BioMedLib Search Engine [ goto HOMEPAGE ]

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Association between BMI and metabolic syndrome and adenomatous colonic polyps in Korean men.

Obesity and insulin resistance are associated with the risk of colon cancer.

Adenomatous colonic polyps are precancerous lesions of colon cancer.

We investigated whether BMI and the metabolic syndrome are associated with the presence of adenomatous colonic polyps in Korean men.

Multiple logistic regression analysis was used to evaluate the association between BMI and the metabolic syndrome and adenomatous polyps.

Compared with men in the 1st quintile of the BMI, the adjusted odds ratio (OR) and 95% confidence interval (CI) for adenomatous polyps in men in the 2nd, 3rd, 4th, and 5th quintiles of the BMI were 1.55 (1.10-2.19), 1.57 (1.10-2.24), 1.94 (1.34-2.81), and 1.99 (1.31-3.01), respectively (P for trend <0.0001).

Men with triglycerides (TGs) > or = 150 mg/dl were significantly more likely to have adenomatous polyps than were men with TG <150 mg/dl (OR 1.29; 95% CI 1.03-1.62).

As a function of the number of metabolic risk factors, the ORs for adenomatous polyps were 1.41 (1.03-1.93), 1.52 (1.08-2.12), 1.46 (1.01-2.12), and 1.77 (1.08-2.90) for 1, 2, 3, and > or = 4 risk factors, respectively (P for trend <0.05).

Adenomatous colonic polyps were significantly associated with increased BMI levels.

Subjects with even one component of the metabolic syndrome had a significantly higher risk for developing adenomatous polyps compared to those subjects without any component in Korean men.

[MeSH-major] Adenomatous Polyps / epidemiology. Body Mass Index. Colonic Polyps / epidemiology. Metabolic Syndrome X / physiopathology

MedlinePlus Health Information. consumer health - Colonic Polyps.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18388894.001).

[ISSN] 1930-7381

[Journal-full-title] Obesity (Silver Spring, Md.)

[ISO-abbreviation] Obesity (Silver Spring)

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Triglycerides

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Synchronous ileal carcinoid and primary colonic neoplasms: a case report.

Primary colonic tumours with synchronous ileal carcinoid tumours are rare in occurrence and are mainly found incidentally on autopsies or pathological examination of resected surgical specimens.

This article describes a case of adenomatous colonic polyps, adenocarcinoma of sigmoid colon and concurrent malignant carcinoid tumour of ileocaecal junction, detected on colonoscopic examination.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Tunis Med. 2007 Jul;85(7):607-9 [18064997.001]

[Cites] Aust N Z J Surg. 1997 Oct;67(10):739-41 [9322730.001]

[Cites] Ann Oncol. 2001 Jan;12(1):101-3 [11249034.001]

[Cites] Dis Colon Rectum. 1982 May-Jun;25(4):375-82 [7044728.001]

[Cites] Cancer. 1973 Jul;32(1):216-22 [4716775.001]

[Cites] J Natl Med Assoc. 1996 May;88(5):310-2 [8667441.001]

(PMID = 19918418.001).

[ISSN] 1757-1626

[Journal-full-title] Cases journal

[ISO-abbreviation] Cases J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2769428

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Clinical studies have successfully used tissue autofluorescence with conventional white light endoscopy and biopsy for detecting adenomatous colonic polyps, differentiating benign hyperplastic from adenomas with acceptable sensitivity and specificity.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18167619.001).

[ISSN] 1537-744X

[Journal-full-title] TheScientificWorldJournal

[ISO-abbreviation] ScientificWorldJournal

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers

[Number-of-references] 93

   

Advertisement

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Gardner syndrome is a variant of familial adenomatous polyposis characterized by intestinal adenomatous polyps, which can progress to adenocarcinoma, and a variety of extraintestinal manifestations, including skin cysts, osteomas, soft tissue fibrous tumours and a characteristic ocular lesion.

Gardner syndrome was considered only after excision of subcutaneous fibrous tumours from the mastoid region and paraspinal area and was confirmed by genetic testing in spite of the patient's refusal to undergo colonic endoscopic examination.

Subsequent resection revealed approximately 70 adenomatous colonic polyps in the colon and rectum but no invasive tumour, highlighting the benefits of genetic testing in treatment planning.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16353862.001).

[ISSN] 1479-666X

[Journal-full-title] The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland

[ISO-abbreviation] Surgeon

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Scotland

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Clinicopathologic study of colorectal polyps and obesity in Korean adult].

Numerous epidemiologic studies have shown a positive association between obesity and colorectal polyps.

There are few studies investigating the association between colorectal adenomatous polyps and body fat composition in Korea.

We tried to examine the relationship between body fatness and colorectal adenomatous polyps in health check-up subjects in Korea.

METHODS: Six thousand seven hundred and six routine health check-up subjects, who visited our hospital between March 2002 and April 2005 and underwent distal colon examimation with sigmoidoscopy, were enrolled in this study.

Among them, colonoscopy was done in 860 patients to evaluate the entire colon.

We tried to reveal the relationship between body mass index (BMI) and size, location, number and histopathological type of polyps.

RESULTS: The mean value of BMI in total polyp-free group (23.8+/-2.9) was not different from that of the polyp group (24.5+/-2.8, p=0.09).

The frequency of rectosigmoid polyps in obese patients (20.4%) was higher than that in non-obese patients (16.0%, p<0.05).

The frequency of adenomatous polyp was not different between obese and non-obese group.

Number of polyps (> or=4) correlated well with obesity.

Moreover, age and triglyceride level in patients with colonic adenoma were significantly higher than in patients without colonic adenom.

CONCLUSIONS: This study shows that obesity is not associated with colonic adenomatous polyp in Korean population.

However, we observed that obesity may be associated with rectosigmoid colon polyps.

Furthermore, age and triglyceride level might be the risk factors of colonic adenomatous polyps in Korean population.

[MeSH-major] Adenomatous Polyps / complications. Colonic Neoplasms / complications. Obesity / complications

[MeSH-minor] Adult. Aged. Aged, 80 and over. Body Mass Index. Colonic Polyps / complications. Colonic Polyps / epidemiology. Colonic Polyps / pathology. Comorbidity. Female. Humans. Korea. Male. Middle Aged. Retrospective Studies. Sigmoidoscopy

Genetic Alliance. consumer health - Obesity.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18167428.001).

[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)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Working through a diagnostic challenge: colonic polyposis, Amsterdam criteria, and a mismatch repair mutation.

The two most common causes of hereditary colorectal cancer are Lynch syndrome and familial adenomatous polyposis (FAP).

The phenotype of Lynch syndrome, also known as hereditary nonpolyposis colorectal cancer (HNPCC), is differentiated in part from FAP by the lack of profuse colonic polyposis.

Here we describe a proband who presented with greater than 50 adenomatous colonic polyps prior to developing cancer of the colon and urinary bladder, and a family history that fulfills the Amsterdam criteria.

We outline evidence supporting the pathogenicity of the identified hMSH6 mutation (arg772trp) and suggest possible etiologies for the unexplained colonic adenomatous polyposis.

[MeSH-major] Adenocarcinoma / diagnosis. Adenomatous Polyposis Coli / complications. Colonic Neoplasms / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. DNA-Binding Proteins

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Gastroenterol. 2002 Jul;97(7):1822-7 [12135043.001]

[Cites] Clin Genet. 1998 Oct;54(4):368-70 [9831355.001]

[Cites] Gut. 1997 Aug;41(2):235-8 [9301504.001]

[Cites] Gene. 2001 Jul 11;272(1-2):301-13 [11470537.001]

[Cites] Gastroenterology. 1999 Jun;116(6):1453-6 [10348829.001]

[Cites] Gastroenterology. 2004 Jan;126(1):42-8 [14699485.001]

[Cites] Hum Mol Genet. 2001 Apr;10(7):721-33 [11257105.001]

[Cites] Hum Mutat. 2004 Mar;23(3):285 [14974087.001]

[Cites] Int J Cancer. 2006 Aug 15;119(4):807-14 [16557584.001]

[Cites] Int J Colorectal Dis. 2006 Jan;21(1):79-83 [16676398.001]

[Cites] J Med Genet. 1999 Oct;36(10 ):790-3 [10528862.001]

[Cites] Dis Colon Rectum. 1991 May;34(5):424-5 [2022152.001]

[Cites] Int J Colorectal Dis. 2006 Dec;21(8):847-50 [16525781.001]

[Cites] J Bacteriol. 1994 Sep;176(17):5393-400 [8071216.001]

[Cites] Hum Genet. 2006 Mar;119(1-2):206-11 [16408224.001]

[Cites] Gut. 2003 Jun;52(6):898-9 [12740349.001]

[Cites] Fam Cancer. 2007;6(1):43-51 [17039270.001]

[Cites] Fam Cancer. 2003;2(1):43-55 [14574166.001]

[Cites] Clin Gastroenterol Hepatol. 2005 Oct;3(10):1022-8 [16234049.001]

[Cites] J Biol Chem. 2002 Mar 29;277(13):11135-42 [11801590.001]

[Cites] Proc Natl Acad Sci U S A. 2003 May 13;100(10):5908-13 [12732731.001]

[Cites] Int J Cancer. 2002 Feb 10;97(5):643-8 [11807791.001]

(PMID = 18176851.001).

[ISSN] 1389-9600

[Journal-full-title] Familial cancer

[ISO-abbreviation] Fam. Cancer

[Language] eng

[Grant] United States / NCRR NIH HHS / RR / M01 RR000043; United States / NCI NIH HHS / CA / R25 CA085771; United States / NCRR NIH HHS / RR / M01 RR00043; United States / NCI NIH HHS / CA / R25 CA85771

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

[Publication-country] Netherlands

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Computed tomographic virtual colonoscopy computer-aided polyp detection in a screening population.

BACKGROUND & AIMS: The sensitivity of computed tomographic (CT) virtual colonoscopy (CT colonography) for detecting polyps varies widely in recently reported large clinical trials.

Our objective was to determine whether a computer program is as sensitive as optical colonoscopy for the detection of adenomatous colonic polyps on CT virtual colonoscopy.

Our enhanced gold standard combined segmental unblinded optical colonoscopy and retrospective identification of precise polyp locations.

The data were randomized into separate training (n = 394) and test (n = 792) sets for analysis by a computer-aided polyp detection (CAD) program.

RESULTS: For the test set, per-polyp and per-patient sensitivities for CAD were both 89.3% (25/28; 95% confidence interval, 71.8%-97.7%) for detecting retrospectively identifiable adenomatous polyps at least 1 cm in size.

The false-positive rate was 2.1 (95% confidence interval, 2.0-2.2) false polyps per patient.

At both 8-mm and 10-mm adenoma size thresholds, the per-patient sensitivities of CAD were not significantly different from those of optical colonoscopy before segmental unblinding.

CONCLUSIONS: The per-patient sensitivity of CT virtual colonoscopy CAD in an asymptomatic screening population is comparable to that of optical colonoscopy for adenomas > or = 8 mm and is generalizable to new CT virtual colonoscopy data.

MedlinePlus Health Information. consumer health - Colonic Polyps.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Radiology. 2001 Apr;219(1):51-9 [11274534.001]

[Cites] Radiology. 2001 Feb;218(2):375-83 [11161149.001]

[Cites] Radiology. 2000 Sep;216(3):704-11 [10966698.001]

[Cites] Radiology. 2000 Jul;216(1):284-90 [10887263.001]

[Cites] AJR Am J Roentgenol. 2000 Jun;174(6):1543-9 [10845478.001]

[Cites] J Comput Assist Tomogr. 2004 May-Jun;28(3):318-26 [15100534.001]

[Cites] Radiology. 2001 Jun;219(3):685-92 [11376255.001]

[Cites] Radiology. 2001 Sep;220(3):781-6 [11526282.001]

[Cites] Radiology. 2001 Sep;220(3):787-94 [11526283.001]

[Cites] Gastroenterology. 2003 Aug;125(2):304-10 [12891529.001]

[Cites] Acad Radiol. 2005 Feb;12(2):182-90 [15721595.001]

[Cites] Lancet. 2005 Jan 22-28;365(9456):305-11 [15664225.001]

[Cites] Ann Intern Med. 2004 Sep 7;141(5):352-9 [15353426.001]

[Cites] Radiology. 2004 Nov;233(2):328-37 [15358854.001]

[Cites] AJR Am J Roentgenol. 2005 Jan;184(1):105-8 [15615958.001]

[Cites] JAMA. 2004 Jul 28;292(4):432; author reply 433 [15280338.001]

[Cites] JAMA. 2004 Jul 28;292(4):432-3; author reply 433 [15280337.001]

[Cites] JAMA. 2004 Jul 28;292(4):431-2; author reply 433 [15280336.001]

[Cites] JAMA. 2004 Jul 28;292(4):431; author reply 433 [15280335.001]

[Cites] IEEE Trans Med Imaging. 2004 Jun;23(6):661-75 [15191141.001]

[Cites] Eur Radiol. 2004 Jun;14(6):1025-33 [14872280.001]

[Cites] Med Phys. 2004 Apr;31(4):860-72 [15125004.001]

[Cites] JAMA. 2004 Apr 14;291(14):1713-9 [15082698.001]

[Cites] CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29 [14974761.001]

[Cites] Acad Radiol. 2004 Jan;11(1):103-5 [14746409.001]

[Cites] N Engl J Med. 2003 Dec 4;349(23):2191-200 [14657426.001]

[Cites] AJR Am J Roentgenol. 2003 Dec;181(6):1599-606 [14627581.001]

[Cites] Gastroenterology. 2003 Sep;125(3):688-95 [12949715.001]

[Cites] AJR Am J Roentgenol. 2003 Sep;181(3):799-805 [12933484.001]

[Cites] Gastroenterology. 2003 Aug;125(2):311-9 [12891530.001]

[Cites] IEEE Trans Med Imaging. 2001 Dec;20(12):1251-60 [11811825.001]

[Cites] IEEE Trans Med Imaging. 2001 Dec;20(12):1261-74 [11811826.001]

[Cites] Eur Radiol. 2002 Jan;12(1):77-81 [11868078.001]

[Cites] Eur Radiol. 2002 Jun;12(6):1405-9 [12042946.001]

[Cites] Radiographics. 2002 Jul-Aug;22(4):963-79 [12110726.001]

[Cites] Radiology. 2002 Nov;225(2):391-9 [12409571.001]

[Cites] IEEE Trans Med Imaging. 2002 Dec;21(12):1461-7 [12588030.001]

[Cites] Radiology. 2003 May;227(2):378-84 [12732696.001]

[CommentOn] Gastroenterology. 2005 Dec;129(6):2103-6 [16344077.001]

(PMID = 16344052.001).

[ISSN] 0016-5085

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] ENG

[Grant] United States / CLC NIH HHS / CL / Z01 CL040003-03; United States / Intramural NIH HHS / /

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

[Publication-country] United States

[Other-IDs] NLM/ NIHMS11760; NLM/ PMC1576342

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

METHODS: The presence of the d3GHR polymorphism was assessed in 86 acromegalic patients with long-term disease control and related to anthropometric parameters, cardiovascular risk factors, osteoarthritis, bone mineral density, colonic polyps and diverticulae, and dolichocolon.

Carriers of the d3GHR isoform showed increased prevalence of osteoarthritis, especially of the hip [adjusted odds ratio (OR), 5.2; 95% confidence interval (CI), 3.2-7.1], of adenomatous polyps (adjusted OR, 4.1; 95% CI, 2.4-5.6), and dolichocolon (adjusted OR, 3.2; 95% CI, 1.8-4.6).

Anthropometric parameters, cardiovascular risk factors, bone mineral density, and (non)vertebral fractures were not significantly different between patients with and without the d3GHR allele.

CONCLUSION: In patients with long-term cured acromegaly, the d3GHR polymorphism is associated with an increased prevalence of irreversible comorbidities such as osteoarthritis, dolichocolon, and adenomatous colonic polyps, but not with other comorbidities such as cardiovascular risk factors.

[MeSH-minor] Adult. Aged. Aged, 80 and over. Anthropometry. Bone Density / genetics. Bone Density / physiology. Cardiovascular Diseases / epidemiology. Cardiovascular Diseases / genetics. Cohort Studies. Colonic Diseases / epidemiology. Colonic Diseases / genetics. DNA / genetics. DNA / isolation & purification. Female. Gene Deletion. Genetic Predisposition to Disease. Human Growth Hormone / metabolism. Human Growth Hormone / physiology. Humans. Insulin-Like Growth Factor I / metabolism. Male. Middle Aged. Osteoarthritis / epidemiology. Osteoarthritis / genetics. Osteoarthritis / radiography. Osteoporosis / epidemiology. Osteoporosis / genetics. Risk Factors. Spinal Fractures / epidemiology. Spinal Fractures / genetics. Treatment Outcome

Genetic Alliance. consumer health - Acromegaly.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19864451.001).

[ISSN] 1945-7197

[Journal-full-title] The Journal of clinical endocrinology and metabolism

[ISO-abbreviation] J. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Somatotropin; 12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9007-49-2 / DNA

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] An association between obesity and the prevalence of colonic adenoma according to age and gender.

BACKGROUND: Epidemiologic data on obesity as a risk factor for colonic adenoma with respect to gender have not yet been confirmed.

Here, we aimed to compare the prevalence of colonic adenoma and of advanced polyps in age-stratified men and women at baseline, to examine the role of body mass index (BMI) on colonic adenoma risk according to age and gender, and to examine the influence of menopausal status.

BMI was assessed, and histology, size, and location of the adenoma were examined for each patient.

RESULTS: A significant increase in the prevalence of colonic adenoma and of advanced polyps was found to occur with age (P for trend < 0.01).

The prevalences of adenoma and advanced polyps were higher in men in most age groups (P < 0.01), but no significant difference in prevalences was observed between genderes in patients 70 years of age or older.

Moreover, a positive association between BMI and the prevalence of colonic adenoma and advanced polyps was shown in relatively young individuals of both gender (men in their thirties, P < 0.05; women in their forties, P < 0.05), and premenopausal women according to hormonal status (P = 0.01).

CONCLUSIONS: Our data suggest that obesity increases the risk of colonic adenoma in relatively young people and in premenopausal women subject to estrogen effects.

[MeSH-major] Adenoma / epidemiology. Colonic Neoplasms / epidemiology. Obesity / complications

[MeSH-minor] Adult. Age Factors. Aged. Biopsy. Body Mass Index. Colonic Polyps / epidemiology. Colonic Polyps / etiology. Colonic Polyps / pathology. Colonoscopy. Female. Humans. Korea / epidemiology. Male. Menopause. Middle Aged. Prevalence. Retrospective Studies. Risk Factors. Sex Factors

Genetic Alliance. consumer health - Obesity.

MedlinePlus Health Information. consumer health - Obesity.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Int J Cancer. 1992 May 28;51(3):386-9 [1592529.001]

[Cites] Gut. 2002 Aug;51(2):147 [12117867.001]

[Cites] Gastroenterology. 2002 Sep;123(3):882-932 [12198715.001]

[Cites] Br J Cancer. 2001 Aug 3;85(3):346-9 [11487263.001]

[Cites] Cancer Causes Control. 2003 Feb;14(1):75-84 [12708728.001]

[Cites] Gut. 2004 Jan;53(1):156 [14684597.001]

[Cites] Cancer Causes Control. 1998 Aug;9(4):441-6 [9794177.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1212-8 [15894674.001]

[Cites] Br J Cancer. 1993 Jan;67(1):172-6 [8427777.001]

[Cites] J Nutr. 2001 Nov;131(11 Suppl):3109S-20S [11694656.001]

[Cites] Cancer Causes Control. 1995 Mar;6(2):164-79 [7749056.001]

[Cites] Ann Intern Med. 1998 May 1;128(9):705-12 [9556463.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Oct;5(10):779-84 [8896888.001]

[Cites] Gut. 2002 Aug;51(2):191-4 [12117878.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2000 Apr;9(4):443-7 [10794491.001]

[Cites] Am J Epidemiol. 2000 Nov 1;152(9):847-54 [11085396.001]

[Cites] Br J Cancer. 2005 Oct 31;93(9):1062-7 [16234822.001]

[Cites] Gastroenterology. 1993 Jan;104(1):137-44 [8419236.001]

[Cites] J Natl Cancer Inst. 1991 Mar 6;83(5):359-61 [1995919.001]

[Cites] Am J Epidemiol. 1998 Apr 1;147(7):670-80 [9554606.001]

[Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1799-805 [11734596.001]

[Cites] Cancer Causes Control. 2004 Aug;15(6):581-9 [15280637.001]

[Cites] N Engl J Med. 2005 May 19;352(20):2061-8 [15901859.001]

(PMID = 17701124.001).

[ISSN] 0944-1174

[Journal-full-title] Journal of gastroenterology

[ISO-abbreviation] J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Decreased histamine catabolism in the colonic mucosa of patients with colonic adenoma.

INTRODUCTION: Alterations in mucosal histamine degradation play an important role in various gastrotinestinal diseases including colonic adenoma.

METHODS: About 94 colonic biopsies were endoscopically obtained from 23 patients suffering from colonic adenoma and 26 biopsies from six healthy individuals.

RESULTS: In adenoma patients DAO activities were slightly and HNMT activities were significantly decreased in normal mucosa compared to controls.

Activities of both enzymes were significantly lower in adenoma tissue than in healthy mucosa in the same patients.

Histamine concentrations were elevated in adenoma patients.

CONCLUSIONS: Histamine catabolism is decreased in the colonic mucosa of patients with colonic adenoma.

[MeSH-major] Adenoma / metabolism. Colonic Neoplasms / metabolism. Histamine / metabolism. Intestinal Mucosa / metabolism

[MeSH-minor] Adenoma, Villous / metabolism. Adult. Aged. Amine Oxidase (Copper-Containing) / metabolism. Female. Histamine N-Methyltransferase / metabolism. Humans. Male. Middle Aged

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Inflamm Res. 2002 Apr;51 Suppl 1:S91-2 [12013427.001]

[Cites] Agents Actions. 1991 May;33(1-2):4-7 [1897445.001]

[Cites] Br J Surg. 2002 Jul;89(7):845-60 [12081733.001]

[Cites] Inflamm Res. 2001 Apr;50 Suppl 2:S96-7 [11411621.001]

[Cites] Inflamm Res. 1999 Apr;48 Suppl 1:S75-6 [10350171.001]

[Cites] Gut. 1993 Aug;34(8):1091-6 [8174960.001]

[Cites] Agents Actions. 1989 Nov;28(3-4):164-7 [2480702.001]

[Cites] Inflamm Res. 2004 Mar;53 Suppl 1:S87-8 [15054633.001]

[Cites] Z Gastroenterol. 1998 Aug;36(8):645-55 [9773483.001]

[Cites] Life Sci. 1983 Jun 20;32(25):2855-67 [6343748.001]

[Cites] Gut. 1994 Nov;35(11):1632-6 [7828988.001]

[Cites] Br J Clin Pharmacol. 1992 Oct;34(4):322-7 [1457266.001]

[Cites] Inflamm Res. 1995 Apr;44 Suppl 1:S94-5 [8521021.001]

[Cites] Clin Cancer Res. 2001 May;7(5):1118-26 [11350874.001]

[Cites] Biochim Biophys Acta. 1997 Jun 20;1340(1):152-64 [9217025.001]

[Cites] Anal Biochem. 1985 Oct;150(1):76-85 [3843705.001]

[Cites] Agents Actions. 1985 Apr;16(3-4):91-4 [3925736.001]

[Cites] Agents Actions. 1989 Apr;27(1-2):218-20 [2501972.001]

[Cites] Klin Wochenschr. 1982 Sep 1;60(17):873-81 [6182349.001]

[Cites] Inflamm Res. 1999 Jun;48(6):296-300 [10442480.001]

[Cites] Med J Aust. 1998 Nov 2;169(9):493-8 [9847903.001]

[Cites] J Biol Chem. 1959 Nov;234:2948-50 [13804910.001]

[Cites] Semin Gastrointest Dis. 2000 Oct;11(4):185-93 [11057946.001]

[Cites] BMJ. 2000 Oct 7;321(7265):886-9 [11021873.001]

[Cites] Agents Actions. 1984 Apr;14(3-4):325-34 [6428188.001]

[Cites] Gastroenterology. 2000 Sep;119(3):837-53 [10982778.001]

[Cites] Inflamm Res. 2000 Apr;49 Suppl 1:S35-6 [10864411.001]

[Cites] Cancer Cell. 2002 Apr;1(3):233-6 [12086859.001]

[Cites] Agents Actions. 1988 Apr;23(3-4):354-6 [3134803.001]

[Cites] Ann N Y Acad Sci. 1998 Nov 17;859:262-6 [9928401.001]

[Cites] Agents Actions. 1985 Apr;16(3-4):287-90 [2409778.001]

[Cites] Agents Actions. 1973 Oct;3(3):148-56 [4361531.001]

[Cites] Adv Exp Med Biol. 1988;250:745-52 [3151234.001]

[Cites] Can J Physiol Pharmacol. 1985 Jun;63(6):746-50 [4042010.001]

[Cites] Hoppe Seylers Z Physiol Chem. 1973 Sep;354(9):1021-6 [4807799.001]

[Cites] Clin Exp Allergy. 1993 Dec;23(12):982-5 [10779289.001]

(PMID = 17562176.001).

[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

[Chemical-registry-number] 820484N8I3 / Histamine; EC 1.4.3.21 / Amine Oxidase (Copper-Containing); EC 2.1.1.8 / Histamine N-Methyltransferase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

: 11059 Background: Since the pathologic stage is the most powerful prognostic factor for colorectal cancer (CRC), there is a strong need of non-invasive methods for early detection.

METHODS: cfDNA was extracted from plasma samples from 136 patients with primary CRC at different stages [median age 64 yrs; male/female 78/58; stages I-II, 61; stages III-IV, 75], and from 24 patients with adenomas [median age 67 yrs; male/female 17/7)] and from 55 clean-colon healthy subjects [median age 56 yrs; male/female 13/43).

The levels of cfDNA (ALU-115, ALU-247) of CRC patients (stages I-II and stages III-IV) were compared with those of healthy subjects and patients with adenoma.

RESULTS: The median concentrations of total cfDNA (ALU115) in the plasma samples from patients with stages III-IV and stages I-II CRC, adenoma and normal controls were 52,4, 11.9; 1.9, and 1.7 ng/ml, respectively (p<.0001).

With a cut-off of 4.86 ng/ml, total DNA (ALU115) showed a sensitivity of 78.52 (95% CI 70.6-85.1) and a specificity of 86.08 (95% CI 76.4-92.8) in distinguishing patients with CRC from non-CRC [AUC: 0.860 (95% CI 0.81-0,90), p-value=.0001].

With a cut-off of 3.04, cfDNA tumor-related (ALU247) showed a sensitivity of 77.94 (95% CI 70.0-84.6) and a specificity of 82.28 (95% CI 72.1-90.0) in distinguishing patients with CRC from non-CRC [AUC: 0.864 (95% CI 0.81-0,91), p-value=.0001].

CONCLUSIONS: Both ALU115 and ALU 247 fragments of circulating cfDNA seem promising non-invasive molecular markers of detection and progression of CRC.

The findings of the current study require to be confirmed on larger cohorts of patients with CRC and colonic adenoma.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 27963165.001).

[ISSN] 1527-7755

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

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinical and pathologic features of an adenomatous polyp of the colon in a domestic ferret (Mustela putorius furo).

A 6-year-old castrated male domestic ferret (Mustela putorius furo) with a 4-week history of intermittent diarrhea and straining during defecation had an intraluminal mass in the descending colon identified by abdominal ultrasound.

The histopathological diagnosis of the resected mass was an adenomatous polyp of the colon.

[MeSH-major] Adenomatous Polyps / veterinary. Colonic Polyps / veterinary. Ferrets

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Am Anim Hosp Assoc. 1997 Mar-Apr;33(2):156-60 [9111726.001]

[Cites] J Am Vet Med Assoc. 1998 May 1;212(9):1402-6 [9589126.001]

[Cites] Vet Surg. 2006 Jun;35(4):337-40 [16756613.001]

[Cites] N Engl J Med. 2006 Dec 14;355(24):2551-7 [17167138.001]

[Cites] BMJ. 2000 Oct 7;321(7265):886-9 [11021873.001]

(PMID = 21286327.001).

[ISSN] 0008-5286

[Journal-full-title] The Canadian veterinary journal = La revue vétérinaire canadienne

[ISO-abbreviation] Can. Vet. J.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Canada

[Other-IDs] NLM/ PMC2957035

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

Genetic Alliance. consumer health - Obesity.

MedlinePlus Health Information. consumer health - Obesity.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinico-epidemiologic study of the metabolic syndrome and lifestyle factors associated with the risk of colon adenoma and adenocarcinoma.

Prevention is clearly important and the present study aimed to clarify risk factors and to promote colon cancer screening.

RESULTS: Low-grade adenoma was more frequent among the elderly and in men.

All of the men and 87.5% of the women with high-grade adenoma or adenocarcinoma were aged≥45 and≥50 years, respectively.

In women, a larger waist circumference (=80 cm) increased the odds ratio for colon adenoma or adenocarcinoma (colon tumors) by 1.033 (95% confidence index (CI), 1.001-1.066; p=0.040).

Metabolic syndrome significantly increased the odds ratio of colon tumors in men, but not in women.

Cigarette smoking, drinking alcohol, and increased physical activity were significant risk factors for colon tumors in men, with odds ratios of 1.001 (95% CI, 1.000-1.002; p=0.001), 1.001 (95% CI, 1.000-1.003; p=0.047), and 1.406 (95% CI 1.038-1.904; p=0.028), respectively.

CONCLUSIONS: Colon tumors have a high prevalence in the elderly.

A larger waist circumference in women and metabolic syndrome in both men and women elevate the risk of colon tumors.

In addition, smoking, drinking, and excessive physical activity are risk factors for adenoma and adenocarcinoma in men.

[MeSH-major] Adenocarcinoma / epidemiology. Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Metabolic Syndrome X / complications

MedlinePlus Health Information. consumer health - Colorectal Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21133610.001).

[ISSN] 2476-762X

[Journal-full-title] Asian Pacific journal of cancer prevention : APJCP

[ISO-abbreviation] Asian Pac. J. Cancer Prev.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Thailand

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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.

MedlinePlus Health Information. consumer health - Hormone Replacement Therapy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer Epidemiol Biomarkers Prev. 2000 Apr;9(4):443-7 [10794491.001]

[Cites] Obstet Gynecol. 1999 May;93(5 Pt 2):880-8 [10912438.001]

[Cites] Cancer Res. 2001 Jan 1;61(1):126-30 [11196149.001]

[Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1799-805 [11734596.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Jul;11(7):622-9 [12101109.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2004 Apr;13(4):546-52 [15066918.001]

[Cites] Lancet. 1970 Sep 12;2(7672):535-7 [4195202.001]

[Cites] Cancer Causes Control. 1994 Jul;5(4):359-66 [8080948.001]

[Cites] Nat Genet. 1994 Aug;7(4):536-40 [7951326.001]

[Cites] J Natl Cancer Inst. 1995 Jul 19;87(14):1067-71 [7616598.001]

[Cites] Cancer Causes Control. 1997 Mar;8(2):130-8 [9134236.001]

[Cites] Cancer Causes Control. 1997 Mar;8(2):146-58 [9134238.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1998 Apr;7(4):329-33 [9568789.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1998 Aug;7(8):653-9 [9718216.001]

[Cites] N Engl J Med. 1999 Jan 14;340(2):101-7 [9887161.001]

[Cites] Dis Colon Rectum. 1999 Feb;42(2):212-7 [10211498.001]

[Cites] Am J Med. 1999 May;106(5):574-82 [10335731.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1219-23 [15894675.001]

[Cites] Cancer Causes Control. 2005 Oct;16(8):965-73 [16132805.001]

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Invasive carcinoma arising from a colonic adenoma with clear cell change.

Clear cell change (CCC) in colonic adenoma is rare, and its biological and clinical significance remains unknown.

Malignant progression of an adenoma with CCC has seldom been reported.

We report a case of a sigmoid adenoma with multiple foci of CCC associated with high-grade dysplasia and invasive carcinoma in a 62-year-old patient.

We evaluated the histochemical and immunohistochemical characteristics of each component of the adenoma.

In contrast to other parts of the adenoma, p53 was strongly and diffusely overexpressed in the areas of CCC, high-grade dysplasia, and carcinoma.

The MIB-1 labeling index was also significantly higher in these components than in other parts of the adenoma.

In conclusion, our findings suggest that CCC in adenoma may be associated with malignant progression of the adenoma.

Hence, for practical purposes, we recommend considering CCC in colonic adenomas as a high-grade dysplasia equivalent and following up the patient accordingly.

[MeSH-major] Adenoma / pathology. Sigmoid Neoplasms / pathology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18602669.001).

[ISSN] 1532-8392

[Journal-full-title] Human pathology

[ISO-abbreviation] Hum. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Carcinoembryonic Antigen; 0 / Tumor Suppressor Protein p53

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Serum insulin levels and the prevalence of adenomatous and hyperplastic polyps in the proximal colon.

BACKGROUND & AIMS: Obesity and diabetes mellitus are associated with an increased incidence of proximal colon cancer.

Colonic adenoma that has been reported to be associated with elevated serum insulin levels and subsets of hyperplastic polyps might serve as a precursor of colon cancer.

In this study, we sought to determine segment-specific associations between serum insulin levels and the prevalence of adenoma and hyperplastic polyps in the proximal and distal colon.

We performed multinomial logistic regression models by using the outcome categories of none (reference), proximal-only, distal-only, and both-segment lesions for the presence of adenoma/hyperplastic polyp with serum insulin, age, gender, lifestyle characteristics, and the presence of other types of lesions as predictors.

RESULTS: Overall, serum insulin levels were significantly associated with adenoma (OR, 1.5; 95% CI, 1.1-2.0; P = .005) and borderline associated with hyperplastic polyps (OR, 1.3; 95% CI, 1.0-1.7; P = .075).

In multinomial logistic regression models, elevated serum insulin levels were significantly associated with proximal-only adenoma (OR, 1.8; 95% CI, 1.2-2.5; P = .002), both-side hyperplastic polyp (OR, 1.7; 95% CI, 1.1-2.5; P = .015), and proximal-only hyperplastic polyp (OR, 1.5; 95% CI, 1.0-2.1; P = .048) and borderline associated with distal-only adenoma (OR, 1.5; 95% CI, 1.0-2.1; P =.059) but not with distal-only hyperplastic polyp.

CONCLUSIONS: Serum insulin levels directly correlate with the presence of adenoma and hyperplastic polyps in the proximal colon and might also less strongly correlate with the presence of distal adenoma.

[MeSH-major] Adenomatous Polyposis Coli / blood. Biomarkers, Tumor / blood. Colonic Polyps / blood. Colonic Polyps / epidemiology. Insulin / blood

MedlinePlus Health Information. consumer health - Colonic Polyps.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[ErratumIn] Clin Gastroenterol Hepatol. 2007 Jan;5(1):137

(PMID = 16979948.001).

[ISSN] 1542-3565

[Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association

[ISO-abbreviation] Clin. Gastroenterol. Hepatol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pseudoinvasion in an adenomatous polyp of the colon mimicking invasive colon cancer.

Pseudoinvasion or pseudocarcinomatous invasion in an adenomatous polyp of the colon can be unfamiliar to an endoscopist.

Pseudoinvasion in an adenomatous polyp represents prolapse of the adenomatous epithelium into its stalk.

In most cases its morphology does not differ from of general adenomatous polyps, but in some cases it can morphologically mimic a malignant polyp with submucosal invasion due to mass-like lesioning of its stalk.

This makes it difficult for endoscopists to differentiate pseudoinvasion in an adenoma from an invasive carcinoma by conventional endoscopy; instead, endoscopic ultrasonography can provide useful information for differentiating these conditions.

We report on an 82-year-old man who presented with a large pedunculated polyp with a thick stalk in the sigmoid colon, which mimicked a submucosal invasive carcinoma.

The patient was diagnosed with pseudoinvasion in an adenomatous polyp after segmental resection of the sigmoid colon.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Pathol. 1973 Jan;26(1):25-31 [4540378.001]

[Cites] Cancer. 1974 Jan;33(1):206-17 [4810096.001]

[Cites] Dis Colon Rectum. 1980 Nov-Dec;23(8):529-35 [7460689.001]

[Cites] Endoscopy. 2001 Aug;33(8):709-18 [11490390.001]

[Cites] Adv Anat Pathol. 2008 Jan;15(1):1-17 [18156808.001]

[Cites] Gastrointest Endosc. 2003 May;57(6):722 [12709708.001]

[Cites] Pathol Int. 2003 Sep;53(9):584-90 [14507314.001]

[Cites] Gastrointest Endosc. 2005 Jan;61(1):1-7 [15672048.001]

[Cites] Am J Surg Pathol. 2002 Feb;26(2):206-15 [11812942.001]

(PMID = 20431736.001).

[ISSN] 2005-1212

[Journal-full-title] Gut and liver

[ISO-abbreviation] Gut Liver

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2852693

[Keywords] NOTNLM ; Adenomatous polyps / EUS / Malignant polyp / Pseudoinvasion

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Disease-associated casein kinase I delta mutation may promote adenomatous polyps formation via a Wnt/beta-catenin independent mechanism.

We speculated that mutations in the autoinhibitory domain of CKIdelta/epsilon might upregulate CKIdelta/epsilon activity and hence Wnt signaling and increase the risk of adenomatous polyps and colon cancer.

Exons encoding the CKIepsilon and CKIdelta regulatory domains were sequenced from DNA obtained from individuals with adenomatous polyps and a family history of colon cancer unaffected by familial adenomatous polyposis or hereditary nonpolyposis colorectal cancer (HNPCC).

A CKIdelta missense mutation, changing a highly conserved residue, Arg324, to His (R324H), was found in an individual with large and multiple polyps diagnosed at a relatively young age.

Second, CKIdelta(R324H) is more potent than wildtype CKIdelta in transformation of RKO colon cancer cells.

This novel human CKIdelta mutation may alter the physiological role and enhance the transforming ability of CKIdelta through a Wnt/beta-catenin independent mechanism and thereby influence colonic adenoma development.

[MeSH-major] Adenomatous Polyps / genetics. Casein Kinase Idelta / genetics. Colonic Neoplasms / genetics

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. (L)-HISTIDINE .

Hazardous Substances Data Bank. (L)-ARGININE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2006 Wiley-Liss, Inc.

(PMID = 17131344.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / PC / N01-PC-3541; United States / NCI NIH HHS / CA / P01 CA73992; United States / NCI NIH HHS / CA / P30 CA42014; United States / NCI NIH HHS / CA / R01 CA40641; United States / NCI NIH HHS / CA / R01 CA80809

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

[Publication-country] United States

[Chemical-registry-number] 0 / Wnt Proteins; 0 / beta Catenin; 4QD397987E / Histidine; 94ZLA3W45F / Arginine; EC 2.7.11.1 / Casein Kinase Idelta

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [The association of obesity and left colonic adenomatous polyps in Korean adult men].

OBJECTIVES: We wanted to evaluate the relationship between obesity and left colonic adenomatous polyps in Korean adult men.

RESULTS: There were 99 cases of colonic adenomatous polyps.

The BMI and WHR were associated with the adenomatous polyps (odds ratio, 1.81 [95% CI=1.02-3.19] for a BMI > or = 25.0 as compared with a BMI < or = 22.9, odds ratio, 3.94 [95% CI = 1.77-8.77] for a WHR > or = 0.95 as compared with a WHR < or = 0.86).

The BMI was not associated with the risk of adenomatous polyps after additional adjustment was made for the WHR, but the association between the WHR and adenomatous polyps was still positive and independent of the BMI (odds ratio, 4.15 [95% CI=1.63-10.59]).

CONCLUSIONS: The results support that obesity, and particularly abdominal obesity, can be associated with an increased risk of incurring colonic adenomatous polyps.

[MeSH-major] Adenomatous Polyps / etiology. Colonic Polyps / etiology. Obesity / complications

Genetic Alliance. consumer health - Obesity.

MedlinePlus Health Information. consumer health - Colonic Polyps.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16358826.001).

[ISSN] 1975-8375

[Journal-full-title] Journal of preventive medicine and public health = Yebang Ŭihakhoe chi

[ISO-abbreviation] J Prev Med Public Health

[Language] kor

[Publication-type] English Abstract; Journal Article

[Publication-country] Korea (South)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Colonic adenoma with squamous metaplasia.

Squamous metaplasia arising within colon adenomas is a rare occurrence, with a 0.4% incidence noted predominantly in elderly males.

A case of squamous metaplasia arising in a tubulovillous adenoma of the cecum, associated with adenocarcinoma, is described.

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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18701516.001).

[ISSN] 1066-8969

[Journal-full-title] International journal of surgical pathology

[ISO-abbreviation] Int. J. Surg. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / beta Catenin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Luminal histological outline and colonic adenoma phenotypes.

BACKGROUND: The luminal appearance of histological sections from colonic adenomas exhibits two different profiles: one regularly smooth and the other asymmetrically lumpy.

MATERIALS AND METHODS: For this purpose, the largest section of 107 consecutive endoscopically removed colonic adenomas was digitalized using an Epson Perfection 4990 PHOTO device.

RESULTS: Asymmetrically lumpy profiles were found in 96% (22/23) of the sections from adenomas measuring > or =15 mm, in 72% (39/54) of those having villous, mixed serrated or microtubular configurations and in 89% (24/27) showing carcinoma according to the Vienna classification.

CONCLUSION: The asymmetrically lumpy profile of sections from endoscopically excised colonic adenomas correlated with the size of the sections, the histological phenotype and the degree of neoplastic transformation.

Studies have been initiated to clinically explore whether the luminal configuration of colonic adenomas can be of help in predicting, before endoscopical removal, accepted histological parameters.

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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17972517.001).

[ISSN] 0250-7005

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Optical biopsy system distinguishing between hyperplastic and adenomatous polyps in the colon during colonoscopy.

BACKGROUND: It has been established that the removal of adenomatous colon polyps drastically reduces the incidence of colorectal cancer (CRC), but polypectomy is not without risk.

The aim was to determine the correlation between the results of an optical biopsy system and the histopathology report of the physical biopsy specimens of the same polyps removed at colonoscopy.

PATIENTS AND METHODS: Paired optical and physical biopsies were performed on 55 polyps with complete polypectomy of the same tissue.

RESULTS: Fifty-three adenomatous polyps and two hyperplastic polyps were identified by the hospital pathologist.

The optical biopsy system identified 52 polyps as suspect (adenomatous) and 2 as non-suspect (hyperplastic).

One villous adenoma could not be optically analyzed due to friability.

CONCLUSION: The WavSTAT Optical Biopsy System provides accurate information to the gastroenterologist to assist in distinguishing between hyperplastic and adenomatous polyps.

[MeSH-major] Adenomatous Polyposis Coli / pathology. Colon / pathology

[MeSH-minor] Adenoma / diagnosis. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Biopsy / methods. Colonic Neoplasms / diagnosis. Colonic Neoplasms / pathology. Colonoscopy / methods. Diagnosis, Differential. Humans. Hyperplasia / diagnosis. Middle Aged. Optics and Photonics / methods. Prospective Studies

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20032428.001).

[ISSN] 1791-7530

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] JC virus T-antigen expression in sporadic adenomatous polyps of the colon.

The hypothesis that JCV DNA sequences and T-antigen (T-Ag) expression may be present in adenomatous polyps of the colon was tested.

METHODS: DNA was extracted from 74 paraffin-embedded adenomatous polyps.

Immunohistochemical staining was performed to localize T-Ag expression in the adenomas using a monoclonal antibody.

RESULTS: JCV T-Ag sequences were found in 82% (61 of 74) of adenomas, and T-Ag protein was expressed in 16% (12 of 74) of these polyps.

The T-Ag staining was localized exclusively in the nuclei of adenoma cells, but never in the cytoplasm or the adjacent nonneoplastic cells.

The prevalence of MSI-H and non-MSI-H (MSI-L/MSS) in adenomatous polyps was 9.5% (7 of 74) and 90.5% (67 of 74), respectively.

Among the 61 adenomas that harbored JCV sequences, 8% (5 of 61) were MSI-H, and similarly among 12 adenomatous polyps expressing T-Ag protein 8% (1 of 12) of the adenomatous polyps were MSI-H.

CONCLUSIONS: JCV T-Ag DNA sequences are frequently present in adenomatous polyps of the colon, and T-Ag is expressed specifically in the nuclei of these premalignant lesions.

This study indicates that JCV T-Ag is present in the early stage of colonic carcinogenesis.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] N Engl J Med. 2000 Jan 13;342(2):69-77 [10631274.001]

[Cites] Clin Cancer Res. 2005 Dec 1;11(23):8332-40 [16322293.001]

[Cites] Mol Cell Biol. 2000 Sep;20(17):6233-43 [10938100.001]

[Cites] Virology. 2000 Aug 15;274(1):165-78 [10936097.001]

[Cites] Int J Colorectal Dis. 2000 Aug;15(4):189-96 [11008717.001]

[Cites] Gastroenterology. 2000 Nov;119(5):1228-35 [11054380.001]

[Cites] J Virol. 2001 Feb;75(4):1996-2001 [11160700.001]

[Cites] Cancer Res. 2001 May 15;61(10):4287-93 [11358858.001]

[Cites] Oncogene. 2001 Aug 9;20(35):4864-70 [11521197.001]

[Cites] Am J Pathol. 2001 Dec;159(6):2107-16 [11733361.001]

[Cites] Gut. 2002 Mar;50(3):382-6 [11839719.001]

[Cites] J Natl Cancer Inst. 2002 Feb 20;94(4):267-73 [11854388.001]

[Cites] Gastroenterology. 2002 Dec;123(6):1804-11 [12454837.001]

[Cites] Cancer Res. 2002 Dec 1;62(23):7093-101 [12460931.001]

[Cites] J Neurovirol. 2002 Dec;8 Suppl 2:138-47 [12491166.001]

[Cites] J Gen Virol. 2003 Jun;84(Pt 6):1499-504 [12771419.001]

[Cites] Oncogene. 2003 Aug 11;22(33):5181-91 [12910255.001]

[Cites] Gastroenterology. 2004 Jan;126(1):42-8 [14699485.001]

[Cites] J Natl Cancer Inst. 2004 Feb 18;96(4):261-8 [14970275.001]

[Cites] Microbiol Immunol. 1982;26(11):1057-64 [6300615.001]

[Cites] J Virol. 1984 Aug;51(2):458-69 [6086957.001]

[Cites] J Virol. 1989 Feb;63(2):863-72 [2536108.001]

[Cites] J Virol. 1990 Mar;64(3):1353-6 [2154613.001]

[Cites] J Virol. 1992 Jul;66(7):3979-85 [1318392.001]

[Cites] Science. 1993 May 7;260(5109):812-6 [8484121.001]

[Cites] Science. 1993 May 7;260(5109):816-9 [8484122.001]

[Cites] Nature. 1993 Jun 10;363(6429):558-61 [8505985.001]

[Cites] Cancer Res. 1994 Apr 1;54(7):1645-8 [8137274.001]

[Cites] Int J Mol Med. 1998 Apr;1(4):647-55 [9852278.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7484-9 [10377441.001]

[Cites] J Gastroenterol Hepatol. 2005 Dec;20(12):1920-6 [16336454.001]

[Cites] Gut. 2006 May;55(5):695-702 [16354798.001]

[Cites] Gastroenterology. 2006 Jun;130(7):1950-61 [16762618.001]

[Cites] Cancer. 2006 Aug 1;107(3):481-8 [16795066.001]

[Cites] Gastroenterology. 2007 Jan;132(1):127-38 [17087942.001]

[Cites] J Neuropathol Exp Neurol. 2004 Nov;63(11):1124-30 [15581180.001]

[Cites] Cancer. 2005 Feb 1;103(3):516-27 [15630684.001]

[Cites] Dis Colon Rectum. 2005 Jan;48(1):86-91 [15690663.001]

[Cites] Am J Gastroenterol. 2005 May;100(5):1143-9 [15842591.001]

[Cites] Anticancer Res. 2005 Mar-Apr;25(2A):1079-85 [15868949.001]

[Cites] Gut. 2005 Sep;54(9):1321-31 [16099799.001]

[Cites] Virchows Arch. 2005 Oct;447(4):723-30 [16021515.001]

[Cites] Gut. 2000 Jul;47(1):37-42 [10861262.001]

(PMID = 18205186.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA098572-05; United States / NCI NIH HHS / CA / R01 CA098572; United States / NCI NIH HHS / CA / R01 CA 98572; United States / NCI NIH HHS / CA / R01 CA098572-05

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / DNA, Viral

[Other-IDs] NLM/ NIHMS187525; NLM/ PMC2855201

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Expression of MMP-2, HIF-1alpha and VEGF in colon adenoma and colon cancer].

BACKGROUND/AIMS: This study was aimed to investigate the expression of matrix metalloproteinase-2 (MMP-2), hypoxia-inducible factor (HIF)-1alpha, and vascular endothelial growth factor (VEGF) in colonic adenoma-carcinoma sequence.

METHODS: Thirty-two tissue samples of colon adenoma, 11 of early colon cancer and 36 of advanced colon cancer were collected by colonoscopic biopsy.

Normal colonic tissues were also collected from the same subjects.

RESULTS: The expression level of MMP-2 mRNA showed a progressive increase in the advance of the colorectal adenoma-carcinoma sequence (p<0.05).

In colon cancer tissues, the expression level of MMP-2 mRNA showed an increasing trend according to differentiation, lymphatic invasion and Dukes' stage (p<0.05).

The mRNA expression levels of HIF-1alpha and VEGF were greater in tissues of early and advanced colon cancer compared with colon adenoma (p<0.05; p<0.001).

CONCLUSIONS: MMP-2, HIF-1alpha, and VEGF may be useful in detecting early carcinogenesis and progression of colon cancer.

[MeSH-major] Adenoma / metabolism. Colonic Neoplasms / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Matrix Metalloproteinase 2 / metabolism. Vascular Endothelial Growth Factor A / metabolism

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18172354.001).

[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)

[Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / Matrix Metalloproteinase 2

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A reduced COX-2 expression and a reduced number of pericryptal myofibroblasts are associated with depressed adenoma of the colon.

The histogenesis of depressed adenoma of the colon has not been sufficiently investigated.

Pericryptal myofibroblasts are stromal cells expressing smooth muscle actin, and are involved in the differentiation and multiplication of epithelial cells in the colonic epithelium.

COX-2 has been reported to be involved in the development of colon adenoma.

We studied the histogenesis of depressed adenoma of the colon by examining the relationship between the presence of pericryptal myofibroblasts and COX-2 expression.

Twenty-one depressed adenomas of the colon that had been resected endoscopically between June 1998 and May 2003 (mild-moderate atypia; mean diameter, 6.7 mm) and 23 elevated adenomas that had been resected endoscopically in 2003 (mild-moderate atypia; mean diameter, 11.7 mm), were studied.

Eighteen (78.3%) of the 23 elevated adenomas and six (28.6%) of the 21 depressed adenomas were positive for pericryptal myofibroblasts immunohistochemically, showing a significant difference (P<0.001).

Seventeen elevated adenomas (73.9%) and eight depressed adenomas (38.1%) were positive for COX-2 expression (P=0.016).

The histogenesis of depressed adenomas differs from that of elevated adenomas.

Our results suggest that a low number of pericryptal myofibroblasts and a low COX-2 expression are associated with depressed adenomas.

[MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Cyclooxygenase 2 / metabolism. Fibroblasts / pathology. Membrane Proteins / metabolism. Myoblasts / pathology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17487390.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / Actins; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Monocyte chemoattractant protein 1 and macrophage cyclooxygenase 2 expression in colonic adenoma.

BACKGROUND AND AIMS: Cyclooxygenase 2 (COX-2) expression in subepithelial macrophages of colorectal adenoma has been suggested as the first in a series of steps leading to colorectal tumorigenesis.

We tested the hypothesis that chemokines released from human colorectal adenoma epithelium might be involved in COX-2 expression in macrophages of the lamina propria.

METHODS: Endoscopic samples of sporadic colorectal adenomas were tested by enzyme linked immunosorbent assay for chemokines involved in macrophage chemotaxis.

Localisation of adenoma macrophage chemoattractant protein 1 (MCP-1) and COX-2 were determined by immunohistochemistry.

RESULTS: MCP-1 levels were markedly higher in adenoma with mild-moderate dysplasia (129.7 (19.9) pg/mg protein) and severe dysplasia (227.9 (35.4) pg/mg protein) than in normal colonic mucosa (55.8 (4.2) pg/mg protein).

Other chemokine levels, macrophage inflammatory proteins (MIP)-1alpha and MIP-1beta, and the chemokine regulated on activation of normal T cell expressed and secreted (RANTES) did not vary significantly between adenoma and normal mucosa.

MCP-1 levels in both adenoma and normal colonic mucosa increased significantly three hours after tissue cultivation in vitro.

MCP-1 immunoreactivity was restricted to the adenoma epithelium, with no reactivity seen in adjacent normal epithelial cells.

Addition of exogenous PGE(2) reversed this inhibitory effect on VEGF release, suggesting that MCP-1 in adenoma epithelial cells might be involved in COX-2 expression and subsequent macrophage activation.

CONCLUSIONS: MCP-1 in colorectal adenoma epithelial cells might be involved in macrophage migration and COX-2 expression, leading to the subsequent development of colonic adenoma.

[MeSH-major] Adenoma / metabolism. Chemokine CCL2 / metabolism. Colorectal Neoplasms / metabolism. Cyclooxygenase 2 / metabolism. Macrophages / enzymology

MedlinePlus Health Information. consumer health - Colorectal Cancer.

Hazardous Substances Data Bank. CELECOXIB .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Biochem Biophys Res Commun. 1999 Nov 2;264(3):751-8 [10544003.001]

[Cites] Int J Cancer. 1999 Nov 12;83(4):470-5 [10508481.001]

[Cites] J Pharmacol Exp Ther. 2000 May;293(2):539-44 [10773026.001]

[Cites] J Clin Invest. 2000 Jun;105(11):1589-94 [10841517.001]

[Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]

[Cites] J Exp Clin Cancer Res. 2000 Jun;19(2):219-23 [10965822.001]

[Cites] J Pharmacol Exp Ther. 2000 Nov;295(2):802-9 [11046121.001]

[Cites] Cancer Res. 2000 Nov 1;60(21):6045-51 [11085526.001]

[Cites] Cancer Res. 2001 Feb 15;61(4):1733-40 [11245490.001]

[Cites] Acta Oncol. 2001;40(5):622-8 [11669335.001]

[Cites] Gastroenterology. 2001 Dec;121(6):1339-47 [11729113.001]

[Cites] Cancer Res. 2002 Mar 15;62(6):1669-75 [11912138.001]

[Cites] Int J Cancer. 2002 Nov 20;102(3):220-4 [12397639.001]

[Cites] J Pathol. 2002 Dec;198(4):435-41 [12434412.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2736-41 [12598658.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]

[Cites] Int J Oncol. 2003 Apr;22(4):773-8 [12632067.001]

[Cites] Gastroenterology. 2003 Aug;125(2):328-36 [12891533.001]

[Cites] Cancer Causes Control. 2003 Jun;14(5):403-11 [12946034.001]

[Cites] Gut. 2003 Oct;52(10):1448-56 [12970138.001]

[Cites] Int J Oncol. 2003 Nov;23(5):1317-22 [14532971.001]

[Cites] Ann Intern Med. 2004 Feb 3;140(3):157-66 [14757613.001]

[Cites] Hum Pathol. 2004 Apr;35(4):488-95 [15116331.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Aug;287(2):G444-51 [15246970.001]

[Cites] J Surg Oncol. 1983 Sep;24(1):83-7 [6887943.001]

[Cites] Am J Surg. 1989 Jan;157(1):175-9 [2535920.001]

[Cites] N Engl J Med. 1991 Dec 5;325(23):1593-6 [1669840.001]

[Cites] Gastroenterology. 1994 Oct;107(4):1183-8 [7926468.001]

[Cites] Proc Natl Acad Sci U S A. 1995 May 9;92(10):4482-6 [7753829.001]

[Cites] N Engl J Med. 1995 Sep 7;333(10):609-14 [7637720.001]

[Cites] J Immunol. 1995 Dec 15;155(12):5769-76 [7499865.001]

[Cites] Eur J Immunol. 1995 Dec;25(12):3482-8 [8566041.001]

[Cites] Cancer Res. 1996 Oct 15;56(20):4625-9 [8840975.001]

[Cites] Cell. 1996 Nov 29;87(5):803-9 [8945508.001]

[Cites] Gastroenterology. 1997 Feb;112(2):387-97 [9024292.001]

[Cites] Arch Intern Med. 1999 Jan 25;159(2):161-6 [9927099.001]

[Cites] Acta Obstet Gynecol Scand. 1999 Mar;78(3):240-4 [10078587.001]

[Cites] Br J Cancer. 1999 Mar;79(9-10):1399-405 [10188882.001]

[Cites] Clin Cancer Res. 1999 May;5(5):1107-13 [10353745.001]

[Cites] Am J Pathol. 2000 Feb;156(2):545-53 [10666384.001]

(PMID = 16085694.001).

[ISSN] 0017-5749

[Journal-full-title] Gut

[ISO-abbreviation] Gut

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / Chemokine CCL2; 0 / Chemokines; 0 / Cyclooxygenase Inhibitors; 0 / Neoplasm Proteins; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone

[Other-IDs] NLM/ PMC1856393

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Analysis of serum gastrin levels in patients with adenomatous polyps of the colon].

Adenomatous polyps are known risk factor of colon cancer.

Gastrin is a peptide hormone involved in the growth of both normal and malignant intestinal tissue, which probably may promote progression through the adenoma-carcinoma sequence.

AIM OF OUR STUDY: To assess the association between serum gastrin levels and size, type and localization of colonic adenomas.

MATERIAL AND METHODS: The study included 60 patients with adenomatous polyps of the colon and 30 healthy volunteers.

RESULTS: We observed higher serum gastrin levels in patients with colonic adenomas compared to control group (59.65 pg/ml vs. 46.89 pg/ml; p < 0.05).

There was no association between gastrin levels and size, number, localisation and histologic type of polyps (p > 0.05).

CONCLUSION: Despite of elevated serum levels in patients with colonic adenomas we did not observe the association between gastrin levels and size, grade of dysplasia and histologic type of polyps.

The exact role of hipergastrinemia in process of colon carcinogenesis remains to be determined.

[MeSH-major] Adenomatous Polyps / blood. Gastrins / blood

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19606697.001).

[ISSN] 1426-9686

[Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego

[ISO-abbreviation] Pol. Merkur. Lekarski

[Language] pol

[Publication-type] English Abstract; Journal Article

[Publication-country] Poland

[Chemical-registry-number] 0 / Gastrins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Dietary calcium supplementation for preventing colorectal cancer and adenomatous polyps.

Intervention studies with colorectal cancer as an endpoint are difficult to perform owing to the large number of patients and the long follow-up required; studies using the appearance of colorectal adenomatous polyps as a surrogate endpoint are therefore considered in reviewing the existing evidence.

OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps.

SELECTION CRITERIA: Randomised controlled trials of the effects of dietary calcium on the development of colonic cancer and adenomatous polyps in humans are reviewed.

Studies of healthy adults and studies of adults at higher risk of colon cancer due to family history, previous adenomatous polyps, or inflammatory bowel disease were considered; data from subjects with familial polyposis coli are excluded.

The primary outcomes were the occurrence of colon cancer, and occurrence or recurrence of any new adenomas of the colon.

Both trials were well designed, double - blind, placebo controlled trials, included participants with previous adenomas.

For the development of recurrent colorectal adenoma, a reduction was found (OR 0.74, CI 0.58,0.95) when the results from both trials were combined.

AUTHORS' CONCLUSIONS: Although the evidence from two RCTs suggests that calcium supplementation might contribute to a moderate degree to the prevention of colorectal adenomatous polyps, this does not constitute sufficient evidence to recommend the general use of calcium supplements to prevent colorectal cancer.

[MeSH-major] Adenomatous Polyps / prevention & control. Calcium, Dietary / therapeutic use. Colorectal Neoplasms / prevention & control. Dietary Supplements

[MeSH-minor] Adenoma / complications. Humans. Randomized Controlled Trials as Topic

Genetic Alliance. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Calcium.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Dietary Supplements.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[UpdateIn] Cochrane Database Syst Rev. 2008;(1):CD003548 [18254022.001]

[UpdateOf] Cochrane Database Syst Rev. 2004;(1):CD003548 [14974021.001]

(PMID = 16034903.001).

[ISSN] 1469-493X

[Journal-full-title] The Cochrane database of systematic reviews

[ISO-abbreviation] Cochrane Database Syst Rev

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Calcium, Dietary

[Number-of-references] 33

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Dietary calcium supplementation for preventing colorectal cancer and adenomatous polyps.

Intervention studies with colorectal cancer as an endpoint are difficult to perform owing to the large number of patients and the long follow-up required; studies using the appearance of colorectal adenomatous polyps as a surrogate endpoint are therefore considered in reviewing the existing evidence.

OBJECTIVES: This systematic review aims to assess the effect of supplementary dietary calcium on the incidence of colorectal cancer and the incidence or recurrence of adenomatous polyps.

SELECTION CRITERIA: Randomised controlled trials of the effects of dietary calcium on the development of colonic cancer and adenomatous polyps in humans are reviewed.

Studies of healthy adults and studies of adults at higher risk of colon cancer due to family history, previous adenomatous polyps, or inflammatory bowel disease were considered; data from subjects with familial polyposis coli are excluded.

The primary outcomes were the occurrence of colon cancer, and occurrence or recurrence of any new adenomas of the colon.

Both trials were well designed, double - blind, placebo controlled trials, included participants with previous adenomas.

For the development of recurrent colorectal adenoma, a reduction was found (OR 0.74, CI 0.58,0.95) when the results from both trials were combined.

AUTHORS' CONCLUSIONS: Although the evidence from two RCTs suggests that calcium supplementation might contribute to a moderate degree to the prevention of colorectal adenomatous polyps, this does not constitute sufficient evidence to recommend the general use of calcium supplements to prevent colorectal cancer.

[MeSH-major] Adenomatous Polyps / prevention & control. Calcium, Dietary / therapeutic use. Colorectal Neoplasms / prevention & control. Dietary Supplements

[MeSH-minor] Adenoma / complications. Humans. Randomized Controlled Trials as Topic

Genetic Alliance. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Calcium.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Dietary Supplements.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[UpdateOf] Cochrane Database Syst Rev. 2005;(3):CD003548 [16034903.001]

(PMID = 18254022.001).

[ISSN] 1469-493X

[Journal-full-title] The Cochrane database of systematic reviews

[ISO-abbreviation] Cochrane Database Syst Rev

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Calcium, Dietary

[Number-of-references] 38

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genetic polymorphisms in vitamin D receptor VDR/RXRA influence the likelihood of colon adenoma recurrence.

No gene-level associations were observed for VDR, nor was any single SNP in VDR related to any metachronous adenoma after correction for multiple comparisons.

Haplotypes within linkage blocks of RXRA support an approximately 30% reduction in odds of metachronous neoplasia arising in the proximal colon among carriers of specific haplotypes, which was strongest (OR(proximal), 0.67; 95% CI, 0.52-0.86) for carriers of a CGGGCA haplotype (rs1805352, rs3132297, rs3132296, rs3118529, rs3118536, and rs7861779).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Hum Mutat. 2006 Nov;27(11):1129-34 [16937379.001]

[Cites] Gastroenterology. 2006 Dec;131(6):1706-16 [17087956.001]

[Cites] Genet Epidemiol. 2007 Jul;31(5):383-95 [17410554.001]

[Cites] J Clin Gastroenterol. 2007 Sep;41(8):731-46 [17700421.001]

[Cites] Nat Rev Drug Discov. 2007 Oct;6(10):793-810 [17906642.001]

[Cites] Gut. 2007 Nov;56(11):1557-63 [17604322.001]

[Cites] J Natl Cancer Inst. 2007 Nov 7;99(21):1594-602 [17971526.001]

[Cites] PLoS One. 2008;3(1):e1483 [18213391.001]

[Cites] Nutr Cancer. 2008;60(1):97-108 [18444141.001]

[Cites] Cell Mol Life Sci. 2008 May;65(10):1523-43 [18278436.001]

[Cites] Int J Cancer. 2008 Aug 1;123(3):586-93 [18470879.001]

[Cites] Carcinogenesis. 2008 May;29(5):944-8 [18375961.001]

[Cites] Nutr Rev. 2008 Oct;66(10 Suppl 2):S98-112 [18844852.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):2958-69 [18990737.001]

[Cites] Carcinogenesis. 2009 May;30(5):769-76 [19255064.001]

[Cites] Carcinogenesis. 2009 Jul;30(7):1170-80 [19403841.001]

[Cites] N Engl J Med. 2000 Apr 20;342(16):1156-62 [10770980.001]

[Cites] Cancer Res. 2000 Apr 15;60(8):2304-12 [10786699.001]

[Cites] Endocrinology. 2000 Nov;141(11):3931-9 [11089522.001]

[Cites] J Cell Biol. 2001 Jul 23;154(2):369-87 [11470825.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2001 Aug;10(8):869-74 [11489753.001]

[Cites] Cancer Causes Control. 2001 Sep;12(7):607-14 [11552708.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2001 Dec;10(12):1267-74 [11751444.001]

[Cites] J Biol Chem. 2002 Jul 12;277(28):25313-22 [12000762.001]

[Cites] Exp Hematol. 2003 Jun;31(6):488-94 [12829024.001]

[Cites] Nat Rev Cancer. 2003 Aug;3(8):601-14 [12894248.001]

[Cites] J Biol Chem. 2003 Aug 8;278(32):29954-62 [12771132.001]

[Cites] Cancer Res. 2003 Nov 15;63(22):7799-806 [14633706.001]

[Cites] J Natl Cancer Inst. 2003 Dec 3;95(23):1765-71 [14652238.001]

[Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2004 Sep;13(9):1502-8 [15342452.001]

[Cites] Int J Epidemiol. 1980 Sep;9(3):227-31 [7440046.001]

[Cites] Lancet. 1989 Nov 18;2(8673):1176-8 [2572900.001]

[Cites] Endocrinology. 1994 Apr;134(4):1710-7 [8137734.001]

[Cites] Cell. 1995 Dec 15;83(6):835-9 [8521507.001]

[Cites] Cancer Res. 1996 Feb 1;56(3):623-32 [8564982.001]

[Cites] J Endocrinol. 1997 Sep;154 Suppl:S57-73 [9379138.001]

[Cites] J Bone Miner Res. 1998 Mar;13(3):325-49 [9525333.001]

[Cites] Hum Genet. 1998 Oct;103(4):462-9 [9856491.001]

[Cites] J Natl Cancer Inst. 2005 Jun 1;97(11):846-53 [15928305.001]

[Cites] Hum Genomics. 2005 Jun;2(2):144-51 [16004730.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2061-3 [16172209.001]

[Cites] Nat Genet. 2005 Nov;37(11):1217-23 [16244653.001]

[Cites] Endocr Rev. 2005 Dec;26(7):898-915 [16126938.001]

[Cites] N Engl J Med. 2006 Feb 16;354(7):684-96 [16481636.001]

[Cites] Am J Hum Genet. 2006 Apr;78(4):629-44 [16532393.001]

[Cites] J Natl Cancer Inst. 2006 Apr 5;98(7):451-9 [16595781.001]

[Cites] Anticancer Res. 2009 Sep;29(9):3511-36 [19667145.001]

[Cites] Am J Hum Genet. 2007 Dec;81(6):1158-68 [17966093.001]

[Cites] EMBO Rep. 2006 Oct;7(10):1030-4 [16936639.001]

(PMID = 20145122.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / K07 CA106269; United States / NCI NIH HHS / CA / CA023074-22S1; United States / NCI NIH HHS / CA / P50 CA095060-01; United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / K07CA106269; United States / NCI NIH HHS / CA / CA95060; United States / NCI NIH HHS / CA / CA77145; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / CA095060-01; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / R01 CA123065; United States / NCI NIH HHS / CA / K07 CA106269-01A1; United States / NCI NIH HHS / CA / P30 CA023074-22S1; United States / NCI NIH HHS / CA / P01 CA041108-13; United States / NCI NIH HHS / CA / P01CA41108; United States / NCI NIH HHS / CA / CA041108-13; United States / NCI NIH HHS / CA / CA106269-01A1

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

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Calcitriol; 0 / Retinoid X Receptor alpha

[Other-IDs] NLM/ NIHMS262521; NLM/ PMC3019606

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Determinants of compliance with colonoscopy in patients with adenomatous colon polyps in a veteran population.

AIM: To determine factors affecting compliance of a follow-up colonoscopy in patients with previously diagnosed adenomatous colon polyps.

METHODS: A retrospective review was performed on patients with adenomatous polyps excised between January and December 1998.

RESULTS: One hundred and nineteen patients with adenomatous colon polyps were identified.

In a univariate analysis, greater number of polyps (P = 0.04), NSAID use (P = 0.02), statin use (P = 0.005), first-degree relatives with colon cancer (P = 0.05) and compliance with out-patient clinic follow-up (P < 0.001) were significantly associated with patient compliance.

Multivariate analysis revealed statin use (P = 0.05), first-degree relatives with colon cancer (P = 0.06) and compliance with out-patient clinic follow-up (P < 0.001) were independent predictors of compliance.

CONCLUSIONS: History of statin use and family history of colon cancer are good predictors of compliance.

Strong efforts should be directed at improving patient education about colon cancer by the physician and facilitating patient compliance.

[MeSH-major] Adenomatous Polyps / pathology. Colonic Neoplasms / pathology. Colonic Polyps / pathology. Colonoscopy. Patient Compliance

MedlinePlus Health Information. consumer health - Colonic Polyps.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17206950.001).

[ISSN] 0269-2813

[Journal-full-title] Alimentary pharmacology & therapeutics

[ISO-abbreviation] Aliment. Pharmacol. Ther.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Apple polyphenols and products formed in the gut differently inhibit survival of human cell lines derived from colon adenoma (LT97) and carcinoma (HT29).

Here, apple polyphenols were studied for effects on the survival of colon adenoma (LT97) and carcinoma-derived (HT29) cell lines.

[MeSH-major] Cell Survival / drug effects. Colonic Neoplasms / pathology. Fermentation. Flavonoids / pharmacology. Fruit / chemistry. Malus / chemistry. Phenols / pharmacology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17378580.001).

[ISSN] 0021-8561

[Journal-full-title] Journal of agricultural and food chemistry

[ISO-abbreviation] J. Agric. Food Chem.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Flavonoids; 0 / Phenols; 0 / Plant Extracts; 0 / Polyphenols

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Obesity is associated with an increased prevalence of advanced adenomatous colon polyps in a male veteran population.

Obesity has been associated with an increased risk for colonic adenomatous polyps (APs) and colorectal cancers, but the influence of obesity on the development of advanced APs is not clear.

[MeSH-major] Adenomatous Polyps / epidemiology. Colonic Neoplasms / epidemiology. Obesity / epidemiology

Genetic Alliance. consumer health - Obesity.

MedlinePlus Health Information. consumer health - Obesity.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Gastroenterol. 2001 Jul;96(7):2238-46 [11467659.001]

[Cites] Am J Clin Nutr. 1988 Feb;47(2):312-7 [3341261.001]

[Cites] J Natl Cancer Inst. 2002 Jul 3;94(13):972-80 [12096082.001]

[Cites] Clin Gastroenterol Hepatol. 2007 Aug;5(8):982-90 [17553754.001]

[Cites] Jpn J Cancer Res. 1989 Jan;80(1):51-8 [2540132.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Dec;5(12):1013-5 [8959325.001]

[Cites] Intern Med. 2009;48(3):123-8 [19182421.001]

[Cites] J Gastroenterol. 2007 Aug;42(8):616-23 [17701124.001]

[Cites] J Nutr. 2001 Nov;131(11 Suppl):3109S-20S [11694656.001]

[Cites] N Engl J Med. 2005 May 26;352(21):2184-92 [15917383.001]

[Cites] Oncogene. 1999 Nov 22;18(49):6853-66 [10602461.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]

[Cites] Gastroenterology. 2005 Aug;129(2):464-75 [16083703.001]

[Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]

[Cites] Int J Colorectal Dis. 1987 Nov;2(4):203-7 [3694018.001]

[Cites] Br J Cancer. 1987 Jun;55(6):687-94 [3620314.001]

[Cites] Nutr Cancer. 1997;27(3):316-20 [9101563.001]

[Cites] Cancer Causes Control. 1996 Mar;7(2):253-63 [8740738.001]

[Cites] Jpn J Cancer Res. 1996 Aug;87(8):798-804 [8797885.001]

[Cites] Lancet. 2004 Apr 24;363(9418):1346-53 [15110491.001]

[Cites] N Engl J Med. 1992 Mar 5;326(10):658-62 [1736104.001]

[Cites] J Clin Invest. 1995 Apr;95(4):1897-905 [7706497.001]

[Cites] Br J Surg. 2001 Jan;88(1):107-13 [11136321.001]

[Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]

[Cites] J Natl Cancer Inst. 1991 Mar 6;83(5):355-8 [1759994.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2082-6 [16172213.001]

[Cites] J Natl Cancer Inst. 1991 Mar 6;83(5):359-61 [1995919.001]

[Cites] Am J Epidemiol. 1998 Apr 1;147(7):670-80 [9554606.001]

[Cites] Scand J Gastroenterol. 1999 Apr;34(4):414-20 [10365903.001]

[Cites] Int J Oncol. 2003 Oct;23(4):1055-69 [12963986.001]

[Cites] N Engl J Med. 1991 Dec 5;325(23):1593-6 [1669840.001]

[Cites] Nutr Cancer. 2001;39(1):50-7 [11588902.001]

(PMID = 19399615.001).

[ISSN] 1573-2568

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The association of elevated HbA1c on the behavior of adenomatous polyps in patients with type-II diabetes mellitus.

The aim of our study was to determine whether poor control of diabetes mellitus (DM) is associated with increased prevalence of colonic adenomatous polyps (APs), especially those that are advanced .

Significant variables by UA were included in a stepwise logistic regression analysis to determine independent predictors of aggressive clinical behavior by the polyps.

Logistic regression, as measured by HbA1c, demonstrated that poorly controlled DM-2 independently predicted a greater prevalence of right-sided AP, a more advanced lesion at the time of presentation, a greater number of polyps, and greater use of exogenous insulin.

[MeSH-major] Adenomatous Polyps / blood. Adenomatous Polyps / pathology. Colonic Neoplasms / blood. Colonic Neoplasms / pathology. Diabetes Mellitus, Type 2 / blood. Hemoglobin A, Glycosylated / metabolism

Genetic Alliance. consumer health - Diabetes.

MedlinePlus Health Information. consumer health - A1C.

MedlinePlus Health Information. consumer health - Diabetes Type 2.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Science. 1978 Apr 7;200(4337):21-7 [635569.001]

[Cites] J Natl Cancer Inst. 2002 Jul 3;94(13):972-80 [12096082.001]

[Cites] Diabetes Care. 2003 Jan;26 Suppl 1:S33-50 [12502618.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):412-8 [12750235.001]

[Cites] Jpn J Cancer Res. 1989 Jan;80(1):51-8 [2540132.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Dec;5(12):1013-5 [8959325.001]

[Cites] Int J Epidemiol. 1998 Oct;27(5):794-8 [9839735.001]

[Cites] J Gen Intern Med. 2000 Aug;15(8):551-5 [10940146.001]

[Cites] Annu Rev Public Health. 2005;26:445-67 [15760297.001]

[Cites] Br J Cancer. 2001 Feb 2;84(3):417-22 [11161410.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):850-5 [15824155.001]

[Cites] Clin Chem. 1986 Oct;32(10 Suppl):B64-70 [3530542.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jun;13(6):915-9 [15184246.001]

[Cites] Gastroenterol Clin North Am. 2002 Dec;31(4):925-43 [12489270.001]

[Cites] Clin Biochem. 1998 Jun;31(4):221-8 [9646944.001]

[Cites] Lancet. 1998 Sep 12;352(9131):837-53 [9742976.001]

[Cites] Semin Gastrointest Dis. 2000 Oct;11(4):194-206 [11057947.001]

[Cites] Gut. 1999 Jul;45(1):45-50 [10369703.001]

[Cites] J Nutr. 2001 Nov;131(11 Suppl):3109S-20S [11694656.001]

[Cites] Ann Intern Med. 1993 Oct 15;119(8):836-43 [8379605.001]

[Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]

[Cites] Gastroenterology. 2005 Aug;129(2):464-75 [16083703.001]

[Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]

[Cites] Nutr Cancer. 1997;27(3):316-20 [9101563.001]

[Cites] Carcinogenesis. 1985 Jul;6(7):1063-6 [4017173.001]

[Cites] Lancet. 2004 Apr 24;363(9418):1346-53 [15110491.001]

[Cites] Am J Epidemiol. 1998 May 1;147(9):816-25 [9583711.001]

[Cites] Cancer Causes Control. 1995 Mar;6(2):164-79 [7749056.001]

[Cites] Arch Intern Med. 2004 Nov 8;164(20):2235-40 [15534160.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2001 Sep;10(9):937-41 [11535544.001]

[Cites] Carcinogenesis. 1993 Apr;14(4):777-9 [8472347.001]

[Cites] J Clin Invest. 1995 Apr;95(4):1897-905 [7706497.001]

[Cites] Br J Surg. 2001 Jan;88(1):107-13 [11136321.001]

[Cites] J Natl Cancer Inst. 1999 Mar 17;91(6):542-7 [10088625.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 1996 Aug;5(8):607-12 [8824362.001]

[Cites] Ann Intern Med. 2004 Jun 1;140(11):945-50 [15172919.001]

[Cites] Diabetes Care. 1992 Jul;15(7):815-9 [1516497.001]

[Cites] Clin Gastroenterol Hepatol. 2006 Oct;4(10):1225-31 [16979948.001]

[Cites] Am J Gastroenterol. 2006 Aug;101(8):1872-9 [16790032.001]

(PMID = 17939046.001).

[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

[Publication-country] United States

[Chemical-registry-number] 0 / Blood Glucose; 0 / Hemoglobin A, Glycosylated; 0 / hemoglobin A1c protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Colonic and duodenal flat adenomas in children with classical familial adenomatous polyposis.

Flat adenomas of the colon and duodenum have been described as associating with familial adenomatous polyposis (FAP), its attenuated variant, and the so-called hereditary nonpolyposis colorectal cancer.

There seem to be no report on the occurrence of flat adenomas in pediatric patients with family history of FAP.

We are reporting 4 children from 2 cancer-prone families in whom colonic and duodenal moderately dysplastic flat adenomas were found.

The colonic videoendoscopy showed in 2/3 siblings hundreds of flat or slightly raised plaques less than 1 cm in diameter as well as some classic polyps throughout the colon.

The colonic videoendoscopy performed on the 9-year-old boy revealed multiple small sessile polyps.

Microscopic study demonstrated tubular adenomas with a few neoplastic crypts, slight disarray of the overall architecture, and moderate (low-grade) dysplasia of the epithelium.

These features were more obvious at the center and superficial areas of the adenomas.

The 4 children had multiple flat adenomas of the colon and duodenum (2/4) matching with those described in adult patients.

Flat adenomas in the context of FAP probably represent early stages of the adenoma development.

[MeSH-major] Adenoma / etiology. Adenomatous Polyposis Coli / complications. Colorectal Neoplasms / etiology. Duodenal Neoplasms / etiology. Precancerous Conditions / etiology

Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

Genetic Alliance. consumer health - Familial Polyposis.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16703174.001).

[ISSN] 1066-8969

[Journal-full-title] International journal of surgical pathology

[ISO-abbreviation] Int. J. Surg. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Helicobacter pylori infection is associated with colon adenomatous polyps detected by high-resolution colonoscopy.

We sought to determine whether H. pylori is associated with colon neoplasia in Japanese population.

A significant increase in the incidence of adenomatous polyps (p < 0.0001) and decrease in normal colonoscopic findings (p < 0.0005) were observed in seropositive patients than those seronegative.

[MeSH-major] Adenomatous Polyps / microbiology. Colonic Neoplasms / microbiology. Colonic Polyps / microbiology. Colonoscopy. Helicobacter Infections. Helicobacter pylori

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Colonoscopy.

MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2005 Wiley-Liss, Inc

[CommentIn] Int J Cancer. 2006 Oct 15;119(8):1999-2000 [16708392.001]

(PMID = 15986436.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Immunoglobulin G

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The long-term use of statins is associated with a decreased incidence of adenomatous colon polyps.

BACKGROUND/AIMS: Studies have suggested that statins may protect against colorectal cancer (CRC), but it is not clear whether that protection results from effects on established adenomatous polyps (APs) or from preventing the development of new APs.

Statin use was associated with a smaller mean number of polyps (2.6 vs. 3.1; p = 0.002), a smaller mean polyp size (7.1 vs. 7.9 mm; p = 0.03) and a significant reduction in the incidence of advanced APs (OR 0.74, 95% CI 0.52-0.96; p = 0.03).

[MeSH-major] Adenomatous Polyps / epidemiology. Colonic Polyps / epidemiology. Colorectal Neoplasms / epidemiology. Hydroxymethylglutaryl-CoA Reductase Inhibitors / administration & dosage

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

MedlinePlus Health Information. consumer health - Statins.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19246916.001).

[ISSN] 1421-9867

[Journal-full-title] Digestion

[ISO-abbreviation] Digestion

[Language] eng

[Publication-type] Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Profile of colonic polyps in a southern Indian population.

BACKGROUND: In Western countries, colonic polyps are usually adenomatous in nature, are evenly distributed along the entire colon in asymptomatic per-sons and show a left-sided predominance in symptomatic patients.

Clinical features, colonoscopic description and histologic findings of all patients with polyps were noted.

Association of the degree of dysplasia with the size, site and type of polyps and the person's age was assessed.

RESULTS: Polyps were seen in 124 (5.1%) of 2412 complete colonoscopies.

Mean age of patients with polyps was 58.1 (SD 19.9) years; ninety were men.

A majority of polyps (92%) were located in the left colon.

They were adenomatous in 99 (79.8%), juvenile in 12 (9.8%), hyperplastic in 11 (8.8 %), inflammatory in 1 (0.8%) and Peutz-Jegher's polyp in 1 (0.8%).

Dysplasia was severe in large (>2 cm) polyps compared to small (< 1 cm) ones (p< 0.001).

Age of patient and location of polyp had no association with degree of dysplasia.

CONCLUSIONS: In southern Indian adults, most colonic polyps are adenomatous and are in the left colon.

Large polyps are associated with severe dysplasia.

[MeSH-major] Colonic Polyps / epidemiology

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17704579.001).

[ISSN] 0254-8860

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

[ISO-abbreviation] Indian J Gastroenterol

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] mRNA expression of minichromosome maintenance 2 in colonic adenoma and adenocarcinoma.

As proliferation is essential for progression from normal cells to tumor, certain markers specific to proliferating cells may permit detection of premalignant lesions.

Here, we aimed to evaluate the possible value of a proliferation marker, minichromosome maintenance 2 (MCM2), in the early diagnosis of colorectal cancer, by analyzing the difference in MCM2 expression among normal mucosa, adenoma, and adenocarcinoma, and investigating the relationship of MCM2 expression in adenomas with clinicopathologic variables.

Using immunohistochemistry and real-time reverse transcription-PCR, we observed that the expression of MCM2 protein was present on basal third to half of colonic crypts in normal mucosa, whereas throughout the epithelium in adenomas and adenocarcinomas, the expression of MCM2 mRNA in adenocarcinomas was significantly higher than in adenomas (P=0.001), whereas the difference between adenoma and normal mucosa was not significant (P=0.184); we also found that the expression of MCM2 mRNA tended to be increased in the adenomas with high-grade dysplasia, or in older patients, respectively, compared with those with low-grade dysplasia, and younger patients.

[MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Cell Cycle Proteins / genetics. Colonic Neoplasms / genetics. Nuclear Proteins / genetics

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19077563.001).

[ISSN] 1473-5709

[Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)

[ISO-abbreviation] Eur. J. Cancer Prev.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] From colonic polyps to colon cancer: pathophysiology, clinical presentation, screening and colonoscopic therapy.

Colon cancer is the most common nondermatologic cancer in Italy and throughout Europe, with about 250,000 cases annually in Europe, about half of whom die.

Yet, colon cancer is largely preventable through intensive, mass screening programs to remove premalignant colonic polyps.

Colon cancer mostly arises from adenomas, recognized as colonic polyps, but may occasionally arise from the sessile serrated adenoma.

Adenomatous polyposis coli (APC) gene mutation is the key molecular step in adenoma formation.

Progression from adenomas to colon cancer is a multistep process, involving mutations of the DCC, k-ras, and p53 genes; loss of heterozygosity in which cells loose one allele of some genes from chromosomal loss; and DNA methylation which can silence DNA expression.

Numerous environmental factors can increase the risk of colon cancer, presumably by modulating these molecular pathways.

While colon cancer in an advanced and incurable stage often produces clinical findings, premalignant adenomatous polyps and early, highly curable, colon cancer are often asymptomatic.

This phenomenon renders adenomas or early cancers difficult to detect by clinical presentation and provides the rationale for mass screening of asymptomatic adults over 50 years old for early detection and prevention of colon cancer.

All polyps identified at colonoscopy are removed by colonoscopic polypectomy.

Endoscopic mucosal resection is required for deeply penetrating noncancerous polyps.

Colonoscopy is repeated every ten years if the index colonoscopy revealed no lesions, but is repeated more frequently if adenomatous polyps were identified at this colonoscopy due to an increased risk of subsequent polyps or colon cancer.

Virtual colonoscopy is controversial as a screening test due to widely variable reported RESULTS: Computerized tomography is standardly used to preoperatively detect distant colon cancer metastases, while endosonography is being increasingly used for locoregional staging of rectal cancer.

[MeSH-major] Adenoma. Colonic Neoplasms. Colonic Polyps / complications. Colonoscopy

[MeSH-minor] Aged. Colon / pathology. Endosonography. Humans. Mass Screening. Middle Aged. Mutation. Neoplasm Staging. Risk Factors. Tomography, X-Ray Computed

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Colonoscopy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18043553.001).

[ISSN] 1121-421X

[Journal-full-title] Minerva gastroenterologica e dietologica

[ISO-abbreviation] Minerva Gastroenterol Dietol

[Language] eng

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

[Publication-country] Italy

[Number-of-references] 113

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Colon adenoma detection using Kubelka-Munk spectral function of DNA and protein bands].

Differential diagnosis of human colon adenoma was studied using the Kubelka-Munk spectral function of the DNA and protein absorption bands at 260 and 280 nm in vitro.

The results of measurement showed that for the spectral range from 590 to 1 064 nm pathological changes of colon epithelial tissues were induced so that there were significant differences in the averaged values of the Kubelka-Munk function f(r infinity) and logarithmic Kubelka-Munk function log [f(r infinity)] of the DNA absorption bands at 260 nm between normal and adenomatous colon epithelial tissues, and the differences were 218% (p < 0.05) and 68.5% (p < 0.05) respectively.

Pathological changes of colon epithelial tissues were induced so that there were significant differences in the averaged values of the Kubelka-Munk function f(r infinity) and logarithmic Kubelka-Munk function log [f(r infinity)] of the protein absorption bands at 280 nm between normal and adenomatous colon epithelial tissues, and the differences were 208% (p < 0.05) and 59.0% (p < 0.05) respectively.

Pathological changes of colon epithelial tissues were induced so that there were significant differences in the averaged values of the Kubelka-Munk function f(r infinity) and logarithmic Kubelka-Munk function log [f(r infinity)] of the beta-carotene absorption bands at 480 nm between normal and adenomatous colon epithelial tissues, and the differences were 41.7% (p < 0.05) and 32.9% (p < 0.05) respectively.

Obviously, pathological changes of colon epithelial tissues were induced so that there were significant changes in the contents of the DNA, protein and beta-carotene of colon epithelial tissues.

The conclusion can be applied to rapid, low-cost and noninvasive optical biopsy of colon adenoma, and provides a useful reference.

[MeSH-major] Adenoma / diagnosis. Colonic Neoplasms / diagnosis. DNA / chemistry. Proteins / chemistry. Spectrum Analysis

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19810511.001).

[ISSN] 1000-0593

[Journal-full-title] Guang pu xue yu guang pu fen xi = Guang pu

[ISO-abbreviation] Guang Pu Xue Yu Guang Pu Fen Xi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Proteins; 9007-49-2 / DNA

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Autoregulatory growth control of adenomatous polyps and carcinogenesis in the colorectal region. Basics of tumor surgery Part I].

Autoregulatory growth control of adenomatous polyps in the colon and rectum is an important factor in the success of sphincter-sparing surgical resections.

Similar to normal mucosa, adenomatous polyps in the colorectum show autoregulatory growth control in their tissues.

While colorectal adenomas have malignant potential, their transformation to cancerous lesions is exceedingly rare (e.g., in familial polyposis, or FAP, with a prevalence of only one in 10,000).

It has been hypothesized that "fully developed adenomas" frequently are a prestage of colorectal cancer.

However, convincing evidence on a molecular level that this so-called adenoma-carcinoma sequence indeed occurs in vivo is lacking.

[MeSH-major] Adenomatous Polyps / pathology. Cell Division / physiology. Colonic Polyps / pathology. Colonic Polyps / surgery. Colorectal Neoplasms / pathology. Colorectal Neoplasms / surgery. Homeostasis / physiology

[MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. Adenomatous Polyposis Coli / surgery. Bone Marrow Cells / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Chromosome Aberrations. Colon / pathology. Colon / surgery. Gene Expression Regulation, Neoplastic / physiology. Humans. Neoplasm Staging. Prognosis. Rectum / pathology. Rectum / surgery

MedlinePlus Health Information. consumer health - Colonic Polyps.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Chirurg. 2006 Nov;77(11):1061-2 [17066270.001]

(PMID = 17068665.001).

[ISSN] 0009-4722

[Journal-full-title] Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen

[ISO-abbreviation] Chirurg

[Language] ger

[Publication-type] English Abstract; Journal Article

[Publication-country] Germany

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Importance of the surrounding colonic mucosa in distinguishing between hyperplastic and adenomatous polyps during acetic acid chromoendoscopy.

AIM: To examine the characteristics of colonic polyps, where it is difficult to distinguish adenomatous polyps from hyperplastic polyps, with the aid of acetic acid chromoendoscopy.

METHODS: Acetic acid spray was applied to colonic polyps smaller than 10 mm before complete excision.

Both pre- and post-sprayed images were shown to 16 examiners, who were asked to interpret the lesions as either hyperplastic or adenomatous polyps.

Regression analysis demonstrated that surrounding colonic mucosa was the only factor that was significantly related to accuracy in discriminating adenomatous from hyperplastic polyps (P < 0.001).

Accuracy was higher for polyps with linear surrounding colonic mucosa than for those with nodular surrounding colonic mucosa (P < 0.001), but was not related to the shape, location, or size of the polyp.

CONCLUSION: The accuracy of predicting histology is significantly related to the pattern of colonic mucosa surrounding the polyp.

Making a histological diagnosis of colon polyps merely by acetic acid spray is helpful for colon polyps with linear, regularly patterned surrounding colonic mucosa, and less so for those with nodular, irregularly patterned surrounding colonic mucosa.

[MeSH-major] Acetic Acid. Adenomatous Polyps. Colonic Polyps. Endoscopy / methods. Hyperplasia. Intestinal Mucosa

MedlinePlus Health Information. consumer health - Colonic Polyps.

MedlinePlus Health Information. consumer health - Endoscopy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Gastrointest Endosc. 2003 Jan;57(1):48-53 [12518130.001]

[Cites] Endoscopy. 2003 May;35(5):437-45 [12701018.001]

[Cites] Ann Surg. 1987 Jun;205(6):659-64 [3592808.001]

[Cites] Gastroenterology. 1996 Apr;110(4):1253-8 [8613016.001]

[Cites] Gastrointest Endosc. 1996 Jul;44(1):8-14 [8836710.001]

[Cites] Endoscopy. 2004 Dec;36(12):1089-93 [15578300.001]

[Cites] Gastrointest Endosc. 2002 May;55(6):687-94 [11979251.001]

[Cites] Gastrointest Endosc. 2006 May;63(6):824-8 [16650546.001]

[Cites] World J Gastroenterol. 2006 Apr 21;12(15):2402-5 [16688833.001]

[Cites] Gastrointest Endosc. 2006 Jun;63(7):1010-7 [16733118.001]

[Cites] CA Cancer J Clin. 2006 May-Jun;56(3):143-59; quiz 184-5 [16737947.001]

[Cites] Endoscopy. 2006 Jun;38(6):613-6 [16612744.001]

[Cites] Gastrointest Endosc. 2006 Jul;64(1):13-6 [16813796.001]

[Cites] World J Gastroenterol. 2006 Mar 7;12(9):1416-20 [16552812.001]

(PMID = 18350630.001).

[ISSN] 1007-9327

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] eng

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

[Publication-country] China

[Chemical-registry-number] Q40Q9N063P / Acetic Acid

[Other-IDs] NLM/ PMC2700415

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] American founder mutation for attenuated familial adenomatous polyposis.

BACKGROUND & AIMS: Specific mutations in the adenomatous polyposis coli (APC) gene can lead to an attenuated form of familial adenomatous polyposis (AFAP).

Although AFAP mutation carriers have a 69% risk of colorectal cancer by age 80, clinical recognition remains a challenge in some cases because they present with few colonic adenomas and are difficult to distinguish clinically from patients with sporadic polyps.

The data show that 36.6% of the mutation-positive family members have fewer than 10 colonic adenomatous polyps, and 3 (6.8%) of these individuals were diagnosed with colorectal cancer.

CONCLUSIONS: In view of the apparent age of this mutation, a notable fraction of both multiple-adenoma patients and perhaps even colon cancer cases in the United States could be related to this founder mutation.

The colon cancer risk associated with the mutation makes genetic testing of considerable importance in patients with a personal or family history of either colonic polyps or cancer at a young age.

Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

Genetic Alliance. consumer health - Familial Polyposis.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Hum Mol Genet. 2000 Sep 22;9(15):2215-21 [11001924.001]

[Cites] Gastroenterology. 2006 May;130(6):1872-85 [16697750.001]

[Cites] Gastroenterology. 2001 Jul;121(1):198-213 [11438509.001]

[Cites] Dis Colon Rectum. 2002 Jan;45(1):127-34; discussion 134-6 [11786778.001]

[Cites] Nat Genet. 2002 Feb;30(2):227-32 [11818965.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):2954-8 [11867715.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8161-6 [12034871.001]

[Cites] Hum Mol Genet. 2002 Nov 1;11(23):2961-7 [12393807.001]

[Cites] N Engl J Med. 2003 Mar 6;348(10):919-32 [12621137.001]

[Cites] Trends Biotechnol. 2003 Mar;21(3):113-6 [12628367.001]

[Cites] Fam Cancer. 2003;2(1):43-55 [14574166.001]

[Cites] Am J Hum Genet. 2003 Dec;73(6):1250-60 [14624392.001]

[Cites] JAMA. 2004 Feb 11;291(6):718-24 [14871915.001]

[Cites] Gastroenterology. 2004 Aug;127(2):444-51 [15300576.001]

[Cites] Hum Hered. 1971;21(6):523-42 [5149961.001]

[Cites] N Engl J Med. 1990 Mar 29;322(13):904-8 [2156161.001]

[Cites] J Med Genet. 1991 May;28(5):289-96 [1650842.001]

[Cites] N Engl J Med. 1992 Mar 5;326(10):658-62 [1736104.001]

[Cites] Cell. 1993 Dec 3;75(5):951-7 [8252630.001]

[Cites] Hum Genet. 1994 Mar;93(3):281-6 [8125478.001]

[Cites] Hum Mutat. 1994;3(2):121-5 [8199592.001]

[Cites] Hum Genet. 1995 Dec;96(6):705-10 [8522331.001]

[Cites] Cancer. 1995 Dec 15;76(12):2427-33 [8625067.001]

[Cites] Ann Intern Med. 1997 Apr 1;126(7):514-9 [9092316.001]

[Cites] Am J Hum Genet. 1998 Jun;62(6):1290-301 [9585611.001]

[Cites] Nat Genet. 1998 Dec;20(4):385-8 [9843214.001]

[Cites] Cancer Res. 1999 Apr 15;59(8):1857-60 [10213492.001]

[Cites] Am J Med Genet. 1999 Oct 8;86(4):321-4 [10494086.001]

[Cites] Hum Genet. 1999 Nov;105(5):388-98 [10598803.001]

[Cites] Am J Hum Genet. 2000 Sep;67(3):582-90 [10924409.001]

[Cites] Cancer Genet Cytogenet. 2005 Apr 1;158(1):70-4 [15771908.001]

[Cites] Gastroenterology. 2005 May;128(6):1696-716 [15887160.001]

[Cites] Gastroenterology. 2001 Jul;121(1):195-7 [11438508.001]

(PMID = 18063416.001).

[ISSN] 1542-7714

[Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association

[ISO-abbreviation] Clin. Gastroenterol. Hepatol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CN / NCI-CN-67000; United States / NCI NIH HHS / CA / P01-CA073992; United States / NCI NIH HHS / CA / R01 CA040641-21; United States / NCI NIH HHS / CA / R01 CA040641; United States / NCI NIH HHS / CA / P01 CA073992-10; United States / NCI NIH HHS / CA / CA040641-21; United States / NCI NIH HHS / CN / N01 CN067000; United States / NCI NIH HHS / CA / R01-CA040641; United States / NCI NIH HHS / CA / P01 CA073992; United States / NCI NIH HHS / CA / CA073992-10

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

[Publication-country] United States

[Other-IDs] NLM/ NIHMS37623; NLM/ PMC2245898

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Role of the endoscopist in the detection of adenomatous polyps during colonoscopy].

[Transliterated title] Papel del Endoscopista en la Detección de Pólipos Adenomatosos Durante la Colonoscopia.

INTRODUCTION: Age, gender and indication for the examination are known predictors of adenomatous polyp detection during colonoscopy.

OBJECTIVES: To determine the role of the endoscopist in detecting adenomatous polyps during colonoscopy MATERIAL AND METHODS: Is retrospective cross-sectional correlational study.

Statistical analysis showed significant differences between endoscopists regarding the detection rate of adenomatous polyps (p = 0.038).

The range for the detection of at least 1 adenomatous polyp by colonoscopy was 14,6-30,0%.

In patients over 50 years, there were also significant differences between endoscopists in detection rate of adenomatous polyps (p = 0.001).

The range for the detection of at least 1 adenomatous polyp was 18,2-37,5% in that group.Also found that age and gender were powerful predictors of adenomatous polyps, both for the total cohort, and patients older than 50 years.

Regarding the indication for colonoscopy, no significant difference between the categories, were found p = 0.288 CONCLUSION S: The endoscopist is as or more important than age, gender or indication for the examination, in predicting the detection of adenomatous polyps during colonoscopy.

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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20066017.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A possible new syndrome with growth-hormone secreting pituitary adenoma, colonic polyposis, lipomatosis, lentigines and renal carcinoma in association with familial testicular germ cell malignancy: A case report.

BACKGROUND: Germ-cell testicular cancer has not been definitively linked to any known hereditary cancer susceptibility disorder.

His evaluation as part of an etiologic study of familial testicular cancer revealed multiple colon polyps (adenomatous, hyperplastic, and hamartomatous) first found in his 50 s, multiple lipomas, multiple hyperpigmented skin lesions, left kidney cancer diagnosed at age 64, and a growth-hormone producing pituitary adenoma with associated acromegaly diagnosed at age 64.

Alternatively, this family's phenotype might represent a novel neoplasm susceptibility disorder.

COS Scholar Universe. author profiles.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Br J Neurosurg. 2004 Dec;18(6):629-31 [15799199.001]

[Cites] Horm Res. 2004;62 Suppl 1:108-15 [15761242.001]

[Cites] Am J Gastroenterol. 2005 Feb;100(2):476-90 [15667510.001]

[Cites] Dig Dis Sci. 2004 Apr;49(4):662-6 [15185875.001]

[Cites] Lancet Oncol. 2004 Jun;5(6):363-71 [15172357.001]

[Cites] Cancer. 2003 Feb 15;97(4):984-92 [12569597.001]

[Cites] J Clin Endocrinol Metab. 2001 Dec;86(12):5658-71 [11739416.001]

[Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4041-6 [11549623.001]

[Cites] J Neurosurg. 2000 Mar;92(3):413-8 [10701527.001]

[Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1354-65 [16174857.001]

[Cites] Science. 2006 May 26;312(5777):1228-30 [16728643.001]

[Cites] Hum Mol Genet. 2006 Feb 1;15(3):443-51 [16407372.001]

(PMID = 17411461.001).

[Journal-full-title] Journal of medical case reports

[ISO-abbreviation] J Med Case Rep

[Language] ENG

[Grant] United States / NCI NIH HHS / CP / N02CP11019

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC1847830

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Decreased expression of cytochrome P450 protein in non-malignant colonic tissue of patients with colonic adenoma.

To estimate the role of cytochrome P450 in carcinogenesis of the colon, expression patterns and protein levels of four representative CYPs (CYP2C, CYP2E1, CYP3A4 and CYP3A5) were determined in colon mucosa of normal and adenomatous colonic tissue of patients with adenomas and disease-free controls.

METHODS: Expression of CYP2C, CYP2E1, CYP3A4, and CYP3A5 in colon mucosa of normal and adenomatous colonic tissue of patients with adenoma and disease-free controls was determined by RT-PCR.

RESULTS: With the exception of CYP3A5, expression of CYP mRNA was similar among groups and tissues (e.g. normal colon mucosa and adenoma).

CYP3A5 mRNA expression was significantly higher in adenoma in comparison to normal tissue of patients with adenoma (approximately 48%).

When comparing protein concentrations of CYPs measured in adenomas with neighboring normal colonic mucosa no differences were found.

However, in normal tissue of patients with adenomas, protein levels of CYP2C8, CYP3A4 and CYP3A5, but not that of CYP2E1, were significantly lower than in biopsies obtained from disease-free controls.

Specifically, in normal colonic mucosa of patients protein concentrations of CYP2C8, CYP3A4, and CYP3A5 were approximately 86%, approximately 69%, and approximately 54%, respectively, lower than in disease-free controls.

CYP2C8, CYP3A4 and CYP3A5) in colon mucosa might contribute to the development of neoplasia in the colon.

[MeSH-major] Adenoma / enzymology. Colon / enzymology. Colonic Neoplasms / enzymology. Cytochrome P-450 CYP2E1 / metabolism. Cytochrome P-450 Enzyme System / metabolism

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Arch Biochem Biophys. 2000 Apr 1;376(1):180-90 [10729204.001]

[Cites] Virchows Arch. 1999 May;434(5):401-11 [10389623.001]

[Cites] Arch Biochem Biophys. 2002 Feb 1;398(1):109-17 [11811955.001]

[Cites] Biochem Biophys Res Commun. 2002 Nov 15;298(5):687-92 [12419308.001]

[Cites] Annu Rev Pharmacol Toxicol. 2003;43:149-73 [12171978.001]

[Cites] J Pharm Pharmacol. 2003 Jan;55(1):59-66 [12625868.001]

[Cites] Front Biosci. 2004 May 1;9:1967-76 [14977602.001]

[Cites] Curr Drug Metab. 2004 Jun;5(3):211-24 [15180491.001]

[Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]

[Cites] Gut. 1991 Apr;32(4):408-12 [1902809.001]

[Cites] Carcinogenesis. 1991 May;12(5):905-9 [2029756.001]

[Cites] Mol Cell Biochem. 1991 Mar 27;102(1):61-9 [2052000.001]

[Cites] Crit Rev Toxicol. 1991;21(6):407-22 [1801846.001]

[Cites] J Biol Chem. 1992 Aug 5;267(22):15765-9 [1639811.001]

[Cites] Cancer Res. 1992 Dec 1;52(23):6567-75 [1423302.001]

[Cites] Gut. 1993 Sep;34(9):1234-9 [8406161.001]

[Cites] Mutat Res. 1993 Nov;290(1):27-33 [7694095.001]

[Cites] Anal Biochem. 1993 Sep;213(2):414-21 [8238918.001]

[Cites] Biochem Pharmacol. 1994 Jul 5;48(1):59-64 [8043031.001]

[Cites] Cancer Chemother Pharmacol. 1994;34(6):497-502 [7923560.001]

[Cites] Pharmacogenetics. 1994 Oct;4(5):247-59 [7894497.001]

[Cites] Biochem Biophys Res Commun. 1995 May 16;210(2):350-5 [7755610.001]

[Cites] Biochem Pharmacol. 1996 Jan 12;51(1):61-9 [8534269.001]

[Cites] Naunyn Schmiedebergs Arch Pharmacol. 1996 Jan;353(2):207-12 [8717162.001]

[Cites] Biochem Biophys Res Commun. 1997 Feb 3;231(1):203-5 [9070249.001]

[Cites] Drug Metab Dispos. 1999 Jul;27(7):804-9 [10383924.001]

[Cites] Curr Drug Metab. 2000 Sep;1(2):107-32 [11465078.001]

(PMID = 16281975.001).

[ISSN] 1471-230X

[Journal-full-title] BMC gastroenterology

[ISO-abbreviation] BMC Gastroenterol

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / cytochrome P-450 CYP2C subfamily; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A

[Other-IDs] NLM/ PMC1310537

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Analysis of mtDNA sequence variants in colorectal adenomatous polyps.

Colorectal tumors mostly arise from sporadic adenomatous polyps.

Polyps are defined as a mass of cells that protrudes into the lumen of the colon.

Adenomatous polyps are benign neoplasms that, by definition display some characteristics of dysplasia.

It has been shown that polyps were benign tumors which may undergo malignant transformation.

Adenomatous polyps have been classified into three histologic types; tubular, tubulovillous, and villous with increasing malignant potential.

The ability to differentially diagnose these colorectal adenomatous polyps is important for therapeutic intervention.

To date, little efforts have been directed to identifying genetic changes involved in adenomatous polyps.

This study was designed to examine the relevance of mitochondrial genome alterations in the three adenomatous polyps.

Using high resolution restriction endonucleases and PCR-based sequencing, fifty-seven primary fresh frozen tissues of adenomatous polyps (37 tumors and 20 matched surrounding normal tissues) obtained from the southern regional Cooperative Human Tissue Network (CHTN) and Grady Memorial Hospital at Atlanta were screened with three mtDNA regional primer pairs that spanned 5.9 kbp.

Notably, a heteroplasmic variant C8515G/T in the MT-ATP 8 gene and a germline variant 8327delA in the tRNAlys was observed in all the tissue samples of the three adenomatous polyps in comparison to the referenced database sequence.

A germline variant G9055A in the MT-ATP 6 gene had a frequency of 100% (17/17) in tubular and 57% (13/23) in villous adenomas; no corresponding variant was in tubulovillous adenomas.

Furthermore, A9006G variant at MT-ATP 6 gene was observed at frequency of 57% (13/23) in villous adenomas only.

Interestingly, variants A9006G and G9055A were absent in the villous tissue samples that were clinicopathological designated as "polyvillous adenomas".

Our current data provide a basis for continued investigation of certain mtDNA variants as predictors of the three adenomatous polyps in a larger number of clinicopathological specimens.

[MeSH-major] Adenomatous Polyps / genetics. Colonic Polyps / genetics. Colorectal Neoplasms / genetics. DNA, Mitochondrial / analysis. Genetic Variation

MedlinePlus Health Information. consumer health - Colonic Polyps.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Surg Pathol. 2004 Nov;28(11):1460-5 [15489649.001]

[Cites] Science. 1987 Oct 9;238(4824):193-7 [2889267.001]

[Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]

[Cites] Gastroenterology. 1990 Feb;98(2):371-9 [2403953.001]

[Cites] Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11164-8 [1454794.001]

[Cites] FEBS Lett. 1995 Jan 16;358(1):1-3 [7821417.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):514-9 [9012815.001]

[Cites] Mol Cancer. 2004 Oct 13;3:30 [15482594.001]

[Cites] Cancer Res. 2005 Mar 1;65(5):1655-63 [15753359.001]

[Cites] Br J Cancer. 2005 Aug 8;93(3):331-7 [15956973.001]

[Cites] Science. 2008 May 2;320(5876):661-4 [18388260.001]

[Cites] Diagn Mol Pathol. 2008 Jun;17(2):94-100 [18382370.001]

[Cites] Carcinogenesis. 2010 Feb;31(2):296-301 [19945968.001]

[Cites] Hum Pathol. 2002 Mar;33(3):372-5 [11979380.001]

(PMID = 20929553.001).

[ISSN] 1746-1596

[Journal-full-title] Diagnostic pathology

[ISO-abbreviation] Diagn Pathol

[Language] eng

[Grant] United States / NIGMS NIH HHS / GM / R25 GM058268

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Mitochondrial

[Other-IDs] NLM/ PMC2959018

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).

Genetic Alliance. consumer health - Familial Polyposis.

MedlinePlus Health Information. consumer health - Lymphatic Diseases.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] An association between colonic adenoma and abdominal obesity: a cross-sectional study.

BACKGROUND: Colorectal adenoma is a precursor lesion of colorectal cancer and thus, it is an important target for preventing colorectal cancer.

Only a few studies suggest an association between colorectal adenoma and obesity, but results show considerable heterogeneity.

In this study, we investigated the association between colorectal adenoma and waist circumference.

METHODS: 165 adenoma cases and 365 polyp-free controls with a normal colon were compared in this cross-sectional study.

And smokers and men were more prevalent among cases than controls.Among the abdominal obese subjects, 45.6% had 1 or more adenoma, and 9.0% of these had advanced adenoma, whereas among subjects with a normal waist circumference, only 25.7% had 1 or more adenomas.

The prevalence of adenoma was higher among abdominal obese group (P < 0.05).

Logistic regression analysis showed that abdominal obesity was associated with an increased risk of colorectal adenoma (OR, 2.74; 95% CI, 1.66~4.51 in men, OR, 2.58; 95% CI, 1.08~6.12 in women).

While BMI was found to be weekly associated with the risk of adenoma among men at the highest BMI levels.

However, BMI was not associated with the risk for adenoma after adjusting for waist circumference.

CONCLUSION: Our data suggest that abdominal obesity is associated with an increased risk of colorectal adenoma.

[MeSH-major] Adenoma / epidemiology. Colorectal Neoplasms / epidemiology. Obesity / complications

Genetic Alliance. consumer health - Obesity.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Jpn J Cancer Res. 1999 Aug;90(8):805-11 [10543250.001]

[Cites] Gut. 2008 Aug;57(8):1166-76 [18628378.001]

[Cites] Nutr Cancer. 2000;37(1):19-26 [10965515.001]

[Cites] Circulation. 2000 Sep 12;102(11):1296-301 [10982546.001]

[Cites] J Natl Cancer Inst. 2000 Oct 4;92(19):1592-600 [11018095.001]

[Cites] Am J Epidemiol. 2000 Nov 1;152(9):847-54 [11085396.001]

[Cites] Br J Cancer. 2001 Aug 3;85(3):346-9 [11487263.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1012-8 [12376501.001]

[Cites] J Endocrinol Invest. 2002 Nov;25(10):876-83 [12508950.001]

[Cites] Am J Prev Med. 2003 Feb;24(2):170-6 [12568823.001]

[Cites] Arch Intern Med. 2003 Feb 10;163(3):309-14 [12578511.001]

[Cites] Am J Epidemiol. 2003 Sep 1;158(5):424-31 [12936897.001]

[Cites] J Clin Invest. 1983 Sep;72(3):1150-62 [6350364.001]

[Cites] Jpn J Cancer Res. 1989 Jan;80(1):51-8 [2540132.001]

[Cites] Int J Cancer. 1990 Feb 15;45(2):372-5 [2406206.001]

[Cites] Cancer Causes Control. 1991 Mar;2(2):117-24 [1873436.001]

[Cites] Gastroenterology. 1992 Apr;102(4 Pt 1):1101-8 [1312970.001]

[Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]

[Cites] Jpn J Cancer Res. 1994 May;85(5):479-84 [8014105.001]

[Cites] Ann Intern Med. 1995 Mar 1;122(5):327-34 [7847643.001]

[Cites] Cancer Causes Control. 1996 Mar;7(2):253-63 [8740738.001]

[Cites] Int J Cancer. 1998 Oct 5;78(2):161-5 [9754646.001]

[Cites] J Natl Cancer Inst. 1999 Apr 7;91(7):620-5 [10203281.001]

[Cites] Am J Epidemiol. 1999 Oct 15;150(8):869-77 [10522658.001]

[Cites] Clin Cancer Res. 2005 May 15;11(10):3642-6 [15897559.001]

[Cites] Diabetes Res Clin Pract. 2007 Jan;75(1):72-80 [16735075.001]

[Cites] Swiss Med Wkly. 2007 Jan 27;137(3-4):50-6 [17299670.001]

[Cites] Gastroenterology. 2007 May;132(6):2208-25 [17498513.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2007 Dec;16(12):2533-47 [18086756.001]

[Cites] Int J Cancer. 2008 Sep 1;123(5):1160-5 [18546286.001]

[Cites] Eur J Cancer Prev. 1999 Dec;8 Suppl 1:S53-60 [10772419.001]

(PMID = 19144203.001).

[ISSN] 1471-230X

[Journal-full-title] BMC gastroenterology

[ISO-abbreviation] BMC Gastroenterol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2635368