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Colorectal cancer and genetic alterations in the Wnt pathway

Oncogene, 2006-12, Vol.25 (57), p.7531-7537

2006

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APC and the three-hit hypothesis

Oncogene, 2009-01, Vol.28 (1), p.146-155

2009

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Disease severity and genetic pathways in attenuated familial adenomatous polyposis vary greatly but depend on the site of the germline mutation

Gut, 2006-10, Vol.55 (10), p.1440-1448

2006

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Investigation of pathogenic mechanisms in multiple colorectal adenoma patients without germline APC or MYH MUTYH mutations

British journal of cancer, 2007-06, Vol.96 (11), p.1729-1734

2007

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Analysis of copy number changes suggests chromosomal instability in a minority of large colorectal adenomas

The Journal of pathology, 2007-11, Vol.213 (3), p.249-256

2007

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Colorectal cancer and genetic alterations in the Wnt pathway: Wnt signaling

Oncogene, 2006, Vol.25 (57), p.7531-7537

2006

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Serum- and Glucocorticoid-induced Kinase Sgk1 Directly Promotes the Differentiation of Colorectal Cancer Cells and Restrains Metastasis

Clinical cancer research, 2019-01, Vol.25 (2), p.629-640

2019

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Hereditary mixed polyposis syndrome is caused by a 40-kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1

Nature genetics, 2012-06, Vol.44 (6), p.699-703

2012

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PHLDA1 Expression Marks the Putative Epithelial Stem Cells and Contributes to Intestinal Tumorigenesis

Cancer research (Chicago, Ill.), 2011-05, Vol.71 (10), p.3709-3719

2011

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Putative direct and indirect Wnt targets identified through consistent gene expression changes in APC-mutant intestinal adenomas from humans and mice

Human molecular genetics, 2008-12, Vol.17 (24), p.3864-3875

2008

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A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts

Gut, 2013-01, Vol.62 (1), p.83-93

2013

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Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

Gut, 2010-12, Vol.59 (12), p.1680-1686

2010

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Down-regulation of serum/glucocorticoid regulated kinase 1 in colorectal tumours is largely independent of promoter hypermethylation

PloS one, 2010-11, Vol.5 (11), p.e13840

2010

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The C-terminus of Apc does not influence intestinal adenoma development or progression

The Journal of pathology, 2012-01, Vol.226 (1), p.73-83

2012

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Activation of AKT and nuclear accumulation of wild type TP53 and MDM2 in anal squamous cell carcinoma

International journal of cancer, 2007-12, Vol.121 (12), p.2668-2673

2007

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551 Hereditary Mixed Polyposis Syndrome is Caused by a 40kb Upstream Duplication That Leads to Increased and Ectopic Expression of the BMP Antagonist Grem1

Gastroenterology (New York, N.Y. 1943), 2012-05, Vol.142 (5), p.S-110-S-111

2012

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Hereditary mixed polyposis syndrome is caused by a 40kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1

Nature genetics, 2012-05, Vol.44 (6), p.699-703

2012

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Severe polyposis in Apc 1322T mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

Gut, 2010-12, Vol.59 (12), p.1680-1686

2010

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Severe polyposis in Apc1322T mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

Gut, 2010-12, Vol.59 (12), p.1680-1686

2010

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Promoter hypermethylation leads to decreased APC mRNA expression in familial polyposis and sporadic colorectal tumours, but does not substitute for truncating mutations

Experimental and molecular pathology, 2008-12, Vol.85 (3), p.201-206

2008

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The Apc1322T Mouse Develops Severe Polyposis Associated With Submaximal Nuclear β-Catenin Expression

Gastroenterology (New York, N.Y. 1943), 2009-06, Vol.136 (7), p.2204-2213.e13

2009

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T1738 Stem Cell Location Throughout the Human Gastrointestinal Tract as Defined by LGR5 mRNA in Situ Hybridisation

Gastroenterology (New York, N.Y. 1943), 2010, Vol.138 (5), p.S-568-S-568

2010

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Mechanisms of intestinal tumorigenesis resulting from APC mutations

Segditsas, Stefania

2007

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The Apc 1322T mouse develops severe polyposis associated with submaximal nuclear beta-catenin expression

Gastroenterology (New York, N.Y. 1943), 2009-06, Vol.136 (7), p.2204-2213.e1-13

2009

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Ceruminous gland tumors: Report of three cases

The Laryngoscope, 1974-03, Vol.84 (3), p.438-443

1974

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Colorectal cancer and genetic alterations in the Wnt pathway

APC and the three-hit hypothesis

Disease severity and genetic pathways in attenuated familial adenomatous polyposis vary greatly but depend on the site of the germline mutation

Investigation of pathogenic mechanisms in multiple colorectal adenoma patients without germline APC or MYH MUTYH mutations

Analysis of copy number changes suggests chromosomal instability in a minority of large colorectal adenomas

Colorectal cancer and genetic alterations in the Wnt pathway: Wnt signaling

Serum- and Glucocorticoid-induced Kinase Sgk1 Directly Promotes the Differentiation of Colorectal Cancer Cells and Restrains Metastasis

Hereditary mixed polyposis syndrome is caused by a 40-kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1

PHLDA1 Expression Marks the Putative Epithelial Stem Cells and Contributes to Intestinal Tumorigenesis

Putative direct and indirect Wnt targets identified through consistent gene expression changes in APC-mutant intestinal adenomas from humans and mice

A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts

Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

Down-regulation of serum/glucocorticoid regulated kinase 1 in colorectal tumours is largely independent of promoter hypermethylation

The C-terminus of Apc does not influence intestinal adenoma development or progression

Activation of AKT and nuclear accumulation of wild type TP53 and MDM2 in anal squamous cell carcinoma

551 Hereditary Mixed Polyposis Syndrome is Caused by a 40kb Upstream Duplication That Leads to Increased and Ectopic Expression of the BMP Antagonist Grem1

Hereditary mixed polyposis syndrome is caused by a 40kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1

Severe polyposis in Apc 1322T mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

Severe polyposis in Apc1322T mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

Promoter hypermethylation leads to decreased APC mRNA expression in familial polyposis and sporadic colorectal tumours, but does not substitute for truncating mutations

The Apc1322T Mouse Develops Severe Polyposis Associated With Submaximal Nuclear β-Catenin Expression

T1738 Stem Cell Location Throughout the Human Gastrointestinal Tract as Defined by LGR5 mRNA in Situ Hybridisation

Mechanisms of intestinal tumorigenesis resulting from APC mutations

The Apc 1322T mouse develops severe polyposis associated with submaximal nuclear beta-catenin expression

Ceruminous gland tumors: Report of three cases

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