals that result in a shortened 3'UTR and loss of regulatory elements. Specific microRNAs have been identified to bind regions within the COX-2 3'UTR and control COX-2 expression. Recent evidence demonstrates the functional significance of the COX-2 3'UTR and how improper recognition of the 3'UTR can contribute to COX-2 overexpression in colorectal cancer.
Curr Colorectal Cancer Rep 2010 Apr
PMID:Posttranscriptional Regulation of Cyclooxygenase 2 Expression in Colorectal Cancer. 2057 75

Although progress in the treatment of patients with colorectal cancer (CRC) has resulted in improved median survival, most patients with metastatic CRC still die of their disease, and essentially all patients with early-stage disease must undergo surgical resection and subsequently face the possibility of adjuvant chemotherapy. As effective screening and prevention strategies for CRC have been developed, identification of individuals with a hereditary predisposition to developing CRC is especially important and provides the opportunity to reduce disease burden in this high-risk population. Increased awareness and improved diagnostic techniques for hereditary CRC syndromes have facilitated more frequent diagnosis and management of a small number of highly penetrant syndromes within families. However, known high-penetrance genetic predisposition syndromes account for a minority of all familial CRC, leaving much of the genetic basis of CRC unexplained. Recent advances in high-throughput genotyping have made possible genome-wide association studies, which have identified novel genetic variants associated with modest increases in CRC risk. While these associations have helped to identify potentially important pathways in CRC carcinogenesis, at the current time, the clinical use of such genetic risk variants in colon cancer risk stratification remains limited.
Clin Colorectal Cancer 2010 Oct
PMID:Diagnosing hereditary colorectal cancer. 2092 Sep 89

The calcium-sensing receptor (CaSR) is expressed abundantly in normal colonic epithelium and lost in colon cancer, but its exact role on a molecular level and within the carcinogenesis pathway is yet to be described. Epidemiologic studies show that inadequate dietary calcium predisposes to colon cancer; this may be due to the ability of calcium to bind and upregulate the CaSR. Loss of CaSR expression does not seem to be an early event in carcinogenesis; indeed it is associated with late stage, poorly differentiated, chemo-resistant tumors. Induction of CaSR expression in neoplastic colonocytes arrests tumor progression and deems tumors more sensitive to chemotherapy; hence CaSR may be an important target in colon cancer treatment. The CaSR has a complex role in colon cancer; however, more investigation is required on a molecular level to clarify its exact function in carcinogenesis. This review describes the mechanisms by which the CaSR is currently implicated in colon cancer and identifies areas where further study is needed.
Clin Colorectal Cancer 2012 Mar
PMID:Review article: loss of the calcium-sensing receptor in colonic epithelium is a key event in the pathogenesis of colon cancer. 2172 93

Colorectal cancer (CRC) is a leading cause of cancer death worldwide. Epidemiological risk factors for CRC included dietary fat intake; consequently, the role of genes in the fatty acid biosynthesis and metabolism pathways is of particular interest. Moreover, hyperlipidaemia has been associated with different type of cancer and serum lipid levels could be affected by genetic factors, including polymorphisms in the lipid metabolism pathway. The aim of this study is to assess the association between single-nucleotide polymorphisms (SNPs) in fatty acid metabolism genes, serum lipid levels, body mass index (BMI) and dietary fat intake and CRC risk; 30 SNPs from 8 candidate genes included in fatty acid biosynthesis and metabolism pathways were genotyped in 1780 CRC cases and 1864 matched controls from the Molecular Epidemiology of Colorectal Cancer study. Information on clinicopathological characteristics, lifestyle and dietary habits were also obtained. Logistic regression and association analysis were conducted. Several LIPC (lipase, hepatic) polymorphisms were found to be associated with CRC risk, although no particular haplotype was related to CRC. The SNP rs12299484 showed an association with CRC risk after Bonferroni correction. We replicate the association between the T allele of the LIPC SNP rs1800588 and higher serum high-density lipoprotein levels. Weak associations between selected polymorphism in the LIPC and PPARG genes and BMI were observed. A path analysis based on structural equation modelling showed a direct effect of LIPC gene polymorphisms on colorectal carcinogenesis as well as an indirect effect mediated through serum lipid levels. Genetic polymorphisms in the hepatic lipase gene have a potential role in colorectal carcinogenesis, perhaps though the regulation of serum lipid levels.
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PMID:Genetic polymorphisms in fatty acid metabolism genes and colorectal cancer. 2229 64


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