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

Annabelle Lewis; Stefania Segditsas; Maesha Deheragoda; Patrick Pollard; Rosemary Jeffery; Emma Nye; Helen Lockstone; Hayley Davis; Susan Clark; Gordon Stamp; Richard Poulsom; Nicholas Wright; Ian Tomlinson

doi:10.1136/gut.2009.193680

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

Annabelle Lewis, Stefania Segditsas, Maesha Deheragoda, Patrick Pollard, Rosemary Jeffery, Emma Nye, Helen Lockstone, Hayley Davis, Susan Clark, Gordon Stamp, Richard Poulsom, Nicholas Wright, Ian Tomlinson

Deanery of Molecular, Genetic and Population Health Sciences

Research output: Contribution to journal › Article › peer-review

Abstract / Description of output

Adenomatous polyposis coli (APC) is a tumour suppressor gene mutated in the germline of patients with familial adenomatous polyposis (FAP) and somatically in most colorectal cancers. APC mutations impair β-catenin degradation, resulting in increased Wnt signalling. The most frequent APC mutation is a codon 1309 truncation that is associated with severe FAP. A previous study compared two mouse models of intestinal tumorigenesis, Apc(R850X) (Min) and Apc(1322T) (1322T), the latter a model of human codon 1309 changes. 1322T mice had more severe polyposis but, surprisingly, these tumours had lower levels of nuclear β-catenin than Min tumours. The consequences of these different β-catenin levels were investigated.

Original language	English
Pages (from-to)	1680-6
Number of pages	7
Journal	Gut
Volume	59
Issue number	12
DOIs	https://doi.org/10.1136/gut.2009.193680
Publication status	Published - Dec 2010

Keywords / Materials (for Non-textual outputs)

Adenomatous Polyposis Coli
Animals
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Genes, APC
Mice
Mice, Inbred C57BL
Microdissection
Neoplasm Proteins
Receptors, G-Protein-Coupled
Signal Transduction
Wnt Proteins

Access to Document

10.1136/gut.2009.193680

Cite this

Lewis, A., Segditsas, S., Deheragoda, M., Pollard, P., Jeffery, R., Nye, E., Lockstone, H., Davis, H., Clark, S., Stamp, G., Poulsom, R., Wright, N., & Tomlinson, I. (2010). Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5. Gut, 59(12), 1680-6. https://doi.org/10.1136/gut.2009.193680

@article{7a3444ef9f3d4f989eb776481ea5f4c6,

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

abstract = "Adenomatous polyposis coli (APC) is a tumour suppressor gene mutated in the germline of patients with familial adenomatous polyposis (FAP) and somatically in most colorectal cancers. APC mutations impair β-catenin degradation, resulting in increased Wnt signalling. The most frequent APC mutation is a codon 1309 truncation that is associated with severe FAP. A previous study compared two mouse models of intestinal tumorigenesis, Apc(R850X) (Min) and Apc(1322T) (1322T), the latter a model of human codon 1309 changes. 1322T mice had more severe polyposis but, surprisingly, these tumours had lower levels of nuclear β-catenin than Min tumours. The consequences of these different β-catenin levels were investigated.",

keywords = "Adenomatous Polyposis Coli, Animals, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genes, APC, Mice, Mice, Inbred C57BL, Microdissection, Neoplasm Proteins, Receptors, G-Protein-Coupled, Signal Transduction, Wnt Proteins",

author = "Annabelle Lewis and Stefania Segditsas and Maesha Deheragoda and Patrick Pollard and Rosemary Jeffery and Emma Nye and Helen Lockstone and Hayley Davis and Susan Clark and Gordon Stamp and Richard Poulsom and Nicholas Wright and Ian Tomlinson",

year = "2010",

month = dec,

doi = "10.1136/gut.2009.193680",

language = "English",

volume = "59",

pages = "1680--6",

journal = "Gut",

issn = "0017-5749",

publisher = "BMJ Publishing Group",

number = "12",

}

TY - JOUR

T1 - Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

AU - Lewis, Annabelle

AU - Segditsas, Stefania

AU - Deheragoda, Maesha

AU - Pollard, Patrick

AU - Jeffery, Rosemary

AU - Nye, Emma

AU - Lockstone, Helen

AU - Davis, Hayley

AU - Clark, Susan

AU - Stamp, Gordon

AU - Poulsom, Richard

AU - Wright, Nicholas

AU - Tomlinson, Ian

PY - 2010/12

Y1 - 2010/12

N2 - Adenomatous polyposis coli (APC) is a tumour suppressor gene mutated in the germline of patients with familial adenomatous polyposis (FAP) and somatically in most colorectal cancers. APC mutations impair β-catenin degradation, resulting in increased Wnt signalling. The most frequent APC mutation is a codon 1309 truncation that is associated with severe FAP. A previous study compared two mouse models of intestinal tumorigenesis, Apc(R850X) (Min) and Apc(1322T) (1322T), the latter a model of human codon 1309 changes. 1322T mice had more severe polyposis but, surprisingly, these tumours had lower levels of nuclear β-catenin than Min tumours. The consequences of these different β-catenin levels were investigated.

AB - Adenomatous polyposis coli (APC) is a tumour suppressor gene mutated in the germline of patients with familial adenomatous polyposis (FAP) and somatically in most colorectal cancers. APC mutations impair β-catenin degradation, resulting in increased Wnt signalling. The most frequent APC mutation is a codon 1309 truncation that is associated with severe FAP. A previous study compared two mouse models of intestinal tumorigenesis, Apc(R850X) (Min) and Apc(1322T) (1322T), the latter a model of human codon 1309 changes. 1322T mice had more severe polyposis but, surprisingly, these tumours had lower levels of nuclear β-catenin than Min tumours. The consequences of these different β-catenin levels were investigated.

KW - Adenomatous Polyposis Coli

KW - Animals

KW - Gene Expression Profiling

KW - Gene Expression Regulation, Neoplastic

KW - Genes, APC

KW - Mice

KW - Mice, Inbred C57BL

KW - Microdissection

KW - Neoplasm Proteins

KW - Receptors, G-Protein-Coupled

KW - Signal Transduction

KW - Wnt Proteins

U2 - 10.1136/gut.2009.193680

DO - 10.1136/gut.2009.193680

M3 - Article

C2 - 20926645

SN - 0017-5749

VL - 59

SP - 1680

EP - 1686

JO - Gut

JF - Gut

IS - 12

ER -

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

Abstract / Description of output

Keywords / Materials (for Non-textual outputs)

Access to Document

Fingerprint

Cite this