Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer

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Standard

Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer. / Isinger-Ekstrand, Anna; Therkildsen, Christina; Bernstein, Inge; Nilbert, Mef.

I: Familial Cancer, Bind 10, Nr. 2, 2011, s. 239.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Isinger-Ekstrand, A, Therkildsen, C, Bernstein, I & Nilbert, M 2011, 'Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer', Familial Cancer, bind 10, nr. 2, s. 239. https://doi.org/10.1007/s10689-010-9406-x

APA

Isinger-Ekstrand, A., Therkildsen, C., Bernstein, I., & Nilbert, M. (2011). Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer. Familial Cancer, 10(2), 239. https://doi.org/10.1007/s10689-010-9406-x

Vancouver

Isinger-Ekstrand A, Therkildsen C, Bernstein I, Nilbert M. Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer. Familial Cancer. 2011;10(2):239. https://doi.org/10.1007/s10689-010-9406-x

Author

Isinger-Ekstrand, Anna ; Therkildsen, Christina ; Bernstein, Inge ; Nilbert, Mef. / Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer. I: Familial Cancer. 2011 ; Bind 10, Nr. 2. s. 239.

Bibtex

@article{efd44d93aad74cb28202bbb3a2835762,
title = "Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer",
abstract = "The Wnt signaling pathway is frequently deranged in colorectal cancer and is a key target for future preventive and therapeutic approaches. Colorectal cancers associated with the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome are characterized by wide-spread microsatellite instability, but show few gross genomic alterations. We characterized expression of the Wnt signaling pathway markers {\ss}-catenin, E-cadherin, TCF-4, and PTEN using immunohistochemical staining in colorectal cancers from individuals with HNPCC. Reduced membranous staining for {\ss}-catenin was found in 64% and for E-cadherin in 80% with strong correlation between these markers (P = 0.001). Nuclear {\ss}-catenin staining was detected in 19% of the tumors. Overexpression of TCF-4, which is activated by {\ss}-catenin, was found in 89% and downregulation of PTEN, which suppresses nuclear accumulation of {\ss}-catenin, was present in 54% of the tumors. In summary, altered expression of target molecules in the Wnt signaling pathway was demonstrated in the vast majority of the HNPCC-associated tumors, which support deranged Wnt-signaling as a central tumorigenic mechanism also in MMR defective colorectal cancer.",
author = "Anna Isinger-Ekstrand and Christina Therkildsen and Inge Bernstein and Mef Nilbert",
year = "2011",
doi = "http://dx.doi.org/10.1007/s10689-010-9406-x",
language = "English",
volume = "10",
pages = "239",
journal = "Familial Cancer",
issn = "1389-9600",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - Deranged Wnt signaling is frequent in hereditary nonpolyposis colorectal cancer

AU - Isinger-Ekstrand, Anna

AU - Therkildsen, Christina

AU - Bernstein, Inge

AU - Nilbert, Mef

PY - 2011

Y1 - 2011

N2 - The Wnt signaling pathway is frequently deranged in colorectal cancer and is a key target for future preventive and therapeutic approaches. Colorectal cancers associated with the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome are characterized by wide-spread microsatellite instability, but show few gross genomic alterations. We characterized expression of the Wnt signaling pathway markers ß-catenin, E-cadherin, TCF-4, and PTEN using immunohistochemical staining in colorectal cancers from individuals with HNPCC. Reduced membranous staining for ß-catenin was found in 64% and for E-cadherin in 80% with strong correlation between these markers (P = 0.001). Nuclear ß-catenin staining was detected in 19% of the tumors. Overexpression of TCF-4, which is activated by ß-catenin, was found in 89% and downregulation of PTEN, which suppresses nuclear accumulation of ß-catenin, was present in 54% of the tumors. In summary, altered expression of target molecules in the Wnt signaling pathway was demonstrated in the vast majority of the HNPCC-associated tumors, which support deranged Wnt-signaling as a central tumorigenic mechanism also in MMR defective colorectal cancer.

AB - The Wnt signaling pathway is frequently deranged in colorectal cancer and is a key target for future preventive and therapeutic approaches. Colorectal cancers associated with the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome are characterized by wide-spread microsatellite instability, but show few gross genomic alterations. We characterized expression of the Wnt signaling pathway markers ß-catenin, E-cadherin, TCF-4, and PTEN using immunohistochemical staining in colorectal cancers from individuals with HNPCC. Reduced membranous staining for ß-catenin was found in 64% and for E-cadherin in 80% with strong correlation between these markers (P = 0.001). Nuclear ß-catenin staining was detected in 19% of the tumors. Overexpression of TCF-4, which is activated by ß-catenin, was found in 89% and downregulation of PTEN, which suppresses nuclear accumulation of ß-catenin, was present in 54% of the tumors. In summary, altered expression of target molecules in the Wnt signaling pathway was demonstrated in the vast majority of the HNPCC-associated tumors, which support deranged Wnt-signaling as a central tumorigenic mechanism also in MMR defective colorectal cancer.

U2 - http://dx.doi.org/10.1007/s10689-010-9406-x

DO - http://dx.doi.org/10.1007/s10689-010-9406-x

M3 - Journal article

VL - 10

SP - 239

JO - Familial Cancer

JF - Familial Cancer

SN - 1389-9600

IS - 2

ER -

ID: 34071068