Cylindromatosis and the CYLD gene: new lessons on the molecular principles of epithelial growth control
(2007) In BioEssays 29(12). p.1203-1214- Abstract
- Analysing cylindromatosis and the associated defects in the CYLD gene is providing novel insights into the molecular principles of epithelial growth control and carcinogenesis in, and beyond, the skin. In this review, we summarize the histopathology and histogenesis of cylindromas, and the available genetic information on patients with these skin appendage tumors. Focusing on recent data concerning the normal functions and signaling interactions of the CYLD gene product, we explain how CYLD interferes with TNF-alpha or TLR-mediated signaling as well as with JNK or NF-kappa B-dependent p65/50 signaling to limit inflammation. In addition, we delineate how CYLD interferes with activation of the proto-oncogene BCl3 and with cyclin D1... (More)
- Analysing cylindromatosis and the associated defects in the CYLD gene is providing novel insights into the molecular principles of epithelial growth control and carcinogenesis in, and beyond, the skin. In this review, we summarize the histopathology and histogenesis of cylindromas, and the available genetic information on patients with these skin appendage tumors. Focusing on recent data concerning the normal functions and signaling interactions of the CYLD gene product, we explain how CYLD interferes with TNF-alpha or TLR-mediated signaling as well as with JNK or NF-kappa B-dependent p65/50 signaling to limit inflammation. In addition, we delineate how CYLD interferes with activation of the proto-oncogene BCl3 and with cyclin D1 expression to limit tumorigenesis, and chart how tumor growth-promoting agents or UV light and inflammatory mediators can activate CYLD. We argue that these recent insights into CYLD function and cylindroma pathogenesis may lead to the development of novel molecular strategies for cancer prevention and treatment. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/966418
- author
- Massoumi, Ramin LU and Paus, Ralf
- organization
- publishing date
- 2007
- type
- Contribution to journal
- publication status
- published
- subject
- in
- BioEssays
- volume
- 29
- issue
- 12
- pages
- 1203 - 1214
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000251526300006
- scopus:36849035347
- ISSN
- 0265-9247
- DOI
- 10.1002/bies.20677
- language
- English
- LU publication?
- yes
- id
- 40c2e067-4db2-439a-9599-fd919ee302a8 (old id 966418)
- date added to LUP
- 2016-04-01 11:43:00
- date last changed
- 2022-05-06 08:10:26
@article{40c2e067-4db2-439a-9599-fd919ee302a8, abstract = {{Analysing cylindromatosis and the associated defects in the CYLD gene is providing novel insights into the molecular principles of epithelial growth control and carcinogenesis in, and beyond, the skin. In this review, we summarize the histopathology and histogenesis of cylindromas, and the available genetic information on patients with these skin appendage tumors. Focusing on recent data concerning the normal functions and signaling interactions of the CYLD gene product, we explain how CYLD interferes with TNF-alpha or TLR-mediated signaling as well as with JNK or NF-kappa B-dependent p65/50 signaling to limit inflammation. In addition, we delineate how CYLD interferes with activation of the proto-oncogene BCl3 and with cyclin D1 expression to limit tumorigenesis, and chart how tumor growth-promoting agents or UV light and inflammatory mediators can activate CYLD. We argue that these recent insights into CYLD function and cylindroma pathogenesis may lead to the development of novel molecular strategies for cancer prevention and treatment.}}, author = {{Massoumi, Ramin and Paus, Ralf}}, issn = {{0265-9247}}, language = {{eng}}, number = {{12}}, pages = {{1203--1214}}, publisher = {{John Wiley & Sons Inc.}}, series = {{BioEssays}}, title = {{Cylindromatosis and the CYLD gene: new lessons on the molecular principles of epithelial growth control}}, url = {{http://dx.doi.org/10.1002/bies.20677}}, doi = {{10.1002/bies.20677}}, volume = {{29}}, year = {{2007}}, }