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The BRAF gene is mutated in 4% to 12% of unselected colorectal cancers, particularly those with high microsatellite instability and in premalignant lesions, such as serrated adenomas and hyperplastic polyps.

To evaluate the role of oncogenic BRAF mutations in non-hereditary nonpolyposis colorectal cancer/non-familial adenomatous polyposis familial colorectal cancer, we did a mutation screening of the most common BRAF mutation, the V600E mutation, in 194 colorectal tumors from patients with a positive family history of the disease.

Interestingly, families with extracolonic tumors showed a much higher mutation frequency (17.5%) compared with families with colonic cancer only (3.5%; P = 0.009).

Subjects from families where the V600E mutation was identified had less adenomas compared with those from families where no BRAF mutation had been found (odds ratio, 8.5; 95% confidence interval, 1.1-64.6).

These findings indicate that adenomas might be less important in the cancer development in the group of families with BRAF-V600E mutations and indirectly support a previous hypothesis that tumors might develop through the hyperplastic polyp-serrated adenoma pathway.

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(PMID = 17119056.001).

[ISSN] 1055-9965

[Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf

   

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DATA SYNTHESIS: Regular use of aspirin reduced the incidence of colonic adenomas in RCTs (relative risk [RR], 0.82 [95% CI, 0.7 to 0.95]), case-control studies (RR, 0.87 [CI, 0.77 to 0.98]), and cohort studies (RR, 0.72 [CI, 0.61 to 0.85]).

CONCLUSIONS: Aspirin appears to be effective at reducing the incidence of colonic adenoma and colorectal cancer, especially if used in high doses for more than 10 years.

[MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control. Primary Prevention

[MeSH-minor] Adenoma / prevention & control. Adult. Cardiovascular Diseases / chemically induced. Colonic Polyps / prevention & control. Female. Gastrointestinal Diseases / chemically induced. Humans. Incidence. Male. United States / epidemiology

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[CommentIn] ACP J Club. 2007 Jul-Aug;147(1):15-6 [17608380.001]

[CommentIn] Gastroenterology. 2007 Aug;133(2):717-8 [17681190.001]

[CommentIn] Ann Intern Med. 2007 Nov 6;147(9):674; author reply 674-5 [17975195.001]

[SummaryForPatientsIn] Ann Intern Med. 2007 Mar 6;146(5):I35 [17339615.001]

(PMID = 17339622.001).

[ISSN] 1539-3704

[Journal-full-title] Annals of internal medicine

[ISO-abbreviation] Ann. Intern. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin

[Number-of-references] 61

   

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[Title] Non-steroidal anti-inflammatory drug use and colorectal polyps in the Prostate, Lung, Colorectal, And Ovarian Cancer Screening Trial.

OBJECTIVES: Non-steroidal anti-inflammatory drugs (NSAIDs) have been documented in animal and human studies to reduce risk for colorectal cancer and adenomatous polyps, but risk modification for subgroups of the population and effects on hyperplastic polyps have been less studied.

Follow-up of detected polyps was accomplished outside the Trial setting and relevant records were sought and abstracted.

Cases (n=4,017) included subjects with a biopsy-proven polyp in the left side of the colon (descending colon, sigmoid, and rectum) detected as a consequence of PLCO screening; controls (n=38,396) were subjects with no left-sided colon polyp.

RESULTS: Regular use of aspirin (≥ 4 times/month) in the past year was inversely associated with hyperplastic polyps (odds ratios (OR)=0.8, 95% confidence interval (CI)=0.7-0.9), adenomatous polyps (OR=0.8, 95% CI=0.8-0.9), and advanced adenomas (OR=0.8, 95% CI=0.7-0.9).

As frequency of aspirin use increased, the prevalence of polyps decreased significantly for each histological classification (P for trend ≤ 0.0004).

Similar patterns were found for adenomas and ibuprofen.

Overall protection was consistent in both the descending colon or sigmoid and the rectum, but more evident in males.

CONCLUSIONS: This study of a large general risk population supports previous work that recent use of aspirin and ibuprofen is associated with a decreased risk of colorectal adenomas and demonstrates that this protective effect may be stronger in certain population subgroups and is also evident for aspirin and hyperplastic polyps.

[MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colonic Polyps / prevention & control. Ibuprofen / therapeutic use

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(PMID = 20808298.001).

[ISSN] 1572-0241

[Journal-full-title] The American journal of gastroenterology

[ISO-abbreviation] Am. J. Gastroenterol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / N01 CN25522; United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin; WK2XYI10QM / Ibuprofen

   

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[Title] [Flat adenomas of the colon].

[MeSH-major] Adenoma / pathology. Adenomatous Polyps / pathology. Colonic Neoplasms / pathology

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(PMID = 17460974.001).

[ISSN] 0040-3660

[Journal-full-title] Terapevticheskiĭ arkhiv

[ISO-abbreviation] Ter. Arkh.

[Language] rus

[Publication-type] Journal Article; Review

[Publication-country] Russia (Federation)

[Number-of-references] 79

   

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The senescence-associated signature of p53 isoform expression (that is, elevated p53beta and reduced Delta133p53) was observed in vivo in colon adenomas with senescent phenotypes.

The increased Delta133p53 and decreased p53beta isoform expression found in colon carcinoma may signal an escape from the senescence barrier during the progression from adenoma to carcinoma.

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(PMID = 19701195.001).

[ISSN] 1476-4679

[Journal-full-title] Nature cell biology

[ISO-abbreviation] Nat. Cell Biol.

[Language] ENG

[Grant] United States / Intramural NIH HHS / / Z01 BC005480-22; United States / Intramural NIH HHS / / ZIA BC010878-02; United Kingdom / Cancer Research UK / / ; United States / Intramural NIH HHS / / Z01 BC005795-13; United States / Intramural NIH HHS / / Z01 BC005795-14; United States / Intramural NIH HHS / / ZIA BC005795-15; United States / Intramural NIH HHS / / Z01 BC010878-01

[Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / MIRN34 microRNA, human; 0 / MicroRNAs; 0 / Protein Isoforms; 0 / Tumor Suppressor Protein p53

[Other-IDs] NLM/ NIHMS161529; NLM/ PMC2802853

   

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[Title] Mucins in the colorectal neoplastic spectrum with reference to conventional and serrated adenomas.

BACKGROUND/AIMS: Alterations in expression of mucins and aberrant expression of various types of mucin genes were observed in colorectal adenomas and carcinomas, though their significance in neoplastic transformation of colorectal epithelium is yet to be determined.

The aim of this study was to determine expression of MUC1, MUC2, MUC5AC, and MUC6 through conventional adenoma-carcinoma sequence and polyps involved in the "serrated" pathway of the colorectum using tissue array technique.

METHODS: In this study, a total of 172 cases including 100 colorectal polyps [8 hyperplastic polyps, 10 sessile serrated adenomas, 19 tubular, 37 tubulovillous, and 26 villous adenomas], 16 adenomas with intramucosal carcinoma, 28 conventional colorectal cancers, and 28 normal mucosae were examined.

Sessile serrated adenomas exhibited the highest MUC5AC expression while adenomatous polyps showed an increase in MUC5AC expression in parallel with neoplastic progression (p<0.001).

Hyperplastic polyps seemed to lie between normal mucosa and sessile serrated adenomas in terms of mucin expression, suggesting that they are morphologically and histogenetically linked.

CONCLUSIONS: Upregulation of MUC1 and MUC6 through the adenoma-carcinoma sequence together with downregulation of MUC2 and MUC5AC at the neoplastic end of the spectrum seem to follow the steps of malignant transformation.

[MeSH-major] Adenoma / metabolism. Colonic Polyps / metabolism. Colorectal Neoplasms / metabolism. Mucins / metabolism

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(PMID = 18080919.001).

[ISSN] 2148-5607

[Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology

[ISO-abbreviation] Turk J Gastroenterol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Turkey

[Chemical-registry-number] 0 / Mucins

   

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Colo-colic intussusception was diagnosed by means of a colonic contrast X-ray.

Hundreds of polyps were seen throughout the entire colon.

The pathology specimen showed an intramucosal carcinoma and multiple adenomas.

[MeSH-major] Adenomatous Polyposis Coli / diagnosis. Colonic Diseases / diagnosis. DNA Glycosylases / genetics. Intussusception / diagnosis

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[CommentIn] Ned Tijdschr Geneeskd. 2008 Jan 5;152(1):56-7; author reply 57 [18240762.001]

(PMID = 17715770.001).

[ISSN] 0028-2162

[Journal-full-title] Nederlands tijdschrift voor geneeskunde

[ISO-abbreviation] Ned Tijdschr Geneeskd

[Language] dut

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase

   

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[Title] Microsatellite instability of selective target genes in HNPCC-associated colon adenomas.

Instability at coding microsatellites (cMS) in specific target genes causes frameshift mutations and functional inactivation of affected proteins, thereby providing a selective growth advantage to MMR deficient cells.

In this study, we examined 30 HNPCC-associated MSI-H colorectal adenomas of different grades of dysplasia for frameshift mutations in 26 cMS-bearing genes, which, according to our previous model, represent Selective Target genes of MSI.

About 30% (8/26) of these genes showed a high mutation frequency (> or =50%) in colorectal adenomas, similar to the frequencies reported for colorectal carcinomas.

Mutations in one gene (PTHL3) occurred significantly less frequently in MSI adenomas compared to published mutation rates in MSI carcinomas (36.0 vs 85.7%, P=0.023).

[MeSH-major] Adenoma / genetics. Adenoma / physiopathology. Cell Transformation, Neoplastic / genetics. Chromosomal Instability. Colonic Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Microsatellite Repeats

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(PMID = 15735733.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

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[Title] Tubulo-villous adenoma of the vagina.

BACKGROUND: Tubulo-villous adenomas are common in the colon and rectum, but extremely rare in the vagina.

As far as we know, only two cases of tubulo-villous adenoma have ever been reported.

We report the third case of enteric-type tubulo-villous adenoma of the vagina.

The tumor was excised and pathologically confirmed as a tubulo-villous adenoma.

CONCLUSION: Because some tubulo-villous adenomas in the colon and rectum can progress to the cancer, this case requires long-term follow-up to detect recurrence and malignant transformation.

[MeSH-major] Adenoma, Villous / pathology. Vaginal Neoplasms / pathology

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(PMID = 15661252.001).

[ISSN] 0090-8258

[Journal-full-title] Gynecologic oncology

[ISO-abbreviation] Gynecol. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 17

   

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Surveillance procedures were classified as: a) Barrett's oesophagus, b) chronic IBD, c) prior adenomatous colorectal polyps and, d) prior surgical resection of colorectal cancer.

Of these, 50 of 133 (37.6%) Barrett's patients, 92 of 213 (43.2%) patients with prior colonic polyps, 36 of 48 (75.0%) patients with prior colonic malignancy and 17 of 47 (36.2%) patients for IBD surveillance were scheduled prematurely.

[MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Barrett Esophagus / diagnosis. Colorectal Neoplasms / diagnosis. Databases as Topic. Great Britain. Humans. Inflammatory Bowel Diseases / diagnosis. Ireland

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(PMID = 18990956.001).

[ISSN] 0332-3102

[Journal-full-title] Irish medical journal

[ISO-abbreviation] Ir Med J

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] Ireland

   

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[Title] Noninvasive detection of candidate molecular biomarkers in subjects with a history of insulin resistance and colorectal adenomas.

We have developed novel molecular methods using a stool sample, which contains intact sloughed colon cells, to quantify colonic gene expression profiles.

For this purpose, the effects of a legume-enriched, low glycemic index, high fermentable fiber diet was evaluated in subjects with four possible combinations of risk factors, including insulin resistance and a history of adenomatous polyps.

Linear discriminant analysis was successfully used to identify the best single genes and two- to three-gene combinations for distinguishing subjects with insulin resistance, a history of polyps, or exposure to a chemoprotective legume-rich diet.

These results support our premise that gene products (RNA) isolated from stool have diagnostic value in terms of assessing colon cancer risk.

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(PMID = 19470793.001).

[ISSN] 1940-6215

[Journal-full-title] Cancer prevention research (Philadelphia, Pa.)

[ISO-abbreviation] Cancer Prev Res (Phila)

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / R01 DK071707-02; United States / NCI NIH HHS / CA / R01 CA129444-01; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2; United States / NIDDK NIH HHS / DK / R01 DK071707-01A2S1; United States / NCI NIH HHS / CA / R01 CA059034-05; United States / NCI NIH HHS / CA / CA059034-12; United States / NCI NIH HHS / CA / CA059034-08; United States / NIEHS NIH HHS / ES / P30ES09106; United States / NCI NIH HHS / CA / R01 CA059034-07; United States / NCI NIH HHS / CA / CA059034-13; United States / NCI NIH HHS / CA / R01 CA059034; United States / NIDDK NIH HHS / DK / DK071707; United States / NCI NIH HHS / CA / R01 CA059034-15; United States / NCI NIH HHS / CA / R01 CA059034-11; United States / NCI NIH HHS / CA / CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-09; United States / NIDDK NIH HHS / DK / R01 DK071707-03; United States / NCI NIH HHS / CA / CA059034-09; United States / NIDDK NIH HHS / DK / DK071707-03; United States / NCI NIH HHS / CA / R01 CA129444-02; United States / NCI NIH HHS / CA / R01 CA059034-08; United States / NCI NIH HHS / CA / CA59034; United States / NCI NIH HHS / CA / CA059034-05; United States / NCI NIH HHS / CA / R01 CA059034-10; United States / NCI NIH HHS / CA / CA129444-01; United States / NCI NIH HHS / CA / CA059034-10; United States / NCI NIH HHS / CA / R01 CA059034-14; United States / NCI NIH HHS / CA / R01 CA059034-12; United States / NIDDK NIH HHS / DK / DK071707-01A2S1; United States / NIDDK NIH HHS / DK / DK071707-01A2; United States / NCI NIH HHS / CA / CA129444-02; United States / NCI NIH HHS / CA / CA059034-15; United States / NIDDK NIH HHS / DK / DK071707-02; United States / NCI NIH HHS / CA / CA059034-11; United States / NCI NIH HHS / CA / CA129444; United States / NCI NIH HHS / CA / CA059034-14; United States / NIDDK NIH HHS / DK / R01 DK071707; United States / NIEHS NIH HHS / ES / P30 ES009106; United States / NCI NIH HHS / CA / CA059034-07; United States / NCI NIH HHS / CA / R01 CA059034-06; United States / NCI NIH HHS / CA / R01 CA059034-13; United States / NCI NIH HHS / CA / R01 CA129444

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger

[Other-IDs] NLM/ NIHMS120536; NLM/ PMC2745241

   

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[Title] [Clinical aspects in polyps of the colon].

[Transliterated title] Aspectos clínicos de los pólipos colónicos.

INTRODUCTION: The colonics polyps according to their number, size, location, age of presentation and mainly, according to their histology, have the potentiality of malignant degeneration, which makes of a continuous study and pursuit susceptible.

OBJECTIVES: To evaluate the relation between the histologic type of the colon polyps, its location, the degree of dysplasia, the size, its possible commitment by carcinoma, the age, sex and the handling that has occurred them, in a series of 684 patients of the National Institute of Enfermedades Neoplásicas (INEN) between the 1 of January from 1974 to the 31 of March of the 2004.

MATERIAL AND METHODS: The revision of clinical histories of 840 patients with the diagnosis of colon polyp was made who attended the service of Gastroenterology of the INEN between the 1 of January from 1974 to the 31 of March of 2004 and a card predesigned for each clinical history filled.

1162 resecteds polyps evaluated themselves in this period.

The final sample was of 684 patients, in whom it was 1057 polyps.

Other endoscopic findings were: internal hemorrhoids (172), colonic diverticulosis (50), anal fissure (4), and nonspecific ulcerative colitis (2).

RESULTS: 1057 polyps extirpated, by means of the endoscopy polipectomy were 1016, with colectomy were 32 and with transanal resection without colectomy they 9.

Within the histology of the 1057 polyps, 331 was briefed (31.3%) that were hyperplasic, 448 (42.4%) adenomas, 278 (26.3%) others and 35 (8.2%) adenocarcinomas on adenomas.

The location but frequence of the adenomas was in the left colon (76.6%).

Adenocarcinoma (carcinomas on adenomas), was present mainly in polyps villous type, with dysplasia severe and greater to 10 mm.

Nevertheless, in smaller polyps of 5mm with dysplasia severe, was a polyp invaded by cancer, that represents the 0,8% of millimetric polyps.

The made handling was mainly endoscopic, with 96% of the resected polyps this way, also slogan transanal resection and segmental colonic resection.

The colectomy was necessary in 3% of all the made interventions, dysplasia severe or carcinoma was made in adenomatous polyps with, and in greater percentage in greater polyps of 20 mm (53%).

On the other hand, in polyps with level of invasion Haggitt 3 and 4, the colectomy was the election treatment.

CONCLUSIONS: The Evaluation of colonic polyps in INEN is predominantly by endoscopy.

The polyps are more frequent over the 50 years and have preferred location in the left colon.

The carcinoma is more probable with severe dysplasia and greater size of the adenoma.

All polyps, from the millimetric ones, including the hyperplasic, must be considered marks of neoplasia and extirpated in its totality.

[MeSH-major] Colonic Polyps / pathology. Colonic Polyps / surgery

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(PMID = 17712391.001).

[ISSN] 1022-5129

[Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú

[ISO-abbreviation] Rev Gastroenterol Peru

[Language] spa

[Publication-type] English Abstract; Journal Article

[Publication-country] Peru

   

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[Title] A case of primary squamous cell colon cancer.

Carcinomas of the colon are a common cancer seen in both inpatient and outpatient settings with approximately 145,000 new cases being diagnosed every year in the USA.

Despite the frequency of these cancers being seen, it continues to be a rarity to see a primary squamous cell cancer of the colon.

While the exact aetiology of this rare tumour is currently still not completely understood, various aetiologies include chronic irritation leading to squamous differentiation, embryonic migration of ectodermal cells to the colon, or adenomas undergoing squamous transformation.

[MeSH-major] Carcinoma, Squamous Cell / pathology. Colonic Neoplasms / pathology

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(PMID = 17621567.001).

[ISSN] 1078-1552

[Journal-full-title] Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners

[ISO-abbreviation] J Oncol Pharm Pract

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

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[Title] Pigmented mesenteric lymphadenopathy in familial adenomatous polyposis - an unusual cause of intraoperative abandonment of ileo-anal pouch.

Familial adenomatous polyposis (FAP) is an autosomal dominant condition with near complete penetrance, characterised by the presence of numerous adenomatous polyps of the colon and rectum.

Melanosis coli describes the brownish-black discolouration of the colon resulting from the accumulation of a granular pigment in the phagosomes of macrophages in the colonic lamina propria.

The presence of melanosis pigment in pericolonic lymph nodes has been reported in patients with coincidental melanosis coli, following segmental colonic resection.

[MeSH-major] Adenomatous Polyposis Coli / surgery. Lymphatic Diseases / complications. Melanosis / complications. Mesentery. Peritoneal Diseases / complications

[MeSH-minor] Adolescent. Colonic Pouches. Female. Humans. Intraoperative Complications / etiology. Proctocolectomy, Restorative. Reoperation

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(PMID = 16884599.001).

[ISSN] 0035-8843

[Journal-full-title] Annals of the Royal College of Surgeons of England

[ISO-abbreviation] Ann R Coll Surg Engl

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC1963935

   

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Gardner syndrome is a variant of familial adenomatous polyposis (FAP) and results in the manifestation of numerous external and internal symptoms including gastrointestinal polyps, osteomas, tumors, and epidermoid cysts.

Stemming from a mutation in the adenomatous polyposis coli (APC) gene, Gardner syndrome shares genetic correlations with the FAP phenotype; as a result, it becomes all the more crucial for physicians to be able to discern Gardner syndrome from other differential diagnoses such as Turcot syndrome, FAP, and other attenuated forms of familial polyposis.

Fortunately, Gardner syndrome has characteristic polyps in the colon, osteomas, and also exhibits abnormalities in the retinal epithelium that discern it from others.

Surgery is the most effective method of management for Gardner syndrome; restorative proctocolectomy with ileal pouch anal anastomosis with mucosectomy is the top choice for colonic malignancies, and skin manifestations can be treated through a variety of excisions and therapy depending on location, size, and number of malignancies.

Currently, there are no specific screening recommendations for Gardner syndrome, but testing following general screening recommendations for extra-colonic malignancies, genetic counseling, and endoscopy are encouraged.

[MeSH-minor] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / pathology. Colorectal Neoplasms, Hereditary Nonpolyposis / therapy. Diagnosis, Differential. Genetic Counseling / methods. Humans. Mutation

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(PMID = 20141232.001).

[ISSN] 1175-0561

[Journal-full-title] American journal of clinical dermatology

[ISO-abbreviation] Am J Clin Dermatol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] New Zealand

[Number-of-references] 29

   

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[Title] ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition.

RESULTS: ITF-2B is strongly expressed in colon adenomas but frequently down-regulated in carcinomas because of LOH at 18q21.

Loss of ITF-2B expression correlates with loss of p21(Cip1) expression in primary colon carcinomas.

ITF-2B, which is up-regulated during early colorectal carcinogenesis because of loss of adenomatous polyposis coli, is a target for LOH on chromosome 18q, along with deleted in colorectal carcinoma and Smad4.

This finding, along with the fact that ITF-2B is a regulator of the key cell cycle inhibitor p21(Cip1), indicates that ITF-2B is a tumor suppressor that has an important function at the adenoma to carcinoma transition.

[MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics

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(PMID = 19394332.001).

[ISSN] 1528-0012

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors

   

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[Title] Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.

CpG island methylation has been observed in aberrant crypt foci (ACF) and adenomas in the colon, implicating it in the earliest aspects of colon cancer formation.

In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in the colon mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk of colon adenomas and colon cancer.

We investigated the methylation status in the promoter regions of the CDKN2A/p16, hMLH1, and MGMT genes in human non-neoplastic rectal mucosa and evaluated whether these methylation markers may predict the presence of adenomatous polyps in the colon.

The promoter methylation patterns of these genes were examined in rectal biopsies (mucosa samples) of 97 colorectal adenoma cases and 94 healthy controls using methylation-specific PCR (MSP) assays.

The methylation status of these genes in rectal mucosa biopsies detected by MSP assays may not distinguish between patients with and without adenomas in the colon.

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(PMID = 16820927.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA95103; United States / NCI NIH HHS / CA / R01CA97386

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] Greece

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase

   

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[Title] Serrated adenoma is a risk factor for subsequent adenomatous polyps.

BACKGROUND: Serrated adenomas (SA) are histologically defined by the presence of both hyperplastic and adenomatous features.

These uncommon polyps are thought to play an important role in the development of sporadic colorectal cancers (CRC) with microsatellite instability (MSI).

This study was undertaken to define the relationship between SA and the future development of adenomatous polyps.

These were matched to controls by age, sex, indication for colonoscopy, polyp type and number and duration of follow-up.

Of these, 80 patients (0.5%) with SA were found, and of these SA, 80% were found in the left colon.

On follow-up examination four patients (24%) and no controls had adenomatous polyps (P = 0.01).

Serrated adenomas appear to be found more commonly in the left colon and in older patients.

This study found a significant association between SA and the subsequent development of adenomatous polyps.

[MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Precancerous Conditions / pathology

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(PMID = 18320324.001).

[ISSN] 0163-2116

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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To understand the effects of RNS on BER in vivo, we examined intestinal adenomas for levels of inducible nitric oxide synthase (iNOS) and AAG.

We found AAG to be nitrated in human adenomas, suggesting that this RNS modification is relevant in the human disease.

POLbeta protein was increased in nearly all adenomas compared with adjacent non-tumor tissues, whereas APE1 expression was only increased in approximately half of the adenomas and also was relocalized to the cytoplasm in adenomas.

Collectively, the results suggest that BER is dysregulated in colon adenomas.

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(PMID = 19864471.001).

[ISSN] 1460-2180

[Journal-full-title] Carcinogenesis

[ISO-abbreviation] Carcinogenesis

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / P20 RR017698; United States / NCRR NIH HHS / RR / P20 RR17698; United States / NCI NIH HHS / CA / R01 CA100450; United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Reactive Nitrogen Species; EC 2.7.7.- / DNA Polymerase beta; EC 3.2.2.- / 3-methyladenine-DNA glycosylase; EC 3.2.2.- / DNA Glycosylases; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase

[Other-IDs] NLM/ PMC2792317

   

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[Transliterated title] Precisión diagnóstica de la calprotectina fecal para predecir una colonoscopia patológica.

The colonoscopy is the gold standard method of detecting an organic pathology in the colon.

Fecal calprotectin (FCP) is a marker that may detect organic pathologies of the colon.

People were divided in: normal colonoscopy: 117 people, and 28 colon adenomas, 20 colorectal cancer (CRC) and 25 IBD.

217 mg/kg was the best cut-off for discriminating patients with organic colon disorders.

The measurement of FCP is a non-invasive, inexpensive, reliable and easily measured test.

[MeSH-major] Colonic Diseases / diagnosis. Colonic Neoplasms / diagnosis. Colonoscopy. Feces / chemistry. Inflammatory Bowel Diseases / diagnosis. Leukocyte L1 Antigen Complex / analysis

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(PMID = 16801001.001).

[ISSN] 0025-7753

[Journal-full-title] Medicina clínica

[ISO-abbreviation] Med Clin (Barc)

[Language] spa

[Publication-type] Clinical Trial; English Abstract; Journal Article

[Publication-country] Spain

[Chemical-registry-number] 0 / Leukocyte L1 Antigen Complex

   

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Esophagogastroduodenoscopy, video capsule endoscopy and colonoscopy revealed various sizes of generalized gastrointestinal polyps.

Histological examination of the biopsy specimens obtained from the stomach and the colon showed adenomatous polyp and inflammatory polyp respectively.

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(PMID = 20955587.001).

[ISSN] 1471-230X

[Journal-full-title] BMC gastroenterology

[ISO-abbreviation] BMC Gastroenterol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2972238

   

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[Title] Sporadic adenomatous polyp regression with exisulind is effective but toxic: a randomised, double blind, placebo controlled, dose-response study.

The aim of our study was to investigate if exisulind induces regression of sporadic colonic adenomas.

At baseline colonoscopy, left sided polyps (3-10 mm) were tattooed, measured, and left in place.

Follow up sigmoidoscopy was performed after six months, and removal of any remaining polyps at the 12 month colonoscopy.

The primary efficacy variable was change in polyp size from baseline.

The decrease in median polyp size was significantly greater (p=0.03) in patients who received exisulind 400 mg (-10 mm2) compared with those who received placebo (-4 mm2).

CONCLUSION: Exisulind caused significant regression of sporadic adenomatous polyps but was associated with more toxicity.

This model of polyp regression, short in its term and involving a comparatively small patient sample size, may be the best available tool to assess a therapeutic regimen before launching into large preventive clinical studies.

[MeSH-major] Adenomatous Polyposis Coli / drug therapy. Antineoplastic Agents / therapeutic use. Sulindac / analogs & derivatives

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(PMID = 16150858.001).

[ISSN] 0017-5749

[Journal-full-title] Gut

[ISO-abbreviation] Gut

[Language] eng

[Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone

[Other-IDs] NLM/ PMC1856089

   

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[Title] Colorectal polyps on portal phase contrast-enhanced CT colonography: lesion attenuation and distinction from tagged feces.

OBJECTIVE: The purpose of our study was to determine the attenuation of colorectal polyps on portal phase contrast-enhanced CT colonography (CTC) and evaluate whether enhanced polyps can be clearly distinguished from tagged feces during CTC review.

Forty-eight colonoscopy-proven polyps (6-20 mm) and 41 polypoid tagged feces (6-19 mm) were selected from contrast-enhanced CTC performed without (n = 37 examinations) and with (n = 10 examinations) fecal tagging, respectively.

Attenuation of the polyps and tagged feces was measured.

Four independent blinded radiologists reviewed the polyps and tagged feces at both wide (width, 1,500 H; level -400 H) and soft-tissue (width, 400 H; level, 20 H) window settings to distinguish them by using subjective visual assessment.

RESULTS: Polyp attenuation on the portal phase was not correlated with size (R = -0.003; p = 0.99) and was not different between histologic types (p = 0.884).

Enhanced polyps (mean +/- SD, 119.9 +/- 25.3 H; range, 50-173 H) showed significantly lower attenuation than did tagged feces (1,521.4 +/- 683.6 H; range, 495-2,683 H) without any overlap (p < 0.0005).

An 8-mm sessile adenomatous polyp was misinterpreted as tagged feces by one reviewer.

CONCLUSION: Polyp attenuation on portal phase contrast-enhanced CTC ranges from 50 to 173 H.

Contrast-enhanced polyps are clearly and consistently distinguished from barium-tagged polypoid feces.

[MeSH-major] Colonic Polyps / radiography. Colonography, Computed Tomographic / methods. Contrast Media / administration & dosage. Feces. Radiographic Image Enhancement / methods. Rectal Diseases / radiography

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(PMID = 17579149.001).

[ISSN] 1546-3141

[Journal-full-title] AJR. American journal of roentgenology

[ISO-abbreviation] AJR Am J Roentgenol

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Contrast Media

   

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We describe a 58-year-old woman who was incidentally found to have gastric and colonic polyposis, hypoalbuminemia, cutaneous hyperpigmentation and onychodystrophy (Cronkhite-Canada syndrome).

Histology of polyps from the stomach showed features of juvenile or retention type (hamartomatous) polyps with Helicobacter pylori (H. pylori) infection.

The large pedunculated colonic polyps showed hamartomatous polyps with adenomatous component and polypectomy was performed.

After the treatment with H. pylori eradication and omeprazole, the gastric polyposis, hypoalbuminemia and anemia regressed, and endoscopic polypectomy of gastric polyps were performed.

[MeSH-major] Anti-Ulcer Agents / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. Omeprazole / therapeutic use. Polyps / complications. Stomach Neoplasms / complications

[MeSH-minor] Colonic Polyps / complications. Colonic Polyps / microbiology. Colonic Polyps / pathology. Female. Humans. Hyperpigmentation / pathology. Middle Aged. Nails, Malformed / pathology. Proton Pump Inhibitors. Syndrome

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(PMID = 16434870.001).

[ISSN] 1598-9992

[Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi

[ISO-abbreviation] Korean J Gastroenterol

[Language] kor

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors; KG60484QX9 / Omeprazole

   

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[Title] Medulloblastoma, acute myelocytic leukemia and colonic carcinomas in a child with biallelic MSH6 mutations.

Background A 13-year-old girl presented with rectal bleeding and was found to have two colonic carcinomas (stage Dukes' C) and multiple colonic polyps.

A three-generation family history identified no relatives with colonic carcinomas or polyposis.

Investigations Immunohistochemical analysis was performed on a sample of colonic adenoma.

[MeSH-major] Cerebellar Neoplasms / genetics. Colonic Neoplasms / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Medulloblastoma / genetics

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(PMID = 17259933.001).

[ISSN] 1743-4262

[Journal-full-title] Nature clinical practice. Oncology

[ISO-abbreviation] Nat Clin Pract Oncol

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein

   

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[Title] Reduction of miss rates of colonic adenomas by zoom chromoendoscopy.

BACKGROUND AND AIMS: The aim of this study was to determine the detection rate of polyps using zoom chromoendoscopy (ZE) compared with standard video colonoscopy.

The second colonoscopy (C2) was done with a zoom colonoscope spraying the whole colon with indigocarmine (0.4%).

During C1, 56 lesions were detected in 26 of 50 patients (34 hyperplastic and 22 adenomatous).

During C2, 19 additional polyps were documented prior to ZE (15% tandem miss rate), and 20 further lesions were detected with ZE (21% additional polyp detection rate compared to C1 and C2 without ZE).

Of the 39 additional lesions removed during C2 after ZE, 29 were hyperplastic and 10 were adenomatous.

Most adenomas detected during the second investigation were found in patients in whom adenomatous polyps had already been removed during the initial colonoscopy (9 of 26 patients vs 1 of 24 patients, p<0.02).

The pit pattern classification allowed a correct differentiation between hyperplastic and adenomatous polyps (accuracy 93%, sensitivity 90%, specificity 97%).

CONCLUSION: Using zoom chromoendoscopy, the rate of detecting colonic polyps can be increased at the cost of a longer retrieval time.

[MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Colonoscopy / methods. Coloring Agents. Diagnostic Errors / prevention & control. Indigo Carmine

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[Cites] Am J Gastroenterol. 2002 Jul;97(7):1696-700 [12135020.001]

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(PMID = 16283340.001).

[ISSN] 0179-1958

[Journal-full-title] International journal of colorectal disease

[ISO-abbreviation] Int J Colorectal Dis

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Coloring Agents; D3741U8K7L / Indigo Carmine

   

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CRC develops from benign adenomas in the colon over a long time.

RESULTS AND INTERPRETATION: Acetylsalicylic-acid, non-steroidal anti-inflammatory drugs and COX-2 inhibitors are shown to reduce adenoma growth, but it remains uncertain whether these drugs reduce the incidence of CRC.

[MeSH-minor] Colon / radiography. Colonoscopy. Early Diagnosis. Evidence-Based Medicine. Humans. Mass Screening. Occult Blood. Prognosis. Randomized Controlled Trials as Topic. Sigmoidoscopy

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(PMID = 17952153.001).

[ISSN] 0807-7096

[Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række

[ISO-abbreviation] Tidsskr. Nor. Laegeforen.

[Language] nor

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Norway

[Number-of-references] 35

   

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We analyzed the DNA of various organs and lesions in Korean patients with Cowden syndrome, their family members, and patients with familial adenomatous polyposis for germline or somatic PTEN mutations.

METHODS: The 11 patients included in this study were 5 patients with Cowden syndrome, 4 of their family members, and 2 patients with familial adenomatous polyposis.

Deletions and mutations in exons 1 to 9 of the PTEN gene were evaluated by polymerase chain reaction-single strand conformation polymorphism and sequencing analysis in esophageal acanthosis, gastric polyps, colonic polyps, skin lesions, and peripheral blood mononuclear cells.

RESULTS: All patients with Cowden syndrome showed several to numerous polyps in the gastrointestinal tract.

Identical mutations were found in all tissue samples, including colonic polyps, from each patient.

No PTEN mutations were found in their family members or in any patient with familial adenomatous polyposis.

[MeSH-major] Adenomatous Polyposis Coli / genetics. Chromosomes, Human, Pair 10. Germ-Line Mutation. Hamartoma Syndrome, Multiple / genetics. Phosphoric Monoester Hydrolases / genetics. Tumor Suppressor Proteins / genetics

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(PMID = 16007494.001).

[ISSN] 0012-3706

[Journal-full-title] Diseases of the colon and rectum

[ISO-abbreviation] Dis. Colon Rectum

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase

   

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The Comet-FISH technique is a useful tool to detect overall and region-specific DNA damage and repair in individual cells.

Whereas the Comet assay allows separating fragmented from non-fragmented DNA, FISH helps to detect specifically labelled DNA sequences of interest, including whole chromosomes.

Thus the combination of both techniques has been applied in particular for detection of site-specific breaks in DNA regions which are relevant for development of different diseases.

This paper reviews the relevant literature and presents three examples on how Comet-FISH was used for studying the induction of DNA damage by genotoxic compounds related to oxidative stress in colon cancer-relevant genes (TP53, APC, KRAS) of a colon adenoma cell line.

A third example relates to measuring repair of specific gene regions using Comet-FISH, a method that can be developed to biomarker application.

Taken together, available data suggests that Comet-FISH helps to get further insights into sensitivity of specific DNA regions and consequently in mechanisms of carcinogenesis.

Although the nature of the measured Comet-FISH endpoint precludes us from stating basically that damage and repair are occurring within the specific gene, it is at least possible to evaluate whether the damage and repair are occurring within the vicinity of the gene of interest.

[MeSH-minor] Cell Line, Tumor. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. Genes, APC / drug effects. Genes, p53 / drug effects. Genes, ras / drug effects. Genetic Markers. Humans. Mutagens / toxicity. Oxidative Stress / genetics. Telomere / drug effects. Telomere / genetics

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(PMID = 18304859.001).

[ISSN] 0027-5107

[Journal-full-title] Mutation research

[ISO-abbreviation] Mutat. Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Genetic Markers; 0 / Mutagens

[Number-of-references] 88

   

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[Title] Adenocarcinoma of the colon associated with hyperplastic polyposis.

[MeSH-major] Adenocarcinoma, Mucinous / pathology. Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Neoplasms, Multiple Primary / pathology. Neoplastic Syndromes, Hereditary / diagnosis

[MeSH-minor] Adenoma, Villous / pathology. Adenoma, Villous / surgery. Adenomatous Polyposis Coli / diagnosis. Adult. Colectomy. Colonoscopy. CpG Islands. DNA Methylation / genetics. Diagnosis, Differential. Female. Humans. Hyperplasia. Proto-Oncogene Proteins B-raf / genetics

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(PMID = 20363055.001).

[ISSN] 0210-5705

[Journal-full-title] Gastroenterología y hepatología

[ISO-abbreviation] Gastroenterol Hepatol

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Spain

[Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf

   

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[Title] Global histone H4 acetylation and HDAC2 expression in colon adenoma and carcinoma.

Chromatin remodeling and activation of transcription are important aspects of gene regulation, but these often go awry in disease progression, including during colon cancer development.

We investigated the status of global histone acetylation (by measuring H3, H4 acetylation of lysine residues, which also occur over large regions of chromatin including coding regions and non-promoter sequences) and expression of histone deacetylase 2 (HDAC2) in colorectal cancer (CRC) tissue microarrays using immunohistochemical staining.

Specifically, HDAC2 and the acetylation of histones H4K12 and H3K18 were evaluated in 134 colonic adenomas, 55 moderate to well differentiated carcinomas, and 4 poorly differentiated carcinomas compared to matched normal tissue.

HDAC2 nuclear expression was detected at high levels in 81.9%, 62.1%, and 53.1% of CRC, adenomas, and normal tissue, respectively (P = 0.002).

HDAC2 expression was correlated significantly with progression of adenoma to carcinoma (P = 0.002), with a discriminative power of 0.74, when comparing cancer and non-cancer cases.

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(PMID = 19057998.001).

[ISSN] 1573-2568

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA122959; United States / NCI NIH HHS / CA / CA122959-02; United States / NCI NIH HHS / CA / R01 CA122959-02; United States / PHS HHS / / A102681; United States / NCI NIH HHS / CA / R01 CA122959

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Histones; EC 3.5.1.98 / Histone Deacetylases

[Other-IDs] NLM/ NIHMS118762; NLM/ PMC2737733

   

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[Title] Colorectal polyps in carriers of the APC I1307K polymorphism.

The prevalence of polyps and adenomas in specimens of colorectal cancer who are carriers and noncarriers of the APC I1307K polymorphism is compared.

METHOD: Prevalence of adenomatous polyps in the pathology specimens of the study participants, stratified by their APC I1307K polymorphism status, was studied in 900 consecutive cases of colorectal cancer diagnosed in northern Israel between 1998 and 2002, within the framework of a population-based, case-controlled study (MECC Study).

Prevalence was higher among Ashkenazi Jews (11.2 percent) than among non-Ashkenazi Jews (2.7 percent) or Arabs (3.1 percent).

After adjustment for age, APC I1307K carriers were significantly more likely than noncarriers to have polyps in their surgical specimen (51.3 percent vs. 32.6 percent, P = 0.002).

Adenomas with a tubular component (either tubular adenomas or tubulovillous adenomas), but not villous adenomas, were significantly more frequent among carriers (37.2 percent vs. 23.6 percent, P = 0.005).

CONCLUSION: Together with former evidence of I1307K being a risk factor for colorectal cancer, these data suggest that colonoscopic surveillance for colorectal adenomas and cancer may be warranted in I1307K carriers, even in the absence of other identifiable risk factors.

[MeSH-major] Adenoma / genetics. Colonic Polyps / genetics. Colorectal Neoplasms / genetics. Genes, APC. Polymorphism, Genetic

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(PMID = 16228836.001).

[ISSN] 0012-3706

[Journal-full-title] Diseases of the colon and rectum

[ISO-abbreviation] Dis. Colon Rectum

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Dose-dependent promoting effect of dextran sodium sulfate on mouse colon carcinogenesis initiated with azoxymethane.

We previously reported a powerful tumor-promoting ability of dextran sodium sulfate (DSS) in a novel mouse model for colitis-related colon carcinogenesis initiated with azoxymethane (AOM).

All animals were sacrificed at week 14 and histological alterations in their colon and nitrotyrosine immunohistochemistry were examined to evaluate the nitrosative stress.

In the mice which received AOM and 2% DSS, the incidences (multiplicity) of colonic tubular adenoma and adenocarcinoma were 75% (1.25+/-1.26/mouse) and 100% (2.75+/-2.22/mouse), respectively.

Mice given AOM and 1% DSS had 80% incidence of adenoma (1.00+/-0.71/mouse) and 60% incidence of adenocarcinoma (1.40+/-2.07/mouse) in the colon.

In a mouse treated with AOM and 0.5% DSS, only one colonic adenoma (20% incidence with 0.20+/-0.45 multiplicity) developed.

Higher frequency of high-grade colonic dysplasia was noted in mice given AOM and 2% or 1% DSS when compared with mice treated with AOM and lower doses of DSS.

Also, scoring of inflammation and nitrotyrosine immunoreactivity suggested that severe inflammation and nitrosation stress caused by high-doses (2% and 1%) of DSS contribute its tumor-promoting effects in mouse colon carcinogenesis initiated with a low dose of AOM.

[MeSH-major] Carcinogens / toxicity. Colonic Neoplasms / chemically induced. Dextran Sulfate / toxicity. Tyrosine / analogs & derivatives

[MeSH-minor] Animals. Azoxymethane / administration & dosage. Azoxymethane / toxicity. Cocarcinogenesis. Colitis / chemically induced. Colitis / pathology. Colonic Diseases / chemically induced. Colonic Diseases / pathology. Dose-Response Relationship, Drug. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Mice. Mice, Inbred ICR. Ulcer / chemically induced. Ulcer / pathology

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(PMID = 15736053.001).

[ISSN] 0213-3911

[Journal-full-title] Histology and histopathology

[ISO-abbreviation] Histol. Histopathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Spain

[Chemical-registry-number] 0 / Carcinogens; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 9042-14-2 / Dextran Sulfate; MO0N1J0SEN / Azoxymethane

   

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[Transliterated title] Manejo anestésico de un paciente con displasia arritmogénica de ventrículo derecho, ascitis y colitis ulcerosa para una cirugía abdominal mayor.

A 43-year-old man with ulcerative colitis was scheduled for pancolectomy owing to adenomatous transformation of polyps.

[MeSH-minor] Adenomatous Polyps / surgery. Adult. Analgesia, Epidural / methods. Atracurium / analogs & derivatives. Catheter Ablation. Colonic Neoplasms / surgery. Colonic Polyps / surgery. Defibrillators, Implantable. Equipment Failure. Fentanyl. Humans. Isoflurane. Male. Monitoring, Intraoperative. Pain, Postoperative / drug therapy. Postoperative Care. Postoperative Complications / surgery. Preanesthetic Medication. Respiration, Artificial. Thiopental

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(PMID = 16435619.001).

[ISSN] 0034-9356

[Journal-full-title] Revista española de anestesiología y reanimación

[ISO-abbreviation] Rev Esp Anestesiol Reanim

[Language] spa

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Spain

[Chemical-registry-number] 64228-79-1 / Atracurium; 76-75-5 / Thiopental; CYS9AKD70P / Isoflurane; QX62KLI41N / cisatracurium; UF599785JZ / Fentanyl

   

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The primary endpoint was the detection of patients having colon cancer or at least one adenoma.

Significantly more neoplastic (adenomatous and cancerous) lesions and more flat adenomas could be detected using high definition endoscopy with surface enhancement.

[MeSH-major] Adenoma / diagnosis. Colonic Polyps / diagnosis. Colonoscopy / methods. Colorectal Neoplasms / diagnosis. Image Enhancement / instrumentation. Image Enhancement / methods

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[Copyright] © Georg Thieme Verlag KG Stuttgart · New York.

[CommentIn] Endoscopy. 2010 Oct;42(10):866-9 [20886407.001]

(PMID = 20803419.001).

[ISSN] 1438-8812

[Journal-full-title] Endoscopy

[ISO-abbreviation] Endoscopy

[Language] eng

[Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial

[Publication-country] Germany

   

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[Title] Bile acid induced gene expression in LT97 colonic adenoma cells.

LT97 human colonic adenoma cells reflecting early premalignant genotype and growth characteristics have been posed to tumor promoting bile acids in order to identify marker genes that permit identification of tumor promoters in vitro.

Physiologically relevant concentrations of desoxycholate (DOC) and chenodesoxycholate (CDC) upregulated expression of c-fos and COX-2 in a concentration- and time-dependent manner.

Transient induction of c-fos was seen with the non-promoting taurodesoxycholate (TDOC) as well as DOC, however extended induction at 3 h was only achieved by DOC and CDC reaching 3-6-fold as compared to the control.

Stimulation of COX-2 expression was completely specific for the tumor promoting analogs DOC and CDC.

Expression of VEGF was stimulated 4-5-fold in the tumor promoter (DOC and CDC) groups and about 2-fold in the non-promoting controls TDOC and GCDC.

At later times the tumor promoter specific difference was lost.

Our results show that all three genes are modulated in a tumor promoter dependent way and that their upregulation in LT97 adenoma cells can be used for in vitro testing of colon tumor promoters and chemopreventive compounds.

[MeSH-major] Adenoma / metabolism. Bile Acids and Salts / pharmacology. Biomarkers, Tumor / metabolism. Colonic Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / drug effects

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(PMID = 15582199.001).

[ISSN] 0278-6915

[Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

[ISO-abbreviation] Food Chem. Toxicol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 005990WHZZ / Deoxycholic Acid; 0GEI24LG0J / Chenodeoxycholic Acid; 516-50-7 / Taurodeoxycholic Acid; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases

   

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[Title] [Emerging concepts in colorectal serrated polyps].

Colorectal serrated polyps are heterogeneous epithelial lesions characterized by a serrated architecture.

They include the classical hyperplastic polyps and the much rarer serrated adenomas and mixed polyps.

Whereas serrated adenomas are composed of an unequivocal adenomatous epithelium with architectural serrated, mixed polyps include two separate hyperplastic and adenomatous components.

During the past few years, another type of serrated polyp with only very subtle proliferation abnormalities has been described.

These atypical serrated polyps may occur either sporadically or in the context of colorectal polyposis.

Despite their close resemblance to traditional hyperplastic polyps, some authors argued that they should be regarded as authentically neoplastic lesions and have proposed to call them "sessile serrated adenomas".

This article reviews the histological features, the endoscopic appearance, the natural history and the molecular phenotype of the different categories of serrated polyps and introduces the concept of "serrated neoplastic pathway" in the development of colorectal cancer.

[MeSH-major] Adenoma / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology

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(PMID = 17273130.001).

[ISSN] 0399-8320

[Journal-full-title] Gastroentérologie clinique et biologique

[ISO-abbreviation] Gastroenterol. Clin. Biol.

[Language] fre

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] France

[Number-of-references] 90

   

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[Title] Noninvasive monitoring of colonic carcinogenesis: feasibility of [(18)F]FDG-PET in the azoxymethane model.

BACKGROUND: Azoxymethane (AOM) is a potent carcinogen that induces colorectal cancer and adenomas in rats.

At present, it is unknown at which stage FDG accumulation occurs during the adenoma carcinoma sequence.

RESULTS: Macroscopic examination revealed 21 tumors (7 located in the small bowel and 14 in the colon) in 19 rats.

On histological examination, we found 10 colonic adenocarcinomas (the first being observed at Week 22) and 7 adenocarcinoma in the small bowel.

In total, seven colon adenomas were found in five rats, six of which expressed high-grade dysplasia.

[(18)F]FDG uptake was lower in adenomas than in carcinomas.

[MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / radionuclide imaging. Colonic Neoplasms / metabolism. Colonic Neoplasms / radionuclide imaging. Disease Models, Animal. Fluorodeoxyglucose F18 / pharmacokinetics

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(PMID = 16546679.001).

[ISSN] 0969-8051

[Journal-full-title] Nuclear medicine and biology

[ISO-abbreviation] Nucl. Med. Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; MO0N1J0SEN / Azoxymethane

   

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[Title] Serrated pathway and APC (conventional)-type colorectal polyps: molecular-morphologic correlations, genetic pathways, and implications for classification.

This review addresses the genetic mutations and cell signaling pathway alterations in colorectal premalignant polyps, focusing on the link between molecular changes and morphologic features.

Biallelic APC (adenomatous polyposis coli) mutations are directly responsible for the specific and characteristic cytologic features of dysplastic cells in conventional tubular adenomas.

Sessile serrated adenomas (SSAs) are the precursor lesions of the serrated neoplasia pathway.

Intracellular butyrate inhibits histone deacetylase, allowing histone hyperacetylation and, eventually, transcriptional activation of specific genes.

Progressive loss of cell cycle control and decreased and altered cytoplasmic differentiation produce the characteristic constellation of morphologic changes of SSAs and traditional serrated adenomas.

[MeSH-major] Adenomatous Polyposis Coli / pathology. Colonic Polyps / pathology

[MeSH-minor] Adaptor Proteins, Signal Transducing. Adenomatous Polyposis Coli Protein / physiology. Carrier Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Nuclear Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics

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(PMID = 16483003.001).

[ISSN] 0002-9173

[Journal-full-title] American journal of clinical pathology

[ISO-abbreviation] Am. J. Clin. Pathol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adenomatous Polyposis Coli Protein; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf

[Number-of-references] 123

   

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[Title] An anti-adenoma antibody, Adnab-9, may reflect the risk for neoplastic progression in familial hamartomatous polyposis syndromes.

Patients with the hamartomatous polyposis Peutz-Jeghers and familial juvenile polyposis syndromes are predisposed to colorectal cancer but lack early genetic alterations found in adenomatous premalignant lesions.

We studied hamartomatous polyps for the expression of an early preneoplastic colorectal neoplasia risk marker also found in familial adenomatous polyposis patients.

Retrospective, genetic, and hospital archival tissue immunohistochemistry using Adnab-9, a premalignant marker often found in Paneth-like cells (PCs), was performed on sections of polyps from eight patients with Peutz-Jeghers syndrome, eight patients with familial juvenile polyposis, and 36 hyperplastic polyp control sections.

Hamartomatous polyposis patients also underwent specific genetic analysis.

Eighty-nine percent of Peutz-Jeghers syndrome polyps labeled with Adnab-9 compared with 63% for AD5; 88% of familial juvenile polyposis sections also labeled with Adnab-9.

Of the 36 hyperplastic polyp sections, only four (11%) labeled with Adnab-9 and one (3%) with AD5.

Adnab-9 labeling of PCs in the epithelial elements of hamartomatous colonic lesions of hereditary hamartomatous syndrome patients reflects the predisposition to colorectal cancer, further justifying early intervention strategies.

[MeSH-major] Adenomatous Polyposis Coli / pathology. Antibodies, Monoclonal. Biomarkers, Tumor. Colon / pathology. Colonic Polyps / pathology. Peutz-Jeghers Syndrome / pathology

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(PMID = 17934846.001).

[ISSN] 0163-2116

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Adnab-9; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / alpha-defensin 5, human; EC 2.7.1.- / STK11 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases

   

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[Title] [Abdominal obesity, insulin resistance, and the risk of colonic adenoma].

BACKGROUND/AIMS: Abdominal obesity and hyperinsulinemia or insulin resistance are of interest in connection with colon carcinogenesis.

We conducted a prospective case controlled study for the evaluation of relationship between abdominal obesity, insulin resistance, and colorectal adenoma.

METHODS: Fifty patients with colorectal adenoma and fifty healthy subjects were included in this study.

RESULTS: There were no differences in sex, serum insulin, FBS, HOMA-IR, TG, CROL between adenoma and control group.

Subjects with high BMI, WHR, percent body fat, and obesity were more likely to have colonic adenoma.

Multiple logistic regression analysis after adjusting confounding factors, had revealed that WHR was the most important independent risk factor for colon adenoma.

CONCLUSIONS: Abdominal obesity was most closely related to colonic adenoma.

However, insulin resistance was not related to colonic adenoma.

[MeSH-major] Abdominal Fat. Adenoma / etiology. Colonic Neoplasms / etiology. Insulin Resistance. Obesity / complications

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[CommentIn] Korean J Gastroenterol. 2007 Mar;49(3):192-5 [18172350.001]

(PMID = 18172342.001).

[ISSN] 1598-9992

[Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi

[ISO-abbreviation] Korean J Gastroenterol

[Language] kor

[Publication-type] English Abstract; Journal Article

[Publication-country] Korea (South)

   

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Hereditary CRC is conventionally divided into two major categories: hereditary non-polyposis colorectal cancer (HNPCC) and those related to polyposis syndromes including familial adenomatous polyposis (FAP), Peutz-Jegher syndrome (PJS), and juvenile polyposis (JP).

Germ-line mutation of the APC gene induces FAP, an autosomal dominant disorder, characterized by the development of hundreds to thousands of colonic adenomas.

Recently, a mutation on the MYH gene is increasingly being investigated in patients with multiple polyps, and autosomal recessive MYH polyposis is considered to be a new category of polyposis.

Although there is no polyposis, polyps seem to be more villous and dysplastic and appear to grow rapidly into CRCs.

PJS and JP are reported to be characterized by hamartomatous polyps throughout the GI tract and germ-line mutations in the STK11 gene (PJS) and the DPC4/BMPR1A gene (JP).

[MeSH-major] Adenomatous Polyposis Coli / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Intestinal Polyposis / genetics. Peutz-Jeghers Syndrome / genetics

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(PMID = 15725711.001).

[ISSN] 1598-9992

[Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi

[ISO-abbreviation] Korean J Gastroenterol

[Language] kor

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Korea (South)

[Number-of-references] 40

   

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[Title] 2-Dodecylcyclobutanone, a radiolytic product of palmitic acid, is genotoxic in primary human colon cells and in cells from preneoplastic lesions.

Results of previous in vitro studies with primary human colon cells and in vivo experiments with rats fed with 2-alkylcyclobutanones indicated that these radiolytic derivatives may be genotoxic and enhance the progression of colon tumors.

In particular, we explored the relative sensitivities of human colon cells, representing different stages of tumor development and healthy colon tissues, respectively.

HT29clone19A cells, LT97 adenoma cells and primary human epithelial cells were exposed to 2dDCB (150-2097 microM).

Genotoxicity, reflected as strand breaks, was assessed using the alkaline version of the comet assay and chromosomal abnormalities were investigated by 24-color fluorescence-in-situ-hybridization.

2dDCB was cytotoxic in a time- and dose-dependent manner in LT97 adenoma cells and in freshly isolated primary cells but not in the human colon tumor cell line.

Associated with this was a marked induction of DNA damage by 2dDCB in LT97 adenoma cells and in freshly isolated colonocytes, whereas in the HT29clone19A cells no strand breaks were detectable.

A long-term incubation of LT97 adenoma cells with lower concentrations of 2dDCB revealed cytogenetic effects.

In summary, 2dDCB was clearly genotoxic in healthy human colon epithelial cells and in cells representing preneoplastic colon adenoma.

These findings provide additional evidence that this compound may be regarded as a possible risk factor for processes in colon carcinogenesis related to initiation and progression.

[MeSH-major] Colon / drug effects. Cyclobutanes / toxicity. Mutagens / toxicity. Palmitic Acid / metabolism. Precancerous Conditions / genetics

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(PMID = 16153665.001).

[ISSN] 0027-5107

[Journal-full-title] Mutation research

[ISO-abbreviation] Mutat. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Cyclobutanes; 0 / Mutagens; 2V16EO95H1 / Palmitic Acid; 35493-46-0 / 2-dodecylcyclobutanone

   

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[Title] [Serrated, hyperplastic and hyperplasia-like colorectal polyps].

The colorectal hyperplastic polyp has generally been considered a finding of no clinical significance.

Recent research has, however, called attention to the existence of some variants of hyperplastic polyp which are potentially malignant.

The term "advanced serrated polyp" has been coined for such cases, which comprise mixed hyperplastic/adenomatous tissue, serrated adenoma, and sessile serrated polyp, in contrast to the traditional hyperplastic polyp.

Since epithelial dysplasia is an integrated component of mixed hyperplastic/adenomatous polyp and of the serrated adenoma, such a diagnosis would dictate control colonoscopy comparable to the guidelines for subjects with conventional adenomas.

The cytology of the sessile serrated polyp is, however, closer to that of the traditional hyperplastic polyp, whereas the architecture mimics that of the serrated adenoma.

For this reason, a consensus regarding the optimal management of such patients has not been obtained, but if the polyp is sizeable and located in the right colon, control should be considered.

The small, usually left-sided traditional polyp as a rule needs no follow-up, but the context in which such a lesion is found and its morphology may influence the clinical decision.

Future large-scale investigations of serrated colorectal polyps, including interobserver studies, will be required to identify histological details of clinical utility which can be adopted in daily routine practice.

[MeSH-major] Adenoma / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology

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(PMID = 17125655.001).

[ISSN] 1603-6824

[Journal-full-title] Ugeskrift for laeger

[ISO-abbreviation] Ugeskr. Laeg.

[Language] dan

[Publication-type] Comparative Study; English Abstract; Journal Article; Review

[Publication-country] Denmark

[Number-of-references] 40

   

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[Title] The loss of sarco/endoplasmic reticulum calcium transport ATPase 3 expression is an early event during the multistep process of colon carcinogenesis.

To better characterize the role of SERCA3 in colon carcinogenesis, its expression has been investigated in colonic epithelium, benign lesions, adenomas, and adenocarcinomas.

In addition, the regulation of SERCA3 expression was analyzed in the context of the adenomatous polyposis coli/beta-catenin/T-cell factor 4 (TCF4) pathway and of specificity protein 1 (Sp1)-like factor-dependent transcription.

We report that SERCA3 expression increased along the crypts as cells differentiated in normal colonic mucosa and in hyperplastic polyps, was moderately and heterogeneously expressed in colonic adenomas with expression levels inversely correlated with the degree of dysplasia, was barely detectable in well and moderately differentiated adenocarcinomas, and was absent in poorly differentiated tumors.

Inhibition of Sp1-like factor-dependent transcription blocked SERCA3 expression during cell differentiation, and SERCA3 expression was induced by the expression of dominant-negative TCF4 in colon cancer cells.

These data link SERCA3 expression to the state of differentiation of colonic epithelial cells, and relate SERCA3 expression, already decreased in adenomas, to enhanced adenomatous polyposis coli/beta-catenin/TCF4-dependent signaling and deficient Sp1-like factor-dependent transcription.

In conclusion, intracellular calcium homeostasis becomes progressively anomalous during colon carcinogenesis as reflected by deficient SERCA3 expression.

[MeSH-major] Biomarkers, Tumor / analysis. Calcium / metabolism. Calcium-Transporting ATPases / biosynthesis. Colonic Neoplasms / enzymology. Intestinal Mucosa / metabolism

[MeSH-minor] Adenomatous Polyposis Coli Protein / genetics. Blotting, Western. Cell Line, Tumor. Cell Transformation, Neoplastic. Colonic Polyps / enzymology. Cytoskeletal Proteins / genetics. DNA-Binding Proteins. Endoplasmic Reticulum / metabolism. Humans. Immunohistochemistry. Sarcoplasmic Reticulum Calcium-Transporting ATPases. TCF Transcription Factors. Trans-Activators / genetics. Transcription Factor 7-Like 2 Protein. Transcription Factors. Transfection. Transgenes. beta Catenin

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(PMID = 15972967.001).

[ISSN] 0002-9440

[Journal-full-title] The American journal of pathology

[ISO-abbreviation] Am. J. Pathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 2 Protein; 0 / Transcription Factors; 0 / beta Catenin; EC 3.6.3.8 / ATP2A3 protein, human; EC 3.6.3.8 / Calcium-Transporting ATPases; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium

[Other-IDs] NLM/ PMC1603437

   

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Four classes of chemopreventive compounds have demonstrated efficacy in reducing recurrent colorectal adenomas and/or cancer in randomized, controlled trials.

Considerable effort is being expended to define chemopreventive activity, optimal dose, administration schedule, and toxicity for the coxibs in adenoma recurrence prevention trials.

[MeSH-minor] Adenomatous Polyps / complications. Adenomatous Polyps / diagnosis. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Clinical Trials as Topic. Colonic Polyps / diagnosis. Cyclooxygenase Inhibitors / therapeutic use. Female. Forecasting. Humans. Male. Patient Selection. Precancerous Conditions / diagnosis. Precancerous Conditions / therapy. Risk

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(PMID = 15637400.001).

[ISSN] 0732-183X

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA131378; United States / NCI NIH HHS / CA / R01 CA148817; United States / NCI NIH HHS / CA / R01 CA155638

[Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; R16CO5Y76E / Aspirin

[Number-of-references] 167

   

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[Title] The interaction of age and hormone replacement therapy on colon adenoma risk.

BACKGROUND: Several studies have identified a possible interaction between age and hormone replacement therapy on colon neoplasm risk.

RESULTS: There was a significant interaction between age and hormone replacement therapy use (P=0.03) with current estrogen users who were over 56 years of age having a reduced odds of colon adenoma (OR, 0.40; 95% CI, 0.16-0.98) when compared to never users.

Both older women who had used hormone replacement therapy for 3 or less years (OR, 0.07; 95% CI, 0.006-0.81) and those reporting greater than 10 years of use (OR, 0.27; 95% CI, 0.09-0.80) had a reduced adjusted odds for adenomas when compared to non-users.

CONCLUSIONS: Duration of use is not likely to explain the stronger association of hormone replacement therapy use with colon neoplasm in older women.

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(PMID = 17433566.001).

[ISSN] 0361-090X

[Journal-full-title] Cancer detection and prevention

[ISO-abbreviation] Cancer Detect. Prev.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / K07 CA114029; United States / NCI NIH HHS / CA / R01 CA097386-01; United States / NCI NIH HHS / CA / K07 CA114029-01A2; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA095103-01; United States / NCI NIH HHS / CA / CA95103; United States / NCI NIH HHS / CA / CA097386-01; United States / NCI NIH HHS / CA / R01 CA97386

[Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Other-IDs] NLM/ NIHMS24075; NLM/ PMC1949417

   

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[Title] Uranyl nitrilotriacetate, a stabilized salt of uranium, is genotoxic in nontransformed human colon cells and in the human colon adenoma cell line LT97.

To assess possible hazards, we investigated the genotoxic effects of uranyl nitrilotriacetate (U-NTA) in human colon tumor cells (HT29 clone 19A), adenoma cells (LT97), and nontransformed primary colon cells.

Colon cells were incubated with U-NTA.

Cell survival, cytotoxicity, cellular glutathione (GSH) levels, genotoxicity, and DNA repair capacity (comet assay), as well as gene- and chromosome-specific damage combination of comet assay and fluorescence in situ hybridization [FISH], 24-color FISH) were determined.

U-NTA was also genotoxic in LT97 cells and primary colon cells, where it additionally increased migration of TP53 into the comet tail.

[MeSH-major] Colon / drug effects. Uranium / toxicity

[MeSH-minor] Adenoma / genetics. Adenoma / pathology. Cell Line, Tumor. Cell Survival / drug effects. Chromosome Aberrations. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. DNA Damage. Glutathione / analysis. Humans. In Situ Hybridization, Fluorescence. Reactive Oxygen Species. Tumor Suppressor Protein p53 / analysis

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(PMID = 16840563.001).

[ISSN] 1096-6080

[Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology

[ISO-abbreviation] Toxicol. Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; 4OC371KSTK / Uranium; GAN16C9B8O / Glutathione