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

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

Show other versions (1)

Adenomatous polyposis coli (APC ) mutations are found in most colorectal tumours. These mutations are almost always protein-truncating, deleting both central domains that regulate Wnt signalling and C-terminal domains that interact with the cytoskeleton. The importance of Wnt dysregulation for color...

Full description

Bibliographic Details
Main Authors:	Lewis, A, Davis, H, Deheragoda, M, Pollard, P, Nye, E, Jeffery, R, Segditsas, S, East, P, Poulsom, R, Stamp, G, Wright, N, Tomlinson, I
Format:	Journal article
Language:	English
Published:	2012

Similar Items

The C-terminus of Apc does not influence intestinal adenoma development or progression
by: Lewis, A, et al.
Published: (2012)

Putative direct and indirect Wnt targets identified through consistent gene expression changes in APC-mutant intestinal adenomas from humans and mice.
by: Segditsas, S, et al.
Published: (2008)

Severe polyposis in Apc1322T mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5
by: Lewis, A, et al.
Published: (2010)

Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5.
by: Lewis, A, et al.
Published: (2010)

The APC1310T/+ mouse: A novel murine model of intestinal tumorigenesis analogous to the APC-1309 mutation causing severe intestinal polyposis in humans
by: Deheragoda, MG, et al.
Published: (2007)

The Apcl323t/+ mouse: A novel murine model analagous to the APC-1309 mutation causing severe intestinal polyposis in humans
by: Deheragoda, MG, et al.
Published: (2007)

The Apc 1322T mouse develops severe polyposis associated with submaximal nuclear beta-catenin expression.
by: Pollard, P, et al.
Published: (2009)

Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) mice.
by: Alferez, D, et al.
Published: (2008)

Investigation of pathogenic mechanisms in multiple colorectal adenoma patients without germline APC or MYH/MUTYH mutations.
by: Thirlwell, C, et al.
Published: (2007)

APC and the three-hit hypothesis.
by: Segditsas, S, et al.
Published: (2009)

Location in the large bowel influences the APC mutations observed in FAP adenomas.
by: Will, O, et al.
Published: (2010)

APC mutations are sufficient for the growth of early colorectal adenomas.
by: Lamlum, H, et al.
Published: (2000)

The role of cell proliferation and crypt fission in adenoma aggressiveness: a comparison of ileoanal pouch and rectal adenomas in familial adenomatous polyposis.
by: Will, O, et al.
Published: (2011)

Analysis of chromosomal instability in human colorectal adenomas with two mutational hits at APC.
by: Sieber, O, et al.
Published: (2002)

APC in the regulation of intestinal crypt fission.
by: Wasan, H, et al.
Published: (1998)

Promoter hypermethylation leads to decreased APC mRNA expression in familial polyposis and sporadic colorectal tumours, but does not substitute for truncating mutations.
by: Segditsas, S, et al.
Published: (2008)

Myh deficiency enhances intestinal tumorigenesis in multiple intestinal neoplasia (ApcMin/+) mice.
by: Sieber, O, et al.
Published: (2004)

Bottom-up histogenesis of colorectal adenomas: origin in the monocryptal adenoma and initial expansion by crypt fission.
by: Preston, S, et al.
Published: (2003)

APC protein immunoexpression in colorectal adenoma and adenocarcinoma
by: Vivian Sati Oba Bourroul, et al.
Published: (2013-07-01)

The soluble IGF2 receptor reduces small intestine adenoma number in the Apc(Min/+) mouse
by: Howell, J, et al.
Published: (2000)

Genetic basis of variation in adenoma multiplicity in ApcMin/+ Mom1S mice.
by: Haines, J, et al.
Published: (2005)

Soluble IGF2 receptor rescues Apc(Min/+) intestinal adenoma progression induced by Igf2 loss of imprinting.
by: Harper, J, et al.
Published: (2006)

Insulin-like growth factor II supply modifies growth of intestinal adenoma in Apc(Min/+) mice.
by: Hassan, A, et al.
Published: (2000)

A rapid method for the analysis of cell proliferation and survival in intestinal adenoma from the Apc(Min) mouse
by: Burns, J, et al.
Published: (2001)

A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts
by: Leedham, S, et al.
Published: (2013)

A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts.
by: Leedham, S, et al.
Published: (2013)

Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
by: Alferez, D, et al.
Published: (2010)

Top down or bottom up: competing management strategies in the histogenesis of colorectal adenomas
by: Wong, R, et al.
Published: (2002)

Cancer stemness in Apc- vs. Apc/KRAS-driven intestinal tumorigenesis.
by: Mehrnaz Ghazvini, et al.
Published: (2013-01-01)

Vitamin D receptor absence does not enhance intestinal tumorigenesis in ApcPirc/+rats
by: Amy A. Irving, et al.
Published: (2022-07-01)

Dual inhibition of epidermal growth factor and insulin-like 1 growth factor receptors reduce intestinal adenoma burden in the Apc(min/+) mouse.
by: Shaw, P, et al.
Published: (2011)

Germline APC variants in patients with multiple colorectal adenomas, with evidence for the particular importance of E1317Q.
by: Lamlum, H, et al.
Published: (2000)

Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or "multiple" colorectal adenomas.
by: Sieber, O, et al.
Published: (2002)

Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or "multiple" colorectal adenomas
by: Sieber, O, et al.
Published: (2002)

Erratum to: Genetic analysis of intestinal polyp development in Collaborative Cross mice carrying the Apc Min/+ mutation.
by: Dorman, A, et al.
Published: (2016)

Diagnosis of sessile serrated polyps/adenomas: what does this mean for the pathologist, gastroenterologist and patient?
by: Leedham, S, et al.
Published: (2013)

Targeted inactivation of fh1 causes proliferative renal cyst development and activation of the hypoxia pathway.
by: Pollard, P, et al.
Published: (2007)

Five quantitative trait loci control radiation-induced adenoma multiplicity in Mom1R Apc Min/+ mice.
by: Elahi, E, et al.
Published: (2009)

Five quantitative trait loci control radiation-induced adenoma multiplicity in Mom 1R ApcMin/+ mice
by: Elahi, E, et al.
Published: (2009)

Diagnosis of sessile serrated polyps/adenomas: What does this mean for the pathologist, gastroenterologist and patient
by: Leedham, S, et al.
Published: (2013)