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Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy.

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Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy. / Abdel-Haidy, El-Said; Martin-Hirsch, Pierre L.; Duggan-Keen, Maggie; Stern, Peter L.; Moore, James V.; Corbitt, Gerald; Kitchener, Henry C.; Hampson, Ian N.

In: Cancer Research, Vol. 61, No. 1, 01.01.2001, p. 192-196.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Abdel-Haidy, E-S, Martin-Hirsch, PL, Duggan-Keen, M, Stern, PL, Moore, JV, Corbitt, G, Kitchener, HC & Hampson, IN 2001, 'Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy.', Cancer Research, vol. 61, no. 1, pp. 192-196. <http://cancerres.aacrjournals.org/cgi/content/abstract/61/1/192>

APA

Abdel-Haidy, E-S., Martin-Hirsch, P. L., Duggan-Keen, M., Stern, P. L., Moore, J. V., Corbitt, G., Kitchener, H. C., & Hampson, I. N. (2001). Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy. Cancer Research, 61(1), 192-196. http://cancerres.aacrjournals.org/cgi/content/abstract/61/1/192

Vancouver

Abdel-Haidy E-S, Martin-Hirsch PL, Duggan-Keen M, Stern PL, Moore JV, Corbitt G et al. Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy. Cancer Research. 2001 Jan 1;61(1):192-196.

Author

Abdel-Haidy, El-Said ; Martin-Hirsch, Pierre L. ; Duggan-Keen, Maggie ; Stern, Peter L. ; Moore, James V. ; Corbitt, Gerald ; Kitchener, Henry C. ; Hampson, Ian N. / Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy. In: Cancer Research. 2001 ; Vol. 61, No. 1. pp. 192-196.

Bibtex

@article{8385b931566e41899e663b7f7debf80f,
title = "Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy.",
abstract = "Topical 5-aminolevulinic acid-based photodynamic therapy (PDT) has produced complete response rates of >90% for nonmelanoma skin carcinomas, which are mostly human papillomavirus (HPV) negative. Using a similar treatment protocol, we observed a short-term response in only one third (10 of 32) of high-grade vulval intraepithelial neoplasia (VIN 2–3) lesions. Unifocal lesions were found more responsive than multifocal and pigmented lesions. Animal model studies have suggested that long-term PDT response involves an immune reaction in which CTLs play a crucial role. In this study, we have assessed: (a) HPV infection; (b) HLA expression; and (c) immune infiltrating cells in VIN biopsies from responders and nonresponders to determine whether these factors may limit response to topical 5-aminolevulinic acid-based PDT. Tissues from normal vulva (n = 9), vulval carcinoma (n = 11), and VIN (32 patients from which 19 pre- and 43 post-PDT biopsies were taken) were investigated for immune cell infiltration and HLA class I expression by immunohistochemistry and HPV infection by PCR. There was a greater likelihood of HPV positivity associated with a lack of response of VIN to PDT (P = 0.002), and VIN nonresponders were more likely to show HLA class I loss compared with responders (P = 0.030). HLA class I down-regulation was significantly greater in the carcinomas (82%, total loss) than the VIN (28%, 19%, total loss; and 9%, allele loss; P = 0.004). None of the cases with class I down-regulation responded to PDT, whereas 3 of 6 (50%) of cases that showed total class I loss subsequently developed superficial invasion. Compared with normal vulval skin, VIN lesions showed increased infiltration by CD4 (T-helper) and CD68 (macrophages) but not CD1a (Langerhans cells) or CD8 (CTLs). There was, however, a significant increase of CD8 infiltration in posttreatment VIN responders compared with nonresponders (P = 0.0001). These data clearly support the contention that high-risk HPV infection and lack of cell-mediated immunity may play a role in the observed poor response of lower genital lesions to topical PDT.",
author = "El-Said Abdel-Haidy and Martin-Hirsch, {Pierre L.} and Maggie Duggan-Keen and Stern, {Peter L.} and Moore, {James V.} and Gerald Corbitt and Kitchener, {Henry C.} and Hampson, {Ian N.}",
note = "RAE_import_type : Journal article RAE_uoa_type : Allied Health Professions and Studies",
year = "2001",
month = jan,
day = "1",
language = "English",
volume = "61",
pages = "192--196",
journal = "Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Immunological and viral factors assiciated with the response of vulval intraepithelial neoplasia to photodynamic therapy.

AU - Abdel-Haidy, El-Said

AU - Martin-Hirsch, Pierre L.

AU - Duggan-Keen, Maggie

AU - Stern, Peter L.

AU - Moore, James V.

AU - Corbitt, Gerald

AU - Kitchener, Henry C.

AU - Hampson, Ian N.

N1 - RAE_import_type : Journal article RAE_uoa_type : Allied Health Professions and Studies

PY - 2001/1/1

Y1 - 2001/1/1

N2 - Topical 5-aminolevulinic acid-based photodynamic therapy (PDT) has produced complete response rates of >90% for nonmelanoma skin carcinomas, which are mostly human papillomavirus (HPV) negative. Using a similar treatment protocol, we observed a short-term response in only one third (10 of 32) of high-grade vulval intraepithelial neoplasia (VIN 2–3) lesions. Unifocal lesions were found more responsive than multifocal and pigmented lesions. Animal model studies have suggested that long-term PDT response involves an immune reaction in which CTLs play a crucial role. In this study, we have assessed: (a) HPV infection; (b) HLA expression; and (c) immune infiltrating cells in VIN biopsies from responders and nonresponders to determine whether these factors may limit response to topical 5-aminolevulinic acid-based PDT. Tissues from normal vulva (n = 9), vulval carcinoma (n = 11), and VIN (32 patients from which 19 pre- and 43 post-PDT biopsies were taken) were investigated for immune cell infiltration and HLA class I expression by immunohistochemistry and HPV infection by PCR. There was a greater likelihood of HPV positivity associated with a lack of response of VIN to PDT (P = 0.002), and VIN nonresponders were more likely to show HLA class I loss compared with responders (P = 0.030). HLA class I down-regulation was significantly greater in the carcinomas (82%, total loss) than the VIN (28%, 19%, total loss; and 9%, allele loss; P = 0.004). None of the cases with class I down-regulation responded to PDT, whereas 3 of 6 (50%) of cases that showed total class I loss subsequently developed superficial invasion. Compared with normal vulval skin, VIN lesions showed increased infiltration by CD4 (T-helper) and CD68 (macrophages) but not CD1a (Langerhans cells) or CD8 (CTLs). There was, however, a significant increase of CD8 infiltration in posttreatment VIN responders compared with nonresponders (P = 0.0001). These data clearly support the contention that high-risk HPV infection and lack of cell-mediated immunity may play a role in the observed poor response of lower genital lesions to topical PDT.

AB - Topical 5-aminolevulinic acid-based photodynamic therapy (PDT) has produced complete response rates of >90% for nonmelanoma skin carcinomas, which are mostly human papillomavirus (HPV) negative. Using a similar treatment protocol, we observed a short-term response in only one third (10 of 32) of high-grade vulval intraepithelial neoplasia (VIN 2–3) lesions. Unifocal lesions were found more responsive than multifocal and pigmented lesions. Animal model studies have suggested that long-term PDT response involves an immune reaction in which CTLs play a crucial role. In this study, we have assessed: (a) HPV infection; (b) HLA expression; and (c) immune infiltrating cells in VIN biopsies from responders and nonresponders to determine whether these factors may limit response to topical 5-aminolevulinic acid-based PDT. Tissues from normal vulva (n = 9), vulval carcinoma (n = 11), and VIN (32 patients from which 19 pre- and 43 post-PDT biopsies were taken) were investigated for immune cell infiltration and HLA class I expression by immunohistochemistry and HPV infection by PCR. There was a greater likelihood of HPV positivity associated with a lack of response of VIN to PDT (P = 0.002), and VIN nonresponders were more likely to show HLA class I loss compared with responders (P = 0.030). HLA class I down-regulation was significantly greater in the carcinomas (82%, total loss) than the VIN (28%, 19%, total loss; and 9%, allele loss; P = 0.004). None of the cases with class I down-regulation responded to PDT, whereas 3 of 6 (50%) of cases that showed total class I loss subsequently developed superficial invasion. Compared with normal vulval skin, VIN lesions showed increased infiltration by CD4 (T-helper) and CD68 (macrophages) but not CD1a (Langerhans cells) or CD8 (CTLs). There was, however, a significant increase of CD8 infiltration in posttreatment VIN responders compared with nonresponders (P = 0.0001). These data clearly support the contention that high-risk HPV infection and lack of cell-mediated immunity may play a role in the observed poor response of lower genital lesions to topical PDT.

M3 - Journal article

VL - 61

SP - 192

EP - 196

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 1

ER -