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Oncoimmunology. 2014 Jan 1;3(1):e28288. Epub 2014 Apr 15.

The transmembrane channel-like protein family and human papillomaviruses: Insights into epidermodysplasia verruciformis and progression to squamous cell carcinoma.

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1
Laboratory of Experimental Medicine; John A. Burns School of Medicine; Honolulu, HI USA ; Department of Cell and Molecular Biology; John A. Burns School of Medicine; Honolulu, HI USA.
2
Laboratory of Experimental Medicine; John A. Burns School of Medicine; Honolulu, HI USA ; Department of Cell and Molecular Biology; John A. Burns School of Medicine; Honolulu, HI USA ; Chaminade University; Honolulu, HI USA.

Abstract

Epidermodysplasia verruciformis (EV) is a rare genodermatosis characterized by increased sensitivity to infection by the β-subtype of human papillomaviruses (β-HPVs), causing persistent, tinea versicolor-like dermal lesions. In a majority of affected individuals, these macular lesions progress to invasive cutaneous squamous cell carcinoma (CSCC) in sun-exposed areas. While mutations in transmembrane channel-like 6 (TMC6 / EVER1) and 8 (TMC8 / EVER2) have been causally linked to EV, their molecular functions are unclear. It is likely that their protective effects involve regulation of the β-HPV life cycle, host keratinocyte apoptosis vs. survival balance and/or T-cell interaction with infected host cells.

KEYWORDS:

EVER1; EVER2; Epidermodysplasia verruciformis; TMC6; TMC8; cutaneous squamous cell carcinoma; papillomavirus

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