Article first published online: 10 AUG 2007
British Journal of Dermatology
Volume 157, Issue 3, pages 634–635, September 2007
How to Cite
(2007), Errata. British Journal of Dermatology, 157: 634–635. doi: 10.1111/j.1365-2133.2007.08155.x
- Issue published online: 10 AUG 2007
- Article first published online: 10 AUG 2007
Vol. 157, Issue 2, 228–241, Article first published online: 6 JUN 2007
The oncogenic potential of human papillomaviruses: a review on the role of host genetics and environmental cofactors. Br J Dermatol 2007, Madkan et al.
In the above mentioned article1 there were a number of errors in the section headed ‘Susceptibility loci (EVER1, EVER2)’. The section as it should have appeared is below.
Susceptibility loci (EV1, EV2)
EV is a rare genetic disorder characterized by development of lesions associated with HPV in early childhood and malignant transformation in approximately half of patients during adulthood. Defective cellular immunity causes prolonged infection with one or several HPV types and is a characteristic feature in EV. The mechanism for the malignant transformation is thought to centre around oncogenic HPVs and the antioncogene products, p53 and pRb, in cell cycle regulation, DNA repair, and the execution of programmed cell death (apoptosis).3
Although it is known that HPV is required for the malignant transformation of cervical epithelial cells, HPV may also be associated with the malignant transformation of keratinocytes in SCCs of the skin. HPV is probably not a necessary requirement for skin carcinogenesis, but certain HPV types, especially those associated with EV, are noted to be translationally active in many SCCs of the skin.31,32
Using genetic linkage analysis on EV families, researchers have recently identified two susceptibility loci, known as EV1 and EV2 on chromosome 17 and chromosome 2, respectively Nonsense mutations of two genes (EVER1/TMC6 and EVER2/ TMC8) have been identified on the EV1 locus in affected patients. Researchers propose that proteins encoded by these genes are partly responsible for controlling EV-HPV infection.33 Such host genetic mutations may therefore be responsible for infection with carcinogenic HPV types that would have been controlled in individuals without the mutations. It is also possible that susceptibility loci exist which are involved in regulating non-EV-type HPV infections.33 Further research may discover these loci and characterize their role in HPV carcinogenesis in patients without EV.
As well as this, the affiliation details for Dr Madkan should have given as the Center for Clinical Studies and the Department of Dermatology, UT-Houston School of Medicine.
The publisher apologises for this error.