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PubMed2002

Considering virtual colonoscopy.

Virtual colonoscopy continues to show promise as a colorectal cancer screening test and is technically evolving rapidly. It has particular advantages with regard to acceptability by both radiologists and patients. Important steps to achieve implementation include clear delineation of all of the technical components necessary to produce consistent high performance and development of clear-cut recommendations for interpretation and management of polyps of various sizes and the range of extracolonic findings identified. Development of an effective methodology to perform the test without bowel preparation or demonstration of cost-effectiveness for identification and treatment of one or more significant extracolonic diseases would be major breakthroughs, provided they are still accompanied by effective detection of significant colon neoplasms. Issues regarding general effectiveness and cost-effectiveness must be resolved before virtual colonoscopy is endorsed for widespread colorectal cancer screening or utilized for that purpose.

Colonic Polyps↗
PubMed1998

Risk of colon cancer associated with a family history of cancer or colorectal polyps: the diet, activity, and reproduction in colon cancer study.

The Diet, Activity, and Reproduction in Colon Cancer (DARCC) study is a large, multi-center case-control study of colon cancer. We examined family histories of cancer among first-degree relatives obtained by computer-assisted in-person interviews from the DARCC to study the impact of family histories of several cancers and colorectal polyps on colon cancer risk. We examined familial cancer risks both by treating a family history of polyps or cancer as a covariate in a logistic regression model, and by comparing cancer or polyp incidence among relatives of cases to incidence among relatives of controls in a proportional hazards model. There were few differences between the odds ratios (OR) or confidence intervals (CI) generated from logistic regression models and the hazard rate ratios (HRR) generated from the proportional hazards models. Overall, the OR of colon cancer among subjects with a family history of colorectal cancer was 1.77. There were only minor differences in risk by sex, age and subsite. A family history of colorectal polyps also increased risk by about the same amount as a family history of colorectal cancer. The increased risk associated with a family history of polyps did not appear to decrease with age.

Adult↗
PubMed1984

Detection of in vitro tetraploidy in heritable colon cancer syndromes. Confirmation by three different assays.

The incidence of in vitro tetraploidy during logarithmic growth in dermal fibroblast monolayer cultures from normals without a family cancer history and affected with heritable colon cancer syndromes, familial polyposis coli (FPC) and the Gardner syndrome (GS) was assayed by (1) examination of metaphase preparations for percentage of tetraploids (4N nuclei); (2) determination of [3H]thymidine incorporation (average cpm/cell); and (3) measurement by flow cytophotometry of the percentage of cells with greater than 4C DNA content. For each monolayer culture assayed, if cell density was standardized, concurrence was observed between the first two assays and with the third assay when done. In cultures of individuals with a low level of in vitro tetraploidy (37 normals without a family cancer history, 9 FPC, and 1 GS patient) incidence of this parameter, as measured by all three assays, was not significantly influenced by variation in cell density. However, in cultures with increased in vitro tetraploidy (17 FPC and 6 GS patients) all three assays revealed an inverse relationship between the incidence of tetraploidy and cell density, i.e., tetraploidy increased with decreasing cell density. Only at cell densities below 4.0 X 10(3) cells/cm2 growth area was increased tetraploidy consistently observed by any of the three assays. Above this density its incidence was indistinguishable in all cultures. The use of these three independent assays (two of which are automated) for the determination of tetraploidy in duplicate subcultures from the same dermal monolayer culture should allow reliable detection of this in vitro expression of some cancer-related genes in extensive human kindreds.

Cells, Cultured↗
PubMed1987

Alterations in DNA methylation in human colon neoplasia.

A review of studies on DNA methylation in colonic neoplasia is presented. Hypomethylation of a wide variety of genes from throughout the genome was seen in all colon cancers studied. These changes preceded malignancy because benign adenomas were also affected.

Adenocarcinoma↗
PubMed1997

Aspirin and gastrointestinal cancer.

In rodents, nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin inhibit chemically induced adenomas and early carcinomas of the colon. The NSAID Sulindac inhibits the growth of polyps of the colon and rectum in two randomized trials of patients with familial adenomatous polyposis (FAP), although the inhibition is not complete. Eight epidemiologic studies have found a 40-50% reduction in polyps or colorectal cancer among persons who regularly use aspirin or other NSAIDs compared to those who do not. Two epidemiologic studies show a slight increase in risk. Interpretation of the epidemiologic studies is complicated, because bleeding induced by aspirin may enhance the diagnosis and early treatment of cancer, and at least in theory, the symptoms of cancer could cause patients to avoid aspirin. Clinical trials designed specifically to investigate the aspirin hypothesis in humans at high risk of colorectal polyps or cancer are needed to establish causality, and to define the optimal dose and drug. Experimental studies should further define the mechanism of tumor inhibition in animals.

Adenoma↗
PubMed1995

DNA ploidy and proliferating cell nuclear antigen in colonic adenomas and adenocarcinomas.

To investigate the colonic adenoma-adenocarcinoma progression sequence, DNA ploidy analysis was performed on hyperplastic polyps to adenocarcinomas. DNA ploidy data were then compared with immunocytochemical staining for proliferating cell nuclear antigen (PCNA). In hyperplastic polyps to villous adenomas, all cases were diploid except one aneuploid villous adenoma. In three adenomas, diploid in situ adenocarcinomas were present. As diploid percentages decreased from hyperplastic polyps to villous adenomas, aneuploid percentages increased. In adenocarcinomas, the Dukes classification corresponded well to DNA ploidy status: all four stage A carcinomas were diploid, whereas three cases each of stage C1 and C2 carcinomas were aneuploid or multiploid. A surprising finding was that S-phase percentage in adenocarcinomas was not parallel with PCNA-positive tumor cell numbers. It is concluded that multistep adenoma-adenocarcinoma progression was partially reflected in DNA ploidy pattern from hyperplastic polyps to villous adenomas. In adenocarcinomas, the Dukes classification paralleled well the DNA ploidy status from stage A diploid to stage D aneuploid, but was not accompanied by increasing PCNA-positive cell numbers.

Adenocarcinoma↗
PubMed1988

DNA aneuploidy in solitary colonic adenomas and the future risk of colorectal cancer.

Flow cytometric DNA analysis was performed on the colonic adenomas of 24 patients who had resection of an invasive colorectal carcinoma subsequent to polypectomy. The incidence of DNA aneuploidy among these adenomas was only 13 percent. Thus, simple recognition of colonic adenomas as being DNA diploid or DNA aneuploid is unlikely to be helpful for identifying patients with adenoma who are at high risk for developing a future colorectal carcinoma.

Aneuploidy↗
PubMed1998

Diminutive cancers of the colon and rectum: comparison between flat and polypoid cancers.

A comparative study of polypoid and flat colorectal cancers less than 20 mm in size was made. A review of the characteristics of 56 polypoid cancers and 29 flat cancers treated between April 1989 and January 1996 was performed. Both groups of cancers showed similar age and location distribution. Polypoid cancers were more likely to be well differentiated (38%) than were flat cancers (17%) (P < 0.05). Flat cancers were more likely to have reached the serosa (52% vs 12%; P < 0.01) and also demonstrated a higher frequency of lymph node involvement (41% vs p 9%) (P < 0.01) when compared to polypoid cancers. Flat colorectal cancers belong to a distinct subset which demonstrates greater biological aggressiveness than polypoid cancers of equivalent size.

Aged↗
PubMed1991

Lecithin organogels as matrix for the transdermal transport of drugs.

The stable, transparent, thermoreversible organogels which are prepared by adding a minute amount of water to a solution of lecithin in isopropylpalmitate are studied as matrices for promoting the transdermal transport of drugs throughout the skin. In this work we study this process by using two model drug substances, scopolamine (already well known as a transdermally active substance) and broxaterol, a new drug against asthma. It is found that the transport of scopolamine is much more effective in gel than in aqueous solution and that the transport of broxaterol is also proceeding well. Since the same can be observed with a variety of substances differing in the chemical structure, we speculate on the application of lecithin gels as general matrices for the transdermal transport.

Adenocarcinoma↗
PubMed2003

Frequent CpG island methylation in serrated adenomas of the colorectum.

Serrated adenomas are characterized by a saw-toothed growth pattern with epithelial dysplasia (intraepithelial neoplasia). The CpG island methylator phenotype (CIMP) is a recently described mechanism for tumorigenesis in colorectal carcinomas and adenomas characterized by methylation of multiple CpG islands. The role of these epigenetic alterations in the pathogenesis of serrated adenomas is not clear. We therefore evaluated CIMP in 22 sporadic serrated adenomas and 6 serrated adenomas with multiple (6 to 10) hyperplastic polyps, including 5 with admixed hyperplastic glands and adenomatous glands, and compared the results with 34 conventional adenomas. Bisulfite methylation-specific polymerase chain reaction was used for the p16 and hMLH1 genes, and three MINT (methylated in tumor) loci (MINT1, MINT2, and MINT31). Patients with sporadic serrated adenomas had a higher frequency of hyperplastic polyps (1.3 +/- 1.6) as compared to patients with tubular adenomas (0.4 +/- 0.9, P = 0.02). Mean number of methylated sites was significantly higher in sporadic serrated adenomas (2.0 +/- 1.7) than in tubular adenomas (0.8 +/- 0.9, P = 0.00001). Sporadic serrated adenomas had significantly more frequent methylation of MINT1 (48%, 10 of 22) and MINT2 (71%, 15 of 21) than tubular adenomas (9%, 3 of 34, P = 0.001; and 18%, 6 of 34, P = 0.0001), respectively. Concordant methylation of two or more sites (CIMP-high) was also more frequent in sporadic serrated adenomas (68%, 15 of 22) than in tubular adenomas (18%, 6 of 34, P = 0.0005). All five serrated adenomas with admixed hyperplastic glands and adenomatous glands were CIMP-high. Our results indicate that CpG island methylation is common in sporadic serrated adenomas and may play an important role in their pathogenesis.

Adaptor Proteins, Signal Transducing↗
PubMed2003

The relationship between hypomethylation and CpG island methylation in colorectal neoplasia.

Tumors are often characterized by an imbalance in cytosine methylation as manifested both by hypermethylation of CpG islands and by genome hypomethylation. These epigenetic changes were assessed in colorectal neoplasia to determine whether they arose through a common mechanism or indeed were distinct and unrelated phenomena. Fresh representative samples of adenomas, hyperplastic polyps, colorectal cancers, and normal mucosa were used in this study. Global methylation levels were measured by analyzing the methyl-accepting capacity of DNA. Methylation of p16, hMLH1, and MINT 1, 2, 12, and 31 were assessed by bisulfite polymerase chain reaction. Microsatellite status was determined by polymerase chain reaction using six markers and hMLH1 and proliferating cell nuclear antigen expression was assessed by immunohistochemistry. Normal colonic mucosa had a higher endogenous 5-methyl cytosine content than all proliferative lesions of the colon (P < 0.001). The extent of demethylation in hyperplastic polyps and adenomas was significantly related to its proliferative rate. Right-sided hyperplastic polyps were more likely to be methylated than adenomas (odds ratio, 2.3; confidence interval, 1.1 to 4.6). There was no relationship between the level of global hypomethylation and hypermethylation. Some hyperplastic colorectal polyps have a propensity to develop dense CpG island methylation. Hypermethylation and hypomethylation contribute separately to the process of carcinogenesis.

Adaptor Proteins, Signal Transducing↗
PubMed1999

[Explanation of enigmas of the Lynch syndrome thanks to a new carcinogenesis model characterized by an unorthodox initiation process].

The genotype-phenotype relationship of Lynch syndrome displays many enigmatic features which cannot be explained satisfactorily by the prevailing concepts of carcinogenesis and genetic predisposition to cancer. We propose here a new model of carcinogenesis divided into two and only two evolutive phases: a) a preliminary phase starting with the counter-selective loss of mismatch repair function, in which most clones with the RER mutator phenotype are eliminated through apoptosis or an accelerated ageing process; b) an explosive phase that is initiated only if mutations blocking apoptosis and senescence, rapidly acquired during the short life span of the non-transformed RER+ clones, eventually rescue one mismatch repair-deficient cell that gives rise to the malignant clone. Carcinogenesis is proposed here to progress irreversibly and very rapidly once initiated. We shall show how this model provides a meaningful etiologic and pathogenic interpretation of all the curious features of Lynch syndrome.

Adenoma↗
PubMed1995

Plasminogen activators and inhibitor type 1 in neoplastic colonic tissue from patients with familial adenomatous polyposis.

The plasminogen activation cascade is involved in carcinogenesis, invasion and metastasis. In this study plasminogen activators and their type 1 inhibitor were evaluated in colonic tissue from 19 patients with familial adenomatous polyposis coli, an inherited disorder characterised by the presence of thousands of adenomatous polyps in the colorectum which predispose to colorectal cancer. The conversion of normal-appearing colonic mucosa to neoplastic tissue in these patients was associated with an increase in urokinase-type plasminogen activator and plasminogen activator inhibitor type 1, accompanied by a decreased level of tissue-type plasminogen activator. These observations are essentially similar to those found in solitary adenomas and carcinomas of the colon, and illustrate the uniform involvement of the plasminogen activation system in colorectal carcinogenesis.

Adenocarcinoma↗
PubMed2003

Is the distal hyperplastic polyp a marker for proximal neoplasia?

CONTEXT: The current literature is unclear about the association between distal hyperplastic polyps and synchronous neoplasia (adenomatous polyps and cancer) in the proximal colon. OBJECTIVE: To estimate the prevalence of proximal neoplasia associated with distal hyperplastic polyps. DATA SOURCES: Database searches (medline and embase from 1966 to 2001) and manual search of the bibliographies of included and excluded studies, case reports, editorials, review articles, and textbooks of Gastroenterology. STUDY SELECTION: Studies describing the prevalence of proximal neoplasia in persons with distal hyperplastic polyps. DATA EXTRACTION: Demographics, clinical variables, study design, and prevalence of proximal neoplasia associated with various distal colorectal findings. DATA SYNTHESIS: Of 18 included studies, 12 involved asymptomatic individuals in which the pooled absolute risk of any proximal neoplasia associated with distal hyperplastic polyps was 25% (95% confidence interval [95% CI], 21% to 29%). In 4 studies where colonoscopy was performed irrespective of distal findings, the absolute risk was 21% (95% CI, 14% to 28%). The relative risk of finding any proximal neoplasia in persons with distal hyperplastic polyps was 1.3 (95% CI, 0.9 to 1.8) compared to those with no distal polyps. Among 6 studies of patients with symptoms or risk factors for neoplasia, the absolute risk of proximal neoplasia was 35% (95% CI, 32% to 39%) in persons with distal hyperplastic polyps. In 2 studies of screening colonoscopy, advanced proximal neoplasia (cancer, or a polyp with villous histology or severe dysplasia, or a tubular adenoma >/=1 cm) was present in 4% to 5% of persons with distal hyperplastic polyps, which was 1.5 to 2.6 times greater than in those with no distal polyps. CONCLUSIONS: In asymptomatic persons, a distal hyperplastic polyp is associated with a 21% to 25% risk for any proximal neoplasia and a 4% to 5% risk of advanced proximal neoplasia, and may justify examination of the proximal colon. Further study is needed to determine the risk of advanced proximal neoplasia associated with size and number of distal hyperplastic polyps.

Colonic Neoplasms↗
PubMed2002

Colonic cancer and polyps.

Colorectal cancer (CRC) is one of the best studied cancers. It is easily accessible and develops slowly over several years from premalignant lesions (adenomatous polyps) to invasive cancers. The key molecular events in this sequence have been characterized. Different screening strategies have proven to be effective in lowering both the mortality and the incidence of CRC. Nevertheless, CRC is still the second leading cause of cancer-related deaths for both men and women in the USA and other Western countries. An estimated 130 000 new cases and more than 50 000 deaths have been diagnosed in the USA in 2000. Surgical resection remains the only curative treatment, and the likelihood of cure is greater when the disease is detected at an early stage. Hereditary non-polyposis colorectal cancer (HNPCC) and the different polyposis syndromes such as familial adenomatous polyposis (FAP) or Peutz-Jeghers disease are rare causes of CRC but have been a major focus of research in past years, helping with the understanding of the molecular events in carcinogenesis. This review summarizes our current knowledge of the pathogenesis and management of colorectal polyps and polyposis syndromes as well as sporadic CRC.

Adenomatous Polyposis Coli↗
PubMed2002

CDX2 regulates liver intestine-cadherin expression in normal and malignant colon epithelium and intestinal metaplasia.

BACKGROUND & AIMS: The intestine-specific caudal-related homeobox transcription factor CDX2 seems to play a key role in intestinal development and differentiation. Inactivation of one Cdx2 allele predisposes mice to develop colon polyps, and loss of CDX2 expression is a feature of some poorly differentiated colon carcinomas in humans. Conversely, aberrant CDX2 expression is often seen in intestinal metaplasias in the stomach and esophagus and in some gastric carcinomas. To better understand CDX2 function, we sought to define CDX2-regulated genes. METHODS: HT-29 colon cancer cells with minimal endogenous CDX2 expression were engineered to express exogenous CDX2, and gene expression changes relative to control cells were assessed using high-density oligonucleotide arrays. RESULTS: The gene for liver intestine (LI)-cadherin (cadherin 17) was strongly induced by CDX2 in HT-29. In other colorectal cancer lines, endogenous CDX2 and LI-cadherin expression were well correlated. Activation of a ligand-regulated form of CDX2 rapidly induced LI-cadherin gene expression, even in the presence of protein synthesis inhibitor. Analysis of the 5'-flanking region of the LI-cadherin gene defined 2 CDX2 responsive elements, and chromatin immunoprecipitation assays indicate CDX2 binds to the elements. In primary colorectal cancers and intestinal metaplasias in the stomach, CDX2 and LI-cadherin expression were tightly correlated. CONCLUSIONS: CDX2 regulates LI-cadherin gene expression in normal, metaplastic, and neoplastic tissues of the gastrointestinal tract via binding to elements in the 5'-flanking region of the gene. Given the well-established roles of cadherins in morphogenesis and differentiation, LI-cadherin may be a key factor mediating CDX2 function in intestinal cell fate determination.

Animals↗