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1
adenoma of large intestine 2005:2010[pubdate] *count=100
982 results
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Items 1 to 100 of about 982
1.
Menigatti M, Cattaneo E, Sabates-Bellver J, Ilinsky VV, Went P, Buffoli F, Marquez VE, Jiricny J, Marra G:
The protein tyrosine phosphatase receptor type R gene is an early and frequent target of silencing in human colorectal tumorigenesis.
Mol Cancer
; 2009 Dec 16;8:124
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[Title]
The protein tyrosine phosphatase receptor type R gene is an early and frequent target of silencing in human
colorectal
tumorigenesis.
RESULTS: A recent high-throughput gene expression analysis conducted by our group identified numerous genes whose transcription was markedly diminished in
colorectal
tumors.
Here, we show that levels of both major PTPRR transcript variants are markedly decreased (compared with normal mucosal levels) in precancerous and cancerous
colorectal
tumors, as well in
colorectal
cancer cell lines.
The expression of the PTPRR-1 isoform was inactivated in
colorectal
cancer cells as a result of
de
novo CpG island methylation and enrichment of transcription-repressive histone-tail marks, mainly H3K27me3.
De
novo methylation of the PTPRR-1 transcription start site was demonstrated in 29/36 (80%)
colorectal adenomas
, 42/44 (95%)
colorectal
adenocarcinomas, and 8/8 (100%) liver metastases associated with the latter tumors.
CONCLUSIONS: Epigenetic downregulation of PTPRR seems to be an early alteration in
colorectal
cell transformation, which is maintained during the clonal selection associated with tumor progression.
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[Cites]
Cancer Res. 2006 Sep 1;66(17):8430-8
[
16951153.001
]
[Cites]
Genes Chromosomes Cancer. 2004 Oct;41(2):117-24
[
15287024.001
]
[Cites]
Nat Rev Mol Cell Biol. 2006 Nov;7(11):833-46
[
17057753.001
]
[Cites]
Nat Rev Cancer. 2006 Dec;6(12):924-35
[
17109012.001
]
[Cites]
Nat Genet. 2007 Feb;39(2):232-6
[
17200670.001
]
[Cites]
Cell. 2007 Feb 23;128(4):683-92
[
17320506.001
]
[Cites]
Gastroenterology. 2007 Feb;132(2):628-32
[
17320548.001
]
[Cites]
J Neurochem. 2007 May;101(3):829-40
[
17266727.001
]
[Cites]
Genes Dev. 2007 May 1;21(9):1050-63
[
17437993.001
]
[Cites]
Nature. 2007 Nov 15;450(7168):415-9
[
17928865.001
]
[Cites]
Mol Cancer Res. 2007 Dec;5(12):1263-75
[
18171984.001
]
[Cites]
FEBS J. 2008 Mar;275(5):816-30
[
18298790.001
]
[Cites]
N Engl J Med. 2008 Mar 13;358(11):1148-59
[
18337604.001
]
[Cites]
Oncogene. 2008 Jul 24;27(32):4503-8
[
18391979.001
]
[Cites]
PLoS Genet. 2008;4(8):e1000145
[
18670629.001
]
[Cites]
Oncogene. 2009 Feb 12;28(6):899-909
[
19060925.001
]
[Cites]
Cell Death Differ. 2009 Mar;16(3):368-77
[
18846109.001
]
[Cites]
Cerebellum. 2009 Jun;8(2):80-8
[
19137382.001
]
[Cites]
Mol Cancer Ther. 2009 Jun;8(6):1579-88
[
19509260.001
]
[Cites]
Cell. 1987 Sep 11;50(6):823-9
[
3113737.001
]
[Cites]
Anat Rec. 2000 Mar 1;258(3):221-34
[
10705342.001
]
[Cites]
Nature. 2001 May 17;411(6835):355-65
[
11357143.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7164-9
[
11416201.001
]
[Cites]
Nature. 2002 Jun 27;417(6892):949-54
[
12068308.001
]
[Cites]
J Biol Chem. 2002 Aug 16;277(33):29503-9
[
12042304.001
]
[Cites]
Nature. 2002 Aug 29;418(6901):934
[
12198537.001
]
[Cites]
Nucleic Acids Res. 2001 May 1;29(9):e45
[
11328886.001
]
[Cites]
Genes Dev. 2002 Nov 15;16(22):2893-905
[
12435631.001
]
[Cites]
Cancer Res. 2002 Nov 15;62(22):6390-4
[
12438221.001
]
[Cites]
Gastroenterology. 2002 Dec;123(6):1941-8
[
12454851.001
]
[Cites]
Science. 2003 Apr 4;300(5616):131-5
[
12649488.001
]
[Cites]
Biochem J. 2003 May 15;372(Pt 1):193-201
[
12583813.001
]
[Cites]
Nat Rev Cancer. 2003 Jun;3(6):459-65
[
12778136.001
]
[Cites]
Oncogene. 2003 Sep 25;22(41):6319-31
[
14508512.001
]
[Cites]
Nat Genet. 2004 Apr;36(4):417-22
[
15034581.001
]
[Cites]
Science. 2004 May 21;304(5674):1164-6
[
15155950.001
]
[Cites]
Cell. 2004 Jun 11;117(6):699-711
[
15186772.001
]
[Cites]
Genes Dev. 2004 Jul 1;18(13):1592-605
[
15231737.001
]
[Cites]
Nat Genet. 1998 Jun;19(2):187-91
[
9620779.001
]
[Cites]
Nature. 1998 May 28;393(6683):386-9
[
9620804.001
]
[Cites]
EMBO J. 1998 Dec 15;17(24):7337-50
[
9857190.001
]
[Cites]
Oncogene. 1999 Jan 21;18(3):813-22
[
9989833.001
]
[Cites]
Biochem Biophys Res Commun. 1999 Mar 5;256(1):52-6
[
10066421.001
]
[Cites]
Am J Physiol. 1999 Sep;277(3 Pt 1):G631-41
[
10484389.001
]
[Cites]
J Hum Genet. 2005;50(4):159-67
[
15824892.001
]
[Cites]
Nat Rev Genet. 2006 Jan;7(1):21-33
[
16369569.001
]
[Cites]
Nature. 2006 Feb 16;439(7078):871-4
[
16357870.001
]
[Cites]
Nat Rev Cancer. 2006 Feb;6(2):107-16
[
16491070.001
]
[Cites]
Nat Rev Cancer. 2006 Apr;6(4):307-20
[
16557282.001
]
[Cites]
Biochem J. 2006 May 1;395(3):483-91
[
16441242.001
]
[Cites]
Gastroenterology. 2006 Oct;131(4):1096-109
[
17030180.001
]
(PMID = 20015382.001).
[ISSN]
1476-4598
[Journal-full-title]
Molecular cancer
[ISO-abbreviation]
Mol. Cancer
[Language]
ENG
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger; EC 3.1.3.48 / PTPRR protein, human; EC 3.1.3.48 / Receptor-Like Protein Tyrosine Phosphatases, Class 7
[Other-IDs]
NLM/ PMC2801661
2.
Pufulete M:
Intake of dairy products and risk of colorectal neoplasia.
Nutr Res Rev
; 2008 Jun;21(1):56-67
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[Title]
Intake of dairy products and risk of
colorectal
neoplasia.
Prospective cohort studies suggest that higher intakes of dairy products, in particular milk, are associated with a decreased risk of
colorectal
cancer (CRC).
Randomised controlled trials with Ca supplements have been conducted with both
colorectal
adenoma
and CRC as endpoints.
Results suggest that Ca supplementation at a level of 1000-2000 mg/d reduces
adenoma
recurrence in individuals with a previous
adenoma
but has no effect on CRC incidence.
[MeSH-major]
Anticarcinogenic Agents / administration & dosage. Calcium, Dietary / administration & dosage.
Colorectal
Neoplasms / epidemiology.
Colorectal
Neoplasms / prevention & control. Dairy Products
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consumer health - Colorectal Cancer
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(PMID = 19079854.001).
[ISSN]
1475-2700
[Journal-full-title]
Nutrition research reviews
[ISO-abbreviation]
Nutr Res Rev
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Calcium, Dietary; 1406-16-2 / Vitamin D
[Number-of-references]
113
3.
Kaindl U, Eyberg I, Rohr-Udilova N, Heinzle C, Marian B:
The dietary antioxidants resveratrol and quercetin protect cells from exogenous pro-oxidative damage.
Food Chem Toxicol
; 2008 Apr;46(4):1320-6
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In
the colorectal
epithelium oxidative stress is observed endogenously in premalignant
adenoma
cells or induced by nutritional factors like fatty acid hydroperoxides (LOOH).
Our study used
colorectal
adenoma
and carcinoma cell lines to assess antioxidant protective effects of resveratrol and quercetin.
For reduction of endogenous H2O2 levels in
colorectal
tumor cells higher antioxidant-concentrations are needed in all cell lines.
Quercetin (10 microM) alone even increased H2O2 in LT97
adenoma
cells and stimulated VEGF production.
MedlinePlus Health Information.
consumer health - Antioxidants
.
Hazardous Substances Data Bank.
QUERCETIN
.
Hazardous Substances Data Bank.
RESVERATROL
.
Hazardous Substances Data Bank.
HYDROGEN PEROXIDE
.
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(PMID = 17936464.001).
[ISSN]
0278-6915
[Journal-full-title]
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
[ISO-abbreviation]
Food Chem. Toxicol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antioxidants; 0 / Oxidants; 0 / Stilbenes; 0 / Vascular Endothelial Growth Factor A; 63231-63-0 / RNA; 9IKM0I5T1E / Quercetin; BBX060AN9V / Hydrogen Peroxide; K7Q1JQR04M / Dinoprostone; Q369O8926L / resveratrol
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4.
Sarebø M, Skjelbred CF, Breistein R, Lothe IM, Hagen PC, Bock G, Hansteen IL, Kure EH:
Association between cigarette smoking, APC mutations and the risk of developing sporadic colorectal adenomas and carcinomas.
BMC Cancer
; 2006 Mar 17;6:71
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[Title]
Association between cigarette smoking, APC mutations and the risk of developing sporadic
colorectal adenomas
and carcinomas.
BACKGROUND: The association between
colorectal
cancer (CRC) and smoking has not been consistent.
METHODS: To evaluate the hypothesis that cigarette smoking is associated with
adenoma
and carcinoma development and further to investigate whether this association is due to mutations in the APC gene, we used a study population consisting of 133 cases (45
adenomas
and 88 carcinomas) and 334 controls.
An overall case-control association was detected for
adenomas
and "ever smoking" OR = 1.73 (95% CI 0.83-3.58).
When cases were divided based on APC truncation mutation status, an association was detected in
adenomas
without APC mutation in relation to "ever smoking", with an OR = 3.97 (1.26-12.51).
CONCLUSION: Our data suggest an association between smoking and
adenoma
and CRC development.
[MeSH-major]
Adenoma
/ genetics. Carcinoma / genetics.
Colorectal
Neoplasms / genetics. DNA, Neoplasm / genetics. Genes, APC. Smoking / adverse effects
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consumer health - Colorectal Cancer
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[Cites]
N Engl J Med. 2000 Jul 20;343(3):162-8
[
10900274.001
]
[Cites]
Cancer Lett. 2005 Nov 8;229(1):85-91
[
15946795.001
]
[Cites]
Mol Genet Metab. 2000 Dec;71(4):639-45
[
11136557.001
]
[Cites]
J Natl Cancer Inst. 2000 Nov 15;92(22):1831-6
[
11078760.001
]
[Cites]
Int J Colorectal Dis. 2001 Apr;16(2):102-7
[
11355315.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 Jul;10(7):725-31
[
11440957.001
]
[Cites]
Carcinogenesis. 2001 Oct;22(10):1681-4
[
11577009.001
]
[Cites]
Cancer Res. 2002 Jan 15;62(2):363-6
[
11809680.001
]
[Cites]
Lancet Oncol. 2002 Feb;3(2):83-8
[
11905459.001
]
[Cites]
Gastrointest Endosc Clin N Am. 2002 Jan;12(1):1-9, v
[
11916153.001
]
[Cites]
Jpn J Clin Oncol. 2002 Jun;32(6):196-201
[
12110635.001
]
[Cites]
Scand J Gastroenterol. 2002 Oct;37(10):1184-93
[
12408524.001
]
[Cites]
Carcinogenesis. 2003 Feb;24(2):283-90
[
12584179.001
]
[Cites]
Carcinogenesis. 2003 Mar;24(3):565-71
[
12663519.001
]
[Cites]
Scand J Gastroenterol. 2003 Jun;38(6):635-42
[
12825872.001
]
[Cites]
Nat Rev Cancer. 2003 Oct;3(10):733-44
[
14570033.001
]
[Cites]
Carcinogenesis. 2004 Jul;25(7):1219-26
[
14976131.001
]
[Cites]
Mol Cancer. 2003 Dec 12;2:41
[
14672538.001
]
[Cites]
IARC Monogr Eval Carcinog Risks Hum. 2004;83:1-1438
[
15285078.001
]
[Cites]
Semin Cancer Biol. 2004 Dec;14(6):473-86
[
15489140.001
]
[Cites]
Am J Epidemiol. 1986 Sep;124(3):453-69
[
3740045.001
]
[Cites]
N Engl J Med. 1988 Sep 1;319(9):525-32
[
2841597.001
]
[Cites]
J Clin Epidemiol. 1990;43(12):1327-35
[
2254769.001
]
[Cites]
Cell. 1991 Aug 9;66(3):589-600
[
1651174.001
]
[Cites]
J Am Diet Assoc. 1992 Jun;92(6):686-93
[
1607564.001
]
[Cites]
Nature. 1992 Sep 17;359(6392):235-7
[
1528264.001
]
[Cites]
Hum Mol Genet. 1992 Jul;1(4):229-33
[
1338904.001
]
[Cites]
Cancer Res. 1994 Jun 1;54(11):3011-20
[
8187091.001
]
[Cites]
J Natl Cancer Inst. 1996 Dec 4;88(23):1717-30
[
8944002.001
]
[Cites]
Jpn J Cancer Res. 1997 Aug;88(8):718-24
[
9330602.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Oct 28;94(22):12122-7
[
9342373.001
]
[Cites]
Hum Mutat. 1998;11(2):114-20
[
9482574.001
]
[Cites]
J Natl Cancer Inst. 1999 Jun 2;91(11):916-32
[
10359544.001
]
[Cites]
Am J Epidemiol. 2005 May 1;161(9):806-15
[
15840612.001
]
[Cites]
Eur J Cancer Prev. 2000 Jun;9(3):193-203
[
10954259.001
]
(PMID = 16545110.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Neoplasm
[Other-IDs]
NLM/ PMC1475604
5.
Skjelbred CF, Saebø M, Hjartåker A, Grotmol T, Hansteen IL, Tveit KM, Hoff G, Kure EH:
Meat, vegetables and genetic polymorphisms and the risk of colorectal carcinomas and adenomas.
BMC Cancer
; 2007 Dec 19;7:228
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[Title]
Meat, vegetables and genetic polymorphisms and the risk of
colorectal
carcinomas and
adenomas
.
BACKGROUND: The risk of sporadic
colorectal
cancer (CRC) is mainly associated with lifestyle factors, particularly dietary factors.
In this study we aimed to evaluate the role of dietary factors in combination with genetic factors in the different stages of
colorectal
carcinogenesis in a Norwegian population.
METHODS: We used a case-control study design (234 carcinomas, 229 high-risk
adenomas
, 762 low-risk
adenomas
and 400 controls) to test the association between dietary factors (meat versus fruit, berries and vegetables) genetic polymorphisms in biotransformation genes (GSTM1, GSTT1, GSTP1 Ile105Val, EPHX1 Tyr113His and EPHX1 His139Arg), and risk of
colorectal
carcinomas and
adenomas
.
RESULTS: A higher ratio of total meat to total fruit, berry and vegetable intake was positively associated with both high and low-risk
adenomas
, with approximately twice the higher risk in the 2nd quartile compared to the lowest quartile.
For the high-risk
adenomas
this positive association was more obvious for the common allele (Tyr allele) of the EPHX1 codon 113 polymorphism.
An association was also observed for the EPHX1 codon 113 polymorphism in the low-risk
adenomas
, although not as obvious.
CONCLUSION: Although, the majority of the comparison groups are not significant, our results suggest an increased risk of
colorectal adenomas
in individuals for some of the higher ratios of total meat to total fruit, berry and vegetable intake.
In addition the study supports the notion that the biotransformation enzymes GSTM1, GSTP1 and EPHX1 may modify the effect of dietary factors on the risk of developing
colorectal
carcinoma and
adenoma
.
[MeSH-major]
Adenoma
/ etiology. Carcinoma / etiology.
Colorectal
Neoplasms / etiology. Eating / physiology. Meat. Polymorphism, Genetic. Vegetables
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[Cites]
Int J Cancer. 2004 Nov 1;112(2):259-64
[
15352038.001
]
[Cites]
Forum Nutr. 2006;59:130-53
[
16917177.001
]
[Cites]
J Natl Cancer Inst. 1981 Jun;66(6):1191-308
[
7017215.001
]
[Cites]
Biochim Biophys Acta. 1983 Dec 29;695(3-4):251-70
[
6418203.001
]
[Cites]
Am J Epidemiol. 1986 Sep;124(3):453-69
[
3740045.001
]
[Cites]
Nucleic Acids Res. 1988 Feb 11;16(3):1215
[
3344216.001
]
[Cites]
J Clin Epidemiol. 1990;43(12):1327-35
[
2254769.001
]
[Cites]
J Natl Cancer Inst. 1992 Jan 15;84(2):91-8
[
1310511.001
]
[Cites]
J Am Diet Assoc. 1992 Jun;92(6):686-93
[
1607564.001
]
[Cites]
Am J Epidemiol. 2000 Jan 1;151(1):7-32
[
10625170.001
]
[Cites]
Mutat Res. 2000 Oct;463(3):285-308
[
11018745.001
]
[Cites]
J Epidemiol. 2000 Sep;10(5):349-60
[
11059519.001
]
[Cites]
Cancer Res. 2001 Mar 15;61(6):2381-5
[
11289100.001
]
[Cites]
Nutr Rev. 2001 Feb;59(2):37-47
[
11310774.001
]
[Cites]
Eur J Cancer. 2001 May;37(8):948-65
[
11334719.001
]
[Cites]
Ann Intern Med. 1993 Jan 15;118(2):91-5
[
8416323.001
]
[Cites]
Pharmacogenetics. 1991 Oct;1(1):4-19
[
1844821.001
]
[Cites]
J Natl Cancer Inst. 1993 Jun 2;85(11):884-91
[
8388061.001
]
[Cites]
BMJ. 1993 Jul 31;307(6899):277-8
[
8397026.001
]
[Cites]
Hum Mol Genet. 1994 Mar;3(3):421-8
[
7516776.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):439-46
[
11352852.001
]
[Cites]
Mutat Res. 2001 Jul 25;494(1-2):21-9
[
11423342.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 Aug;10(8):875-82
[
11489754.001
]
[Cites]
Int J Hyg Environ Health. 2001 Oct;204(1):31-8
[
11725342.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 Dec;10(12):1239-48
[
11751440.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Jan;11(1):15-21
[
11815396.001
]
[Cites]
Int J Cancer. 2002 Mar 10;98(2):241-56
[
11857415.001
]
[Cites]
Cancer Res. 2002 Apr 15;62(8):2248-52
[
11956078.001
]
[Cites]
Carcinogenesis. 2002 Nov;23(11):1839-49
[
12419832.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1332-52
[
12433710.001
]
[Cites]
Gastroenterol Clin North Am. 2002 Dec;31(4):925-43
[
12489270.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 Jan;12(1):14-22
[
12540498.001
]
[Cites]
J Womens Health (Larchmt). 2003 Mar;12(2):173-82
[
12737716.001
]
[Cites]
Scand J Gastroenterol. 2003 Jun;38(6):635-42
[
12825872.001
]
[Cites]
Cancer Causes Control. 2004 Apr;15(3):225-36
[
15090717.001
]
[Cites]
Carcinogenesis. 2004 Jul;25(7):1211-8
[
14988221.001
]
[Cites]
Biochem Biophys Res Commun. 1995 Jan 17;206(2):748-55
[
7826396.001
]
[Cites]
Biochem J. 1995 Mar 1;306 ( Pt 2):565-9
[
7887912.001
]
[Cites]
Biochem J. 1995 Oct 15;311 ( Pt 2):453-9
[
7487881.001
]
[Cites]
Crit Rev Biochem Mol Biol. 1995;30(6):445-600
[
8770536.001
]
[Cites]
Lancet. 1997 Aug 30;350(9078):630-3
[
9288046.001
]
[Cites]
Eur J Cancer Prev. 1997 Oct;6(5):415-7
[
9466112.001
]
[Cites]
J Mol Biol. 1998 May 8;278(3):687-98
[
9600848.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1998 Aug;7(8):647-52
[
9718215.001
]
[Cites]
Pharmacogenetics. 1998 Oct;8(5):441-7
[
9825836.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1999 Apr;8(4 Pt 1):289-92
[
10207630.001
]
[Cites]
Br J Cancer. 1999 Jan;79(1):168-71
[
10408710.001
]
[Cites]
Environ Health Perspect. 1999 Feb;107 Suppl 1:37-47
[
10229705.001
]
[Cites]
Eur J Cancer Prev. 1999 Jul;8(3):173-4
[
10443942.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):152-7
[
15668489.001
]
[Cites]
World J Gastroenterol. 2005 Mar 14;11(10):1473-80
[
15770723.001
]
[Cites]
Annu Rev Pharmacol Toxicol. 2005;45:51-88
[
15822171.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1350-2
[
15894702.001
]
[Cites]
Eur J Cancer Prev. 2005 Aug;14(4):373-9
[
16030428.001
]
[Cites]
Cancer Lett. 2005 Nov 8;229(1):85-91
[
15946795.001
]
[Cites]
Int J Cancer. 1975 Apr 15;15(4):617-31
[
1140864.001
]
(PMID = 18093316.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 3.3.2.- / Epoxide Hydrolases; EC 3.3.2.9 / EPHX1 protein, human
[Other-IDs]
NLM/ PMC2228310
6.
Sharma S, Iwasaki M, Kunieda C, Cao X, Ishihara J, Hamada G, Miyajima NT, Tsugane S, Le Marchand L:
Development of a quantitative food frequency questionnaire for assessing food, nutrient, and heterocyclic aromatic amines intake in Japanese Brazilians for a colorectal adenoma case-control study.
Int J Food Sci Nutr
; 2009;60 Suppl 7:128-39
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[Title]
Development of a quantitative food frequency questionnaire for assessing food, nutrient, and heterocyclic aromatic amines intake in Japanese Brazilians for a
colorectal
adenoma
case-control study.
PRIMARY OBJECTIVE: To develop of a quantitative food frequency questionnaire (QFFQ) to assess intake of specific foods, nutrients and heterocyclic aromatic amines (HAAs) in a case-control study of
colorectal
adenoma
.
CONCLUSIONS: We have developed a QFFQ appropriate for Japanese Brazilians that will allow us to estimate HAA intake and will be used to examine our hypotheses related to foods, nutrients and HAAs, and diet-gene interactions in
colorectal
neoplasia in this population.
[MeSH-major]
Adenoma
. Amines / administration & dosage.
Colorectal
Neoplasms. Diet. Diet Surveys. Food Analysis. Polycyclic Hydrocarbons, Aromatic / administration & dosage
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(PMID = 19381993.001).
[ISSN]
1465-3478
[Journal-full-title]
International journal of food sciences and nutrition
[ISO-abbreviation]
Int J Food Sci Nutr
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R03 CA119682
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Amines; 0 / Polycyclic Hydrocarbons, Aromatic
7.
Yamaji T, Iwasaki M, Sasazuki S, Tsugane S:
Interaction between adiponectin and leptin influences the risk of colorectal adenoma.
Cancer Res
; 2010 Jul 1;70(13):5430-7
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[Title]
Interaction between adiponectin and leptin influences the risk of
colorectal
adenoma
.
Obesity has been associated with an increased risk of
colorectal
neoplasia, but the mechanisms of this potential association have not been elucidated.
We hypothesized that the adipokines adiponectin, leptin, and tumor necrosis factor-alpha (TNF-alpha) may mediate an association between obesity and
colorectal
cancer.
An inverse association of total and HMW adiponectin was observed with
colorectal
adenoma
(P trend < 0.001 and 0.03, respectively).
Further, total adiponectin interacted with leptin, but not TNF-alpha, in relation to
colorectal
adenoma
(P interaction = 0.007).
An inverse association of total adiponectin with
colorectal
adenoma
was apparent in the highest two tertiles of leptin, particularly the middle (P trend < 0.001), whereas a positive association of leptin was obvious in the lowest tertile of total adiponectin (P trend = 0.01) after adjusting for potential confounders and body mass index, which is a major determinant of insulin resistance.
Adiponectin may exert an anticarcinogenic effect on the
large intestine
by interfering with leptin, whereas leptin could conversely exert a carcinogenic effect under conditions of a lower abundance of adiponectin.
Our findings provide the first epidemiologic evidence for interactive effects of adiponectin and leptin in the early stage of
colorectal
tumorigenesis, distinct from their involvement in insulin resistance.
[MeSH-major]
Adenoma
/ blood.
Colorectal
Neoplasms / blood. Leptin / blood
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[Copyright]
Copyright 2010 AACR.
(PMID = 20516125.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ADIPOQ protein, human; 0 / Adiponectin; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha
8.
Zhang W, Bauer M, Croner RS, Pelz JO, Lodygin D, Hermeking H, Stürzl M, Hohenberger W, Matzel KE:
DNA stool test for colorectal cancer: hypermethylation of the secreted frizzled-related protein-1 gene.
Dis Colon Rectum
; 2007 Oct;50(10):1618-26; discussion 1626-7
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[Title]
DNA stool test for
colorectal
cancer: hypermethylation of the secreted frizzled-related protein-1 gene.
PURPOSE: To investigate a potential mode of noninvasive screening for
colorectal
cancer, we evaluated the hypermethylation of the secreted frizzled-related protein-1 gene promoter in human stool DNA.
METHODS: In stool samples from 36 patients with
colorectal
neoplasia (7
adenoma
, 29
colorectal
cancer) and 17 healthy control subjects, isolated DNA was treated with sodium bisulfite and analyzed by methylation-specific polymerase chain reaction with primers specific for methylated or unmethylated promoter sequences of the secreted frizzled-related protein-1 gene.
RESULTS: Hypermethylation of the secreted frizzled-related protein-1 promoter was present in the stool DNA of patients with
adenoma
and
colorectal
cancer.
A sensitivity of 89 percent and specificity of 86 percent were achieved in the detection of
colorectal
neoplasia.
The difference in hypermethylation status of the secreted frizzled-related protein-1 promoter between the patients with
colorectal
neoplasia and the control group was statistically highly significant (P < 0.001).
Adenoma
and early tumor Stage I (International Union Against Cancer) displayed both unmethylated and methylated secreted frizzled-related protein-1 promoter sequences, whereas advanced tumor stages showed only methylated secreted frizzled-related protein-1 (P = 0.05).
It has the potential of a clinically useful test for the early detection of
colorectal
cancer.
[MeSH-major]
Adenoma
/ metabolism. Carcinoma / metabolism.
Colorectal
Neoplasms / metabolism. DNA Methylation. Feces. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / metabolism
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(PMID = 17762966.001).
[ISSN]
0012-3706
[Journal-full-title]
Diseases of the colon and rectum
[ISO-abbreviation]
Dis. Colon Rectum
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / SFRP1 protein, human
9.
Lobach I, Carroll RJ, Spinka C, Gail MH, Chatterjee N:
Haplotype-based regression analysis and inference of case-control studies with unphased genotypes and measurement errors in environmental exposures.
Biometrics
; 2008 Sep;64(3):673-84
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Inferences with measurement error corrections are complicated by the fact that the Wald test often behaves poorly in the presence
of large
amounts of measurement error.
An application of our method is illustrated using a population-based case-control study of the association between calcium intake and the risk of
colorectal
adenoma
.
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[Cites]
Biometrics. 2001 Sep;57(3):795-802
[
11550930.001
]
[Cites]
Cancer Causes Control. 2002 Dec;13(10):937-46
[
12588090.001
]
[Cites]
Am J Epidemiol. 2003 Jul 1;158(1):1-13
[
12835280.001
]
[Cites]
Am J Hum Genet. 2003 Dec;73(6):1316-29
[
14631556.001
]
[Cites]
Genet Epidemiol. 2004 Nov;27(3):192-201
[
15372619.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2004 Dec;13(12):2181-6
[
15598778.001
]
[Cites]
Genet Epidemiol. 2005 Sep;29(2):108-27
[
16080203.001
]
(PMID = 18047538.001).
[ISSN]
1541-0420
[Journal-full-title]
Biometrics
[ISO-abbreviation]
Biometrics
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA057030; United States / NCI NIH HHS / CA / R25 CA090301; United States / NCI NIH HHS / CA / CA57030; United States / NCI NIH HHS / CA / R37 CA057030-20; United States / NCI NIH HHS / CA / R01 CA057030; United States / NCI NIH HHS / CA / CA90301; United States / NCI NIH HHS / CA / CA057030-20; United States / NCI NIH HHS / CA / R37 CA057030; United States / NIEHS NIH HHS / ES / P30 ES009106; United States / NIEHS NIH HHS / ES / P30-ES09106
[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 / Calcium, Dietary
[Other-IDs]
NLM/ NIHMS101403; NLM/ PMC2672569
10.
Oh K, Willett WC, Fuchs CS, Giovannucci E:
Dietary marine n-3 fatty acids in relation to risk of distal colorectal adenoma in women.
Cancer Epidemiol Biomarkers Prev
; 2005 Apr;14(4):835-41
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[Title]
Dietary marine n-3 fatty acids in relation to risk of distal
colorectal
adenoma
in women.
Epidemiologic studies of dietary marine n-3 fatty acids and risk of
colorectal
cancer have been inconsistent, and their relation to risk of
colorectal
adenoma
has not been evaluated in detail.
We examined dietary marine n-3 fatty acids and the ratio of marine n-3 to total n-6 fatty acids (n-3/n-6 ratio) in relation to risk
of adenoma
of the distal colon or rectum among 34,451 U.S. women who were initially free of
colorectal
cancer or polyps, who completed a semiquantitative food frequency questionnaire in 1980, and who underwent endoscopy from 1980 to 1998.
We documented 1,719 distal
colorectal
adenoma
cases (705
large
adenomas
, 897 small
adenomas
, 1,280 distal colon
adenomas
, and 505 rectal
adenomas
) during 18 years of follow-up.
Neither dietary marine n-3 fatty acids nor n-3/n-6 ratio were associated with risk of total distal
colorectal
adenoma
after adjustment for age and established risk factors [multivariable relative risk (RR) for extreme quintiles of dietary marine n-3 fatty acids = 1.04; 95% confidence interval (95% CI), 0.84-1.27, P(trend) = 0.66; RR for extreme quintiles of n-3/n-6 ratio = 1.02; 95% CI, 0.83-1.25; P(trend) = 0.86].
Similarly, no significant associations were observed separately for distal colon or rectal
adenoma
.
However, higher intake of dietary marine n-3 fatty acids was nonsignificantly but suggestively inversely associated with
large adenoma
(RR, 0.74; 95% CI, 0.54-1.01; P(trend) = 0.16) but directly associated with small
adenoma
(RR, 1.36; 95% CI, 1.02-1.81; P(trend) = 0.09).
Our findings do not support the hypothesis that a higher intake of marine n-3 fatty acids or a higher n-3/n-6 ratio reduces the risk of distal
colorectal
adenoma
but are suggestive that higher intake may reduce the progression of small
adenomas
to
large
adenomas
.
[MeSH-major]
Adenoma
/ prevention & control.
Colorectal
Neoplasms / prevention & control. Diet. Fatty Acids, Omega-3 / therapeutic use
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[CommentIn]
Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):406-7
[
16492940.001
]
(PMID = 15824153.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA 87969; United States / NCI NIH HHS / CA / CA55075
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Fatty Acids, Omega-3; 0 / Fatty Acids, Omega-6; 0RBV727H71 / alpha-Linolenic Acid
11.
Das P, Jain D, Vaiphei K, Wig JD:
Abberant crypt foci -- importance in colorectal carcinogenesis and expression of p53 and mdm2: a changing concept.
Dig Dis Sci
; 2008 Aug;53(8):2183-8
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[Title]
Abberant crypt foci -- importance in
colorectal
carcinogenesis and expression of p53 and mdm2: a changing concept.
BACKGROUND: The presence of aberrant crypt foci (ACF) represents an important preneoplastic condition of the
large intestine
.
AIMS: To study the significance of ACF in carcinogenesis, the incidence of ACF in
colorectal
carcinoma (CRC) patients and the expression profiles of the tumor repressor protein p53 and the murine double minute (mdm2) protein in ACF.
RESULT: Aberrant crypt foci were present in a
large
number of cases (84.4%), of which 65% were hyperplastic.
This results suggests that the conventional
adenoma
-carcinoma sequence is not completely correct.
[MeSH-major]
Adenocarcinoma / chemistry. Cell Transformation, Neoplastic / chemistry.
Colorectal
Neoplasms / chemistry. Precancerous Conditions / chemistry. Proto-Oncogene Proteins c-mdm2 / analysis. Tumor Suppressor Protein p53 / analysis
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[Cites]
Oncogene. 1998 Dec 24;17(25):3287-99
[
9916991.001
]
[Cites]
Cancer Sci. 2004 Oct;95(10):792-7
[
15504245.001
]
[Cites]
Carcinogenesis. 1999 Jun;20(6):1005-9
[
10357780.001
]
[Cites]
Cancer Res. 1999 Jan 1;59(1):63-6
[
9892186.001
]
[Cites]
Mol Med. 1999 Feb;5(2):71-83
[
10203572.001
]
[Cites]
Carcinogenesis. 2006 Jun;27(6):1153-9
[
16474178.001
]
[Cites]
Asian Pac J Cancer Prev. 2004 Apr-Jun;5(2):126-32
[
15244513.001
]
[Cites]
Hum Pathol. 1991 Mar;22(3):287-94
[
1706308.001
]
[Cites]
Chem Biol Interact. 2005 Jun 30;155(1-2):1-9
[
15904905.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):391-400
[
12750232.001
]
[Cites]
Br J Cancer. 1999 Jul;80 Suppl 1:1-5
[
10466753.001
]
[Cites]
Cancer Res. 1995 Nov 1;55(21):4743-6
[
7585496.001
]
[Cites]
Oncogene. 1996 Apr 18;12(8):1767-72
[
8622897.001
]
[Cites]
BMC Cancer. 2003 Nov 06;3:29
[
14604438.001
]
[Cites]
Colorectal Dis. 2002 Mar;4(2):76-89
[
12780627.001
]
[Cites]
Cell. 1990 Jun 1;61(5):759-67
[
2188735.001
]
[Cites]
Cancer Res. 2000 Jul 1;60(13):3323-7
[
10910031.001
]
[Cites]
Cell. 1996 Oct 18;87(2):159-70
[
8861899.001
]
[Cites]
Jpn J Cancer Res. 1994 Jul;85(7):692-8
[
7915263.001
]
[Cites]
Nutr Cancer. 2002;43(1):1-21
[
12467130.001
]
[Cites]
Appl Immunohistochem Mol Morphol. 2004 Dec;12(4):350-5
[
15536336.001
]
[Cites]
Cancer Surv. 1989;8(1):189-200
[
2680070.001
]
[Cites]
Pathologe. 2003 Feb;24(1):44-8
[
12601477.001
]
[Cites]
Int J Mol Med. 2002 Apr;9(4):353-8
[
11891526.001
]
[Cites]
Am J Gastroenterol. 2005 Jun;100(6):1283-9
[
15929758.001
]
[Cites]
Cancer. 1995 Mar 15;75(6 Suppl):1527-33
[
7889486.001
]
[Cites]
Cancer Res. 2000 Apr 1;60(7):1777-88
[
10766157.001
]
[Cites]
Clin Gastroenterol Hepatol. 2005 Mar;3(3):271-8
[
15765447.001
]
[Cites]
Cytobios. 1993;73(293):73-88
[
8319499.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15095-100
[
12415112.001
]
[Cites]
N Engl J Med. 1998 Oct 29;339(18):1277-84
[
9791143.001
]
[Cites]
World J Gastroenterol. 2001 Jun;7(3):352-6
[
11819789.001
]
[Cites]
Cancer Lett. 1987 Oct 30;37(2):147-51
[
3677050.001
]
[Cites]
Cancer Res. 2003 May 15;63(10):2388-92
[
12750256.001
]
[Cites]
Hum Pathol. 1996 Oct;27(10):1050-5
[
8892589.001
]
(PMID = 18080767.001).
[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]
0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.3.2.27 / MDM2 protein, human; EC 2.3.2.27 / Proto-Oncogene Proteins c-mdm2
12.
Fracchia M, Galatola G, Sarotto I, Guraldo V, Perona M, Pera A, Risio M:
Serum bile acids, programmed cell death and cell proliferation in the mucosa of patients with colorectal adenomas.
Dig Liver Dis
; 2005 Jul;37(7):509-14
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[Title]
Serum bile acids, programmed cell death and cell proliferation in the mucosa of patients with
colorectal adenomas
.
BACKGROUND: Deoxycholic acid induced programmed cell death and an imbalance with cell proliferation may favour
colorectal
tumourigenesis according to 'in vitro' studies, but information is lacking on the relationships occurring 'in vivo' in humans.
METHODS: In 10 patients with
colorectal adenomas
, we measured fasting serum levels of bile acids; and, in normal colonic mucosa, programmed cell death by the TUNEL technique and cell proliferation by immunohistochemical staining with anti-Ki67.
[MeSH-major]
Adenoma
/ blood. Apoptosis / drug effects. Bile Acids and Salts / blood. Cell Proliferation / drug effects.
Colorectal
Neoplasms / blood. Deoxycholic Acid / blood. Deoxycholic Acid / pharmacology. Intestinal Mucosa / cytology
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.
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DEOXYCHOLIC ACID
.
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(PMID = 15975538.001).
[ISSN]
1590-8658
[Journal-full-title]
Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
[ISO-abbreviation]
Dig Liver Dis
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antibodies, Antinuclear; 0 / Antibodies, Monoclonal; 0 / Bile Acids and Salts; 0 / Ki-67 Antigen; 0 / MIB-1 antibody; 005990WHZZ / Deoxycholic Acid
13.
Heijink DM, Kleibeuker JH, Jalving M, Boersma-van Ek W, Koornstra JJ, Wesseling J, de Jong S:
Independent induction of caspase-8 and cFLIP expression during colorectal carcinogenesis in sporadic and HNPCC adenomas and carcinomas.
Cell Oncol
; 2007;29(5):409-19
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[Title]
Independent induction of caspase-8 and cFLIP expression during
colorectal
carcinogenesis in sporadic and HNPCC
adenomas
and carcinomas.
METHODS: The aim of this study was to investigate basic expression of caspase-8 and cFLIP in normal
colorectal
epithelium (n=20),
colorectal adenomas
(n=66) and
colorectal
carcinomas (n=44) using immunohistochemistry performed on both sporadic and Hereditary Non-Polyposis
Colorectal
Cancer (HNPCC or Lynch syndrome)-associated
adenomas
and carcinomas.
Expression of caspase-8 in
colorectal adenomas
and carcinomas was increased when compared to normal colon tissue (P=0.02).
Immunohistochemistry revealed an upregulation of cFLIP in
colorectal
carcinomas in comparison to normal epithelium and
colorectal adenomas
(P<0.001).
A
large
variation in the caspase-8/cFLIP ratio was observed between the individual
adenomas
and carcinomas.
CONCLUSION: Caspase-8 and cFLIP are upregulated during
colorectal
carcinogenesis.
Upregulation of caspase-8 and/or downregulation of cFLIP may be interesting approaches to maximize TRAIL sensitivity in
colorectal
neoplasms.
[MeSH-major]
Adenoma
/ enzymology. CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism. Caspase 8 / biosynthesis.
Colorectal
Neoplasms, Hereditary Nonpolyposis / enzymology
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(PMID = 17726263.001).
[ISSN]
1570-5870
[Journal-full-title]
Cellular oncology : the official journal of the International Society for Cellular Oncology
[ISO-abbreviation]
Cell. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; EC 3.4.22.- / Caspase 8
[Other-IDs]
NLM/ PMC4617989
14.
Pufulete M, Al-Ghnaniem R, Khushal A, Appleby P, Harris N, Gout S, Emery PW, Sanders TA:
Effect of folic acid supplementation on genomic DNA methylation in patients with colorectal adenoma.
Gut
; 2005 May;54(5):648-53
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[Title]
Effect of folic acid supplementation on genomic DNA methylation in patients with
colorectal
adenoma
.
BACKGROUND AND AIMS: A low dietary folate intake can cause genomic DNA hypomethylation and may increase the risk of
colorectal
neoplasia.
The hypothesis that folic acid supplementation increases DNA methylation in leucocytes and
colorectal
mucosa was tested in 31 patients with histologically confirmed
colorectal
adenoma
using a randomised, double blind, placebo controlled, parallel design.
[MeSH-major]
Adenoma
/ genetics.
Colorectal
Neoplasms / genetics. DNA Methylation / drug effects. Dietary Supplements. Folic Acid / pharmacology
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.
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.
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FOLIC ACID
.
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[Cites]
Dis Colon Rectum. 1994 Dec;37(12):1340-1
[
7995171.001
]
[Cites]
J Biol Chem. 2000 Sep 22;275(38):29318-23
[
10884384.001
]
[Cites]
Eur J Cancer Prev. 1994 Nov;3(6):473-9
[
7858479.001
]
[Cites]
J Natl Cancer Inst. 1995 Feb 15;87(4):265-73
[
7707417.001
]
[Cites]
Am J Clin Nutr. 2000 Oct;72(4):998-1003
[
11010943.001
]
[Cites]
Cancer Res. 2000 Oct 1;60(19):5434-40
[
11034085.001
]
[Cites]
Am J Gastroenterol. 2001 Jan;96(1):184-95
[
11197251.001
]
[Cites]
Am J Clin Nutr. 2001 Mar;73(3):613-21
[
11237940.001
]
[Cites]
Cancer Res. 2001 Oct 1;61(19):6991-5
[
11585722.001
]
[Cites]
Gut. 2002 Apr;50(4):520-4
[
11889073.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5606-11
[
11929966.001
]
[Cites]
Gastroenterology. 2002 May;122(5):1376-87
[
11984524.001
]
[Cites]
Pharmacogenetics. 2002 Jun;12(4):339-42
[
12042673.001
]
[Cites]
Br J Nutr. 2002 Apr;87(4):383-90
[
12064348.001
]
[Cites]
Cancer Res. 2002 Nov 15;62(22):6442-6
[
12438232.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1611-21
[
12496052.001
]
[Cites]
Clin Cancer Res. 2003 Feb;9(2):743-8
[
12576444.001
]
[Cites]
Am J Pathol. 2003 Apr;162(4):1043-5
[
12651596.001
]
[Cites]
Am J Pathol. 2003 Apr;162(4):1361-71
[
12651628.001
]
[Cites]
Gastroenterology. 2003 May;124(5):1240-8
[
12730865.001
]
[Cites]
Cancer Res. 2003 Jun 15;63(12):3133-7
[
12810640.001
]
[Cites]
Cancer Detect Prev. 2003;27(4):297-304
[
12893078.001
]
[Cites]
Clin Cancer Res. 2003 Dec 1;9(16 Pt 1):5860-5
[
14676107.001
]
[Cites]
Clin Gastroenterol Hepatol. 2004 Jan;2(1):1-8
[
15017625.001
]
[Cites]
Anticancer Res. 2004 Mar-Apr;24(2B):649-54
[
15161007.001
]
[Cites]
Carcinogenesis. 2004 Aug;25(8):1507-15
[
15016659.001
]
[Cites]
J Nutr Biochem. 2004 Sep;15(9):554-60
[
15350988.001
]
[Cites]
Nature. 1983 Jan 6;301(5895):89-92
[
6185846.001
]
[Cites]
Science. 1985 Apr 12;228(4696):187-90
[
2579435.001
]
[Cites]
Br J Cancer. 1992 May;65(5):667-72
[
1586594.001
]
[Cites]
J Natl Cancer Inst. 1993 Jun 2;85(11):875-84
[
8492316.001
]
[Cites]
Biochem Biophys Res Commun. 1993 Jun 30;193(3):1184-90
[
8323540.001
]
[Cites]
J Cancer Res Clin Oncol. 1993;119(9):549-54
[
8392076.001
]
[Cites]
Nat Genet. 1994 Aug;7(4):536-40
[
7951326.001
]
[Cites]
Dis Colon Rectum. 1995 Jan;38(1):64-7; discussion 67-8
[
7813348.001
]
[Cites]
Nat Genet. 1995 May;10(1):111-3
[
7647779.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1995 Oct-Nov;4(7):709-14
[
8672986.001
]
[Cites]
Cancer Res. 1996 Nov 1;56(21):4862-4
[
8895734.001
]
[Cites]
Cancer Res. 1997 Mar 15;57(6):1098-102
[
9067278.001
]
[Cites]
Int J Cancer. 1997 Mar 17;70(6):644-8
[
9096643.001
]
[Cites]
J Nutr. 1998 Jul;128(7):1204-12
[
9649607.001
]
[Cites]
Ann Intern Med. 1998 Oct 1;129(7):517-24
[
9758570.001
]
[Cites]
Cancer Res. 1998 Dec 1;58(23):5489-94
[
9850084.001
]
[Cites]
Br J Cancer. 1999 Apr;79(11-12):1917-22
[
10206314.001
]
[Cites]
Clin Nutr. 1998 Apr;17(2):45-9
[
10205316.001
]
[Cites]
Ann Intern Med. 1999 Sep 7;131(5):331-9
[
10475885.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1999 Sep;8(9):825-9
[
10498402.001
]
[Cites]
Genet Epidemiol. 1999 Nov;17(4):298-309
[
10520212.001
]
[Cites]
Cancer Lett. 2000 Apr 14;151(2):181-6
[
10738112.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1999 Aug;8(8):659-68
[
10744125.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2000 Jul;9(7):657-63
[
10919734.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2000 Aug;9(8):849-53
[
10952104.001
]
[CommentIn]
Gut. 2005 May;54(5):579-81
[
15831897.001
]
(PMID = 15831910.001).
[ISSN]
0017-5749
[Journal-full-title]
Gut
[ISO-abbreviation]
Gut
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Randomized Controlled Trial
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Neoplasm; 0LVT1QZ0BA / Homocysteine; 935E97BOY8 / Folic Acid
[Other-IDs]
NLM/ PMC1774481
15.
Ding XW, Yan JJ, An P, Lü P, Luo HS:
Aberrant expression of ether à go-go potassium channel in colorectal cancer patients and cell lines.
World J Gastroenterol
; 2007 Feb 28;13(8):1257-61
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[Title]
Aberrant expression of ether à go-go potassium channel in
colorectal
cancer patients and cell lines.
AIM: To study the expression of ether à go-go (Eag1) potassium channel in
colorectal
cancer and the relation-ship between their expression and clinico-pathological features.
METHODS: The expression levels of Eag1 protein were determined in 76 cancer tissues with paired non-cancerous matched tissues as well as 9
colorectal
adenoma
tissues by immunohistochemistry.
Eag1 mRNA expression was detected in 13
colorectal
cancer tissues with paired non-cancerous matched tissues and 4
colorectal
adenoma
tissues as well as two
colorectal
cancer cell lines (LoVo and HT-29) by reverse transcription PCR.
RESULTS: The frequency of positive expression of Eag1 protein was 76.3% (58/76) and Eag1 mRNA was 76.9% (10/13) in
colorectal
cancer tissue.
Eag1 protein and mRNA were negative in normal
colorectal
tissue, and absolutely negative in
colorectal adenomas
except that one case was positively stained for Eag1 protein.
CONCLUSION: Eag1 protein and mRNA are aberrantly expressed in
colorectal
cancer and occasionally expressed in
colorectal
adenoma
.
[MeSH-major]
Adenoma
/ metabolism. Carcinoma / metabolism.
Colorectal
Neoplasms / metabolism. Ether-A-Go-Go Potassium Channels / metabolism. Gene Expression Regulation, Neoplastic
Genetic Alliance.
consumer health - Colorectal Cancer
.
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.
Guide to Pharmacology.
gene/protein/disease-specific - Kv10.1 - data and references
.
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[Cites]
J Membr Biol. 2001 Jul 1;182(1):1-15
[
11426295.001
]
[Cites]
Receptors Channels. 2001;7(5):345-56
[
11697078.001
]
[Cites]
J Membr Biol. 2002 Jul 15;188(2):137-49
[
12172639.001
]
[Cites]
Cancer Res. 2004 Oct 1;64(19):6996-7001
[
15466192.001
]
[Cites]
Genetics. 1969 Feb;61(2):399-409
[
5807804.001
]
[Cites]
Mol Cancer. 2006;5:41
[
17022810.001
]
[Cites]
J Physiol. 1998 Apr 1;508 ( Pt 1):49-56
[
9490815.001
]
[Cites]
FEBS Lett. 1998 Aug 28;434(1-2):177-82
[
9738473.001
]
[Cites]
EMBO J. 1999 Oct 15;18(20):5540-7
[
10523298.001
]
[Cites]
J Biol Chem. 2006 May 12;281(19):13030-7
[
16537547.001
]
[Cites]
Mol Cancer. 2006;5:42
[
17022811.001
]
[Cites]
Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3438-42
[
8159766.001
]
(PMID = 17451210.001).
[ISSN]
1007-9327
[Journal-full-title]
World journal of gastroenterology
[ISO-abbreviation]
World J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Ether-A-Go-Go Potassium Channels; 0 / KCNH1 protein, human
[Other-IDs]
NLM/ PMC4147004
16.
Petrova TV, Nykänen A, Norrmén C, Ivanov KI, Andersson LC, Haglund C, Puolakkainen P, Wempe F, von Melchner H, Gradwohl G, Vanharanta S, Aaltonen LA, Saharinen J, Gentile M, Clarke A, Taipale J, Oliver G, Alitalo K:
Transcription factor PROX1 induces colon cancer progression by promoting the transition from benign to highly dysplastic phenotype.
Cancer Cell
; 2008 May;13(5):407-19
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However, we show here that PROX1 promotes dysplasia in colonic
adenomas
and
colorectal
cancer progression.
PROX1 expression marks the transition from benign colon
adenoma
to carcinoma in situ, and its loss inhibits growth of human
colorectal
tumor xenografts and intestinal
adenomas
in Apc(min/+) mice, while its transgenic overexpression promotes
colorectal
tumorigenesis.
[MeSH-major]
Adenoma
/ genetics. Colonic Neoplasms / genetics. Homeodomain Proteins / genetics. Tumor Suppressor Proteins / genetics
[MeSH-minor]
Carcinoma in Situ / genetics. Cell Line, Tumor.
Colorectal
Neoplasms / genetics. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Phenotype. beta Catenin / physiology
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Mouse Genome Informatics (MGI)
.
The Lens.
Cited by Patents in
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(PMID = 18455124.001).
[ISSN]
1878-3686
[Journal-full-title]
Cancer cell
[ISO-abbreviation]
Cancer Cell
[Language]
eng
[Grant]
United Kingdom / Worldwide Cancer Research / / 09-0791; United Kingdom / Medical Research Council / / G0301154
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Tumor Suppressor Proteins; 0 / beta Catenin; 0 / prospero-related homeobox 1 protein
17.
Hubner RA, Muir KR, Liu JF, Logan RF, Grainge M, Armitage N, Shepherd V, Popat S, Houlston RS, United Kingdom Colorectal Adenoma Prevention Consortium:
Genetic variants of UGT1A6 influence risk of colorectal adenoma recurrence.
Clin Cancer Res
; 2006 Nov 1;12(21):6585-9
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[Title]
Genetic variants of UGT1A6 influence risk of
colorectal
adenoma
recurrence.
Functional polymorphisms of UGT1A6 (T181A and R184S) and CYP2C9 (R144C and I359L) have been reported to modify the protective effect of aspirin on
colorectal
adenoma
risk.
We aimed to further investigate the effect of these genetic variants on the development of
colorectal
neoplasia.
EXPERIMENTAL DESIGN: We examined the relationship between UGT1A6 and CYP2C9 genotype and
colorectal
adenoma
recurrence in 546 patients participating in a randomized placebo-controlled aspirin intervention trial.
RESULTS: Although
colorectal
adenoma
recurrence was not significantly influenced by CYP2C9 genotype, carriers of variant UGT1A6 alleles were at significantly reduced risk of
colorectal
neoplasia recurrence [relative risk (RR), 0.68; 95% confidence interval (95% CI), 0.52-0.89].
CONCLUSIONS: These findings confirm that UGT1A6 variants influence
colorectal
carcinogenesis independent of aspirin intake and suggest that they may have clinical value in secondary prevention programs for patients diagnosed with
colorectal
adenoma
.
[MeSH-major]
Adenoma
/ genetics.
Colorectal
Neoplasms / genetics. Genetic Predisposition to Disease. Glucuronosyltransferase / genetics. Neoplasm Recurrence, Local / genetics
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consumer health - Colorectal Cancer
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(PMID = 17085674.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; EC 2.4.1.- / UDP-glucuronosyltransferase, UGT1A6; EC 2.4.1.17 / Glucuronosyltransferase; R16CO5Y76E / Aspirin
18.
Zhu XL, Liang L, Ding YQ:
[Galectin-1 expression in human colorectal carcinoma and its clinical significance].
Nan Fang Yi Ke Da Xue Xue Bao
; 2007 Sep;27(9):1331-4
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[Title]
[Galectin-1 expression in human
colorectal
carcinoma and its clinical significance].
OBJECTIVE: To investigate the correlation between galectin-1 expression and the biological behaviors of human
colorectal
carcinoma.
METHODS: SP immunohistochemistry was used to detect the expression of galectin-1 in 158 paraffin-embedded specimens including 30 normal mucosa, 25
adenoma
, 65
colorectal
carcinoma and 38 metastatic tumor specimens.
Real-time RT-PCR was used to detect galectin-1 mRNA expression in 32 fresh specimens of
colorectal
carcinoma and normal mucosa.
RESULTS: The positive expression level of galectin-1 was significantly different between normal mucosa,
adenoma
,
colorectal
carcinomas and metastatic tumors, with positivity rate of 0, 8%, 66% and 86%, respectively (P<0.05).
Galectin-1 expression in moderately or well differentiated
colorectal
carcinomas was significantly lower than that in poorly differentiated ones (P=0.031), and its expression in invasive carcinomas was significantly higher than that in non-invasive carcinomas (P=0.000).
Galectin-1 expression in
colorectal
carcinomas was significantly related with lymph node metastasis (P=0.004).
In poorly differentiated
colorectal
carcinomas, the expression of galectin-1 mRNA was about 2.27 times that in moderately or well differentiated
colorectal
carcinomas (P=0.00); galectin-1 mRNA expression in invasive carcinoma was 1.98 times that in non-invasive carcinoma (P=0.002).
CONCLUSION: Galectin-1 can be involved in the development and progression of
colorectal
carcinoma, and may relate to the infiltration, differentiation and lymph node metastasis of
colorectal
carcinoma.
[MeSH-major]
Colorectal
Neoplasms / genetics.
Colorectal
Neoplasms / pathology. Galectin 1 / genetics. Galectin 1 / metabolism. Gene Expression Regulation, Neoplastic
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(PMID = 17884770.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Galectin 1; 0 / RNA, Messenger
19.
Dai Q, Shrubsole MJ, Ness RM, Schlundt D, Cai Q, Smalley WE, Li M, Shyr Y, Zheng W:
The relation of magnesium and calcium intakes and a genetic polymorphism in the magnesium transporter to colorectal neoplasia risk.
Am J Clin Nutr
; 2007 Sep;86(3):743-51
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[Title]
The relation of magnesium and calcium intakes and a genetic polymorphism in the magnesium transporter to
colorectal
neoplasia risk.
BACKGROUND: Mean magnesium intake in the US population does not differ from that in East Asian populations with traditionally low risks of
colorectal
cancer and other chronic diseases, but the ratio of calcium to magnesium (Ca:Mg) intake is much higher in the US population.
OBJECTIVE: We aimed to test whether the association of
colorectal
polyps with intake of calcium, magnesium, or both and Thr1482Ile polymorphism in the TRPM7 gene is modified by the Ca:Mg intake.
DESIGN: Included in the study were a total of 688
adenoma
cases, 210 hyperplastic polyp cases, and 1306 polyp-free controls from the Tennessee
Colorectal
Polyp Study.
RESULTS: We found that total magnesium consumption was linked to a significantly lower risk of
colorectal
adenoma
, particularly in those subjects with a low Ca:Mg intake.
The subjects who carried >or=1 1482Ile allele and who consumed diets with a high Ca:Mg intake were at a higher risk
of adenoma
(odds ratio: 1.60; 95% CI: 1.12, 2.29) and hyperplastic polyps (odds ratio: 1.85; 95% CI: 1.09, 3.14) than were the subjects who did not carry the polymorphism.
CONCLUSION: These findings, if confirmed, may provide a new avenue for the personalized prevention of magnesium deficiency and, thus,
colorectal
cancer.
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[Cites]
N Engl J Med. 1999 Jan 14;340(2):101-7
[
9887161.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1998 Feb;7(2):163-8
[
9488592.001
]
[Cites]
Eur J Clin Nutr. 2004 Dec;58(12):1604-11
[
15199383.001
]
[Cites]
Biochim Biophys Acta. 2004 Dec 24;1739(1):26-32
[
15607114.001
]
[Cites]
J Am Soc Nephrol. 2005 Jan;16(1):15-26
[
15574510.001
]
[Cites]
JAMA. 2005 Jan 5;293(1):86-9
[
15632340.001
]
[Cites]
Curr Mol Med. 2005 May;5(3):309-22
[
15892650.001
]
[Cites]
Int J Cancer. 2005 Oct 20;117(1):137-44
[
15880532.001
]
[Cites]
Proc Natl Acad Sci U S A. 2005 Aug 9;102(32):11510-5
[
16051700.001
]
[Cites]
Pflugers Arch. 2005 Oct;451(1):228-34
[
16075242.001
]
[Cites]
Public Health Nutr. 2005 Dec;8(8):1293-9
[
16372925.001
]
[Cites]
Am J Epidemiol. 2006 Feb 1;163(3):232-5
[
16319289.001
]
[Cites]
J Natl Cancer Inst. 2007 Jan 17;99(2):129-36
[
17227996.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Oct;15(10):2006-9
[
17035414.001
]
[Cites]
N Engl J Med. 2006 Feb 16;354(7):684-96
[
16481636.001
]
[Cites]
Arch Biochem Biophys. 2007 Feb 1;458(1):24-32
[
16564020.001
]
[Cites]
Br J Cancer. 2007 Feb 12;96(3):510-3
[
17285123.001
]
[Cites]
J Natl Cancer Inst. 2000 Jul 19;92(14):1151-8
[
10904088.001
]
[Cites]
Histopathology. 2000 Oct;37(4):295-301
[
11012735.001
]
[Cites]
Lancet. 2000 Oct 14;356(9238):1300-6
[
11073017.001
]
[Cites]
Physiol Rev. 2001 Jan;81(1):239-297
[
11152759.001
]
[Cites]
J Natl Cancer Inst. 2001 Sep 5;93(17):1307-13
[
11535705.001
]
[Cites]
Annu Rev Physiol. 2002;64:529-49
[
11826278.001
]
[Cites]
Eur J Nutr. 2002 Oct;41(5):197-202
[
12395213.001
]
[Cites]
Int J Epidemiol. 2003 Feb;32(1):1-22
[
12689998.001
]
[Cites]
J Womens Health (Larchmt). 2003 Mar;12(2):173-82
[
12737716.001
]
[Cites]
Cell. 2003 Jul 25;114(2):191-200
[
12887921.001
]
[Cites]
J Natl Cancer Inst. 2003 Dec 3;95(23):1765-71
[
14652238.001
]
[Cites]
JAMA. 2003 Dec 10;290(22):2959-67
[
14665657.001
]
[Cites]
Diabetes Care. 2004 Jan;27(1):134-40
[
14693979.001
]
[Cites]
J Am Coll Nutr. 2004 Feb;23(1):63-70
[
14963055.001
]
[Cites]
Cell Mol Biol (Noisy-le-grand). 2003 Dec;49(8):1295-304
[
14984001.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2894-9
[
14976260.001
]
[Cites]
Adv Data. 2004 Apr 27;(341):1-5
[
15114720.001
]
[Cites]
J Natl Cancer Inst. 2004 Jul 7;96(13):1015-22
[
15240785.001
]
[Cites]
Natl Cancer Inst Monogr. 1979 Nov;(53):175-9
[
119916.001
]
[Cites]
J Clin Endocrinol Metab. 1978 Oct;47(4):800-6
[
263326.001
]
[Cites]
Am Heart J. 1984 Jul;108(1):188-93
[
6375330.001
]
[Cites]
Magnes Trace Elem. 1990;9(3):143-51
[
2248695.001
]
[Cites]
J Nutr. 1991 Jan;121(1):13-23
[
1992050.001
]
[Cites]
J Clin Epidemiol. 1991;44(6):571-8
[
2037862.001
]
[Cites]
Annu Rev Physiol. 1991;53:259-71
[
2042962.001
]
[Cites]
Am J Clin Nutr. 1992 May;55(5):1018-23
[
1315120.001
]
[Cites]
Am J Epidemiol. 1994 Jan 1;139(1):16-29
[
8296771.001
]
[Cites]
Br J Cancer. 1996 Jul;74(1):145-51
[
8679449.001
]
[Cites]
Epidemiology. 1996 May;7(3):264-8
[
8728439.001
]
[Cites]
Epidemiology. 1996 Nov;7(6):590-7
[
8899384.001
]
[Cites]
Am J Clin Nutr. 1997 Nov;66(5):1172-7
[
9356535.001
]
[Cites]
Am J Clin Nutr. 1964 Jun;14:242-90
[
14168977.001
]
(PMID = 17823441.001).
[ISSN]
0002-9165
[Journal-full-title]
The American journal of clinical nutrition
[ISO-abbreviation]
Am. J. Clin. Nutr.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / P50 CA 95103; United States / NCI NIH HHS / CA / R01 CA072784; United States / NCI NIH HHS / CA / R01 CA072784-05; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / R01 CA97386; United States / NCI NIH HHS / CA / CA072784-05
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Calcium, Dietary; 0 / TRPM Cation Channels; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / TRPM7 protein, human; I38ZP9992A / Magnesium
[Other-IDs]
NLM/ NIHMS33891; NLM/ PMC2082111
20.
Borda Martín A, Martínez-Peñuela JM, Muñoz-Navas M, Borda Celaya F, Jiménez Pérez J, Carretero Ribón C:
[Do metachronous colorectal adenomas show proximal shift?].
Gastroenterol Hepatol
; 2010 Jun-Jul;33(6):419-24
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[Title]
[Do metachronous
colorectal adenomas
show proximal shift?].
[Transliterated title]
¿Presentan un desplazamiento hacia segmentos más proximales los
adenomas
metacrónicos en el cáncer colorrectal?
OBJECTIVE: To study the possibility of shift toward more proximal sites in
colorectal
cancer (CRC) after resection of tumors and synchronous lesions.
The localization of metachronous
adenomas
was compared with that of synchronous lesions overall and by sex, tumoral size and the number of synchronous lesions.
The frequency of exclusively proximal localization in first-, second- and third-generation metachronous
adenomas
was compared with that of synchronous
adenomas
.
RESULTS: A total of 54.5% of patients with CRC had synchronous
adenomas
.
After a median follow-up of 48 months, with 2.74+/-1.47 colonoscopies/case, 42.4% developed metachronous
adenomas
, 16.8% second-generation
adenomas
and 7.3% third-generation lesions.
Proximal shift was found in metachronous
adenomas
in both sexes, independently of tumoral size and the number of initial lesions.
The frequency of exclusively proximal localization in
adenomas
was 21.2% in synchronous lesions, 39.5% in first-generation metachronous
adenomas
(p=0.0001; OR=2.46 [1.50-3.95]), 42.6% in second-generation metachronous
adenomas
(p=0.0008; OR=2.77 [1.44-5.31]) and 39.3% in third-generation metachronous lesions (p=0.0003; OR=2.41 [0.97-5.93]).
CONCLUSIONS: We found a high incidence of synchronous and metachronous
adenomas
.
Metachronous
adenomas
showed a proximal shift, independently of sex, tumoral size and the number of synchronous lesions.
This tendency was maintained in successive generations of metachronous
adenomas
, thus demonstrating the need to perform complete colonoscopies throughout the postoperative follow-up period.
[MeSH-major]
Adenoma
/ pathology. Colon / pathology.
Colorectal
Neoplasms / pathology. Neoplasms, Second Primary / pathology
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[Copyright]
Copyright 2009 Elsevier España, S.L. All rights reserved.
(PMID = 20374971.001).
[ISSN]
0210-5705
[Journal-full-title]
Gastroenterología y hepatología
[ISO-abbreviation]
Gastroenterol Hepatol
[Language]
spa
[Publication-type]
English Abstract; Journal Article; Multicenter Study
[Publication-country]
Spain
21.
Durno CA, Holter S, Sherman PM, Gallinger S:
The gastrointestinal phenotype of germline biallelic mismatch repair gene mutations.
Am J Gastroenterol
; 2010 Nov;105(11):2449-56
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The aim of this study was to characterize patients with GI small
bowel
and/or
colorectal
cancers (CRCs) who have germline biallelic MMR mutations.
Among the 29 patients with CRCs, the mean age of first cancer
diagnosis
was 16.4 years (range: 5-28).
More than one-third of patients had multiple
colorectal adenomas
(>10 polyps).
Six individuals with biallelic MMR gene mutations have been reported with small
bowel
adenocarcinoma (mean age 20 years (range: 11-41)).
CONCLUSIONS: Biallelic MMR mutations are an underrecognized cause of small
bowel
and colonic cancers in children and young adults.
[MeSH-major]
Alleles.
Colorectal
Neoplasms / genetics. DNA Mismatch Repair. Genetic Predisposition to Disease. Germ-Line Mutation. Intestinal Neoplasms / genetics
[MeSH-minor]
Adolescent. Adult. Child. Child, Preschool. DNA Mutational Analysis. Databases, Factual. Humans.
Intestine
, Small. Microsatellite Instability. Phenotype. Registries
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(PMID = 20531397.001).
[ISSN]
1572-0241
[Journal-full-title]
The American journal of gastroenterology
[ISO-abbreviation]
Am. J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
22.
Holt PR, Kozuch P, Mewar S:
Colon cancer and the elderly: from screening to treatment in management of GI disease in the elderly.
Best Pract Res Clin Gastroenterol
; 2009;23(6):889-907
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Colorectal
cancer is one of the commonest tumours in the Westernized world affecting mainly the elderly.
Effective screening permits discovery of
colorectal
cancer at an early highly treatable stage and allows for detection and removal of premalignant
colorectal adenomas
.
Screening methods that focus on cancer detection use fecal assays for the presence of blood or altered DNA, those for detection of
adenomas
(and early cancer) use endoscopic or computerised radiologic techniques.
Broad use of screening methods has lowered
colorectal
cancer development by about 50%.
Since 1996 the chemotherapeutic armamentarium for metastatic
colorectal
cancer has grown beyond 5-fluorouracil to include an oral 5-fluorouracil prodrug, capecitabine as well as irinotecan and oxaliplatin.
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[Cites]
J Natl Cancer Inst. 2003 Dec 3;95(23):1765-71
[
14652238.001
]
[Cites]
Biochem Biophys Res Commun. 2004 Jan 16;313(3):784-8
[
14697260.001
]
[Cites]
J Clin Oncol. 2004 Jan 15;22(2):229-37
[
14657227.001
]
[Cites]
Gut. 2004 Feb;53(2):284-90
[
14724165.001
]
[Cites]
N Engl J Med. 2004 Mar 4;350(10):991-1004
[
14999111.001
]
[Cites]
Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):11-27
[
15000146.001
]
[Cites]
J Clin Oncol. 2004 Apr 1;22(7):1201-8
[
14993230.001
]
[Cites]
Dis Colon Rectum. 2004 May;47(5):665-73
[
15054679.001
]
[Cites]
Ann Surg. 2004 Jun;239(6):818-25; discussion 825-7
[
15166961.001
]
[Cites]
N Engl J Med. 2004 Jun 3;350(23):2343-51
[
15175436.001
]
[Cites]
Trends Mol Med. 2004 Jul;10(7):324-30
[
15242680.001
]
[Cites]
Ann Surg. 2005 May;241(5):715-22, discussion 722-4
[
15849507.001
]
[Cites]
J Clin Oncol. 2005 May 20;23(15):3545-51
[
15908665.001
]
[Cites]
J Pharmacol Exp Ther. 2005 Jul;314(1):1-8
[
15805430.001
]
[Cites]
N Engl J Med. 2005 Jun 30;352(26):2696-704
[
15987918.001
]
[Cites]
Gastroenterology. 2005 Jul;129(1):34-41
[
16012932.001
]
[Cites]
J Clin Oncol. 2005 Aug 1;23(22):4866-75
[
15939922.001
]
[Cites]
Mech Ageing Dev. 2005 Sep;126(9):987-1002
[
15893363.001
]
[Cites]
Science. 2005 Aug 5;309(5736):886-7
[
16081723.001
]
[Cites]
Gastroenterology. 2005 Sep;129(3):837-45
[
16143123.001
]
[Cites]
Eur J Cancer. 2005 Oct;41(15):2297-303
[
16140008.001
]
[Cites]
Gastroenterology. 2005 Oct;129(4):1163-70
[
16230070.001
]
[Cites]
J Clin Oncol. 2008 Jul 20;26(21):3523-9
[
18640933.001
]
[Cites]
Br J Cancer. 2008 Aug 5;99(3):532-5
[
18628760.001
]
[Cites]
J Clin Oncol. 2005 Dec 1;23(34):8671-8
[
16314627.001
]
[Cites]
Am J Gastroenterol. 2006 Feb;101(2):255-62
[
16454827.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):189-93
[
16492904.001
]
[Cites]
Br J Cancer. 2006 Apr 10;94(7):969-75
[
16552438.001
]
[Cites]
JAMA. 2006 May 24;295(20):2357-65
[
16720821.001
]
[Cites]
Dis Colon Rectum. 2006 Jun;49(6):816-24
[
16741639.001
]
[Cites]
Nat Genet. 2006 Jul;38(7):787-93
[
16804544.001
]
[Cites]
J Clin Oncol. 2006 Sep 1;24(25):4085-91
[
16943526.001
]
[Cites]
N Engl J Med. 2006 Aug 31;355(9):873-84
[
16943400.001
]
[Cites]
N Engl J Med. 2006 Aug 31;355(9):885-95
[
16943401.001
]
[Cites]
Int J Colorectal Dis. 2007 Jan;22(1):77-83
[
16538491.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2418-21
[
17164364.001
]
[Cites]
Mod Pathol. 2007 Jan;20(1):15-22
[
17086168.001
]
[Cites]
Gastroenterology. 2006 Dec;131(6):1683-9
[
17188959.001
]
[Cites]
J Natl Cancer Inst. 2007 Jan 17;99(2):129-36
[
17227996.001
]
[Cites]
Clin Gastroenterol Hepatol. 2007 Jan;5(1):111-7
[
17161655.001
]
[Cites]
Ann Intern Med. 2007 Mar 6;146(5):361-4
[
17339621.001
]
[Cites]
Cancer Detect Prev. 2007;31(1):3-11
[
17289293.001
]
[Cites]
Hum Pathol. 2007 Apr;38(4):585-92
[
17239930.001
]
[Cites]
Oncologist. 2007 Mar;12(3):312-9
[
17405895.001
]
[Cites]
J Clin Oncol. 2007 May 1;25(13):1658-64
[
17470858.001
]
[Cites]
Dis Colon Rectum. 2007 May;50(5):604-10
[
17160571.001
]
[Cites]
JAMA. 2007 Jun 6;297(21):2351-9
[
17551129.001
]
[Cites]
JAMA. 2007 Aug 15;298(7):754-64
[
17699009.001
]
[Cites]
J Clin Oncol. 2007 Aug 20;25(24):3644-8
[
17704414.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2007 Sep;16(9):1745-52
[
17855692.001
]
[Cites]
J Clin Oncol. 2007 Sep 20;25(27):4224-30
[
17548839.001
]
[Cites]
J Clin Oncol. 2007 Sep 20;25(27):4217-23
[
17548840.001
]
[Cites]
J Natl Cancer Inst. 2007 Oct 3;99(19):1462-70
[
17895475.001
]
[Cites]
Gut. 2007 Nov;56(11):1585-9
[
17591622.001
]
[Cites]
J Clin Oncol. 2007 Oct 20;25(30):4779-86
[
17947725.001
]
[Cites]
N Engl J Med. 2007 Nov 15;357(20):2040-8
[
18003960.001
]
[Cites]
J Clin Oncol. 2007 Dec 1;25(34):5390-6
[
18048820.001
]
[Cites]
Cancer Res. 2007 Dec 15;67(24):11594-600
[
18089788.001
]
[Cites]
Gastroenterology. 2008 Jan;134(1):29-38
[
18022173.001
]
[Cites]
JAMA. 2008 Mar 5;299(9):1027-35
[
18319413.001
]
[Cites]
J Clin Oncol. 2001 Nov 1;19(21):4097-106
[
11689577.001
]
[Cites]
Cancer. 2002 Apr 1;94(7):1931-8
[
11932894.001
]
[Cites]
Am J Clin Oncol. 2002 Apr;25(2):126-30
[
11943888.001
]
[Cites]
Ann Surg. 2002 Jun;235(6):759-66
[
12035031.001
]
[Cites]
World J Gastroenterol. 2008 Jul 28;14(28):4429-33
[
18680219.001
]
[Cites]
Crit Rev Oncol Hematol. 2008 Sep;67(3):255-62
[
18400508.001
]
[Cites]
N Engl J Med. 2008 Sep 18;359(12):1207-17
[
18799557.001
]
[Cites]
Br J Cancer. 2008 Oct 7;99(7):1046-9
[
18797465.001
]
[Cites]
Cancer Res. 2008 Oct 15;68(20):8541-6
[
18922929.001
]
[Cites]
Ann Intern Med. 2008 Nov 4;149(9):627-37
[
18838716.001
]
[Cites]
J Clin Oncol. 2008 Nov 20;26(33):5326-34
[
18854571.001
]
[Cites]
Br J Cancer. 2008 Dec 16;99(12):1991-2000
[
19034277.001
]
[Cites]
Ann Intern Med. 2009 Jan 6;150(1):1-8
[
19075198.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):196-203
[
19124498.001
]
[Cites]
Gut. 2009 Feb;58(2):241-8
[
18852257.001
]
[Cites]
J Clin Oncol. 2002 Jun 1;20(11):2651-7
[
12039926.001
]
[Cites]
J Nutr. 2002 Aug;132(8 Suppl):2413S-2418S
[
12163703.001
]
[Cites]
J Clin Oncol. 2002 Aug 15;20(16):3478-83
[
12177109.001
]
[Cites]
Ann Intern Med. 2002 Oct 1;137(7):603-12
[
12353948.001
]
[Cites]
Mech Ageing Dev. 2002 Nov;123(12):1543-52
[
12470892.001
]
[Cites]
Gastroenterology. 2003 Mar;124(3):600-7
[
12612897.001
]
[Cites]
N Engl J Med. 2003 Mar 6;348(10):879-80
[
12621130.001
]
[Cites]
N Engl J Med. 2003 Mar 6;348(10):891-9
[
12621133.001
]
[Cites]
Prog Exp Tumor Res. 2003;37:1-24
[
12795046.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 Aug;12(8):755-62
[
12917207.001
]
[Cites]
J Clin Invest. 2003 Nov;112(9):1351-60
[
14597761.001
]
[Cites]
Cancer Prev Res (Phila). 2008 Jun;1(1):32-8
[
18841250.001
]
[Cites]
Ann Oncol. 2009 Jan;20(1):5-16
[
18922882.001
]
[Cites]
Br J Cancer. 2009 Feb 24;100(4):611-6
[
19209175.001
]
[Cites]
J Natl Cancer Inst. 2009 Feb 18;101(4):267-76
[
19211442.001
]
[Cites]
J Natl Cancer Inst. 2009 Feb 18;101(4):256-66
[
19211452.001
]
[Cites]
Gastroenterology. 2009 Mar;136(3):741-54
[
19166855.001
]
[Cites]
Am J Gastroenterol. 2009 Mar;104(3):739-50
[
19240699.001
]
[Cites]
Cancer Chemother Pharmacol. 2009 May;63(6):1017-22
[
18781300.001
]
[Cites]
N Engl J Med. 2009 Apr 2;360(14):1408-17
[
19339720.001
]
[Cites]
Crit Rev Oncol Hematol. 2009 May;70(2):134-44
[
19111473.001
]
[Cites]
Cancer. 2009 May 1;115(9):1967-76
[
19235249.001
]
[Cites]
J Clin Oncol. 2009 Jul 1;27(19):3109-16
[
19451431.001
]
[Cites]
J Surg Oncol. 2009 Oct 1;100(5):364-71
[
19235181.001
]
[Cites]
Gut. 2010 Jan;59(1):62-8
[
19671542.001
]
[Cites]
J Clin Oncol. 2000 Jan;18(1):136-47
[
10623704.001
]
[Cites]
Lancet. 2000 Apr 8;355(9211):1211-4
[
10770302.001
]
[Cites]
Eur J Cancer Prev. 1999 Dec;8 Suppl 1:S73-86
[
10772421.001
]
[Cites]
Curr Top Microbiol Immunol. 2000;249:101-18
[
10802941.001
]
[Cites]
N Engl J Med. 2000 Jun 29;342(26):1946-52
[
10874062.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8403-8
[
10900004.001
]
[Cites]
J Clin Oncol. 2000 Aug;18(16):2938-47
[
10944126.001
]
[Cites]
World J Surg. 2000 Sep;24(9):1081-90
[
11036286.001
]
[Cites]
Lancet. 2000 Sep 16;356(9234):968-74
[
11041397.001
]
[Cites]
Nat Cell Biol. 2001 Apr;3(4):433-8
[
11283620.001
]
[Cites]
J Clin Oncol. 2001 Apr 15;19(8):2282-92
[
11304782.001
]
[Cites]
J Natl Cancer Inst. 2001 Aug 15;93(16):1264-6
[
11504772.001
]
[Cites]
N Engl J Med. 2001 Oct 11;345(15):1091-7
[
11596588.001
]
[Cites]
Ann Surg. 2004 Sep;240(3):438-47; discussion 447-50
[
15319715.001
]
[Cites]
Cancer Res. 2004 Oct 1;64(19):6919-23
[
15466182.001
]
[Cites]
Lancet. 2004 Oct 2-8;364(9441):1219-28
[
15464182.001
]
[Cites]
Cancer. 1967 Sep;20(9):1520-61
[
6038396.001
]
[Cites]
Int J Cancer. 1985 Aug 15;36(2):179-86
[
4018911.001
]
[Cites]
J Clin Oncol. 1987 Oct;5(10):1559-65
[
2443619.001
]
[Cites]
Cancer. 1988 Dec 1;62(11):2373-7
[
3179952.001
]
[Cites]
Gastroenterology. 1988 Dec;95(6):1556-63
[
3181679.001
]
[Cites]
J Clin Oncol. 1989 Oct;7(10):1407-18
[
2476530.001
]
[Cites]
Cell. 1990 Jun 1;61(5):759-67
[
2188735.001
]
[Cites]
N Engl J Med. 1992 Mar 5;326(10):653-7
[
1736103.001
]
[Cites]
J Natl Cancer Inst. 1992 Oct 21;84(20):1572-5
[
1404450.001
]
[Cites]
N Engl J Med. 1993 May 13;328(19):1365-71
[
8474513.001
]
[Cites]
N Engl J Med. 1993 Dec 30;329(27):1977-81
[
8247072.001
]
[Cites]
Arch Intern Med. 1995 Sep 11;155(16):1741-8
[
7654107.001
]
[Cites]
Int J Colorectal Dis. 1996;11(1):45-8
[
8919342.001
]
[Cites]
Lancet. 1996 Nov 30;348(9040):1472-7
[
8942775.001
]
[Cites]
Cancer. 1997 Sep 1;80(5):858-64
[
9307184.001
]
[Cites]
Br J Surg. 1998 Jul;85(7):897-901
[
9692559.001
]
[Cites]
Lancet. 1998 Oct 31;352(9138):1413-8
[
9807987.001
]
[Cites]
N Engl J Med. 1999 Jan 14;340(2):101-7
[
9887161.001
]
[Cites]
Ann Pharmacother. 2005 Jan;39(1):128-35
[
15590869.001
]
[Cites]
Am J Gastroenterol. 2005 Feb;100(2):390-4
[
15667497.001
]
[Cites]
Clin Gastroenterol Hepatol. 2005 Feb;3(2):150-8
[
15704049.001
]
[Cites]
CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108
[
15761078.001
]
[Cites]
N Engl J Med. 2005 Mar 17;352(11):1071-80
[
15713944.001
]
[Cites]
Dig Dis Sci. 2005 Nov;50(11):2147-52
[
16240230.001
]
[Cites]
Eur J Surg Oncol. 2008 Apr;34(4):428-32
[
17466484.001
]
[Cites]
J Clin Oncol. 2008 Mar 20;26(9):1443-51
[
18349394.001
]
[Cites]
Aliment Pharmacol Ther. 2008 Apr;27(8):697-712
[
18248653.001
]
[Cites]
Lancet. 2008 Mar 22;371(9617):1007-16
[
18358928.001
]
[Cites]
Anticancer Drugs. 2008 Jun;19(5):447-64
[
18418212.001
]
[Cites]
J Clin Oncol. 2008 Apr 20;26(12):2006-12
[
18421053.001
]
[Cites]
J Clin Oncol. 2008 May 10;26(14):2311-9
[
18390971.001
]
[Cites]
Cancer Res. 2008 Jun 1;68(11):4465-78
[
18519710.001
]
[Cites]
Gastroenterology. 2008 Jul;135(1):82-90
[
18482589.001
]
[Cites]
Am J Clin Nutr. 2008 Jul;88(1):176-84
[
18614739.001
]
(PMID = 19942166.001).
[ISSN]
1532-1916
[Journal-full-title]
Best practice & research. Clinical gastroenterology
[ISO-abbreviation]
Best Pract Res Clin Gastroenterol
[Language]
ENG
[Grant]
United States / NCATS NIH HHS / TR / UL1 TR000043; United States / NCRR NIH HHS / RR / UL1RR024143; United States / NCRR NIH HHS / RR / UL1 RR024143; United States / NCI NIH HHS / CA / U54CA100926; United States / NCI NIH HHS / CA / U54 CA100926
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
Netherlands
[Number-of-references]
163
[Other-IDs]
NLM/ NIHMS160270; NLM/ PMC3742312
23.
Pinsky PF, Fleshman J, Mutch M, Rall C, Charabaty A, Seligson D, Dry S, Umar A, Schoen RE:
One year recurrence of aberrant crypt foci.
Cancer Prev Res (Phila)
; 2010 Jul;3(7):839-43
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Aberrant crypt foci (ACF) are putative precursors of
colorectal adenomas
and have been postulated as a potential biomarker for
colorectal
cancer.
Subjects enrolled in the Prostate, Lung,
Colorectal
, and Ovarian Cancer Screening Trial were recruited for a study of ACF.
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[Copyright]
2010 AACR.
[Cites]
Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S
[
11189684.001
]
[Cites]
Gastrointest Endosc. 2009 Aug;70(2):322-30
[
19539919.001
]
[Cites]
Int J Cancer. 2004 Sep 10;111(4):633-9
[
15239144.001
]
[Cites]
N Engl J Med. 1993 Apr 1;328(13):901-6
[
8446136.001
]
[Cites]
N Engl J Med. 1998 Oct 29;339(18):1277-84
[
9791143.001
]
[Cites]
J Gastroenterol Hepatol. 2005 Feb;20(2):173-81
[
15683417.001
]
[Cites]
Clin Gastroenterol Hepatol. 2005 Mar;3(3):271-8
[
15765447.001
]
[Cites]
Clin Gastroenterol Hepatol. 2007 May;5(5):526-33
[
17433788.001
]
[Cites]
Gastrointest Endosc. 2008 Jun;67(7):1097-102
[
18178205.001
]
[Cites]
Clin Gastroenterol Hepatol. 2009 Jan;7(1):86-92
[
18829395.001
]
[Cites]
Cancer Prev Res (Phila). 2008 Jun;1(1):4-8
[
19138929.001
]
[Cites]
Cancer Prev Res (Phila). 2008 Jun;1(1):21-31
[
19138933.001
]
[Cites]
Clin Gastroenterol Hepatol. 2009 May;7(5):568-74
[
19418605.001
]
[Cites]
Cancer Causes Control. 2009 Jul;20(5):653-61
[
19067190.001
]
[Cites]
Am J Gastroenterol. 2002 Jun;97(6):1524-9
[
12094877.001
]
(PMID = 20570885.001).
[ISSN]
1940-6215
[Journal-full-title]
Cancer prevention research (Philadelphia, Pa.)
[ISO-abbreviation]
Cancer Prev Res (Phila)
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z99 CA999999
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS195702; NLM/ PMC2900400
24.
Rubio CA:
Serrated neoplasias and de novo carcinomas in ulcerative colitis: a histological study in colectomy specimens.
J Gastroenterol Hepatol
; 2007 Jul;22(7):1024-31
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[Title]
Serrated neoplasias and
de
novo carcinomas in ulcerative colitis: a histological study in colectomy specimens.
BACKGROUND AND AIM: Cancer in ulcerative colitis (UC) originates in dysplastic crypts, adenomatous growths (UCAG), and UC-associated
adenomas
(UCAD).
The aim of the present study was to compare the histological phenotypes between UCAG, UCAD, and sporadic
colorectal adenomas
in non-colitics (non-UCAD), as well as between UC-associated carcinomas (UCC) and carcinomas in non-colitic patients (non-UCC).
Six UCC (5.6%) were
de
novo carcinomas.
This is the first study reporting the occurrence of serrated and microtubular UCAG and of
de
novo carcinomas in UC.
[MeSH-major]
Adenoma
/ pathology.
Adenoma
/ surgery. Colectomy. Colitis, Ulcerative / pathology. Colitis, Ulcerative / surgery. Colonic Neoplasms / pathology. Colonic Neoplasms / surgery.
Colorectal
Neoplasms / pathology.
Colorectal
Neoplasms / surgery
Genetic Alliance.
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.
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(PMID = 17559365.001).
[ISSN]
0815-9319
[Journal-full-title]
Journal of gastroenterology and hepatology
[ISO-abbreviation]
J. Gastroenterol. Hepatol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
25.
Maaser K, Grabowski P, Oezdem Y, Krahn A, Heine B, Stein H, Buhr H, Zeitz M, Scherübl H:
Up-regulation of the peripheral benzodiazepine receptor during human colorectal carcinogenesis and tumor spread.
Clin Cancer Res
; 2005 Mar 1;11(5):1751-6
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[Title]
Up-regulation of the peripheral benzodiazepine receptor during human
colorectal
carcinogenesis and tumor spread.
In Unio Internationale Contra Cancrum (UICC) III
colorectal
cancers, a high level of PBR overexpression correlates with poor prognosis.
However, little is known about the role of PBR in the development and progression of
colorectal
cancer.
This study addresses the up-regulation of PBR during
colorectal
carcinogenesis and tumor spread.
One hundred sixteen consecutive patients undergoing surgery for
colorectal
cancer with either regional (59 patients) or distant metastases (57 patients) were followed-up for 5 years or until death.
UICC stage III patients with
colorectal
primaries highly overexpressing PBR developed metastases significantly more often than patients with low PBR overexpression in their primary carcinoma.
In 54 of the 116 patients
adenomas
and/or metastases and/or recurrences were available to be studied for PBR up-regulation during
colorectal
carcinogenesis and tumor spread.
PBR was found to be overexpressed in 86% of early and late
adenomas
.
The extent of PBR protein overexpression was equivalent in
colorectal adenomas
and carcinomas but slightly increased in metastases.
These data suggest a functional role of PBR during
colorectal
carcinogenesis and tumor spread.
[MeSH-major]
Adenoma
/ genetics.
Adenoma
/ pathology. Carcinoma / genetics. Carcinoma / pathology. Cell Transformation, Neoplastic / genetics.
Colorectal
Neoplasms / genetics.
Colorectal
Neoplasms / pathology. Neoplasm Metastasis. Receptors, GABA / biosynthesis
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[ErratumIn]
Clin Cancer Res. 2005 Sep 1;11(17):6408
(PMID = 15755996.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Receptors, GABA; 0 / TSPO protein, human
26.
Su Y, Shrubsole MJ, Ness RM, Cai Q, Kataoka N, Washington K, Zheng W:
Immunohistochemical expressions of Ki-67, cyclin D1, beta-catenin, cyclooxygenase-2, and epidermal growth factor receptor in human colorectal adenoma: a validation study of tissue microarrays.
Cancer Epidemiol Biomarkers Prev
; 2006 Sep;15(9):1719-26
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[Title]
Immunohistochemical expressions of Ki-67, cyclin D1, beta-catenin, cyclooxygenase-2, and epidermal growth factor receptor in human
colorectal
adenoma
: a validation study of tissue microarrays.
OBJECTIVES: In this study, we evaluated the validity and reliability of using TMA to assess biomarkers in
colorectal adenomas
.
METHODS: Sixty-three consecutive patients with
colorectal adenomas
were recruited in this study.
Two TMA blocks were constructed using four punches from each
adenoma
(one periphery, one deep, and two middle zones).
RESULTS:
Colorectal
adenoma
exhibited zonal, heterogeneous expression patterns for all five markers.
CONCLUSION: Our study indicates that TMA can be used to reliably assess the expression levels of Ki-67, cyclin D1, beta-catenin, cyclooxygenase-2, and epidermal growth factor receptor in
colorectal
adenoma
tissues.
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NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 16985035.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA95103; United States / NCI NIH HHS / CA / R01 CA97386
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Validation Studies
[Publication-country]
United States
[Chemical-registry-number]
0 / Ki-67 Antigen; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
27.
Berndt SI, Huang WY, Fallin MD, Helzlsouer KJ, Platz EA, Weissfeld JL, Church TR, Welch R, Chanock SJ, Hayes RB:
Genetic variation in base excision repair genes and the prevalence of advanced colorectal adenoma.
Cancer Res
; 2007 Feb 1;67(3):1395-404
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[Title]
Genetic variation in base excision repair genes and the prevalence of advanced
colorectal
adenoma
.
Base excision repair (BER) corrects DNA damage caused by oxidative stress and low folate intake, which are putative risk factors for
colorectal
neoplasia.
To examine the relationship between genetic variation in BER genes and
colorectal
adenoma
risk, we conducted a case-control study of 767 cases of advanced
colorectal
adenoma
and 773 controls from the baseline screening exam of the Prostate, Lung,
Colorectal
, and Ovarian Cancer Screening Trial.
Cases included participants diagnosed with advanced left-sided
adenoma
, and controls were subjects without evidence of a left-sided polyp by sigmoidoscopy, frequency-matched to cases on race and gender.
Twenty single nucleotide polymorphisms were genotyped in four BER genes (APEX1, PARP1, POLB, and XRCC1), and conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for the association with
colorectal
adenoma
.
The APEX1 51H variant was associated with a borderline significant decreased risk of
colorectal
adenoma
(OR, 0.66; 95% CI, 0.44-1.00), and the XRCC1 399Q variant was inversely associated with risk among Caucasians (OR, 0.80; 95% CI, 0.64-0.99).
Homozygotes at two PARP1 loci (A284A and IVS13+118G>A) were also associated with a decreased risk of
colorectal
adenoma
compared with wild-type carriers (OR, 0.70; 95% CI, 0.49-0.98 for both), which was restricted to advanced
adenomas
displaying histologically aggressive characteristics (OR, 0.51; 95% CI, 0.33-0.78, P = 0.002 for PARP1 A284A).
This study suggests that polymorphisms in APEX1, XRCC1, and PARP1 may be associated with advanced
colorectal
adenoma
.
[MeSH-major]
Adenomyoma / epidemiology. Adenomyoma / genetics.
Colorectal
Neoplasms / epidemiology.
Colorectal
Neoplasms / genetics. DNA Repair / genetics
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(PMID = 17283177.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Intramural
[Publication-country]
United States
28.
Snover DC, Jass JR, Fenoglio-Preiser C, Batts KP:
Serrated polyps of the large intestine: a morphologic and molecular review of an evolving concept.
Am J Clin Pathol
; 2005 Sep;124(3):380-91
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[Title]
Serrated polyps of the
large intestine
: a morphologic and molecular review of an evolving concept.
Serrated polyps of the
large intestine
, including traditional hyperplastic polyps, traditional serrated
adenomas
, and more recently described sessile serrated
adenomas
, have gained increased recognition in recent years because of growing evidence that one of these lesions, the sessile serrated
adenoma
, might be the precursor lesion for some cases of microsatellite unstable
colorectal
carcinoma.
Nevertheless, there has been some reluctance to embrace the concept of sessile serrated
adenoma
, and numerous diagnostic challenges exist.
Haggitt Gastrointestinal Pathology Society Forum presented in Vancouver, Canada, March 6, 2004 as part of the annual meeting of the United States-Canadian Academy of Pathology, reviews the morphologic and molecular evidence for the concept of various polyps in the general category of serrated polyps of the
large intestine
, in particular the lesion known as the sessile serrated
adenoma
, and provides a conceptual framework for
diagnosis
of these lesions.
[MeSH-major]
Colonic Polyps / pathology.
Colorectal
Neoplasms / pathology. Intestinal Polyps / pathology
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[CommentIn]
Am J Clin Pathol. 2006 Jun;125(6):951; author reply 952-3
[
16761354.001
]
(PMID = 16191506.001).
[ISSN]
0002-9173
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
36
29.
Deng ZL, Xie DW, Bostick RM, Miao XJ, Gong YL, Zhang JH, Wargovich MJ:
Novel genetic variations of the p53R2 gene in patients with colorectal adenoma and controls.
World J Gastroenterol
; 2005 Sep 7;11(33):5169-73
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[Title]
Novel genetic variations of the p53R2 gene in patients with
colorectal
adenoma
and controls.
METHODS: We screened the p53R2 gene coding regions and a regulatory region which contains a p53 binding sequence in 100 patients with
colorectal
adenoma
and 100 control subjects using PCR, cold SSCP, and direct DNA sequencing.
Additionally, we determined the frequency of these p53R2 variants in a recently concluded case-control study of incident sporadic
colorectal adenomas
(163 cases and 210 controls).
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(PMID = 16127747.001).
[ISSN]
1007-9327
[Journal-full-title]
World journal of gastroenterology
[ISO-abbreviation]
World J. Gastroenterol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA066539; United States / NCI NIH HHS / CA / R03 CA092773
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Protein p53; EC 1.17.4.- / Ribonucleotide Reductases; EC 1.17.4.- / ribonucleotide reductase R2 subunit
[Other-IDs]
NLM/ PMC4320390
30.
Hundt S, Haug U, Brenner H:
Comparative evaluation of immunochemical fecal occult blood tests for colorectal adenoma detection.
Ann Intern Med
; 2009 Feb 3;150(3):162-9
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[Title]
Comparative evaluation of immunochemical fecal occult blood tests for
colorectal
adenoma
detection.
BACKGROUND: Different immunochemical fecal occult blood tests (FOBTs) have been proposed for noninvasive
colorectal
cancer screening.
Large
-scale, colonoscopy-based screening studies that allow evaluation of these tests for the detection of precursor lesions are scarce.
OBJECTIVE: To determine and compare performance characteristics of 6 qualitative immunochemical FOBTs for identifying
colorectal adenomas
among adults who attended screening colonoscopy examinations.
PATIENTS: 1319 participants at average risk for
colorectal
neoplasia who were undergoing screening colonoscopy (mean age, 63 years; 50% men).
MEASUREMENTS: 6 different qualitative immunochemical FOBTs were done with stool samples collected before
bowel
preparation for colonoscopy.
RESULTS: Overall, 405 participants (31%) had an
adenoma
and 130 participants (10%) had an advanced
adenoma
.
For the 2 best-performing tests (immoCARE-C [CAREdiagnostica, Voerde, Germany] and FOB advanced [ulti med, Ahrensburg, Germany]), the sensitivity for detection of advanced
adenomas
was 25% (95% CI, 18% to 34%) and 27% (CI, 20% to 35%), respectively; specificity was 97% (CI, 95% to 98%) and 93% (CI, 91% to 95%); and the positive likelihood ratio was 3.5 (CI, 2.2 to 5.4) and 2.5 (CI, 1.9 to 3.5).
CONCLUSION: Qualitative immunochemical FOBTs could be an option for future
colorectal
cancer screening because they showed better performance characteristics for precursor lesions than guaiac-based FOBTs and are practical for mass screening.
However, given the
large
differences in diagnostic performance among tests, careful evaluation of the different test variants is important.
[MeSH-major]
Adenoma
/
diagnosis
.
Colorectal
Neoplasms /
diagnosis
. Immunohistochemistry / methods. Occult Blood
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[SummaryForPatientsIn]
Ann Intern Med. 2009 Feb 3;150(3):I34
[
19189901.001
]
(PMID = 19189905.001).
[ISSN]
1539-3704
[Journal-full-title]
Annals of internal medicine
[ISO-abbreviation]
Ann. Intern. Med.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Indicators and Reagents; 9000-29-7 / Guaiac
31.
Mitrou PN, Watson MA, Loktionov AS, Cardwell C, Gunter MJ, Atkin WS, Macklin CP, Cecil T, Bishop TD, Primrose J, Bingham SA:
MTHFR (C677T and A1298C) polymorphisms and risk of sporadic distal colorectal adenoma in the UK Flexible Sigmoidoscopy Screening Trial (United Kingdom).
Cancer Causes Control
; 2006 Aug;17(6):793-801
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[Title]
MTHFR (C677T and A1298C) polymorphisms and risk of sporadic distal
colorectal
adenoma
in the UK Flexible Sigmoidoscopy Screening Trial (United Kingdom).
OBJECTIVE: The purpose of this study was to further evaluate the role of low activity MTHFR variants as well as to explore interactive effects between alcoholic drink consumption and MTHFR variants and risk of distal
colorectal
adenomatous polyps.
METHODS: We examined the relationship between MTHFR C677T and A1298C gene polymorphisms and risk of distal
adenomas
in one of the largest case control studies of 946 polyp-free controls and 894 cases, all participants of the UK Flexible Sigmoidoscopy Screening Trial (UKFSS).
RESULTS: Investigation of the effect of the MTHFR C677T polymorphism in this
large
UKFSS study revealed no overall association on
adenoma
risk (P>0.05).
However the MTHFR 1298C allele was linked, for the first time, to high risk
adenomas
, although in males only (odds ratio (OR) for A/C+C/C compared with A/A 1.55; 95% confidence interval (CI), 1.08-2.22; P=0.018).
CONCLUSIONS: In this, the largest study of these polymorphisms in relation to
colorectal
adenoma
, there was no evidence for an interaction with alcohol in combination with the variant forms of MTHFR (P>0.05).
[MeSH-major]
5,10-Methylenetetrahydrofolate Reductase (FADH2) / genetics.
Adenoma
/ genetics. Adenomatous Polyps / genetics.
Colorectal
Neoplasms / genetics. Polymorphism, Single Nucleotide / genetics
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(PMID = 16783607.001).
[ISSN]
0957-5243
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / A4994; United Kingdom / Medical Research Council / / G9615910
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 1.5.1.20 / 5,10-Methylenetetrahydrofolate Reductase (FADH2)
32.
Miller PE, Lesko SM, Muscat JE, Lazarus P, Hartman TJ:
Dietary patterns and colorectal adenoma and cancer risk: a review of the epidemiological evidence.
Nutr Cancer
; 2010;62(4):413-24
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[Title]
Dietary patterns and
colorectal
adenoma
and cancer risk: a review of the epidemiological evidence.
A number of studies exploring associations between individual dietary components and
colorectal
adenoma
or cancer risk have yielded conflicting results.
Results from prospective cohort and population-based case-control studies examining associations between dietary patterns and
colorectal
cancer or
adenoma
risk were evaluated and described in this review.
Despite notable differences in population characteristics, study design, and methods used for characterizing dietary patterns across the different studies, two general dietary patterns were found to modestly predict
colorectal
adenoma
and cancer risk.
A healthier pattern consisting of greater intakes of fruits and vegetables, and lower intakes of red and processed meat, appeared protective against
colorectal
adenoma
and cancer incidence.
Continued research efforts are needed to evaluate the cumulative and interactive effects of numerous dietary exposures on
colorectal
cancer risk.
[MeSH-major]
Adenoma
/ epidemiology.
Colorectal
Neoplasms / epidemiology. Diet
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(PMID = 20432162.001).
[ISSN]
1532-7914
[Journal-full-title]
Nutrition and cancer
[ISO-abbreviation]
Nutr Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Dietary Carbohydrates; 0 / Dietary Fats
[Number-of-references]
49
33.
Hall MJ, Liberman E, Dulkart O, Galazan L, Sagiv E, Shmueli E, Kazanov D, Hallak A, Moshkowitz M, Figer A, Kraus S, Inbar M, Neugut AI, Arber N:
Risk of colorectal neoplasia associated with the adenomatous polyposis coli E1317Q variant.
Ann Oncol
; 2009 Sep;20(9):1517-21
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[Title]
Risk of
colorectal
neoplasia associated with the adenomatous polyposis coli E1317Q variant.
BACKGROUND: Reports of the risk of
colorectal
neoplasia associated with a variant of the adenomatous polyposis coli (APC E1317Q) gene are conflicting.
Subjects underwent colonoscopic evaluation (+/-biopsy and/or polypectomy) and had cancer history and
colorectal
neoplasia risk factors assessed.
When stratified by neoplasia type,
adenoma
risk was significantly elevated in carriers (OR 4.1, 95% CI 1.8-9.4) but
colorectal
cancer risk was not (OR 2.1, 95% CI 0.8-5.3).
After adjustment, the E1317Q variant remained a significant predictor of
colorectal
adenoma
(OR 4.6, 95% CI 2.0-10.8).
CONCLUSIONS: The APC E1317Q variant is associated with
colorectal
neoplasia, particularly
colorectal adenomas
, but further studies are still needed.
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(PMID = 19474113.001).
[ISSN]
1569-8041
[Journal-full-title]
Annals of oncology : official journal of the European Society for Medical Oncology
[ISO-abbreviation]
Ann. Oncol.
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein
34.
Ye C, Shrubsole MJ, Cai Q, Ness R, Grady WM, Smalley W, Cai H, Washington K, Zheng W:
Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without colorectal adenomas.
Oncol Rep
; 2006 Aug;16(2):429-35
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[Title]
Promoter methylation status of the MGMT, hMLH1, and CDKN2A/p16 genes in non-neoplastic mucosa of patients with and without
colorectal adenomas
.
CpG island methylation has been observed in aberrant crypt foci (ACF) and
adenomas
in the colon, implicating it in the earliest aspects of colon cancer formation.
In addition, some investigators have identified an age-related increase in DNA methylation of the ESR1 locus in the colon mucosa, suggesting that DNA methylation may be a pre-neoplastic change that increases the risk of colon
adenomas
and colon cancer.
The promoter methylation patterns of these genes were examined in rectal biopsies (mucosa samples) of 97
colorectal
adenoma
cases and 94 healthy controls using methylation-specific PCR (MSP) assays.
The frequency of CDKN2A/p16 promoter methylation was very rare in normal
colorectal
tissue with a frequency of approximately 2%.
The methylation status of these genes in rectal mucosa biopsies detected by MSP assays may not distinguish between patients with and without
adenomas
in the colon.
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(PMID = 16820927.001).
[ISSN]
1021-335X
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / P50 CA95103; United States / NCI NIH HHS / CA / R01CA97386
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Greece
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Nuclear Proteins; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase
35.
Jenkins PJ:
Cancers associated with acromegaly.
Neuroendocrinology
; 2006;83(3-4):218-23
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More recently, it has become apparent that patients with acromegaly may also have an increased prevalence of
colorectal adenomas
and cancer.
This may be due to elevated IGF-I, which is implicated in the development of sporadic
colorectal
cancer, and environmental factors, such as the bile acid deoxycholic acid, the levels of which are also increased in acromegaly.
Large
-scale epidemiological studies are required to clarify this issue.
[MeSH-major]
Acromegaly / complications. Breast Neoplasms / etiology.
Colorectal
Neoplasms / etiology. Prostatic Neoplasms / etiology
[MeSH-minor]
Adenoma
/ blood.
Adenoma
/ epidemiology.
Adenoma
/ etiology. Carcinoma / blood. Carcinoma / epidemiology. Carcinoma / etiology. Female. Human Growth Hormone / blood. Humans. Male
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(PMID = 17047386.001).
[ISSN]
0028-3835
[Journal-full-title]
Neuroendocrinology
[ISO-abbreviation]
Neuroendocrinology
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone
[Number-of-references]
56
36.
Moslehi R, Chatterjee N, Church TR, Chen J, Yeager M, Weissfeld J, Hein DW, Hayes RB:
Cigarette smoking, N-acetyltransferase genes and the risk of advanced colorectal adenoma.
Pharmacogenomics
; 2006 Sep;7(6):819-29
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[Title]
Cigarette smoking, N-acetyltransferase genes and the risk of advanced
colorectal
adenoma
.
BACKGROUND: Cigarette use is associated with greater risk for
colorectal
adenoma
, a
colorectal
cancer precursor.
Our interest is in the polymorphisms within the NAT1 and NAT2 genes that influence the tobacco-
colorectal
tumor relationship by impacting on the metabolic activation and detoxification of tobacco smoke-derived carcinogens.
METHODS: In the Prostate, Lung,
Colorectal
and Ovarian (PLCO) cancer screening trial, we compared NAT1 and NAT2 gene variant distributions for 772 cases with left-sided advanced
adenoma
and 777 gender and age-matched controls.
RESULTS: Risks for advanced
colorectal
adenoma
were significantly increased among recent smokers (current smokers or those who quit less than 10 years ago) (odds ratio [OR] = 2.3, 95% confidence interval [CI]: 1.7-3.1) and among those who smoked more than 20 cigarettes per day (OR = 1.7, 95% CI: 1.3-2.2), compared with nonsmokers.
CONCLUSIONS: Our study indicated that NAT2 gene variants associated with a slow acetylator phenotype were more susceptible to the effects of tobacco smoking with respect to
adenoma
risk, providing leads for disease prevention.
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(PMID = 16981843.001).
[ISSN]
1462-2416
[Journal-full-title]
Pharmacogenomics
[ISO-abbreviation]
Pharmacogenomics
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA-34627; United States / NCI NIH HHS / CA / CA034627-21; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA034627; United States / NCI NIH HHS / CA / R01 CA034627-21
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
England
[Chemical-registry-number]
0 / Isoenzymes; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / N-acetyltransferase 1; EC 2.3.1.5 / NAT2 protein, human
37.
Hassan C, Zullo A, Winn S, Eramo A, Tomao S, Rossini FP, Morini S:
The colorectal malignant polyp: scoping a dilemma.
Dig Liver Dis
; 2007 Jan;39(1):92-100
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[Title]
The colorectal
malignant polyp: scoping a dilemma.
Colorectal adenomas
containing invasive carcinoma represent the majority of early
colorectal
cancers.
[MeSH-major]
Adenomatous Polyps / pathology. Colonic Polyps / pathology.
Colorectal
Neoplasms / pathology
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(PMID = 17113842.001).
[ISSN]
1590-8658
[Journal-full-title]
Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
[ISO-abbreviation]
Dig Liver Dis
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Number-of-references]
80
38.
Ayanian JZ, Sequist TD, Zaslavsky AM, Johannes RS:
Physician reminders to promote surveillance colonoscopy for colorectal adenomas: a randomized controlled trial.
J Gen Intern Med
; 2008 Jun;23(6):762-7
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[Title]
Physician reminders to promote surveillance colonoscopy for
colorectal adenomas
: a randomized controlled trial.
BACKGROUND: Most
colorectal
cancers develop from adenomatous polyps.
PATIENTS: Seven hundred seventeen patients who had
colorectal adenomas
removed during 1995 through 2000 and no follow-up colonoscopy identified via automated review of electronic records through March, 2006.
MEASUREMENTS AND MAIN RESULTS: The use of colonoscopy and detection of new
adenomas
or cancer were assessed at 6 months by a blinded medical record review in all patients.
New
adenomas
or cancer were detected in 14 (3.9%) intervention patients and 6 (1.7%) control patients (P = 0.06), representing 42.4% and 37.5% of patients who underwent colonoscopy in each group, respectively.
CONCLUSIONS: Among patients with prior
colorectal adenomas
, physician reminders increased the use of surveillance colonoscopy, but better systems are needed to identify eligible patients (ClinicalTrials.gov ID number NCT00397969).
[MeSH-major]
Adenomatous Polyps /
diagnosis
. Appointments and Schedules. Colonic Polyps /
diagnosis
. Colonoscopy / utilization.
Colorectal
Neoplasms /
diagnosis
. Reminder Systems
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[Cites]
Gastrointest Endosc. 2000 Apr;51(4 Pt 1):433-7
[
10744815.001
]
[Cites]
Arch Intern Med. 2007 Mar 12;167(5):507-12
[
17353500.001
]
[Cites]
Gut. 2001 Jun;48(6):812-5
[
11358901.001
]
[Cites]
J Gen Intern Med. 2001 Aug;16(8):531-7
[
11556929.001
]
[Cites]
Ann Intern Med. 2002 May 7;136(9):641-51
[
11992299.001
]
[Cites]
Gastroenterology. 2003 Feb;124(2):544-60
[
12557158.001
]
[Cites]
Am J Med. 2003 Aug 1;115(2):129-33
[
12893399.001
]
[Cites]
Med Care Res Rev. 2003 Sep;60(3):294-331
[
12971231.001
]
[Cites]
Arch Intern Med. 2003 Dec 8-22;163(22):2733-6
[
14662627.001
]
[Cites]
Ann Intern Med. 2004 Aug 17;141(4):264-71
[
15313742.001
]
[Cites]
Cancer. 2004 Sep 1;101(5 Suppl):1188-200
[
15316914.001
]
[Cites]
N Engl J Med. 1993 Apr 1;328(13):901-6
[
8446136.001
]
[Cites]
N Engl J Med. 1993 Dec 30;329(27):1977-81
[
8247072.001
]
[Cites]
N Engl J Med. 1995 Mar 30;332(13):861-7
[
7870142.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1999 Jul;8(7):587-93
[
10428195.001
]
[Cites]
J Am Med Inform Assoc. 2005 Jul-Aug;12(4):431-7
[
15802479.001
]
[Cites]
J Am Med Inform Assoc. 2006 Jan-Feb;13(1):5-11
[
16221941.001
]
[Cites]
CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30
[
16514137.001
]
[Cites]
Arch Intern Med. 2006 Mar 27;166(6):675-81
[
16567608.001
]
[Cites]
Gastroenterology. 2006 May;130(6):1872-85
[
16697750.001
]
[Cites]
Arch Intern Med. 2006 Jul 10;166(13):1374-9
[
16832002.001
]
[Cites]
Gastrointest Endosc. 2006 Oct;64(4):614-26
[
16996358.001
]
[Cites]
Ann Intern Med. 2006 Nov 7;145(9):646-53
[
17088577.001
]
[Cites]
Ann Intern Med. 2006 Nov 7;145(9):654-9
[
17088578.001
]
[Cites]
Arch Intern Med. 2006 Nov 13;166(20):2237-43
[
17101942.001
]
[Cites]
Arch Intern Med. 2006 Nov 13;166(20):2272-7
[
17101947.001
]
[Cites]
Health Aff (Millwood). 2006 Nov-Dec;25(6):w496-507
[
17035341.001
]
[Cites]
Ann Intern Med. 2007 Feb 20;146(4):270-7
[
17310051.001
]
[Cites]
Prev Med. 2000 Oct;31(4):429-39
[
11006069.001
]
(PMID = 18386103.001).
[ISSN]
1525-1497
[Journal-full-title]
Journal of general internal medicine
[ISO-abbreviation]
J Gen Intern Med
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00397969
[Grant]
United States / NCI NIH HHS / CA / R21 CA112365; United States / NCI NIH HHS / CA / R21-CA112365
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2517870
39.
Hariri LP, Tumlinson AR, Besselsen DG, Utzinger U, Gerner EW, Barton JK:
Endoscopic optical coherence tomography and laser-induced fluorescence spectroscopy in a murine colon cancer model.
Lasers Surg Med
; 2006 Apr;38(4):305-13
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BACKGROUND AND OBJECTIVES: The diagnostic feasibility of optical coherence tomography (OCT) and laser-induced fluorescence (LIF) have been evaluated for human
colorectal
cancer.
This study applies these technologies to a murine model of
colorectal
adenoma
.
One
adenoma
was histologically identified; OCT visualized mucosal thickening/abnormal mass development over the imaging timepoints.
CONCLUSIONS: These preliminary data indicate endoscopic OCT-LIF has the potential to identify
colorectal adenomas
in murine models.
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[Copyright]
Copyright 2006 Wiley-Liss, Inc.
(PMID = 16596657.001).
[ISSN]
0196-8092
[Journal-full-title]
Lasers in surgery and medicine
[ISO-abbreviation]
Lasers Surg Med
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA109385; United States / NCI NIH HHS / CA / CA083148; United States / NCI NIH HHS / CA / CA095060; United States / NCI NIH HHS / CA / CA109385
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
40.
Noffsinger AE, Hart J:
Serrated adenoma: a distinct form of non-polypoid colorectal neoplasia?
Gastrointest Endosc Clin N Am
; 2010 Jul;20(3):543-63
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[Title]
Serrated
adenoma
: a distinct form of non-polypoid
colorectal
neoplasia?
Until recently, 2 major forms of
colorectal
polyp were recognized: the
adenoma
and the hyperplastic polyp.
Adenomas
were known to represent a precursor to
colorectal
cancer, whereas hyperplastic polyps were viewed as nonneoplastic, having no potential for progression to malignancy.
We now recognize, however, that the lesions diagnosed as hyperplastic polyps in the past represent a heterogeneous group of polyps, some of which truly are hyperplastic, and others that truly have a significant risk for transformation to
colorectal
cancer.
These polyps have a characteristic serrated architecture, and include not only hyperplastic polyps but also the recently recognized serrated
adenomas
.
Serrated
adenomas
occur in 2 forms: the traditional serrated
adenoma
, which is usually a polypoid lesion endoscopically, and the sessile serrated
adenoma
, a flat or slightly raised, usually right-sided lesion.
Serrated
adenomas
of both types show characteristic molecular alterations not commonly seen in traditional
colorectal adenomas
, and probably progress to
colorectal
cancer by means of a different pathway, the so-called serrated neoplasia pathway.
The morphologic features of serrated
colorectal
lesions, the molecular alterations that characterize them, and their role in
colorectal
cancer development are discussed.
[MeSH-major]
Adenoma
/
diagnosis
.
Colorectal
Neoplasms, Hereditary Nonpolyposis /
diagnosis
[MeSH-minor]
Apoptosis. Colonic Polyps /
diagnosis
. Colonic Polyps / genetics. Colonic Polyps / pathology. CpG Islands / genetics. DNA Methylation. Disease Progression. Humans. Microsatellite Instability. Mutation. Phenotype. Polymorphism, Genetic. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Receptor, EphB2 / genetics. Risk Assessment. ras Proteins / genetics
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[Copyright]
Copyright 2010 Elsevier Inc. All rights reserved.
(PMID = 20656251.001).
[ISSN]
1558-1950
[Journal-full-title]
Gastrointestinal endoscopy clinics of North America
[ISO-abbreviation]
Gastrointest. Endosc. Clin. N. Am.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, EphB2; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
41.
Yamaji Y, Okamoto M, Yoshida H, Kawabe T, Wada R, Mitsushima T, Omata M:
The effect of body weight reduction on the incidence of colorectal adenoma.
Am J Gastroenterol
; 2008 Aug;103(8):2061-7
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[Title]
The effect of body weight reduction on the incidence of
colorectal
adenoma
.
OBJECTIVES: Obesity is thought to be associated with
colorectal
cancer and
adenoma
.
We aimed to investigate the effect of body weight on the risk of
colorectal
adenoma
both in cross-sectional and longitudinal analyses.
METHODS: This is a retrospective cohort study in a
large
-scale health appraisal institution in Japan.
The association with the prevalence of
colorectal
adenoma
was evaluated according to the body mass index (BMI) at the initial examination.
The incidence of
colorectal
adenoma
at the second colonoscopy was investigated according to the initial BMI and body weight changes during the year.
RESULTS: The prevalence of
colorectal
adenoma
increased in relation to increases in the BMI: 15.4%, 20.6%, 22.7%, and 24.2%, respectively, in the first (BMI < 21.350), second (21.350 < or = BMI < 23.199), third (23.199 < or = BMI < 25.156), and fourth (25.156 < or = BMI) quartiles.
The incidence rates of
colorectal
adenoma
after 1 yr also increased proportionally according to the initial BMI: Group Q1 (12.9%), Group Q2 (15.7%), Group Q3 (18.3%), and Group Q4 (19.0%).
CONCLUSIONS: Obesity was associated with the risk for
colorectal
adenoma
, and body weight reduction was suggested to decrease this risk.
[MeSH-major]
Adenoma
/ epidemiology.
Colorectal
Neoplasms / epidemiology. Obesity / complications. Weight Loss
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(PMID = 18796100.001).
[ISSN]
1572-0241
[Journal-full-title]
The American journal of gastroenterology
[ISO-abbreviation]
Am. J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
42.
Hisamuddin IM, Wehbi MA, Yang VW:
Pharmacogenetics and diseases of the colon.
Curr Opin Gastroenterol
; 2007 Jan;23(1):60-6
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They affect the management of inflammatory
bowel
disease,
colorectal
cancer and the chemoprevention of
colorectal
adenoma
by influencing the metabolism of their respective substrates, azathioprine/6-mercaptopurine, 5-fluorouracil and sulindac.
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[Cites]
Hum Genet. 1999 Jan;104(1):1-9
[
10071185.001
]
[Cites]
Ann Intern Med. 1998 Nov 1;129(9):716-8
[
9841604.001
]
[Cites]
Clin Cancer Res. 2004 Dec 15;10(24):8357-62
[
15623613.001
]
[Cites]
Clin Cancer Res. 1999 Apr;5(4):883-9
[
10213225.001
]
[Cites]
Genomics. 1998 Aug 1;51(3):391-400
[
9721209.001
]
[Cites]
Am J Gastroenterol. 2005 Oct;100(10):2239-47
[
16181376.001
]
[Cites]
Ther Drug Monit. 2005 Oct;27(5):647-54
[
16175140.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2366-9
[
16214918.001
]
[Cites]
Invest New Drugs. 2005 Dec;23(6):523-32
[
16267626.001
]
[Cites]
Cancer Invest. 2006 Mar;24(2):215-7
[
16537192.001
]
[Cites]
Intern Med J. 2005 Oct;35(10):580-5
[
16207256.001
]
[Cites]
J Gastroenterol Hepatol. 2005 Aug;20(8):1149-57
[
16048561.001
]
[Cites]
J Natl Cancer Inst. 1999 Dec 1;91(23):2001-8
[
10580024.001
]
[Cites]
Gastroenterology. 2000 Apr;118(4):705-13
[
10734022.001
]
[Cites]
Clin Cancer Res. 2000 Apr;6(4):1322-7
[
10778957.001
]
[Cites]
Biochem Pharmacol. 2000 Jul 1;60(1):7-17
[
10807940.001
]
[Cites]
Nature. 2001 Feb 15;409(6822):860-921
[
11237011.001
]
[Cites]
Nature. 2001 Feb 15;409(6822):928-33
[
11237013.001
]
[Cites]
Clin Cancer Res. 2001 May;7(5):1149-53
[
11350878.001
]
[Cites]
Nat Rev Genet. 2001 Dec;2(12):930-42
[
11733746.001
]
[Cites]
Pharmacogenomics J. 2001;1(4):254-61
[
11908768.001
]
[Cites]
N Engl J Med. 2002 Apr 4;346(14):1054-9
[
11932472.001
]
[Cites]
Nat Rev Drug Discov. 2002 Jan;1(1):37-44
[
12119608.001
]
[Cites]
N Engl J Med. 2002 Aug 8;347(6):417-29
[
12167685.001
]
[Cites]
Drug Metab Dispos. 2002 Oct;30(10):1043-52
[
12228178.001
]
[Cites]
N Engl J Med. 2003 Feb 6;348(6):529-37
[
12571261.001
]
[Cites]
Int J Dermatol. 2003 May;42(5):335-41
[
12755967.001
]
[Cites]
Int J Clin Oncol. 2003 Jun;8(3):127-31
[
12851835.001
]
[Cites]
Hum Mutat. 2003 Sep;22(3):209-13
[
12938085.001
]
[Cites]
Biochem Biophys Res Commun. 2003 Dec 26;312(4):1005-10
[
14651971.001
]
[Cites]
Gastroenterology. 2004 Feb;126(2):425-31
[
14762779.001
]
[Cites]
Mayo Clin Proc. 2004 Mar;79(3):376-84
[
15008610.001
]
[Cites]
Drug Discov Today. 2004 Jul 1;9(13):574-81
[
15203093.001
]
[Cites]
Ther Drug Monit. 2004 Apr;26(2):186-91
[
15228163.001
]
[Cites]
Nat Rev Drug Discov. 2004 Sep;3(9):739-48
[
15340384.001
]
[Cites]
Am J Hum Genet. 1980 Sep;32(5):651-62
[
7191632.001
]
[Cites]
J Pharmacol Exp Ther. 1982 Jul;222(1):174-81
[
7086699.001
]
[Cites]
N Engl J Med. 1993 May 6;328(18):1313-6
[
8385741.001
]
[Cites]
Annu Rev Pharmacol Toxicol. 1993;33:179-99
[
8494339.001
]
[Cites]
Pharmacogenetics. 1992 Aug;2(4):148-59
[
1306116.001
]
[Cites]
J Clin Oncol. 1994 Nov;12(11):2248-53
[
7964939.001
]
[Cites]
DNA Cell Biol. 1995 Jan;14(1):1-6
[
7832988.001
]
[Cites]
Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):949-53
[
7862671.001
]
[Cites]
Blood. 1995 Apr 1;85(7):1897-902
[
7703493.001
]
[Cites]
Clin Pharmacol Ther. 1995 Nov;58(5):512-22
[
7586945.001
]
[Cites]
DNA Cell Biol. 1996 Jan;15(1):17-30
[
8561894.001
]
[Cites]
Am J Hum Genet. 1996 Apr;58(4):694-702
[
8644731.001
]
[Cites]
Gut. 1996 Apr;38(4):578-81
[
8707091.001
]
[Cites]
Ann Intern Med. 1997 Apr 15;126(8):608-14
[
9103127.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6444-9
[
9177237.001
]
[Cites]
J Inherit Metab Dis. 1997 Jul;20(3):335-8
[
9266349.001
]
[Cites]
Hum Genet. 1997 Dec;101(3):333-8
[
9439663.001
]
[Cites]
Br J Cancer. 1998;77(1):79-86
[
9459149.001
]
[Cites]
Leukemia. 1998 Mar;12(3):346-52
[
9529129.001
]
[Cites]
Eur J Cancer. 1998 Jan;34(1):92-7
[
9624244.001
]
[Cites]
Am J Hum Genet. 1998 Jul;63(1):11-6
[
9634537.001
]
(PMID = 17133087.001).
[ISSN]
0267-1379
[Journal-full-title]
Current opinion in gastroenterology
[ISO-abbreviation]
Curr. Opin. Gastroenterol.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK052230; United States / NIDDK NIH HHS / DK / DK064399-05; United States / NCI NIH HHS / CA / R01 CA084197-09; United States / NIDDK NIH HHS / DK / R24 DK064399-05; United States / NCI NIH HHS / CA / CA084197-09; United States / NIDDK NIH HHS / DK / R01 DK052230-11; United States / NCI NIH HHS / CA / R01 CA084197; United States / NIDDK NIH HHS / DK / R24 DK064399; United States / NIDDK NIH HHS / DK / DK52230; United States / NIDDK NIH HHS / DK / DK052230-11; United States / NCI NIH HHS / CA / CA84197
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
57
[Other-IDs]
NLM/ NIHMS37179; NLM/ PMC2213557
43.
Speake D, Biyani D, Frizelle FA, Watson AJ:
Flat adenomas.
ANZ J Surg
; 2007 Jan-Feb;77(1-2):4-8
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[Title]
Flat
adenomas
.
This article was presented at the conjoint CSSA and RACS (
colorectal
section) spring meeting Queensland, Australia, September 2004.
The
adenoma
-carcinoma sequence describes a succession of events from polypoid
adenoma
to
colorectal
cancer.
However, this model only accounts for up to two-thirds of
colorectal
cancers.
There is growing evidence that flat
adenomas
are precursor lesions to a flat type of
colorectal
cancer and certain subtypes of these polyps are at greater risk of malignant transformation.
If confirmed, the implications for screening, endoscopic recognition and management will become of increasing importance if we are to decrease the incidence of
colorectal
cancer.
[MeSH-major]
Adenocarcinoma / physiopathology.
Adenoma
/ physiopathology. Colonic Neoplasms / physiopathology. Colonic Polyps / physiopathology
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(PMID = 17295810.001).
[ISSN]
1445-1433
[Journal-full-title]
ANZ journal of surgery
[ISO-abbreviation]
ANZ J Surg
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Australia
[Number-of-references]
72
44.
Alberts DS, Martínez ME, Hess LM, Einspahr JG, Green SB, Bhattacharyya AK, Guillen J, Krutzsch M, Batta AK, Salen G, Fales L, Koonce K, Parish D, Clouser M, Roe D, Lance P, Phoenix and Tucson Gastroenterologist Networks:
Phase III trial of ursodeoxycholic acid to prevent colorectal adenoma recurrence.
J Natl Cancer Inst
; 2005 Jun 1;97(11):846-53
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[Title]
Phase III trial of ursodeoxycholic acid to prevent
colorectal
adenoma
recurrence.
We conducted a phase III, double-blind placebo-controlled trial of UDCA to evaluate its ability to prevent
colorectal
adenoma
recurrence.
METHODS: We randomly assigned 1285 individuals who had undergone removal of a
colorectal
adenoma
within the past 6 months to daily treatment with UDCA (8-10 mg/kg of body weight; 661 participants) or with placebo (624 participants) for 3 years or until follow-up colonoscopy.
Recurrence rates (number of recurrent
adenomas
per unit time) were compared by use of a Huber-White variance estimator.
Proportions of participants with one or more recurrent
adenomas
were compared with a Pearson chi-square statistic; adjusted odds ratios (ORs) were obtained by logistic regression.
RESULTS: We observed a non-statistically significant 12% reduction in the
adenoma
recurrence rate associated with UDCA treatment, compared with placebo treatment.
However, UDCA treatment was associated with a statistically significant reduction (P = .03) in the recurrence of
adenomas
with high-grade dysplasia (adjusted OR = 0.61, 95% confidence interval = 0.39 to 0.96).
We observed no statistically significant differences between UDCA and placebo groups in recurrence with regard to
adenoma
size, villous histology, or location.
CONCLUSIONS: UDCA treatment was associated with a non-statistically significant reduction in total
colorectal
adenoma
recurrence but with a statistically significant 39% reduction in recurrence of
adenomas
with high-grade dysplasia.
Because severely dysplastic lesions have a high risk of progression to invasive
colorectal
carcinoma, this finding indicates that future chemoprevention trials of UDCA in individuals with such lesions should be considered.
[MeSH-major]
Adenoma
/ prevention & control. Antineoplastic Agents / therapeutic use.
Colorectal
Neoplasms / prevention & control. Neoplasm Recurrence, Local / prevention & control. Ursodeoxycholic Acid / therapeutic use
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(PMID = 15928305.001).
[ISSN]
1460-2105
[Journal-full-title]
Journal of the National Cancer Institute
[ISO-abbreviation]
J. Natl. Cancer Inst.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / P01-CA-41108
[Publication-type]
Clinical Trial; Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 724L30Y2QR / Ursodeoxycholic Acid
45.
Wang JY, Wang YH, Jao SW, Lu CY, Kuo CH, Hu HM, Hsieh JS, Chong IW, Cheng TL, Lin SR:
Molecular mechanisms underlying the tumorigenesis of colorectal adenomas: correlation to activated K-ras oncogene.
Oncol Rep
; 2006 Dec;16(6):1245-52
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[Title]
Molecular mechanisms underlying the tumorigenesis of
colorectal adenomas
: correlation to activated K-ras oncogene.
Mutations of K-ras gene have been demonstrated in 40-50% of
colorectal
cancer and
large adenoma
(>1 cm).
This study was intended to clarify the correlation between the existence of K-ras oncogene and the pathological features of
colorectal adenomas
using our recently developed membrane arrays.
Moreover, the downstream genes regulated by K-ras oncogene were explored to serve as potential biomarkers in the early
diagnosis
and risk assessment of patients with
colorectal
adenoma
.
Specimens were collected from 70 patients with
colorectal
adenoma
.
Furthermore, activated K-ras oncogene was identified in 18 of 70 (25.7%)
adenoma
by membrane arrays.
The analysis of the correlation between the experimental data and pathological characteristics
of adenoma
showed that activated K-ras oncogenes were significantly associated with the size, number and histology of
adenomas
(all P<0.001).
Finally, we found the downstream genes activated by K-ras oncogene, including B-cell CLL/lymphoma 2 (BCL2), Homo sapiens H2A histone family, member Z (H2AFZ), Homo sapiens RAP1B, member of RAS oncogene family (RAP1B), Homo sapiens T-box 19 (TBX19), Homo sapiens E2F transcription factor 4, p107/p130-binding (E2F4) and matrix metallopeptidase 1 (MMP1), of which were overexpressed in most of all examined
adenomas
.
Therefore, we propose that activated K-ras oncogene in
colorectal adenomas
may play an important role in the subsequent
colorectal
carcinogenesis through a group of K-ras-related molecular targets.
[MeSH-major]
Adenoma
/ genetics.
Adenoma
/ pathology.
Colorectal
Neoplasms / genetics.
Colorectal
Neoplasms / pathology. Genes, ras
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(PMID = 17089045.001).
[ISSN]
1021-335X
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / DNA Primers
46.
Vinikoor LC, Schroeder JC, Millikan RC, Satia JA, Martin CF, Ibrahim J, Galanko JA, Sandler RS:
Consumption of trans-fatty acid and its association with colorectal adenomas.
Am J Epidemiol
; 2008 Aug 1;168(3):289-97
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[Title]
Consumption of trans-fatty acid and its association with
colorectal adenomas
.
To investigate the association between
colorectal adenomas
and trans-fatty acid consumption, the authors utilized data from a cross-sectional study of 622 individuals who underwent complete colonoscopy between 2001 and 2002 at the University of North Carolina Hospitals.
Participants were interviewed about demographic, lifestyle, and dietary factors thought to be related to
colorectal
cancer. trans-Fatty acid consumption, energy adjusted by the residual method, was categorized into quartiles based on its distribution in controls.
Compared with participants in the lowest quartile of consumption, those in the highest quartile had an increased prevalence of
colorectal adenomas
, with an adjusted prevalence odds ratio of 1.86 (95% confidence interval: 1.04, 3.33).
The authors further investigated the relation between trans-fatty acid consumption and
colorectal
neoplasia by examining the
adenoma
characteristics, with the adjusted prevalence odds ratios showing little or no difference by
adenoma
location, size, or number.
These results suggest that consumption of high amounts of trans-fatty acid may increase the risk of
colorectal
neoplasia, and they provide additional support to recommendations to limit trans-fatty acid consumption.
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[Cites]
Gastroenterology. 2002 Dec;123(6):1770-7
[
12454832.001
]
[Cites]
Gastroenterology. 2007 Jul;133(1):42-7
[
17631129.001
]
[Cites]
N Engl J Med. 2000 Apr 20;342(16):1149-55
[
10770979.001
]
[Cites]
Epidemiology. 2000 Jul;11(4):469-73
[
10874557.001
]
[Cites]
Am J Epidemiol. 2000 Aug 1;152(3):279-86
[
10933275.001
]
[Cites]
Med Sci Sports Exerc. 2000 Sep;32(9 Suppl):S498-504
[
10993420.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2000 Dec;9(12):1271-9
[
11142411.001
]
[Cites]
Ann Epidemiol. 2001 Feb;11(2):145-53
[
11164131.001
]
[Cites]
J Natl Cancer Inst. 2001 Sep 5;93(17):1282-3
[
11535695.001
]
[Cites]
J Nutr. 2001 Nov;131(11 Suppl):3109S-20S
[
11694656.001
]
[Cites]
Nutr Cancer. 2001;39(2):170-5
[
11759276.001
]
[Cites]
Am J Epidemiol. 2001 Dec 15;154(12):1089-99
[
11744511.001
]
[Cites]
J Am Diet Assoc. 2002 Feb;102(2):212-25
[
11846115.001
]
[Cites]
Am J Gastroenterol. 2002 Jun;97(6):1524-9
[
12094877.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1012-8
[
12376501.001
]
[Cites]
Int J Epidemiol. 2003 Apr;32(2):200-9
[
12714537.001
]
[Cites]
Br J Nutr. 2003 May;89(5):631-9
[
12720583.001
]
[Cites]
Fed Regist. 2003 Jul 11;68(133):41433-1506
[
12856667.001
]
[Cites]
Gastroenterology. 2003 Aug;125(2):328-36
[
12891533.001
]
[Cites]
Am J Clin Nutr. 2004 Apr;79(4):606-12
[
15051604.001
]
[Cites]
Can J Surg. 1978 May;21(3):206-8
[
647507.001
]
[Cites]
Am J Epidemiol. 1985 Nov;122(5):794-804
[
3876763.001
]
[Cites]
Am J Epidemiol. 1986 Jul;124(1):17-27
[
3521261.001
]
[Cites]
J Natl Cancer Inst. 1992 Jan 15;84(2):91-8
[
1310511.001
]
[Cites]
Ann Intern Med. 1993 Jan 15;118(2):91-5
[
8416323.001
]
[Cites]
J Nutr. 1993 Nov;123(11):1808-17
[
8229295.001
]
[Cites]
Cancer Causes Control. 1995 Jan;6(1):45-56
[
7718735.001
]
[Cites]
Cancer Res. 1995 Jun 1;55(11):2293-8
[
7757978.001
]
[Cites]
J Natl Cancer Inst. 1995 Dec 6;87(23):1760-6
[
7473832.001
]
[Cites]
Gastroenterology. 1997 Aug;113(2):423-9
[
9247459.001
]
[Cites]
Am J Clin Nutr. 1997 Dec;66(6 Suppl):1564S-1571S
[
9394716.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1999 Jan;8(1):69-75
[
9950242.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1999 Jun;8(6):519-24
[
10385142.001
]
[Cites]
Am J Epidemiol. 2004 Nov 15;160(10):1011-22
[
15522858.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):2059-60
[
16103463.001
]
[Cites]
Am J Gastroenterol. 2005 Dec;100(12):2789-95
[
16393237.001
]
[Cites]
Atheroscler Suppl. 2006 May;7(2):37-9
[
16713388.001
]
[Cites]
Nutr Rev. 2006 Aug;64(8):364-72
[
16958313.001
]
[Cites]
Nutr Clin Pract. 2006 Oct;21(5):505-12
[
16998148.001
]
[Cites]
Am J Clin Nutr. 2006 Nov;84(5):981-8
[
17093147.001
]
[Cites]
J Nutr. 2006 Dec;136(12):3054-61
[
17116719.001
]
[Cites]
CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66
[
17237035.001
]
[Cites]
N Engl J Med. 2007 May 17;356(20):2017-21
[
17507699.001
]
[Cites]
Am J Epidemiol. 2007 Jul 15;166(2):181-95
[
17493949.001
]
[Cites]
N Engl J Med. 2003 Mar 6;348(10):891-9
[
12621133.001
]
(PMID = 18587137.001).
[ISSN]
1476-6256
[Journal-full-title]
American journal of epidemiology
[ISO-abbreviation]
Am. J. Epidemiol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA044684; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NCI NIH HHS / CA / R01CA44684; United States / NIDDK NIH HHS / DK / P30DK34987; United States / NIDDK NIH HHS / DK / T32 DK007634; United States / NIDDK NIH HHS / DK / T32DK07634
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Trans Fatty Acids
[Other-IDs]
NLM/ NIHMS64890; NLM/ PMC2533637
47.
Otani T, Iwasaki M, Ikeda S, Kozu T, Saito H, Mutoh M, Wakabayashi K, Tsugane S:
Serum triglycerides and colorectal adenoma in a case-control study among cancer screening examinees (Japan).
Cancer Causes Control
; 2006 Dec;17(10):1245-52
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[Title]
Serum triglycerides and
colorectal
adenoma
in a case-control study among cancer screening examinees (Japan).
OBJECTIVE: Most epidemiologic studies have shown serum triglycerides to be associated with
colorectal
adenoma
.
We cross-sectionally investigated the association of serum triglycerides with the risk
of adenoma
by smoking status.
METHODS: We identified 782 newly diagnosed
adenoma
cases from the examinees of a
colorectal
cancer screening program.
We determined 738 controls without present illness or past history
of adenoma
from among the examinees.
We calculated odds ratios (OR) and 95% confidence intervals (CI) of
colorectal
adenoma
for serum triglycerides.
RESULTS: High serum triglycerides were associated with
colorectal
adenoma
(OR 1.5; 95% CI 1.1-2.0 for the highest versus the lowest quartile, P (trend, )0.030).
A stronger association was observed between three or more
adenoma
cases and study controls (OR 2.3; 95% CI 1.3-4.2, P (trend,) < 0.0010).
CONCLUSIONS: Our results suggested that a higher serum triglyceride level may be related to a larger number of
adenomas
.
Adenoma
development involving an elevated serum triglyceride level may be modified by smoking.
[MeSH-major]
Adenoma
/ blood.
Adenoma
/
diagnosis
.
Colorectal
Neoplasms / blood.
Colorectal
Neoplasms /
diagnosis
. Mass Screening. Triglycerides / blood
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(PMID = 17111255.001).
[ISSN]
0957-5243
[Journal-full-title]
Cancer causes & control : CCC
[ISO-abbreviation]
Cancer Causes Control
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Triglycerides
48.
Caswell S, Anderson AS, Steele RJ:
Diet and physical activity in patients with colorectal adenomas: directions for intervention programmes.
J Hum Nutr Diet
; 2008 Oct;21(5):494-501
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[Title]
Diet and physical activity in patients with
colorectal adenomas
: directions for intervention programmes.
The aim of the current exploratory research was to identify diet and activity habits in adults diagnosed with
colorectal adenomas
on screening colonoscopy in order to inform the development of an intervention study in this patient group.
[MeSH-major]
Adenoma
/ prevention & control.
Colorectal
Neoplasms / prevention & control. Diet. Exercise
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(PMID = 18631284.001).
[ISSN]
1365-277X
[Journal-full-title]
Journal of human nutrition and dietetics : the official journal of the British Dietetic Association
[ISO-abbreviation]
J Hum Nutr Diet
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Dietary Carbohydrates; 0 / Dietary Fats; 0 / Dietary Proteins
49.
Fujimoto T, Yoshimatsu K, Watanabe K, Yokomizo H, Otani T, Matsumoto A, Osawa G, Onda M, Ogawa K:
Overexpression of human X-box binding protein 1 (XBP-1) in colorectal adenomas and adenocarcinomas.
Anticancer Res
; 2007 Jan-Feb;27(1A):127-31
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[Title]
Overexpression of human X-box binding protein 1 (XBP-1) in
colorectal adenomas
and adenocarcinomas.
To investigate the involvement of XBP-1 in
colorectal
tumorigenecity, the expression of XBP-1 was examined in four colon cancer cell lines, six
colorectal
polyps and five
colorectal
carcinomas.
MATERIALS AND METHODS: The study population consisted of eleven patients who had undergone resection for
colorectal
cancer or
adenoma
from 2000 to 2002.
RESULTS: The XBP-1 gene was overexpressed in four cases out of five primary
colorectal
carcinomas and in four cases out of six
colorectal adenomas
.
[MeSH-major]
Adenocarcinoma / metabolism.
Adenoma
/ metabolism.
Colorectal
Neoplasms / metabolism. DNA-Binding Proteins / biosynthesis. Nuclear Proteins / biosynthesis
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(PMID = 17352224.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / regulatory factor X transcription factors
50.
Greenhough A, Wallam CA, Hicks DJ, Moorghen M, Williams AC, Paraskeva C:
The proapoptotic BH3-only protein Bim is downregulated in a subset of colorectal cancers and is repressed by antiapoptotic COX-2/PGE(2) signalling in colorectal adenoma cells.
Oncogene
; 2010 Jun 10;29(23):3398-410
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[Title]
The proapoptotic BH3-only protein Bim is downregulated in a subset of
colorectal
cancers and is repressed by antiapoptotic COX-2/PGE(2) signalling in
colorectal
adenoma
cells.
Overexpression of cyclooxygenase-2 (COX-2) and elevated levels of its enzymatic product prostaglandin E2 (PGE(2)) occur in the majority of
colorectal
cancers and have important roles in
colorectal
tumorigenesis.
Here, we have shown that PGE(2) suppresses apoptosis via repression of the proapoptotic BH3-only protein Bim in human
colorectal
adenoma
cells.
Reduction of Bim expression using RNA interference reduced spontaneous apoptosis in
adenoma
cells and abrogated PGE(2)-dependent apoptosis suppression.
Treatment of COX-2-expressing
colorectal
carcinoma cells with COX-2-selective NSAIDs-induced Bim expression, suggesting that Bim repression via PGE(2) signalling may be opposed by COX-2 inhibition.
Examination of Bim expression in two established in vitro models of the
adenoma
-carcinoma sequence revealed that downregulation of Bim expression was associated with tumour progression towards an anchorage-independent phenotype.
Finally, immunohistochemical analyses revealed that Bim expression is markedly reduced in approximately 40% of human
colorectal
carcinomas in vivo.
These observations highlight the COX-2/PGE(2) pathway as an important negative regulator of Bim expression in
colorectal
tumours and suggest that Bim repression may be an important step during
colorectal
cancer tumorigenesis.
[MeSH-major]
Adenoma
/ etiology. Apoptosis Regulatory Proteins / physiology.
Colorectal
Neoplasms / etiology. Cyclooxygenase 2 / physiology. Dinoprostone / physiology. Membrane Proteins / physiology. Proto-Oncogene Proteins / physiology. Signal Transduction / physiology
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[Cites]
Nat Cell Biol. 2003 Aug;5(8):733-40
[
12844146.001
]
[Cites]
Oncogene. 2003 Oct 2;22(43):6785-93
[
14555991.001
]
[Cites]
J Biol Chem. 2004 Mar 5;279(10):8837-47
[
14681225.001
]
[Cites]
Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6164-9
[
15079075.001
]
[Cites]
J Biol Chem. 2004 Jul 9;279(28):29797-804
[
15123663.001
]
[Cites]
Cancer Cell. 2004 Sep;6(3):285-95
[
15380519.001
]
[Cites]
Cancer Res. 1989 Mar 1;49(5):1282-6
[
2917357.001
]
[Cites]
Cancer Res. 1990 Aug 1;50(15):4724-30
[
2369746.001
]
[Cites]
Oncogene. 1994 Nov;9(11):3367-70
[
7936663.001
]
[Cites]
J Cell Sci. 1994 Dec;107 ( Pt 12):3569-77
[
7706406.001
]
[Cites]
Cancer Res. 2005 Mar 1;65(5):1822-9
[
15753380.001
]
[Cites]
Oncogene. 2008 Dec 4;27(57):7150-61
[
18806830.001
]
[Cites]
Cell. 2008 Dec 12;135(6):1074-84
[
19062087.001
]
[Cites]
Mol Cell. 2009 Jan 16;33(1):109-16
[
19150432.001
]
[Cites]
Cell Death Differ. 2009 Mar;16(3):368-77
[
18846109.001
]
[Cites]
Carcinogenesis. 2009 Mar;30(3):377-86
[
19136477.001
]
[Cites]
Cell. 2009 Mar 20;136(6):1136-47
[
19303855.001
]
[Cites]
J Cell Biol. 2009 Apr 20;185(2):279-90
[
19380879.001
]
[Cites]
Trends Mol Med. 2009 May;15(5):225-33
[
19362056.001
]
[Cites]
Oncogene. 2010 Feb 11;29(6):781-8
[
19946329.001
]
[Cites]
Science. 1999 Nov 26;286(5445):1735-8
[
10576740.001
]
[Cites]
Cancer Cell. 2005 Mar;7(3):227-38
[
15766661.001
]
[Cites]
N Engl J Med. 2005 Mar 17;352(11):1092-102
[
15713943.001
]
[Cites]
Oncogene. 2005 Mar 31;24(14):2317-29
[
15688014.001
]
[Cites]
J Clin Oncol. 2005 Apr 20;23(12):2840-55
[
15837998.001
]
[Cites]
Cancer Res. 1995 May 1;55(9):1811-6
[
7728743.001
]
[Cites]
Cancer Res. 1996 May 15;56(10):2273-6
[
8625297.001
]
[Cites]
Cancer Res. 1996 May 15;56(10):2422-7
[
8625322.001
]
[Cites]
Biochem Pharmacol. 1996 Jul 26;52(2):237-45
[
8694848.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):681-6
[
9435252.001
]
[Cites]
Nat Med. 1998 Apr;4(4):392-3
[
9546780.001
]
[Cites]
Cell. 1999 Mar 19;96(6):857-68
[
10102273.001
]
[Cites]
Cancer Res. 2004 Nov 15;64(22):8148-51
[
15548677.001
]
[Cites]
Mol Cell. 2005 Feb 4;17(3):393-403
[
15694340.001
]
[Cites]
Oncogene. 2005 Feb 17;24(8):1348-58
[
15608680.001
]
[Cites]
Cell Death Differ. 2005 Aug;12(8):1008-14
[
15947788.001
]
[Cites]
Science. 2005 Dec 2;310(5753):1504-10
[
16293724.001
]
[Cites]
Cancer Res. 2006 Mar 15;66(6):3106-13
[
16540660.001
]
[Cites]
Cancer Cell. 2006 May;9(5):351-65
[
16697956.001
]
[Cites]
Cancer Res. 2006 Jul 1;66(13):6683-91
[
16818642.001
]
[Cites]
Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14907-12
[
16997913.001
]
[Cites]
Cell Death Differ. 2007 Jan;14(1):137-45
[
16645643.001
]
[Cites]
Nat Cell Biol. 2007 Feb;9(2):210-7
[
17220880.001
]
[Cites]
Science. 2007 Feb 9;315(5813):856-9
[
17289999.001
]
[Cites]
Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):3787-92
[
17360431.001
]
[Cites]
Oncogene. 2007 May 10;26(21):3006-19
[
17130837.001
]
[Cites]
EMBO J. 2007 Jun 20;26(12):2856-67
[
17525735.001
]
[Cites]
Cell. 2007 Jun 29;129(7):1337-49
[
17604722.001
]
[Cites]
Int J Cancer. 2007 Nov 15;121(10):2172-80
[
17583570.001
]
[Cites]
Oncogene. 2007 Oct 25;26(49):7038-48
[
17486061.001
]
[Cites]
PLoS Med. 2007 Oct;4(10):1669-79; discussion 1680
[
17973572.001
]
[Cites]
PLoS Med. 2007 Oct;4(10):1681-89; discussion 1690
[
17973573.001
]
[Cites]
PLoS Med. 2007 Oct 9;4(10):e294
[
17927446.001
]
[Cites]
Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59
[
18097445.001
]
[Cites]
Carcinogenesis. 2008 Apr;29(4):849-57
[
18204076.001
]
[Cites]
Oncogene. 2008 Apr 17;27(18):2648-55
[
18059344.001
]
[Cites]
Clin Cancer Res. 2008 Sep 15;14(18):5810-8
[
18794091.001
]
[Cites]
Pigment Cell Melanoma Res. 2008 Oct;21(5):534-44
[
18715233.001
]
[Cites]
Nature. 2008 Oct 23;455(7216):1076-81
[
18948948.001
]
[Cites]
J Clin Invest. 2008 Nov;118(11):3651-9
[
18949058.001
]
[Cites]
Carcinogenesis. 2000 Jan;21(1):69-77
[
10607736.001
]
[Cites]
Cell. 2000 Jan 7;100(1):57-70
[
10647931.001
]
[Cites]
Am J Pathol. 2000 Aug;157(2):449-61
[
10934149.001
]
[Cites]
Curr Biol. 2000 Oct 5;10(19):1201-4
[
11050388.001
]
[Cites]
J Biol Chem. 2001 May 25;276(21):18075-81
[
11278548.001
]
[Cites]
Mol Cell. 2001 Sep;8(3):705-11
[
11583631.001
]
[Cites]
FASEB J. 2001 Dec;15(14):2742-4
[
11606477.001
]
[Cites]
Cell. 2002 Jan 25;108(2):153-64
[
11832206.001
]
[Cites]
Nature. 2002 Jun 27;417(6892):949-54
[
12068308.001
]
[Cites]
Cancer Cell. 2002 Sep;2(3):183-92
[
12242151.001
]
[Cites]
J Pathol. 2002 Dec;198(4):428-34
[
12434411.001
]
[Cites]
Oncogene. 2003 Mar 6;22(9):1281-93
[
12618753.001
]
[Cites]
J Biol Chem. 2003 May 23;278(21):18811-6
[
12646560.001
]
[Cites]
Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8921-6
[
12837940.001
]
(PMID = 20348947.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / A5301; United Kingdom / Cancer Research UK / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / bcl-Associated Death Protein; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex; K7Q1JQR04M / Dinoprostone
[Other-IDs]
NLM/ PMC2883743; NLM/ UKMS28872
51.
Hsu CH, Taylor JM, Long Q, Alberts DS:
Analysis of colorectal adenoma recurrence data subject to informative censoring.
Cancer Epidemiol Biomarkers Prev
; 2009 Mar;18(3):712-7
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[Title]
Analysis of
colorectal
adenoma
recurrence data subject to informative censoring.
The treatment effect of a
colorectal
polyp prevention trial is often evaluated from
the colorectal
adenoma
recurrence status at the end of the trial.
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.
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[Cites]
Br J Surg. 2002 Jul;89(7):845-60
[
12081733.001
]
[Cites]
Gastroenterology. 2003 Feb;124(2):544-60
[
12557158.001
]
[Cites]
Stat Med. 1988 Nov;7(11):1139-45
[
3201039.001
]
[Cites]
Biometrics. 1992 Sep;48(3):951-9
[
1420849.001
]
[Cites]
Stat Med. 1992 Sep 15;11(12):1569-78
[
1439361.001
]
[Cites]
Biometrics. 1996 Mar;52(1):137-51
[
8934589.001
]
[Cites]
J Natl Cancer Inst. 2005 Jun 1;97(11):846-53
[
15928305.001
]
[Cites]
CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30
[
16514137.001
]
[Cites]
Stat Med. 2006 Oct 30;25(20):3503-17
[
16345047.001
]
[Cites]
Stat Med. 2007 Mar 30;26(7):1567-78
[
16850435.001
]
(PMID = 19240239.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / P30 CA023074-30; United States / NCI NIH HHS / CA / CA041108-22; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / CA041108-21; United States / NCI NIH HHS / CA / P30 CA023074-28; None / None / / P30 CA023074-30; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / P01 CA041108-21; United States / NCI NIH HHS / CA / P01 CA041108-22; United States / NCI NIH HHS / CA / CA41108
[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 / Cholagogues and Choleretics; 724L30Y2QR / Ursodeoxycholic Acid
[Other-IDs]
NLM/ NIHMS104698; NLM/ PMC2668929
52.
Bertagnolli MM:
Cox-2 and cancer chemoprevention: picking up the pieces.
Recent Results Cancer Res
; 2007;174:73-8
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The recent reports of cardiovascular adverse events in patients treated with selective Cox-2 inhibitors for
colorectal
adenoma
prevention remind us that all therapies carry risks as well as benefits.
This article will discuss the biologic rationale for using selective Cox-2 inhibitors in cancer chemoprevention, and outline new avenues of research necessary to allow their successful use in patients at risk for
colorectal
cancer.
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(PMID = 17302187.001).
[ISSN]
0080-0015
[Journal-full-title]
Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
[ISO-abbreviation]
Recent Results Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; EC 1.14.99.1 / Cyclooxygenase 2
[Number-of-references]
41
53.
Kang HW, Kim D, Kim HJ, Kim CH, Kim YS, Park MJ, Kim JS, Cho SH, Sung MW, Jung HC, Lee HS, Song IS:
Visceral obesity and insulin resistance as risk factors for colorectal adenoma: a cross-sectional, case-control study.
Am J Gastroenterol
; 2010 Jan;105(1):178-87
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[Title]
Visceral obesity and insulin resistance as risk factors for
colorectal
adenoma
: a cross-sectional, case-control study.
OBJECTIVES:
Colorectal
adenoma
is known to be associated with obesity, but the association between
colorectal
adenoma
and visceral adipose tissue (VAT) area measured by abdominal computed tomography (CT) has not been documented clearly.
In addition, the relationship between insulin resistance and
colorectal adenomas
, which underlies the mechanism that links obesity and
colorectal
adenoma
, has not been studied extensively.
The aim of this study was to examine VAT area and insulin resistance as risk factors of
colorectal
adenoma
.
VAT, subcutaneous adipose tissue (SAT), and homeostatic metabolic assessment (HOMA) index were evaluated as potential risk factors of
colorectal
adenoma
in 2,244 age- and sex-matched subjects.
RESULTS: According to univariate analysis, the prevalences of smoking, hypertension, metabolic syndrome, and family history of
colorectal
cancer were higher in the
adenoma
group than in the normal control group.
According to the multivariate analysis adjusted for multiple confounders, VAT area was independently associated with the risk of
colorectal
adenoma
(odds ratio (OR)=3.09, 95% confidence interval (CI): 2.19-4.36, highest quintile vs. lowest quintile).
Mean HOMA index was higher in the
adenoma
group than in the control group (OR=1.99, 95% CI: 1.35-2.92, highest vs. lowest quintile).
CONCLUSIONS: Visceral obesity was found to be an independent risk factor of
colorectal
adenoma
, and insulin resistance was associated with the presence of
colorectal
adenoma
.
[MeSH-major]
Adenoma
/ etiology.
Colorectal
Neoplasms / etiology. Insulin Resistance. Intra-Abdominal Fat / pathology. Obesity / complications
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.
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[CommentIn]
Am J Gastroenterol. 2010 Jul;105(7):1677
[
20606672.001
]
(PMID = 19755965.001).
[ISSN]
1572-0241
[Journal-full-title]
The American journal of gastroenterology
[ISO-abbreviation]
Am. J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Lipids
54.
Bresalier RS, Sandler RS, Quan H, Bolognese JA, Oxenius B, Horgan K, Lines C, Riddell R, Morton D, Lanas A, Konstam MA, Baron JA, Adenomatous Polyp Prevention on Vioxx (APPROVe) Trial Investigators:
Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial.
N Engl J Med
; 2005 Mar 17;352(11):1092-102
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[Title]
Cardiovascular events associated with rofecoxib in a
colorectal
adenoma
chemoprevention trial.
We report on the cardiovascular outcomes associated with the use of the selective COX-2 inhibitor rofecoxib in a long-term, multicenter, randomized, placebo-controlled, double-blind trial designed to determine the effect of three years of treatment with rofecoxib on the risk of recurrent neoplastic polyps of the
large
bowel
in patients with a history of
colorectal adenomas
.
METHODS: A total of 2586 patients with a history of
colorectal adenomas
underwent randomization: 1287 were assigned to receive 25 mg of rofecoxib daily, and 1299 to receive placebo.
CONCLUSIONS: Among patients with a history of
colorectal adenomas
, the use of rofecoxib was associated with an increased cardiovascular risk.
[MeSH-major]
Adenomatous Polyps / prevention & control. Cardiovascular Diseases / chemically induced.
Colorectal
Neoplasms / prevention & control. Cyclooxygenase Inhibitors / adverse effects. Lactones / adverse effects. Sulfones / adverse effects. Thrombosis / chemically induced
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meta-databases - Pharmacogenomic Annotation 827850865 for PMID:15713943 [PharmGKB]
.
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.
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.
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Cited by Patents in
.
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[Copyright]
Copyright 2005 Massachusetts Medical Society.
[CommentIn]
N Engl J Med. 2006 Jul 13;355(2):203-4; author reply 203-5
[
16801355.001
]
[CommentIn]
N Engl J Med. 2006 Jul 13;355(2):204; author reply 204-5
[
16838442.001
]
[CommentIn]
N Engl J Med. 2006 Jul 13;355(2):113-7
[
16801354.001
]
[CommentIn]
N Engl J Med. 2005 Mar 17;352(11):1133-5
[
15713946.001
]
[CommentIn]
ACP J Club. 2005 Jul-Aug;143(1):2
[
15989290.001
]
[CommentIn]
N Engl J Med. 2005 Mar 17;352(11):1131-2
[
15713947.001
]
[ErratumIn]
N Engl J Med. 2006 Jul 13;355(2):221
(PMID = 15713943.001).
[ISSN]
1533-4406
[Journal-full-title]
The New England journal of medicine
[ISO-abbreviation]
N. Engl. J. Med.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 0 / Lactones; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; R16CO5Y76E / Aspirin
55.
Bresalier RS:
Chemoprevention of colorectal cancer: why all the confusion?
Curr Opin Gastroenterol
; 2008 Jan;24(1):48-50
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[Title]
Chemoprevention of
colorectal
cancer: why all the confusion?
PURPOSE OF REVIEW: Chemoprevention provides an opportunity to complement screening for the prevention of
colorectal
neoplasia.
RECENT FINDINGS: A recent prospective randomized trial demonstrates that folic acid supplementation in patients with a previous history of
colorectal adenomas
does not reduce future
colorectal
adenoma
risk, and may possibly increase the risk of
colorectal
neoplasia.
[MeSH-major]
Colorectal
Neoplasms / prevention & control. Diet. Folic Acid / pharmacology
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.
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FOLIC ACID
.
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CALCIUM, ELEMENTAL
.
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(PMID = 18043232.001).
[ISSN]
1531-7056
[Journal-full-title]
Current opinion in gastroenterology
[ISO-abbreviation]
Curr. Opin. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 935E97BOY8 / Folic Acid; SY7Q814VUP / Calcium
[Number-of-references]
13
56.
Taylor JC, Kendall CA, Stone N, Cook TA:
Optical adjuncts for enhanced colonoscopic diagnosis.
Br J Surg
; 2007 Jan;94(1):6-16
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[Title]
Optical adjuncts for enhanced colonoscopic
diagnosis
.
BACKGROUND: Optical techniques using previously unexploited properties of light interaction with tissue may be valuable in the detection,
diagnosis
and staging of
colorectal
neoplasia.
METHODS: A Medline search (1990 to present) was conducted on optical diagnostics in the detection of
colorectal
neoplasia.
RESULTS AND CONCLUSION: Chromoendoscopy is the only optical adjunct to colonoscopy that has been tested in
large
randomized clinical trials.
It improves the detection of small and flat
colorectal adenomas
, and of neoplasia in chronic ulcerative colitis and hereditary non-polyposis
colorectal
cancer.
Optical techniques may, however, permit immediate clinical
diagnosis
, removing the need for histological analysis.
They may also improve
the diagnosis
of early colonic neoplasia.
[MeSH-major]
Colonoscopy / methods.
Colorectal
Neoplasms /
diagnosis
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[Copyright]
Copyright 2007 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
(PMID = 17205497.001).
[ISSN]
0007-1323
[Journal-full-title]
The British journal of surgery
[ISO-abbreviation]
Br J Surg
[Language]
eng
[Grant]
United Kingdom / Department of Health / / CSA/03/07/017
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
87
57.
Wang J, Wang X, Gong W, Mi B, Liu S, Jiang B:
Increased expression of beta-catenin, phosphorylated glycogen synthase kinase 3beta, cyclin D1, and c-myc in laterally spreading colorectal tumors.
J Histochem Cytochem
; 2009 Apr;57(4):363-71
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[Title]
Increased expression of beta-catenin, phosphorylated glycogen synthase kinase 3beta, cyclin D1, and c-myc in laterally spreading
colorectal
tumors.
Laterally spreading tumors (LSTs) are considered a special subtype of superficial
colorectal
tumor.
This study was performed to characterize the clinicopathological features and examine activation of the Wnt/beta-catenin pathway in LSTs and protruded-type
colorectal adenomas
(PAs).
[MeSH-major]
Colorectal
Neoplasms / metabolism. Cyclin D1 / biosynthesis. Glycogen Synthase Kinase 3 / biosynthesis. Proto-Oncogene Proteins c-myc / biosynthesis. beta Catenin / biosynthesis
[MeSH-minor]
Adenoma
/ metabolism.
Adenoma
/ pathology. Biomarkers, Tumor / biosynthesis. Humans. Immunohistochemistry. Phosphorylation
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[Cites]
Cancer Res. 2000 Jul 1;60(13):3323-7
[
10910031.001
]
[Cites]
Histopathology. 2008 Apr;52(5):569-77
[
18370954.001
]
[Cites]
Gastrointest Endosc. 2001 Jul;54(1):62-6
[
11427843.001
]
[Cites]
J Gastroenterol Hepatol. 2001 Jul;16(7):770-6
[
11446885.001
]
[Cites]
Nat Rev Cancer. 2001 Oct;1(1):55-67
[
11900252.001
]
[Cites]
Br J Cancer. 2002 Apr 8;86(7):1124-9
[
11953860.001
]
[Cites]
Virchows Arch. 2002 May;440(5):453-60
[
12021919.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8683-8
[
12072559.001
]
[Cites]
Cell. 2002 Oct 18;111(2):241-50
[
12408868.001
]
[Cites]
J Gastroenterol Hepatol. 2002 Dec;17(12):1344-5
[
12423287.001
]
[Cites]
Dig Liver Dis. 2003 Mar;35(3):165-71
[
12779070.001
]
[Cites]
Biochim Biophys Acta. 2003 Jun 5;1653(1):1-24
[
12781368.001
]
[Cites]
Cancer Cell. 2004 Jan;5(1):5-6
[
14749120.001
]
[Cites]
Endoscopy. 2004 Apr;36(4):306-12
[
15057679.001
]
[Cites]
Cell. 1990 Jun 1;61(5):759-67
[
2188735.001
]
[Cites]
Endoscopy. 1993 Sep;25(7):455-61
[
8261988.001
]
[Cites]
Oncology. 1996 Mar-Apr;53(2):89-93
[
8604246.001
]
[Cites]
Science. 1998 Sep 4;281(5382):1438-9, 1441
[
9750112.001
]
[Cites]
Biochem Biophys Res Commun. 2005 Sep 9;334(4):1365-73
[
16043125.001
]
[Cites]
Gut. 2005 Oct;54(10):1504-5
[
16162961.001
]
[Cites]
J Gastroenterol Hepatol. 2005 Oct;20(10):1584-90
[
16174078.001
]
[Cites]
J Pathol. 2006 Jan;208(1):91-9
[
16278819.001
]
[Cites]
Gastrointest Endosc. 2006 Jan;63(1):178-83
[
16377346.001
]
[Cites]
Br J Cancer. 2006 Jan 30;94(2):311-7
[
16404419.001
]
[Cites]
J Gastroenterol. 2006 Apr;41(4):325-31
[
16741611.001
]
[Cites]
Gastroenterology. 2006 Aug;131(2):379-89
[
16890591.001
]
[Cites]
Cancer Lett. 2006 Sep 28;241(2):203-12
[
16298038.001
]
[Cites]
Eur J Cancer. 2006 Nov;42(17):3065-72
[
17011185.001
]
[Cites]
Oncogene. 2006 Dec 4;25(57):7531-7
[
17143297.001
]
[Cites]
Mod Pathol. 2007 Jan;20(1):139-47
[
17143260.001
]
[Cites]
J Gastroenterol Hepatol. 2007 Jan;22(1):30-6
[
17201877.001
]
[Cites]
Curr Opin Cell Biol. 2007 Apr;19(2):150-8
[
17306971.001
]
[Cites]
Mol Carcinog. 2008 Jan;47(1):1-8
[
17620311.001
]
[Cites]
Int J Cancer. 2001 May 20;95(3):194-7
[
11307154.001
]
(PMID = 19064714.001).
[ISSN]
0022-1554
[Journal-full-title]
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
[ISO-abbreviation]
J. Histochem. Cytochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / beta Catenin; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
[Other-IDs]
NLM/ PMC2664982
58.
Arslan N, Dehdashti F, Siegel BA:
FDG uptake in colonic villous adenomas.
Ann Nucl Med
; 2005 Jun;19(4):331-4
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[Title]
FDG uptake in colonic villous
adenomas
.
Colonic
adenomas
constitute 70-80% of all
colorectal
polyps, and their clinical significance relates primarily to their relationship with
colorectal
cancer.
The malignant potential of the polyps detected by FDG-PET is unknown, as not all the colonic lesions identified by FDG-PET represent
colorectal
malignancies.
The purpose of this study was to investigate the rate of FDG-PET positivity within colonic villous
adenomas
.
A pathology database search was performed to identify all patients diagnosed with colonic villous
adenoma
between June 1, 1996 and December 1, 2000.
Patients with a pathologic
diagnosis
of colonic villous
adenoma
and who also had a FDG-PET study up to 1 month before colonoscopy were included in this study.
Of more than 4,000 patients, six patients were diagnosed with colonic
adenoma
on subsequent colonoscopy following FDG-PET study.
Based on the pathological findings, these 6 patients had a total of 2 villous and 9 tubulovillous
adenomas
.
Five of the 6 patients showed foci of increased FDG uptake in the region of the colon that corresponded to the villous
adenoma
(s) detected on colonoscopy, which accounted for a true-positive rate of 83.3% (5/6 subjects).
Focal lesions in the colon seen on FDG-PET examinations need to be investigated further, even though some of these will prove to be villous
adenomas
rather than
colorectal
carcinomas.
[MeSH-major]
Adenoma
, Villous / radionuclide imaging.
Colorectal
Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18 / pharmacokinetics. Positron-Emission Tomography / methods
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(PMID = 16097645.001).
[ISSN]
0914-7187
[Journal-full-title]
Annals of nuclear medicine
[ISO-abbreviation]
Ann Nucl Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
59.
Li ZX, Zeng SD, Liu YD, Liao YJ, Hua WF, Lin F, Xie D:
[Clinicopathological significance of expression and amplification of P21-activated kinase 1 gene in colorectal carcinoma].
Zhonghua Wei Chang Wai Ke Za Zhi
; 2009 Mar;12(2):185-8
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[Title]
[Clinicopathological significance of expression and amplification of P21-activated kinase 1 gene in
colorectal
carcinoma].
OBJECTIVE: To investigate the clinicopathological value of the expression and amplification of P21-activated kinase 1 gene (PAK1) in
colorectal
carcinoma(CRC).
METHODS: Immunohistochemistry (IHC), fluorescence in situ hybridization (FISH) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling(TUNEL) methods were used to examine the protein expression, amplification of PAK1 and cell apoptosis in 80 cases of CRC and 30 cases of
colorectal
adenoma
by tissue microarray.
RESULTS: IHC showed an overexpression of PAK1 protein in 26% of
colorectal adenomas
and 62% of CRCs.
CONCLUSIONS: Overexpression of PAK1 protein may play an important role in development and progression of
colorectal
neoplasms and it is closely associated with the malignant histological and invasive phenotype of CRCs.
[MeSH-major]
Colorectal
Neoplasms / genetics.
Colorectal
Neoplasms / pathology. p21-Activated Kinases / genetics
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(PMID = 19296259.001).
[ISSN]
1671-0274
[Journal-full-title]
Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery
[ISO-abbreviation]
Zhonghua Wei Chang Wai Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
EC 2.7.11.1 / PAK1 protein, human; EC 2.7.11.1 / p21-Activated Kinases
60.
Boutron-Ruault MC, Marteau P, Lavergne-Slove A, Myara A, Gerhardt MF, Franchisseur C, Bornet F, Eripolyp Study Group:
Effects of a 3-mo consumption of short-chain fructo-oligosaccharides on parameters of colorectal carcinogenesis in patients with or without small or large colorectal adenomas.
Nutr Cancer
; 2005;53(2):160-8
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[Title]
Effects of a 3-mo consumption of short-chain fructo-oligosaccharides on parameters of
colorectal
carcinogenesis in patients with or without small or
large
colorectal adenomas
.
Intervention studies of
colorectal
adenoma
recurrence have demonstrated the need for surrogate markers of the cancer risk.
We investigated differences in biological markers between
adenoma
and
adenoma
-free subjects, before and after 3 mo of daily intake of 10 g sc-FOS, within a multicenter study.
After a full colonoscopy, 3 groups were studied at baseline and after 3 mo: 26 subjects with small
colorectal
adenoma
(s), 18 with
large adenoma
(s), and 30 with no
adenoma
.
At baseline, the mean fecal butyrate concentration was significantly lower in the
adenoma
groups than in the
adenoma
-free group (12.01 +/- 5.08 vs. 17.28 +/- 7.34 mmol/g dry weight) but was significantly increased in that group after 3-mo ingestion of sc-FOS (15.7 +/- 8.0 mmol/g; P = 0.02).
In subjects without
adenoma
, sc-FOS ingestion was associated with a decrease in fecal lithocholic acid (P = 0.02) and an increase in cholic acid (P = 0.02), chenodeoxycholic acid (P = 0.04), total primary bile acids (P = 0.03), and ursodeoxycholic acid (P = 0.05).
In subjects with and without
adenoma
, sc-FOS affects some aspects of the colonic environment, which may be involved in prevention of
colorectal
neoplasia.
[MeSH-major]
Adenoma
/ drug therapy.
Colorectal
Neoplasms / drug therapy. Feces / chemistry. Oligosaccharides / pharmacology
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.
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(PMID = 16573377.001).
[ISSN]
0163-5581
[Journal-full-title]
Nutrition and cancer
[ISO-abbreviation]
Nutr Cancer
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Bile Acids and Salts; 0 / Biomarkers; 0 / Butyrates; 0 / Oligosaccharides; 0 / fructooligosaccharide; 724L30Y2QR / Ursodeoxycholic Acid
61.
Mroczko B, Groblewska M, Wereszczynska-Siemiatkowska U, Kedra B, Konopko M, Szmitkowski M:
The diagnostic value of G-CSF measurement in the sera of colorectal cancer and adenoma patients.
Clin Chim Acta
; 2006 Sep;371(1-2):143-7
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[Title]
The diagnostic value of G-CSF measurement in the sera of
colorectal
cancer and
adenoma
patients.
Cancer cells, including
colorectal
cancer, can produce this cytokine.
The aim of this study was to compare the diagnostic value of measurement of G-CSF and classic tumor markers--carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA 19-9) in the sera of
colorectal
cancer with
adenoma
patients and to determine its usefulness in
the diagnosis
of
colorectal
cancer and polyps.
PATIENTS AND METHODS: The serum levels of G-CSF and tumor markers were assayed in 76
colorectal
cancer, 35
colorectal
adenoma
patients and in 65 healthy subjects.
RESULTS: Median values of G-CSF and tumor markers were significantly higher in
colorectal
cancer patients than those in healthy subjects.
There were significant differences in the serum levels of G-CSF between
adenoma
patients and healthy subjects.
The concentrations of tumor markers in
colorectal
cancer patients were higher than those in polyps.
Combined use of G-CSF with CEA improved their diagnostic sensitivity in
colorectal
cancer.
CONCLUSIONS: Measurement of G-CSF might be useful in
the diagnosis
of
colorectal
cancer patients, but not in the differentiation between
colorectal
cancer and polyps.
[MeSH-major]
Adenoma
/
diagnosis
. Biomarkers, Tumor / blood.
Colorectal
Neoplasms /
diagnosis
. Granulocyte Colony-Stimulating Factor / blood
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(PMID = 16603145.001).
[ISSN]
0009-8981
[Journal-full-title]
Clinica chimica acta; international journal of clinical chemistry
[ISO-abbreviation]
Clin. Chim. Acta
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Biomarkers, Tumor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
62.
Baron JA:
Statins and the colorectum: hope for chemoprevention?
Cancer Prev Res (Phila)
; 2010 May;3(5):573-5
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This perspective on Bertagnolli et al. (beginning on p. 588 in this issue of the journal) and Lipkin et al. (beginning on p. 597) considers the likelihood that statins have chemopreventive efficacy in the
large
bowel
.
An observational analysis within a clinical trial of celecoxib found no benefit of statin use on the risk of
colorectal adenomas
(and some suggestions of an adverse effect).
On the other hand, variation in the 3-hydroxy-3-methylglutaryl coenzyme A reductase gene modified the association of statins with risk of
colorectal
cancer.
[MeSH-major]
Chemoprevention / methods.
Colorectal
Neoplasms / prevention & control. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use
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.
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[CommentOn]
Cancer Prev Res (Phila). 2010 May;3(5):588-96
[
20403998.001
]
[CommentOn]
Cancer Prev Res (Phila). 2010 May;3(5):597-603
[
20403997.001
]
(PMID = 20403999.001).
[ISSN]
1940-6215
[Journal-full-title]
Cancer prevention research (Philadelphia, Pa.)
[ISO-abbreviation]
Cancer Prev Res (Phila)
[Language]
eng
[Publication-type]
Comment; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Anticholesteremic Agents; 0 / Antineoplastic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors
[Number-of-references]
27
63.
Kloor M, Michel S, Buckowitz B, Rüschoff J, Büttner R, Holinski-Feder E, Dippold W, Wagner R, Tariverdian M, Benner A, Schwitalle Y, Kuchenbuch B, von Knebel Doeberitz M:
Beta2-microglobulin mutations in microsatellite unstable colorectal tumors.
Int J Cancer
; 2007 Jul 15;121(2):454-8
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[Title]
Beta2-microglobulin mutations in microsatellite unstable
colorectal
tumors.
MSI-H cancers may develop either sporadically or in the context of the hereditary nonpolyposis
colorectal
cancer (HNPCC) syndrome that is caused by germline mutations of MMR genes.
In
colorectal
cancer (CRC), MSI-H is characterized by a dense lymphocytic infiltration, reflecting a high immunogenicity of these cancers.
To examine the implications of beta2m mutations during MSI-H
colorectal
tumor development, we analyzed the prevalence of beta2m mutations in MSI-H
colorectal adenomas
(n=38) and carcinomas (n=104) of different stages.
Mutations were observed in 6/38 (15.8%) MSI-H
adenomas
and 29/104 (27.9%) MSI-H CRCs.
The high frequency of beta2m mutations in HNPCC-associated MSI-H CRCs is in line with the hypothesis that immunoselection may be particularly pronounced in HNPCC patients with inherited predisposition to develop MSI-H cancers. beta2m mutations were positively related to stage in tumors without distant metastases (UICC I-III), suggesting that loss of beta2m expression may promote local progression of
colorectal
MSI-H tumors.
[MeSH-major]
Colorectal
Neoplasms / pathology. Microsatellite Repeats / genetics. Mutation. beta 2-Microglobulin / genetics
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 17373663.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / beta 2-Microglobulin; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
64.
Ulrich CM, Whitton J, Yu JH, Sibert J, Sparks R, Potter JD, Bigler J:
PTGS2 (COX-2) -765G > C promoter variant reduces risk of colorectal adenoma among nonusers of nonsteroidal anti-inflammatory drugs.
Cancer Epidemiol Biomarkers Prev
; 2005 Mar;14(3):616-9
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[Title]
PTGS2 (COX-2) -765G > C promoter variant reduces risk of
colorectal
adenoma
among nonusers of nonsteroidal anti-inflammatory drugs.
For
colorectal
adenoma
, odds ratios (OR) compared with PTGS2 -765GG as reference were GC 1.00 [95% confidence interval (95% CI), 0.74-1.35] and CC 0.53 (95% CI, 0.22-1.28).
Among nonusers of aspirin or other NSAIDs, the CC genotype conferred a significant decrease in risk
of adenoma
(OR, 0.26; 95% CI, 0.07-0.89).
Use of aspirin or other NSAIDs reduced risk
of adenoma
only among those with the -765GG (wild type) and possibly -765CG genotypes (OR, 0.66; 95% CI, 0.48-0.92 and OR, 0.64; 95% CI, 0.40-1.02, respectively).
These data suggest that COX-2 expression or activity may be beneficially suppressed, and risk of
colorectal
polyps reduced, by aspirin or other NSAIDs in PTGS2 -765GG (wild type) individuals and by the -765 CC variant genotype in nonusers of NSAIDs.
[MeSH-major]
Adenoma
/ genetics.
Adenoma
/ prevention & control.
Colorectal
Neoplasms / genetics.
Colorectal
Neoplasms / prevention & control. Peroxidases / genetics. Polymorphism, Genetic. Prostaglandin-Endoperoxide Synthases / genetics
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[ErratumIn]
Cancer Epidemiol Biomarkers Prev. 2005 Dec;14(12):3020
(PMID = 15767339.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01CA59045; United States / NCI NIH HHS / CA / R01CA89445
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Membrane Proteins; EC 1.11.1.- / Peroxidases; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
65.
Cai H, Dong RZ, Wu JH, Zhu HY, Wang YN, Shi YQ, Mo SJ:
[Clinical analysis of 168 cases of multiple primary colorectal carcinoma].
Zhonghua Wai Ke Za Zhi
; 2008 Mar 1;46(5):370-4
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[Title]
[Clinical analysis of 168 cases of multiple primary
colorectal
carcinoma].
OBJECTIVE: To study the incidence rate of multiple primary
colorectal
carcinomas (MPCC) in
colorectal
carcinoma and to evaluate its clinical and pathological characteristics.
METHODS: One hundred and sixty-eight (4.6%) patients from 3663 cases with
colorectal
carcinoma were diagnosed with MPCC from January 1985 to December 2003.
The clinical data of the patients were collected retrospectively to investigate
the diagnosis
and treatment of MPCC.
RESULTS: Of the 168 patients, 81 were diagnosed as synchronous
colorectal
carcinoma (SC), 72 with metachronous
colorectal
carcinoma (MC), 15 with both SC and MC.
The median age at time of
diagnosis
of
colorectal
carcinoma was 58 years old (range from 20 to 82 years old).
Eighteen cases (10.7%) were verified with hereditary non-polyposis
colorectal
cancer (HNPCC) while another 9 cases were highly suspected.
Fourteen patients (8.3%) were found with other malignancies out
of large intestine
, 41 patients (24.4%) with
colorectal adenomas
, 72 (42.9%) with
adenoma
carcinogenesis.
Among the 96 SC patients, 91 were given preoperative colonoscopy and 65 (71.4%) got
the diagnosis
.
CONCLUSIONS: MPCC should be paid more attention in
colorectal
cancer management.
Colonoscopic surveillance is much more important in
diagnosis
and follow-up of MPCC for reducing the misdiagnosis of SC and detecting more MC in time.
Prompt treatment
of adenoma
can reduce the occurrence of MPCC, and active and standard surgical treatment should be done for MPCC.
[MeSH-major]
Colorectal
Neoplasms. Neoplasms, Multiple Primary
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(PMID = 18785535.001).
[ISSN]
0529-5815
[Journal-full-title]
Zhonghua wai ke za zhi [Chinese journal of surgery]
[ISO-abbreviation]
Zhonghua Wai Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
66.
Moreira LR, Schenka AA, Filho PL, Lima CS, Trevisan MA, Vassallo J:
Comparison of blood neoangiogenesis and lymphatic vascularization in colorectal adenomas from patients with and without concomitant colorectal cancer.
Braz J Med Biol Res
; 2009 Jul;42(7):593-8
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[Title]
Comparison of blood neoangiogenesis and lymphatic vascularization in
colorectal adenomas
from patients with and without concomitant
colorectal
cancer.
Most
colorectal
carcinomas develop from
adenomas
(
adenoma
-carcinoma sequence) in a process due to accumulation of molecular genetic alterations.
Adenomas
from patients with carcinoma showed significantly higher values of total vascular area determined by immunostaining for CD105 (cutoff value = 4386 microm(2); P = 0.019) and of lymphatic microvessel density determined by immunostaining with D2-40 (cutoff value = 11.5; P = 0.041) when compared with those from patients without cancer.
The present data indicate a significant increase in blood microvascular area and in lymphatic microvascular counts in
adenomas
removed from patients with cancer.
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(PMID = 19466284.001).
[ISSN]
1414-431X
[Journal-full-title]
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
[ISO-abbreviation]
Braz. J. Med. Biol. Res.
[Language]
ENG
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Brazil
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 0 / Biomarkers; 0 / ENG protein, human; 0 / Receptors, Cell Surface; 0 / monoclonal antibody D2-40
67.
Rowan A, Halford S, Gaasenbeek M, Kemp Z, Sieber O, Volikos E, Douglas E, Fiegler H, Carter N, Talbot I, Silver A, Tomlinson I:
Refining molecular analysis in the pathways of colorectal carcinogenesis.
Clin Gastroenterol Hepatol
; 2005 Nov;3(11):1115-23
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[Title]
Refining molecular analysis in the pathways of
colorectal
carcinogenesis.
BACKGROUND & AIMS: In the stepwise model, specific genetic and epigenetic changes accumulate as
colorectal adenomas
progress to carcinomas (CRCs).
[MeSH-major]
Carcinoma / genetics.
Colorectal
Neoplasms / genetics
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(PMID = 16271343.001).
[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
68.
Martínez ME, Jacobs ET, Ashbeck EL, Sinha R, Lance P, Alberts DS, Thompson PA:
Meat intake, preparation methods, mutagens and colorectal adenoma recurrence.
Carcinogenesis
; 2007 Sep;28(9):2019-27
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[Title]
Meat intake, preparation methods, mutagens and
colorectal
adenoma
recurrence.
Red meat intake has been shown to be associated with higher risk of
colorectal
cancer.
We prospectively assessed the relation between type of meat, meat preparation method, doneness, a metric of HCAs and other mutagens and
colorectal
adenoma
recurrence among 869 participants in a chemoprevention trial of ursodeoxycholic acid.
Most meat variables assessed were positively but weakly associated with recurrence of any
adenoma
.
In contrast, recurrence of advanced or multiple
adenomas
was more strongly associated with a number of the meat exposure variables evaluated.
Significant positive associations were shown for recurrence of multiple
adenomas
and the following variables: processed meat (OR = 1.83; 95% CI = 1.10-3.04), pan-fried red meat (OR = 1.63; 95% CI = 1.01-2.61), well/very well done red meat (OR = 1.68; 95% CI = 1.03-2.74), 2-amino-3,4,8-trimethylimidazo[4,5,-f]quinoxaline (OR = 1.74; 95% CI = 1.07-2.82) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (OR = 1.68; 95% CI = 1.03-2.75).
[MeSH-major]
Adenoma
/ epidemiology.
Colorectal
Neoplasms / epidemiology. Cooking / methods. Meat / analysis. Mutagens / analysis
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(PMID = 17690112.001).
[ISSN]
0143-3334
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / CA-41108; United States / NCI NIH HHS / CA / CA106269; United States / NCI NIH HHS / CA / CA95060
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / Mutagens; 724L30Y2QR / Ursodeoxycholic Acid
69.
Heitman SJ, Ronksley PE, Hilsden RJ, Manns BJ, Rostom A, Hemmelgarn BR:
Prevalence of adenomas and colorectal cancer in average risk individuals: a systematic review and meta-analysis.
Clin Gastroenterol Hepatol
; 2009 Dec;7(12):1272-8
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[Title]
Prevalence of
adenomas
and
colorectal
cancer in average risk individuals: a systematic review and meta-analysis.
BACKGROUND & AIMS: There is an extensive yet inconsistent body of literature reporting on the prevalence of adenomatous polyps (
adenomas
) and
colorectal
cancer among average risk individuals.
The objectives of our study were to determine the pooled prevalence of
adenomas
and
colorectal
cancer, as well as nonadvanced and advanced
adenomas
, among average risk North Americans.
Two reviewers independently selected cross-sectional studies reporting
adenoma
and
colorectal
cancer prevalence rates in average risk individuals and assessed studies for inclusion and quality, and extracted the data for analysis.
Pooled
adenoma
and
colorectal
cancer prevalence rates were estimated using fixed and random effects models.
RESULTS: Based on 18 included studies, the pooled prevalence of
adenomas
,
colorectal
cancer, nonadvanced
adenomas
, and advanced
adenomas
was 30.2%, 0.3%, 17.7%, and 5.7%, respectively.
Heterogeneity was observed in the pooled prevalence rates for overall
adenomas
, advanced
adenomas
, and
colorectal
cancer and was explained by the mean age (> or = 65 years vs < 65 years) with older cohorts reporting higher prevalence rates.
CONCLUSIONS: The high prevalence of advanced
adenomas
and
colorectal
cancer, especially among older screen-eligible individuals, provides impetus for expanding
colorectal
cancer screening programs.
[MeSH-major]
Adenoma
/ epidemiology.
Colorectal
Neoplasms / epidemiology
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(PMID = 19523536.001).
[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]
Canada / Canadian Institutes of Health Research / /
[Publication-type]
Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
40
70.
Cao J, Chen XP, Li WL, Xia J, Du H, Tang WB, Wang H, Chen XW, Xiao HQ, Li YY:
Decreased fragile histidine triad expression in colorectal cancer and its association with apoptosis inhibition.
World J Gastroenterol
; 2007 Feb 21;13(7):1018-26
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The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
[Title]
Decreased fragile histidine triad expression in
colorectal
cancer and its association with apoptosis inhibition.
AIM: To detect the expression of fragile histidine triad (FHIT) in normal
colorectal
tissue,
colorectal
adenoma
and
colorectal
cancer (CRC) tissue, and to analyze its relationship with the clinicopathological features of CRC, and apoptosis-associated proteins (Bcl-2, Bax, survivin) and apoptosis in
colorectal
cancer.
Tissue microarray (TMA) was established to detect the expression of FHIT, Bcl-2, Bax and survivin genes in 80 CRC tissue specimens, 16
colorectal
adenoma
tissue specimens and 16 hemorrhoid (PPH) tissue specimens during the same period of time as the control.
RESULTS: Ten out of 26 (38.5%) CRC tissue specimens expressed aberrant FHIT transcripts, none of the aberrant FHIT transcripts was observed in the matched normal tissue and
colorectal
adenoma
tissue by nested RT-PCR assay.
The positive rate of FHIT gene expression in normal
colorectal
tissue,
colorectal
adenoma
and carcinoma tissue was 93.75%, 68.75% and 46.25%, respectively.
CONCLUSION: The FHIT gene plays an important role in the regulation of apoptosis and decreased FHIT expression plays a key role in the initiation and progression of
colorectal
carcinoma.
[MeSH-major]
Acid Anhydride Hydrolases / metabolism. Adenocarcinoma / metabolism.
Adenoma
/ metabolism. Apoptosis / physiology.
Colorectal
Neoplasms / metabolism. Neoplasm Proteins / metabolism
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[Cites]
Cancer Res. 2000 Jan 1;60(1):18-21
[
10646844.001
]
[Cites]
Neoplasia. 2005 Aug;7(8):741-7
[
16207476.001
]
[Cites]
Scand J Gastroenterol. 2000 Jun;35(6):637-41
[
10912665.001
]
[Cites]
Mol Med. 2001 Jul;7(7):442-53
[
11683369.001
]
[Cites]
Oncogene. 2003 Nov 24;22(53):8581-9
[
14634620.001
]
[Cites]
J Cell Biol. 1994 Jan;124(1-2):1-6
[
8294493.001
]
[Cites]
Cell. 1995 Jan 27;80(2):285-91
[
7834748.001
]
[Cites]
Cell. 1996 Feb 23;84(4):587-97
[
8598045.001
]
[Cites]
Cancer Res. 1996 Jul 1;56(13):2936-9
[
8674044.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9770-5
[
8790406.001
]
[Cites]
Cancer Res. 1997 Feb 1;57(3):504-12
[
9012482.001
]
[Cites]
Hum Mol Genet. 1997 Feb;6(2):193-203
[
9063739.001
]
[Cites]
Cancer Res. 1997 May 15;57(10):1981-5
[
9157994.001
]
[Cites]
Cancer Res. 1997 Jun 1;57(11):2121-3
[
9187107.001
]
[Cites]
Biochim Biophys Acta. 1997 Jun 7;1332(3):M65-70
[
9196019.001
]
[Cites]
Jpn J Cancer Res. 1997 Apr;88(4):385-8
[
9197530.001
]
[Cites]
Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13771-6
[
9391102.001
]
[Cites]
Nat Med. 1998 Jul;4(7):844-7
[
9662379.001
]
[Cites]
Cell. 1999 Jan 22;96(2):245-54
[
9988219.001
]
[Cites]
Cancer Res. 1999 Aug 15;59(16):3866-9
[
10463571.001
]
[Cites]
J Clin Oncol. 2005 Jan 10;23(2):378-91
[
15637400.001
]
[Cites]
World J Gastroenterol. 2005 Aug 14;11(30):4685-8
[
16094710.001
]
[Cites]
Cancer Res. 2000 Apr 1;60(7):1949-60
[
10766185.001
]
(PMID = 17373735.001).
[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]
0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; 0 / fragile histidine triad protein; EC 3.6.- / Acid Anhydride Hydrolases
[Other-IDs]
NLM/ PMC4146863
71.
Sun Y, Tian H, Xiao FM, Xie XY, Song YG:
[PI3K p85alpha expression and its role in the progression of colorectal cancer].
Nan Fang Yi Ke Da Xue Xue Bao
; 2009 Mar;29(3):416-8
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[Title]
[PI3K p85alpha expression and its role in the progression of
colorectal
cancer].
OBJECTIVE: To investigate the expression of PI3K p85alpha in normal
colorectal
tissue,
colorectal
adenoma
and primary
colorectal
carcinoma and explore its significance in the progression of
colorectal
cancer.
METHODS: The expression of PI3K p85alpha was detected in 116 normal
colorectal
tissue,
colorectal
adenoma
and primary
colorectal
carcinoma specimens using immunohistochemical staining, and the relationship between the expression of PI3K p85alpha protein and the clinicopathological factors was analyzed.
RESULTS: The positivity rates of the expression of PI3K p85alpha protein increased gradually in the progression of
colorectal
cancer and showed significant differences between the tissues (P<0.05).
A significant difference was also noted in the positivity rates of the PI3K p85alpha expression in
colorectal
carcinoma tissues at different Dukes' stages (P<0.05).
CONCLUSIONS: Abnormal PI3K p85alpha expression occurs in the progression of
colorectal
cancer in close relation to the clinical stage, and the PI3K/AKT pathway plays an important role in the progression of
colorectal
cancer.
[MeSH-major]
Carcinoma / enzymology.
Colorectal
Neoplasms / enzymology. Disease Progression. Phosphatidylinositol 3-Kinases / metabolism
[MeSH-minor]
Adenoma
/ enzymology.
Adenoma
/ pathology. Adult. Aged. Humans. Immunohistochemistry. Middle Aged. Signal Transduction. Young Adult
Genetic Alliance.
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(PMID = 19304514.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
EC 2.7.1.- / Phosphatidylinositol 3-Kinases
72.
Ramadas A, Kandiah M:
Food intake and colorectal adenomas: a case-control study in Malaysia.
Asian Pac J Cancer Prev
; 2009;10(5):925-32
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[Title]
Food intake and
colorectal adenomas
: a case-control study in Malaysia.
It is well established that almost all
colorectal
cancers arise from benign, neoplastic adenomatous polyps.
In previous studies, intake of fruits, vegetables and legumes were found to decrease the risk for
colorectal adenomas
(CRA) and
colorectal
cancer.
In conclusion, our data support protective roles for soy, fruits and vegetables in the aetiology of
colorectal adenomas
and increase in risk in those with high intakes of red meat and tubers.
[MeSH-major]
Adenoma
/ etiology.
Adenoma
/ prevention & control.
Colorectal
Neoplasms / etiology.
Colorectal
Neoplasms / prevention & control. Diet. Eating
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(PMID = 20104992.001).
[ISSN]
2476-762X
[Journal-full-title]
Asian Pacific journal of cancer prevention : APJCP
[ISO-abbreviation]
Asian Pac. J. Cancer Prev.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Thailand
73.
Bobe G, Sansbury LB, Albert PS, Cross AJ, Kahle L, Ashby J, Slattery ML, Caan B, Paskett E, Iber F, Kikendall JW, Lance P, Daston C, Marshall JR, Schatzkin A, Lanza E:
Dietary flavonoids and colorectal adenoma recurrence in the Polyp Prevention Trial.
Cancer Epidemiol Biomarkers Prev
; 2008 Jun;17(6):1344-53
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[Title]
Dietary flavonoids and
colorectal
adenoma
recurrence in the Polyp Prevention Trial.
Two recent case-control studies suggested that some flavonoid subgroups may play a role in preventing
colorectal
cancer.
The Polyp Prevention Trial was a randomized dietary intervention trial, which examined the effectiveness of a low-fat, high-fiber, high-fruit, and high-vegetable diet on
adenoma
recurrence.
Multivariate logistic regression models (adjusted for age, body mass index, sex, regular non-steroidal anti-inflammatory use, and dietary fiber intake) were used to estimate odds ratios and 95% confidence intervals for both any and advanced
adenoma
recurrence within quartiles of energy-adjusted flavonoid intake (baseline, during the trial, and change during the trial).
Total flavonoid intake was not associated with any or advanced
adenoma
recurrence.
However, high intake of flavonols, which are at greater concentrations in beans, onions, apples, and tea, was associated with decreased risk of advanced
adenoma
recurrence (4th versus 1st quartile during the trial; odds ratio, 0.24; 95% confidence interval, 0.11, 0.53; P(trend) = 0.0006).
Our data suggest that a flavonol-rich diet may decrease the risk of advanced
adenoma
recurrence.
[MeSH-major]
Adenoma
/ prevention & control.
Colorectal
Neoplasms / prevention & control. Flavonoids / administration & dosage. Neoplasm Recurrence, Local / prevention & control
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[Cites]
N Engl J Med. 2000 Apr 20;342(16):1149-55
[
10770979.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):684-93
[
17416758.001
]
[Cites]
Carcinogenesis. 2000 Jun;21(6):1149-55
[
10837003.001
]
[Cites]
Carcinogenesis. 2000 Sep;21(9):1655-60
[
10964096.001
]
[Cites]
Am J Clin Nutr. 2001 Sep;74(3):387-401
[
11522565.001
]
[Cites]
J Agric Food Chem. 2001 Oct;49(10):4924-9
[
11600045.001
]
[Cites]
Cancer Causes Control. 2001 Nov;12(9):789-96
[
11714106.001
]
[Cites]
Annu Rev Nutr. 2002;22:19-34
[
12055336.001
]
[Cites]
Cancer Causes Control. 2002 May;13(4):373-82
[
12074507.001
]
[Cites]
Am J Clin Nutr. 2002 Sep;76(3):560-8
[
12198000.001
]
[Cites]
J Am Diet Assoc. 2002 Oct;102(10):1414-20
[
12396158.001
]
[Cites]
Med Res Rev. 2003 Jul;23(4):519-34
[
12710022.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):391-400
[
12750232.001
]
[Cites]
Teratog Carcinog Mutagen. 2003;Suppl 2:93-102
[
14691983.001
]
[Cites]
Am J Clin Nutr. 2004 Feb;79(2):274-81
[
14749234.001
]
[Cites]
Mol Pharmacol. 2004 Sep;66(3):683-93
[
15322261.001
]
[Cites]
J Clin Epidemiol. 1990;43(12):1327-35
[
2254769.001
]
[Cites]
Carcinogenesis. 1991 Jul;12(7):1193-6
[
2070483.001
]
[Cites]
Nutr Cancer. 1993;20(1):21-9
[
8415127.001
]
[Cites]
Nutr Cancer. 1993;20(3):199-204
[
8108270.001
]
[Cites]
Cancer Lett. 1996 Jul 19;105(1):61-70
[
8689634.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1996 May;5(5):375-83
[
9162304.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1996 May;5(5):385-92
[
9162305.001
]
[Cites]
Oncology. 1997 Mar-Apr;54(2):118-21
[
9075782.001
]
[Cites]
Am J Epidemiol. 1997 Aug 1;146(3):223-30
[
9247006.001
]
[Cites]
Eur J Nutr. 1999 Feb;38(1):28-34
[
10338685.001
]
[Cites]
Nutr Cancer. 1999;34(1):88-99
[
10453447.001
]
[Cites]
J Biol Chem. 2005 Feb 18;280(7):5636-45
[
15533929.001
]
[Cites]
J Nutr Biochem. 2005 Mar;16(3):155-62
[
15741050.001
]
[Cites]
Carcinogenesis. 2005 Aug;26(8):1450-6
[
15831530.001
]
[Cites]
In Vivo. 2005 Sep-Oct;19(5):895-909
[
16097445.001
]
[Cites]
J Med Food. 2005 Fall;8(3):281-90
[
16176136.001
]
[Cites]
Crit Rev Food Sci Nutr. 2006;46(2):161-83
[
16431408.001
]
[Cites]
J Nutr Biochem. 2006 Mar;17(3):165-76
[
16169200.001
]
[Cites]
Cancer Res. 2006 Apr 1;66(7):3942-53
[
16585224.001
]
[Cites]
J Nutr. 2006 Jul;136(7):1896-903
[
16772456.001
]
[Cites]
Mol Cell Biochem. 2006 Jul;287(1-2):109-16
[
16645725.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1555-8
[
16896049.001
]
[Cites]
Nutr Cancer. 2006;54(2):243-51
[
16898869.001
]
[Cites]
Int J Cancer. 2006 Nov 1;119(9):2213-20
[
16823841.001
]
[Cites]
Arch Pharm Res. 2006 Aug;29(8):633-44
[
16964758.001
]
[Cites]
Am J Epidemiol. 2006 Oct 1;164(7):644-51
[
16923774.001
]
[Cites]
J Nutr. 2007 May;137(5):1244-52
[
17449588.001
]
[Cites]
Mol Carcinog. 2007 Jun;46(6):436-45
[
17219438.001
]
[Cites]
J Am Coll Nutr. 2006 Oct;25(5):370-81
[
17031005.001
]
[Cites]
J Agric Food Chem. 2006 Dec 13;54(25):9322-8
[
17147414.001
]
[Cites]
J Agric Food Chem. 2006 Dec 27;54(26):9798-804
[
17177504.001
]
[Cites]
J Nutr. 2007 Feb;137(2):391-8
[
17237317.001
]
[Cites]
Eur J Pharmacol. 2007 Feb 28;557(2-3):221-9
[
17184768.001
]
[Cites]
J Agric Food Chem. 1999 Jun;47(6):2274-9
[
10794622.001
]
(PMID = 18559549.001).
[ISSN]
1055-9965
[Journal-full-title]
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
[ISO-abbreviation]
Cancer Epidemiol. Biomarkers Prev.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z01 BC010025-12
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Flavonoids
[Other-IDs]
NLM/ NIHMS56510; NLM/ PMC2517243
74.
Wu H, Dai Q, Shrubsole MJ, Ness RM, Schlundt D, Smalley WE, Chen H, Li M, Shyr Y, Zheng W:
Fruit and vegetable intakes are associated with lower risk of colorectal adenomas.
J Nutr
; 2009 Feb;139(2):340-4
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[Title]
Fruit and vegetable intakes are associated with lower risk of
colorectal adenomas
.
Participants were part of the Tennessee
Colorectal
Polyp Study.
Cases had at least one
adenoma
and controls were polyp free.
Associations between dietary intakes and
adenoma
risk were evaluated using unconditional logistic regression with restricted cubic function spline.
In multivariate analyses of 764 cases and 1517 controls, increased intakes of total fruits, berries, fruit juice, and green leafy vegetables were associated with reduced
adenoma
risk.
This study provides additional evidence that high total fruit intake and certain fruit and vegetable intakes may be associated with a reduced risk of
colorectal adenomas
.
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[Cites]
N Engl J Med. 2000 Apr 20;342(16):1149-55
[
10770979.001
]
[Cites]
Semin Cancer Biol. 2007 Oct;17(5):403-10
[
17574861.001
]
[Cites]
J Natl Cancer Inst. 2000 Nov 1;92(21):1740-52
[
11058617.001
]
[Cites]
Am J Epidemiol. 2000 Dec 1;152(11):1081-92
[
11117618.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 Jan;10(1):3-8
[
11205486.001
]
[Cites]
Dig Dis Sci. 2001 Jan;46(1):86-95
[
11270799.001
]
[Cites]
J Natl Cancer Inst. 2001 Apr 4;93(7):525-33
[
11287446.001
]
[Cites]
Am J Epidemiol. 2002 Jun 15;155(12):1104-13
[
12048224.001
]
[Cites]
Eur J Cancer Prev. 2002 Aug;11(4):369-75
[
12195164.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 Mar;12(3):201-8
[
12646508.001
]
[Cites]
Cancer. 2003 Sep 15;98(6):1161-8
[
12973839.001
]
[Cites]
Int J Cancer. 2004 Jan 10;108(2):287-92
[
14639617.001
]
[Cites]
Cancer Causes Control. 2003 Dec;14(10):959-70
[
14750535.001
]
[Cites]
Cell Mol Biol (Noisy-le-grand). 2003 Dec;49(8):1295-304
[
14984001.001
]
[Cites]
Int J Cancer. 2004 May 1;109(5):728-36
[
14999782.001
]
[Cites]
Environ Mol Mutagen. 2004;44(1):10-25
[
15199543.001
]
[Cites]
Nutr Cancer. 2004;49(2):131-8
[
15489205.001
]
[Cites]
Int J Cancer. 1987 Aug 15;40(2):179-88
[
3038756.001
]
[Cites]
Jpn J Cancer Res. 1990 Nov;81(11):1101-8
[
2125036.001
]
[Cites]
Nutr Cancer. 1991;16(1):25-30
[
1656394.001
]
[Cites]
J Natl Cancer Inst. 1993 Jun 2;85(11):884-91
[
8388061.001
]
[Cites]
Int J Cancer. 1993 Sep 9;55(2):213-9
[
8370618.001
]
[Cites]
Cancer Causes Control. 1995 Jul;6(4):292-302
[
7548716.001
]
[Cites]
Epidemiology. 1995 Jul;6(4):356-65
[
7548341.001
]
[Cites]
J Am Diet Assoc. 1996 Oct;96(10):1027-39
[
8841165.001
]
[Cites]
Am J Epidemiol. 1996 Dec 1;144(11):1015-25
[
8942431.001
]
[Cites]
Int J Cancer. 1997 Jul 3;72(1):56-61
[
9212223.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 1997 Sep;6(9):661-70
[
9298572.001
]
[Cites]
Cancer. 1997 Sep 1;80(5):858-64
[
9307184.001
]
[Cites]
Nutrition. 1999 Jun;15(6):523-6
[
10378216.001
]
[Cites]
J Natl Cancer Inst. 2004 Nov 3;96(21):1577-84
[
15523086.001
]
[Cites]
Public Health Nutr. 2005 May;8(3):309-14
[
15918928.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1619-25
[
16030092.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2359-65
[
16214917.001
]
[Cites]
Am J Gastroenterol. 2005 Dec;100(12):2789-95
[
16393237.001
]
[Cites]
Chem Biol Interact. 2006 Mar 10;160(1):1-40
[
16430879.001
]
[Cites]
Cancer Res. 2006 Apr 1;66(7):3942-53
[
16585224.001
]
[Cites]
J Nutr. 2006 Jul;136(7):1896-903
[
16772456.001
]
[Cites]
Am J Med. 2006 Sep;119(9):751-9
[
16945610.001
]
[Cites]
J Nutr. 2007 Apr;137(4):999-1004
[
17374667.001
]
[Cites]
JAMA. 2007 Jun 6;297(21):2351-9
[
17551129.001
]
[Cites]
JAMA. 2007 Jun 6;297(21):2408-9
[
17551134.001
]
[ErratumIn]
J Nutr. 2010 Mar;140(3):667
(PMID = 19091801.001).
[ISSN]
1541-6100
[Journal-full-title]
The Journal of nutrition
[ISO-abbreviation]
J. Nutr.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA095103; United States / NCI NIH HHS / CA / CA095103-010005; United States / NCI NIH HHS / CA / R01 CA097386-01; United States / NCI NIH HHS / CA / R01 CA097386; United States / NCI NIH HHS / CA / R01CA97386; United States / NCI NIH HHS / CA / P50CA95103; United States / NCI NIH HHS / CA / CA097386-01; United States / NCI NIH HHS / CA / P50 CA095103-010005
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS92794; NLM/ PMC2646202
75.
Oka S, Tanaka S, Yoshida S, Hiyama T, Ueno Y, Ito M, Kitadai Y, Yoshihara M, Chayama K:
A water-soluble extract from culture medium of Ganoderma lucidum mycelia suppresses the development of colorectal adenomas.
Hiroshima J Med Sci
; 2010 Mar;59(1):1-6
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[Title]
A water-soluble extract from culture medium of Ganoderma lucidum mycelia suppresses the development of
colorectal adenomas
.
To confirm cancer-preventive effects of MAK, we performed a no-treatment concurrent controlled trial on patients with
colorectal adenomas
.
Patients who were determined to be carrying
colorectal adenomas
by colonoscopy were enrolled in this study.
Follow-up colonoscopy was performed after 12 months, and the colonoscopists recorded the size, site and macroscopic type of all
adenomas
.
The changes in the number of
adenomas
up to 12 months increased to 0.66 +/- 0.10 (mean +/- SE) in the control group, while decreasing in the MAK group to -0.42 +/- 0.10 (p < 0.01).
The total size of
adenomas
increased to 1.73 +/- 0.28 mm in the control group and decreased to -1.40 +/- 0.64 mm in the MAK group (p < 0.01).
The resultssuggest that MAK suppresses the development of
colorectal adenomas
- precancerous lesions of the
large
bowel
.
[MeSH-major]
Adenoma
/ drug therapy. Antineoplastic Agents / therapeutic use.
Colorectal
Neoplasms / drug therapy. Mycelium / metabolism. Precancerous Conditions / drug therapy. Reishi / metabolism
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(PMID = 20518254.001).
[ISSN]
0018-2052
[Journal-full-title]
Hiroshima journal of medical sciences
[ISO-abbreviation]
Hiroshima J. Med. Sci.
[Language]
eng
[Publication-type]
Controlled Clinical Trial; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Culture Media, Conditioned; 059QF0KO0R / Water
76.
Skjelbred CF, Saebø M, Wallin H, Nexø BA, Hagen PC, Lothe IM, Aase S, Johnson E, Hansteen IL, Vogel U, Kure EH:
Polymorphisms of the XRCC1, XRCC3 and XPD genes and risk of colorectal adenoma and carcinoma, in a Norwegian cohort: a case control study.
BMC Cancer
; 2006 Mar 16;6:67
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[Title]
Polymorphisms of the XRCC1, XRCC3 and XPD genes and risk of
colorectal
adenoma
and carcinoma, in a Norwegian cohort: a case control study.
For
colorectal
cancer the importance of mutations in mismatch repair genes has been extensively documented.
Less is known about other DNA repair pathways in
colorectal
carcinogenesis.
METHODS: We used a case-control study design (157 carcinomas, 983
adenomas
and 399 controls) to test the association between five polymorphisms in these DNA repair genes (XRCC1 Arg194Trp, Arg280His, Arg399Gln, XRCC3 Thr241Met and XPD Lys751Gln), and risk of
colorectal adenomas
and carcinomas in a Norwegian cohort.
RESULTS: The XRCC1 280His allele was associated with an increased risk of
adenomas
(OR 2.30, 95% CI 1.19-4.46).
The XRCC1 399Gln allele was associated with a reduction of risk of high-risk
adenomas
(OR 0.62, 95% CI 0.41-0.96).
Carriers of the variant XPD 751Gln allele had an increased risk of low-risk
adenomas
(OR 1.40, 95% CI 1.03-1.89), while no association was found with risk of carcinomas.
CONCLUSION: Our results suggest an increased risk for advanced
colorectal
neoplasia in individuals with the XRCC1 Arg280His polymorphism and a reduced risk associated with the XRCC1 Arg399Gln polymorphism.
Interestingly, individuals with the XPD Lys751Gln polymorphism had an increased risk of low-risk
adenomas
.
This may suggest a role in regression of
adenomas
.
[MeSH-major]
Adenoma
/ genetics.
Colorectal
Neoplasms / genetics. DNA-Binding Proteins / genetics. Polymorphism, Genetic. Xeroderma Pigmentosum Group D Protein / genetics
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[Cites]
Nat Cell Biol. 2000 Oct;2(10):757-61
[
11025669.001
]
[Cites]
Cancer Lett. 2000 Oct 16;159(1):79-86
[
10974409.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2001 Feb;10(2):119-23
[
11219768.001
]
[Cites]
Carcinogenesis. 2001 Sep;22(9):1437-45
[
11532866.001
]
[Cites]
Pharmacogenetics. 2002 Mar;12(2):145-50
[
11875368.001
]
[Cites]
Hum Mol Genet. 2002 Jun 1;11(12):1399-407
[
12023982.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Sep;11(9):939-43
[
12223443.001
]
[Cites]
Mutat Res. 2002 Nov 30;509(1-2):201-10
[
12427539.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1332-52
[
12433710.001
]
[Cites]
Mutagenesis. 2002 Nov;17(6):463-9
[
12435843.001
]
[Cites]
Nature. 1993 Oct 28;365(6449):852-5
[
8413672.001
]
[Cites]
Cell. 1996 Oct 18;87(2):159-70
[
8861899.001
]
[Cites]
Gut. 1996 Sep;39(3):449-56
[
8949653.001
]
[Cites]
Curr Opin Genet Dev. 1997 Apr;7(2):158-69
[
9115419.001
]
[Cites]
Cancer Res. 1998 Feb 15;58(4):604-8
[
9485007.001
]
[Cites]
EMBO J. 1999 Mar 1;18(5):1357-66
[
10064601.001
]
[Cites]
Mutat Res. 1999 Mar 8;424(1-2):207-19
[
10064862.001
]
[Cites]
Genes Dev. 1999 Apr 1;13(7):768-85
[
10197977.001
]
[Cites]
J Natl Cancer Inst. 1999 Jun 2;91(11):916-32
[
10359544.001
]
[Cites]
Cancer Res. 1999 Jun 1;59(11):2557-61
[
10363972.001
]
[Cites]
Mutat Res. 1999 Jun 23;434(2):75-88
[
10422536.001
]
[Cites]
Biochem Genet. 2004 Dec;42(11-12):453-60
[
15587988.001
]
[Cites]
Am J Epidemiol. 2005 Jan 1;161(1):1-14
[
15615908.001
]
[Cites]
BMC Cancer. 2005 Jan 28;5:12
[
15679883.001
]
[Cites]
Mutat Res. 2005 Apr 4;582(1-2):135-45
[
15781218.001
]
[Cites]
Int J Cancer. 2005 Sep 1;116(3):428-32
[
15800946.001
]
[Cites]
Cancer Lett. 2005 Nov 8;229(1):85-91
[
15946795.001
]
[Cites]
Cancer Genet Cytogenet. 2005 Nov;163(1):38-43
[
16271954.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1513-30
[
12496039.001
]
[Cites]
Am J Hum Genet. 2003 May;72(5):1231-50
[
12704570.001
]
[Cites]
Carcinogenesis. 2003 May;24(5):899-904
[
12771034.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 Jun;12(6):584-5
[
12815008.001
]
[Cites]
Scand J Gastroenterol. 2003 Jun;38(6):635-42
[
12825872.001
]
[Cites]
Br J Cancer. 2003 Jul 21;89(2):333-7
[
12865926.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2003 Nov;12(11 Pt 1):1168-74
[
14652276.001
]
[Cites]
Mutat Res. 2004 Feb 26;546(1-2):65-74
[
14757194.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2004 Jun;13(6):1090-1
[
15184273.001
]
[Cites]
Int J Cancer. 2004 Sep 10;111(4):633-9
[
15239144.001
]
[Cites]
Cancer Lett. 2004 Sep 15;213(1):67-72
[
15312685.001
]
[Cites]
Scand J Gastroenterol. 1986 Sep;21(7):853-62
[
3775252.001
]
[Cites]
Nucleic Acids Res. 1988 Feb 11;16(3):1215
[
3344216.001
]
[Cites]
Cell. 1990 Jun 1;61(5):759-67
[
2188735.001
]
[Cites]
Proc Natl Acad Sci U S A. 1992 Jan 1;89(1):261-5
[
1729695.001
]
[Cites]
J Natl Cancer Inst. 1993 Jun 2;85(11):875-84
[
8492316.001
]
[Cites]
N Engl J Med. 2000 Jul 20;343(3):162-8
[
10900274.001
]
[Cites]
N Engl J Med. 2000 Jul 20;343(3):169-74
[
10900275.001
]
[Cites]
Cancer Res. 2000 Oct 15;60(20):5612-6
[
11059748.001
]
(PMID = 16542436.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; 0 / X-ray repair cross complementing protein 3; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
[Other-IDs]
NLM/ PMC1458350
77.
Rubie C, Frick VO, Wagner M, Schuld J, Gräber S, Brittner B, Bohle RM, Schilling MK:
ELR+ CXC chemokine expression in benign and malignant colorectal conditions.
BMC Cancer
; 2008;8:178
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[Title]
ELR+ CXC chemokine expression in benign and malignant
colorectal
conditions.
Here, we comparatively analyzed their expression profile in resection specimens from patients with
colorectal
adenoma
(CRA) (n = 30) as well as
colorectal
carcinoma (CRC) (n = 48) and corresponding
colorectal
liver metastases (CRLM) (n = 16).
[MeSH-major]
Adenoma
/ metabolism. Carcinoma / metabolism. Chemokines, CXC / biosynthesis.
Colorectal
Neoplasms / metabolism
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[Cites]
Cytokine. 2000 Jan;12(1):78-85
[
10623446.001
]
[Cites]
World J Gastroenterol. 2007 Oct 7;13(37):4996-5002
[
17854143.001
]
[Cites]
Immunity. 2000 Feb;12(2):121-7
[
10714678.001
]
[Cites]
Oncogene. 2000 Jul 20;19(31):3477-86
[
10918606.001
]
[Cites]
Eur J Cancer. 2000 Aug;36(13 Spec No):1706-12
[
10959056.001
]
[Cites]
J Mol Endocrinol. 2000 Oct;25(2):169-93
[
11013345.001
]
[Cites]
J Immunol. 2000 Nov 1;165(9):5269-77
[
11046061.001
]
[Cites]
J Virol. 2001 Jul;75(13):5812-22
[
11390582.001
]
[Cites]
J Intern Med. 2001 Aug;250(2):91-104
[
11489059.001
]
[Cites]
Scand J Gastroenterol. 2001 Aug;36(8):854-64
[
11495082.001
]
[Cites]
J Clin Endocrinol Metab. 2001 Aug;86(8):3968-74
[
11502840.001
]
[Cites]
Cytokine Growth Factor Rev. 2001 Dec;12(4):375-91
[
11544106.001
]
[Cites]
Am J Pathol. 2001 Oct;159(4):1405-14
[
11583968.001
]
[Cites]
Clin Cancer Res. 2001 Oct;7(10):3298-304
[
11595728.001
]
[Cites]
J Leukoc Biol. 2002 Jul;72(1):9-18
[
12101257.001
]
[Cites]
J Immunol. 2004 Mar 1;172(5):2853-60
[
14978086.001
]
[Cites]
Cancer Res. 2004 Mar 1;64(5):1853-60
[
14996749.001
]
[Cites]
Chest. 2004 May;125(5 Suppl):133S
[
15136463.001
]
[Cites]
Curr Opin Oncol. 1991 Feb;3(1):75-92
[
2043698.001
]
[Cites]
J Exp Med. 1991 Dec 1;174(6):1355-62
[
1744577.001
]
[Cites]
Cytokines. 1992;4:96-116
[
1335322.001
]
[Cites]
J Biol Chem. 1995 Nov 10;270(45):27348-57
[
7592998.001
]
[Cites]
Comput Methods Programs Biomed. 1995 Dec;48(3):257-62
[
8925653.001
]
[Cites]
J Immunol. 1997 Jun 1;158(11):5257-66
[
9164944.001
]
[Cites]
Cancer. 1997 Nov 1;80(9):1803-4
[
9351551.001
]
[Cites]
J Leukoc Biol. 1997 Nov;62(5):588-97
[
9365113.001
]
[Cites]
N Engl J Med. 1998 Feb 12;338(7):436-45
[
9459648.001
]
[Cites]
J Clin Invest. 1998 Aug 1;102(3):465-72
[
9691082.001
]
[Cites]
J Immunol Methods. 1998 Nov 1;220(1-2):1-17
[
9839921.001
]
[Cites]
Am J Pathol. 1999 May;154(5):1503-12
[
10329603.001
]
[Cites]
Exp Cell Res. 2005 Feb 15;303(2):331-42
[
15652347.001
]
[Cites]
Mol Cell Probes. 2005 Apr;19(2):101-9
[
15680211.001
]
[Cites]
Clin Exp Metastasis. 2004;21(7):571-9
[
15787094.001
]
[Cites]
Anticancer Res. 2005 Sep-Oct;25(5):3581-4
[
16101183.001
]
[Cites]
Dig Dis Sci. 2006 Jan;51(1):173-7
[
16416232.001
]
[Cites]
Eur J Cancer. 2006 Apr;42(6):768-78
[
16510280.001
]
[Cites]
J Exp Med. 2006 Apr 17;203(4):941-51
[
16567391.001
]
[Cites]
Tumour Biol. 2006;27(3):166-74
[
16641550.001
]
[Cites]
Scand J Immunol. 2006 Jun;63(6):468-77
[
16764701.001
]
[Cites]
Br J Cancer. 2006 Jun 19;94(12):1936-41
[
16721367.001
]
[Cites]
Cancer Lett. 2006 Sep 28;241(2):221-7
[
16458421.001
]
[Cites]
Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):5951-9
[
17062666.001
]
[Cites]
Cancer Lett. 2007 Apr 28;249(1):87-96
[
17275174.001
]
[Cites]
J Leukoc Biol. 2000 Jan;67(1):53-62
[
10647998.001
]
(PMID = 18578857.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / CXCL1 protein, human; 0 / CXCL5 protein, human; 0 / CXCL6 protein, human; 0 / Chemokine CXCL1; 0 / Chemokine CXCL5; 0 / Chemokine CXCL6; 0 / Chemokines, CXC; 0 / RNA, Messenger
[Other-IDs]
NLM/ PMC2459188
78.
Nagel R, le Sage C, Diosdado B, van der Waal M, Oude Vrielink JA, Bolijn A, Meijer GA, Agami R:
Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer.
Cancer Res
; 2008 Jul 15;68(14):5795-802
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[Title]
Regulation of the adenomatous polyposis coli gene by the miR-135 family in
colorectal
cancer.
Inactivation of the adenomatous polyposis coli (APC) gene is a major initiating event in
colorectal
tumorigenesis.
Interestingly, we find a considerable up-regulation of miR-135a&b in
colorectal adenomas
and carcinomas, which significantly correlated with low APC mRNA levels.
Thus, our results uncover a miRNA-mediated mechanism for the control of APC expression and Wnt pathway activity, and suggest its contribution to
colorectal
cancer pathogenesis.
[MeSH-major]
Adenomatous Polyposis Coli Protein / genetics. Adenomatous Polyposis Coli Protein / physiology.
Colorectal
Neoplasms / genetics.
Colorectal
Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics
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(PMID = 18632633.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / 3' Untranslated Regions; 0 / Adenomatous Polyposis Coli Protein; 0 / MicroRNAs; 0 / Wnt Proteins
79.
van den Donk M, Visker MH, Harryvan JL, Kok FJ, Kampman E:
Dietary intake of B-vitamins, polymorphisms in thymidylate synthase and serine hydroxymethyltransferase 1, and colorectal adenoma risk: a Dutch case-control study.
Cancer Lett
; 2007 May 18;250(1):146-53
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[Title]
Dietary intake of B-vitamins, polymorphisms in thymidylate synthase and serine hydroxymethyltransferase 1, and
colorectal
adenoma
risk: a Dutch case-control study.
In a case-control study, including 768 cases and 709 controls, we investigated the associations between
colorectal adenomas
and TS tandem repeat and SHMT1 C1420T polymorphisms, and the interplay with B-vitamins.
The polymorphisms were not associated with
adenomas
, but there was a borderline significant interaction between TS genotype and vitamin B6: the association between vitamin B6 and
adenomas
seemed positive in TS 3R/3R individuals, but inverse in TS 2R/2R individuals.
This study does not provide evidence for a role of SHMT1 genotype in
adenoma
occurrence.
[MeSH-major]
Adenoma
/ genetics.
Colorectal
Neoplasms / genetics. Diet. Glycine Hydroxymethyltransferase / genetics. Polymorphism, Genetic. Thymidylate Synthase / genetics. Vitamin B Complex
MedlinePlus Health Information.
consumer health - B Vitamins
.
MedlinePlus Health Information.
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Hazardous Substances Data Bank.
FOLIC ACID
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CYANOCOBALAMIN
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Riboflavin
.
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(PMID = 17113224.001).
[ISSN]
0304-3835
[Journal-full-title]
Cancer letters
[ISO-abbreviation]
Cancer Lett.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Ireland
[Chemical-registry-number]
12001-76-2 / Vitamin B Complex; 8059-24-3 / Vitamin B 6; 935E97BOY8 / Folic Acid; EC 2.1.1.45 / Thymidylate Synthase; EC 2.1.2.1 / Glycine Hydroxymethyltransferase; EC 2.1.2.1 / SHMT protein, human; P6YC3EG204 / Vitamin B 12; TLM2976OFR / Riboflavin
80.
Bugni JM, Meira LB, Samson LD:
Alkylation-induced colon tumorigenesis in mice deficient in the Mgmt and Msh6 proteins.
Oncogene
; 2009 Feb 5;28(5):734-41
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MGMT expression is lost by epigenetic silencing in a variety of human cancers including nearly half of sporadic
colorectal
cancers, suggesting that this loss maybe causal.
Using mice with a targeted disruption of the Mgmt gene, we tested whether Mgmt protects against azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF), against AOM and dextran sulfate sodium (DSS)-induced
colorectal adenomas
and against spontaneous intestinal
adenomas
in Apc(Min) mice.
In addition, following AOM+DSS treatment Mgmt protected against
adenoma
formation to the same degree as it protected against AOM-induced ACF formation.
Finally, Mgmt deficiency did not affect spontaneous intestinal
adenoma
development in Apc(Min/+) mice, suggesting that Mgmt suppresses intestinal cancer associated with exogenous alkylating agents, and that endogenous alkylation does not contribute to the rapid tumor development seen in Apc(Min/+) mice.
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[Cites]
Nucleic Acids Res. 1991 Nov 25;19(22):6163-7
[
1956775.001
]
[Cites]
Mutat Res. 1985 Jun-Jul;150(1-2):77-84
[
4000169.001
]
[Cites]
Cancer Res. 1992 Dec 1;52(23):6471-5
[
1423294.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Mar 15;90(6):2117-21
[
7681584.001
]
[Cites]
Trends Genet. 1993 Apr;9(4):138-41
[
8516849.001
]
[Cites]
Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6424-8
[
8341649.001
]
[Cites]
Epithelial Cell Biol. 1992 Oct;1(4):147-55
[
1307946.001
]
[Cites]
Carcinogenesis. 1995 Mar;16(3):451-6
[
7697797.001
]
[Cites]
Cancer Res. 1996 Jul 1;56(13):2922-6
[
8674041.001
]
[Cites]
Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13629-34
[
8942985.001
]
[Cites]
Cancer Res. 1997 Jun 15;57(12):2415-8
[
9192819.001
]
[Cites]
Carcinogenesis. 1997 Aug;18(8):1561-7
[
9276631.001
]
[Cites]
Cell. 1997 Nov 14;91(4):467-77
[
9390556.001
]
[Cites]
Mutat Res. 1997 Nov 28;381(2):227-41
[
9434879.001
]
[Cites]
Cancer Res. 1998 Mar 15;58(6):1087-9
[
9515784.001
]
[Cites]
Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5116-20
[
9560238.001
]
[Cites]
Mutat Res. 1999 Mar 8;424(1-2):127-42
[
10064856.001
]
[Cites]
Cancer Res. 1999 Mar 15;59(6):1301-7
[
10096563.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3911-5
[
10097137.001
]
[Cites]
Mutagenesis. 1999 May;14(3):339-47
[
10375003.001
]
[Cites]
Proc Natl Acad Sci U S A. 1999 Sep 14;96(19):10764-9
[
10485900.001
]
[Cites]
Mol Cancer. 2004 Oct 11;3:28
[
15476557.001
]
[Cites]
Cancer Res. 2004 Dec 15;64(24):8876-81
[
15604247.001
]
[Cites]
Biochemistry. 2005 Nov 22;44(46):15396-405
[
16285744.001
]
[Cites]
J Mol Diagn. 2006 Feb;8(1):68-75
[
16436636.001
]
[Cites]
Nat Rev Mol Cell Biol. 2006 May;7(5):335-46
[
16612326.001
]
[Cites]
Oncology. 2006;71(1-2):124-30
[
17347588.001
]
[Cites]
Int J Cancer. 2008 Jun 1;122(11):2429-36
[
18240147.001
]
[Cites]
Carcinogenesis. 1999 Dec;20(12):2355-60
[
10590233.001
]
[Cites]
Carcinogenesis. 2000 Apr;21(4):593-8
[
10753191.001
]
[Cites]
Cancer Res. 2001 Apr 15;61(8):3225-9
[
11309270.001
]
[Cites]
Cancer Res. 2001 Nov 1;61(21):7934-42
[
11691815.001
]
[Cites]
Cancer Res. 2001 Dec 1;61(23):8435-40
[
11731424.001
]
[Cites]
Cancer Res. 2002 Apr 1;62(7):2092-7
[
11929830.001
]
[Cites]
Carcinogenesis. 2002 May;23(5):823-30
[
12016156.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8927-31
[
12060718.001
]
[Cites]
Science. 2002 Jul 19;297(5580):403-5
[
12130785.001
]
[Cites]
Biochem Pharmacol. 2003 Oct 15;66(8):1547-54
[
14555233.001
]
[Cites]
DNA Repair (Amst). 2004 Aug-Sep;3(8-9):1091-101
[
15279797.001
]
[Cites]
Oncogene. 2004 Aug 5;23(35):5931-40
[
15208683.001
]
[Cites]
J Biol Chem. 1984 Jul 10;259(13):8095-100
[
6376499.001
]
[Cites]
Carcinogenesis. 1984 Aug;5(8):1061-4
[
6744514.001
]
[Cites]
Nucleic Acids Res. 1992 Jun 25;20(12):2933-40
[
1620587.001
]
(PMID = 19029948.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
ENG
[Grant]
United States / NIEHS NIH HHS / ES / ES02109; United States / NCI NIH HHS / CA / P30 CA014051; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / CA14051; United States / NCI NIH HHS / CA / CA75576; United States / NCI NIH HHS / CA / R01 CA075576
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Alkylating Agents; 0 / Carcinogens; 0 / DNA-Binding Proteins; 0 / Msh6 protein, mouse; 0 / Tumor Suppressor Proteins; 9042-14-2 / Dextran Sulfate; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, mouse; EC 6.5.1.- / DNA Repair Enzymes; MO0N1J0SEN / Azoxymethane
[Other-IDs]
NLM/ NIHMS74471; NLM/ PMC3557788
81.
Pequin P, Manfredi S, Quentin V, Heresbach D, Boyer J, Siproudhis L, Bretagne JF:
Patients with sporadic duodenal adenoma are a high-risk group for advanced colorectal neoplasia: results of a case-control study.
Aliment Pharmacol Ther
; 2007 Jul 15;26(2):277-82
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[Title]
Patients with sporadic duodenal
adenoma
are a high-risk group for advanced
colorectal
neoplasia: results of a case-control study.
AIM: To evaluate
colorectal
cancer risk among patients with sporadic duodenal neoplasia using a case-control protocol.
METHODS: Cases were 35 patients referred for the management of sporadic duodenal
adenoma
and who underwent colonoscopy.
Colonoscopy findings among cases were compared with those from a control group matched for age and sex (two controls per case) without duodenal
adenoma
.
Colonoscopy findings were categorized as
adenoma
, advanced
adenoma
, cancer or advanced neoplasia.
RESULTS:
Colorectal
adenoma
was present in 31% of cases vs. 24% of controls, advanced neoplasia in 29% vs. 4%, advanced
adenoma
in 23% vs. 3% and adenocarcinoma in 6% vs. 1%.
The relative risks of advanced
colorectal
adenoma
and advanced
colorectal
neoplasia in cases were 10.1 (95% CI: 1.8-100.1, P = 0.003) and 8.9 (95% CI: 2.1-53.3, P = 0.001), respectively.
CONCLUSIONS: The relative risk of advanced
colorectal
adenoma
and advanced neoplasia in cases was nine- to 10-fold that among controls.
Patients with sporadic duodenal
adenoma
represent a high-risk group for advanced
colorectal
neoplasia and should therefore undergo complete colonoscopy.
[MeSH-major]
Adenoma
/ pathology. Colonoscopy.
Colorectal
Neoplasms /
diagnosis
. Duodenal Neoplasms / pathology. Precancerous Conditions / pathology
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(PMID = 17593073.001).
[ISSN]
0269-2813
[Journal-full-title]
Alimentary pharmacology & therapeutics
[ISO-abbreviation]
Aliment. Pharmacol. Ther.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
82.
Nakanishi M, Montrose DC, Clark P, Nambiar PR, Belinsky GS, Claffey KP, Xu D, Rosenberg DW:
Genetic deletion of mPGES-1 suppresses intestinal tumorigenesis.
Cancer Res
; 2008 May 1;68(9):3251-9
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Elevated levels of prostaglandin E(2) (PGE(2)) are often found in
colorectal
cancers.
Thus, nonsteroidal anti-inflammatory drugs, including selective cyclooxygenase-2 (COX-2) inhibitors, are among the most promising chemopreventive agents for
colorectal
cancer.
We report for the first time that genetic deletion of mPGES-1 in Apc-mutant mice results in marked and persistent suppression of intestinal cancer growth by 66%, whereas suppression
of large
adenomas
(>3 mm) was almost 95%.
However, we found that mPGES-1 deficiency was associated with a disorganized vascular pattern within primary
adenomas
as determined by CD31 immunostaining.
[MeSH-major]
Adenoma
/ genetics. Gene Deletion. Intestinal Neoplasms / genetics. Intramolecular Oxidoreductases / genetics
[MeSH-minor]
Animals. Cell Proliferation. Dinoprostone / metabolism. Disease Progression. Female. Homozygote. Intestinal Polyps / genetics. Intestinal Polyps / metabolism. Intestinal Polyps / pathology.
Intestine
, Small / blood supply.
Intestine
, Small / metabolism. Isoenzymes / genetics. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Protein Transport. beta Catenin / metabolism
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(PMID = 18451151.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA-114635
[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 / Isoenzymes; 0 / beta Catenin; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.3 / prostaglandin-E synthase; K7Q1JQR04M / Dinoprostone
83.
Wagner PL, Chen YT, Yantiss RK:
Immunohistochemical and molecular features of sporadic and FAP-associated duodenal adenomas of the ampullary and nonampullary mucosa.
Am J Surg Pathol
; 2008 Sep;32(9):1388-95
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[Title]
Immunohistochemical and molecular features of sporadic and FAP-associated duodenal
adenomas
of the ampullary and nonampullary mucosa.
The pathogenesis of duodenal
adenomas
is not well elucidated.
Much of the literature pertains to ampullary
adenomas
and those associated with familial adenomatous polyposis (FAP).
In this study, we evaluated the molecular features of a series of sporadic duodenal
adenomas
(n=22) that developed distal to the ampulla, and compared them with the features of sporadic ampullary
adenomas
(n=9) and FAP-related polyps (n=12).
Wnt signaling pathway abnormalities occurred in sporadic, nonampullary (82%), and ampullary (77%)
adenomas
at comparable rates, usually reflecting nuclear beta-catenin immunostaining (64% and 44%, respectively), and APC rather than beta-catenin, mutations.
KRAS mutations were infrequent in sporadic, nonampullary
adenomas
(18%), and FAP-related
adenomas
(9%); moderately frequent in ampullary
adenomas
(44%); and none of the cases harbored BRAF mutations.
Only 4 (13%) sporadic
adenomas
showed nuclear p53 staining, but no p53 mutations were detected in exons 5 to 8.
Loss of O-methylguanine methyltransferase immunostaining was identified in 1 sporadic, nonampullary
adenoma
, and none of the polyps in any group showed loss of MLH-1, MSH-2, or MSH-6 staining, or high-frequency microsatellite instability.
We conclude that sporadic and FAP-related
adenomas
show similar molecular features, regardless of their anatomic location.
Similar to
colorectal adenomas
, they harbor APC and KRAS mutations; but BRAF mutations, p53 alterations, and DNA mismatch repair abnormalities are rare.
[MeSH-major]
Adenoma
/ genetics.
Adenoma
/ metabolism. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Duodenal Neoplasms / genetics. Duodenal Neoplasms / metabolism
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(PMID = 18670349.001).
[ISSN]
1532-0979
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Protein p53; 0 / Wnt Proteins
84.
Johnson V, Lipton LR, Cummings C, Eftekhar Sadat AT, Izatt L, Hodgson SV, Talbot IC, Thomas HJ, Silver AJ, Tomlinson IP:
Analysis of somatic molecular changes, clinicopathological features, family history, and germline mutations in colorectal cancer families: evidence for efficient diagnosis of HNPCC and for the existence of distinct groups of non-HNPCC families.
J Med Genet
; 2005 Oct;42(10):756-62
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[Title]
Analysis of somatic molecular changes, clinicopathological features, family history, and germline mutations in
colorectal
cancer families: evidence for efficient
diagnosis
of HNPCC and for the existence of distinct groups of non-HNPCC families.
OBJECTIVE: To analyse somatic molecular changes, clinicopathological features, family history, and germline mutations in families with
colorectal
cancer (CRC).
METHODS: Molecular changes (K-ras and beta-catenin mutations, chromosome 18q allele loss (LOH), APC LOH, microsatellite instability (MSI), and expression of beta-catenin and p53) were examined in four series of CRC patients with proven or probable hereditary disease: hereditary non-polyposis colon cancer (HNPCC); MYH associated polyposis (MAP); multiple (>5)
colorectal adenomas
without familial adenomatous polyposis (FAP); and other families/cases referred to family cancer clinics (FCC series).
RESULTS: There was overlap between genetic pathways followed by each type of CRC, but significant differences included: increased frequency of K-ras mutation and reduced frequency of APC LOH in cancers from MAP, but not from multiple
adenoma
patients; reduced frequency of LOH in HNPCC CRCs; and increased MSI in CRCs from HNPCC, but not from FCC or multiple
adenoma
patients.
Cancers from the FCC, unselected, and multiple
adenoma
series shared similar molecular characteristics.
In the FCC and multiple
adenoma
series, hierarchical cluster analysis using the molecular features of the cancers consistently identified two distinct groups, distinguished by presence or absence of K-ras mutation.
CONCLUSIONS: While K-ras mutation status is known to differentiate hereditary
bowel
cancer syndromes such as MAP and FAP, it may also distinguish groups of non-HNPCC, FCC patients whose disease has different, as yet unknown, genetic origins.
[MeSH-major]
Colorectal
Neoplasms / genetics.
Colorectal
Neoplasms, Hereditary Nonpolyposis / genetics. Genetic Predisposition to Disease. Germ-Line Mutation
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[Cites]
Oncogene. 2005 Feb 24;24(9):1542-51
[
15674332.001
]
[Cites]
Gut. 2005 Feb;54(2):264-7
[
15647192.001
]
[Cites]
Br J Cancer. 2000 May;82(10):1689-93
[
10817505.001
]
[Cites]
N Engl J Med. 2000 Jul 13;343(2):78-85
[
10891514.001
]
[Cites]
Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9719-23
[
11481457.001
]
[Cites]
Nat Genet. 2002 Feb;30(2):227-32
[
11818965.001
]
[Cites]
Int J Cancer. 2002 Feb 20;97(6):823-7
[
11857362.001
]
[Cites]
Eur J Cancer. 2002 May;38(7):858-66
[
11978509.001
]
[Cites]
N Engl J Med. 2003 Feb 27;348(9):791-9
[
12606733.001
]
[Cites]
Cancer Res. 2003 Nov 15;63(22):7595-9
[
14633673.001
]
[Cites]
Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):191-5
[
14734469.001
]
[Cites]
J Natl Cancer Inst. 2004 Feb 18;96(4):261-8
[
14970275.001
]
[Cites]
Hum Mol Genet. 2004 Oct 1;13 Spec No 2:R177-85
[
15358723.001
]
[Cites]
Cell. 1990 Jun 1;61(5):759-67
[
2188735.001
]
[Cites]
Cancer Res. 1990 Nov 15;50(22):7166-73
[
1977514.001
]
[Cites]
Am J Hum Genet. 1993 Feb;52(2):263-72
[
8381579.001
]
[Cites]
Cancer Res. 1994 Jun 1;54(11):3011-20
[
8187091.001
]
[Cites]
Science. 1995 Jun 2;268(5215):1336-8
[
7761852.001
]
[Cites]
Gastroenterology. 1996 Aug;111(2):307-17
[
8690195.001
]
[Cites]
Int J Cancer. 1997 Dec 19;74(6):664-9
[
9421366.001
]
[Cites]
Cancer Res. 1998 Nov 15;58(22):5248-57
[
9823339.001
]
[Cites]
J Clin Oncol. 2004 Dec 15;22(24):4934-43
[
15611508.001
]
[Cites]
Oncogene. 2005 Jan 6;24(1):118-29
[
15531920.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2225-8
[
10681434.001
]
(PMID = 15788729.001).
[ISSN]
1468-6244
[Journal-full-title]
Journal of medical genetics
[ISO-abbreviation]
J. Med. Genet.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1735937
85.
Flood A, Peters U, Jenkins DJ, Chatterjee N, Subar AF, Church TR, Bresalier R, Weissfeld JL, Hayes RB, Schatzkin A, Prostate, Lung, Colorectal, Ovarian (PLCO) Project Team:
Carbohydrate, glycemic index, and glycemic load and colorectal adenomas in the Prostate, Lung, Colorectal, and Ovarian Screening Study.
Am J Clin Nutr
; 2006 Nov;84(5):1184-92
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[Title]
Carbohydrate, glycemic index, and glycemic load and
colorectal adenomas
in the Prostate, Lung,
Colorectal
, and Ovarian Screening Study.
BACKGROUND: It is possible that high-glycemic-load diets, through their hyperinsulinemic effects, can increase the risk of
colorectal
cancer.
OBJECTIVE: We analyzed data from a cancer screening study to determine whether persons with high-glycemic-load diets would be at an increased risk of distal
adenomas
.
DESIGN: We included subjects with no prior
adenoma
or cancer from the Prostate, Lung,
Colorectal
, and Ovarian screening trial and whose results from flexible sigmoidoscopy exams indicated either no lesions (n = 34 817) or >/=1 distal
adenoma
(n = 3696).
Using logistic regression analysis, we calculated, separately for men and women, prevalence odds ratios (ORs) and 95% CIs of sigmoidoscopy-detected, distal
adenomas
for quintiles of energy-adjusted dietary carbohydrate, glycemic index, and glycemic load.
CONCLUSION: Despite expectations that increasing glycemic load and glycemic index would increase the risk
of adenoma
, we observed no association in women and even an inverse association in men.
[MeSH-major]
Adenoma
/ epidemiology.
Colorectal
Neoplasms / epidemiology. Dietary Carbohydrates / administration & dosage. Food Habits
[MeSH-minor]
Adenomatous Polyps /
diagnosis
. Adenomatous Polyps / epidemiology. Adenomatous Polyps / etiology. Aged. Case-Control Studies. Cohort Studies. Confidence Intervals. Female. Glycemic Index. Humans. Hyperglycemia / complications. Logistic Models. Male. Mass Screening. Middle Aged. Multivariate Analysis. Nutrition Assessment. Odds Ratio. Risk Assessment. Risk Factors. Sigmoidoscopy. Surveys and Questionnaires. United States / epidemiology
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.
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consumer health - Colorectal Cancer
.
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(PMID = 17093173.001).
[ISSN]
0002-9165
[Journal-full-title]
The American journal of clinical nutrition
[ISO-abbreviation]
Am. J. Clin. Nutr.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / K07-CA108910-01A1
[Publication-type]
Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Dietary Carbohydrates
86.
Risio M, Malacarne D, Giaretti W:
KRAS transitions and villous growth in colorectal adenomas.
Cell Oncol
; 2005;27(5-6):363-6
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[Title]
KRAS transitions and villous growth in
colorectal adenomas
.
[MeSH-major]
Adenoma
/ genetics.
Adenoma
, Villous / genetics.
Colorectal
Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Genes, ras
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(PMID = 16373972.001).
[ISSN]
1570-5870
[Journal-full-title]
Cellular oncology : the official journal of the International Society for Cellular Oncology
[ISO-abbreviation]
Cell. Oncol.
[Language]
eng
[Publication-type]
Letter; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Other-IDs]
NLM/ PMC4617505
87.
Laurent E, McCoy JW 3rd, Macina RA, Liu W, Cheng G, Robine S, Papkoff J, Lambeth JD:
Nox1 is over-expressed in human colon cancers and correlates with activating mutations in K-Ras.
Int J Cancer
; 2008 Jul 1;123(1):100-7
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This suggests that aberrant expression of Nox1 could contribute to the development of
colorectal
cancer.
Nox1 was overexpressed compared with paired normal tissue in 57% of tumors as early as the
adenoma
stage, with no correlation of expression level with tumor stage.
Transgenic mice expressing K-Ras(G12V) in the intestinal epithelium also expressed markedly elevated Nox1 in both small and
large intestine
.
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[Copyright]
(c) 2008 Wiley-Liss, Inc.
[Cites]
J Biol Chem. 2006 Jun 30;281(26):17718-26
[
16636067.001
]
[Cites]
J Biol Chem. 2006 Jul 21;281(29):20368-82
[
16707484.001
]
[Cites]
Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1447-59
[
16987002.001
]
[Cites]
Free Radic Biol Med. 2007 Aug 1;43(3):319-31
[
17602947.001
]
[Cites]
Free Radic Biol Med. 2007 Aug 1;43(3):332-47
[
17602948.001
]
[Cites]
Science. 1995 Oct 13;270(5234):296-9
[
7569979.001
]
[Cites]
Gene. 2001 May 16;269(1-2):131-40
[
11376945.001
]
[Cites]
Cell. 1996 Oct 18;87(2):159-70
[
8861899.001
]
[Cites]
Science. 1997 Mar 14;275(5306):1649-52
[
9054359.001
]
[Cites]
J Biol Chem. 1998 Jul 17;273(29):17991-4
[
9660749.001
]
[Cites]
Gut. 1999 Jun;44(6):826-33
[
10323885.001
]
[Cites]
Nature. 1999 Sep 2;401(6748):79-82
[
10485709.001
]
[Cites]
Med Clin North Am. 2005 Jan;89(1):1-42, vii
[
15527807.001
]
[Cites]
Prostate. 2005 Feb 1;62(2):200-7
[
15389790.001
]
[Cites]
Cancer Lett. 2005 Apr 18;221(1):97-104
[
15797632.001
]
[Cites]
J Pathol. 2005 Oct;207(2):164-76
[
16086438.001
]
[Cites]
Oncogene. 2006 Jun 22;25(26):3699-707
[
16532036.001
]
[Cites]
J Biol Chem. 2001 May 11;276(19):15609-15
[
11278702.001
]
[Cites]
Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):8010-4
[
10869423.001
]
[Cites]
Physiol Rev. 2002 Jan;82(1):47-95
[
11773609.001
]
[Cites]
IUBMB Life. 2001 Jul;52(1-2):3-6
[
11795590.001
]
[Cites]
Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):715-20
[
11805326.001
]
[Cites]
Circulation. 2002 Mar 26;105(12):1429-35
[
11914250.001
]
[Cites]
Am J Physiol Cell Physiol. 2002 Jun;282(6):C1212-24
[
11997235.001
]