Clinical Characteristics Associated With Development of Recurrence and Progression in Usual-Type Vulvar Intraepithelial Neoplasia

Esch, Edith M.G. van; Dam, Maija C.I.; Osse, Michelle; Putter, Hein; Trimbos, Baptist; Fleuren, G. J.; Burg, Sjoerd H. van der; Poelgeest, Mariëtte I.E. van

doi:10.1097/igc.0b013e3182a57fd6

Cited by 49 publications

(44 citation statements)

References 39 publications

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“…Overall results related to smoking status, history of genital warts and multicentric disease were similar to those reported in the literature [4,14,15]. Our data includes M information on the use of antiretroviral therapy in 78% of women.…”

Section: Discussionsupporting

confidence: 91%

“…The development of vulvar carcinoma had classically been associated with older age even though recent studies suggest it is increasingly affecting premenopausal women [5,27]. Other reported risk factors for progression include immunosuppression, the presence of unifocal lesions and multicentric disease [15,25]. Our results only showed association to HIV infection.…”

Section: Discussionmentioning

confidence: 78%

“…VIN can progress to invasive carcinoma with rates between 3 and 15% been reported in the literature [15,16,25,26]. The development of vulvar carcinoma had classically been associated with older age even though recent studies suggest it is increasingly affecting premenopausal women [5,27].…”

Section: Discussionmentioning

confidence: 97%

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Vulvar intraepithelial neoplasia

Bradbury

Cabrera²,

García-Jiménez³

et al. 2016

Aids

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HIV-positive women are at increased risk of developing VIN and frequently present at a younger age with multifocal and multicentric disease. They have shorter RFS and PFS compared with HIV-negative women. Close surveillance of the lower genital tract is mandatory to enable early recognition and treatment of any suspicious lesions. Close follow-up after treatment of VIN is essential to exclude early recurrence or progression.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 78%

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Vulvar intraepithelial neoplasia

Bradbury

Cabrera²,

García-Jiménez³

et al. 2016

Aids

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“…Previously, we had identified multifocality of uVIN lesions, most often found in relation to larger lesions, as the only clinical prognostic factor for recurrence in this cohort. 34 A larger lesion size was found associated with a lower capacity to respond to therapeutic vaccination. 6 Potentially, intraepithelial myeloid cell infiltration may also influence the outcome of immunotherapeutic approaches since CD141 and CD681 cells were also higher in patients that failed to clear their VIN lesion after imiquimod treatment.…”

Section: Discussionmentioning

confidence: 97%

“…Patients were divided into groups based on the median of infiltrating cells and both an univariate (Log Rank) and multivariate analysis corrected for multifocality of uVIN (Cox proportional hazard model) were performed for RFS analysis, since this was previously identified as prognostic marker in our study cohort. 34 Two sided p-values <0.05 were considered statistical significant. GraphPad Prism 5.04 (Graphpad Software, LA Jolla, CA) was used to illustrate the data by graphs and figures.…”

Section: Discussionmentioning

confidence: 99%

Intraepithelial macrophage infiltration is related to a high number of regulatory T cells and promotes a progressive course of HPV‐induced vulvar neoplasia

Esch

Poelgeest

Trimbos

et al. 2014

Intl Journal of Cancer

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Human papilloma virus (HPV)-induced usual-type vulvar intraepithelial neoplasia (uVIN) is infiltrated by myeloid cells but the type and role of these cells is unclear. We used triple immunofluorescent confocal microscopy to locate, identify and quantify myeloid cells based on their staining pattern for CD14, CD33 and CD163 in a cohort of 43 primary and 20 recurrent uVIN lesions, 21 carcinomas and 26 normal vulvar tissues. The progressive course of uVIN is characterized by an increase in both intraepithelial and stromal mature M1 and M2 macrophages. While the M2 macrophages outnumber M1 macrophages in healthy controls and uVIN, they are matched in number by M1 macrophages in cancer. Importantly, uVIN patients with a dense intraepithelial infiltration with mature CD141 macrophages (irrespective of M1 or M2 type) displayed approximately a six times higher risk to develop a recurrence and a high number of these cells constituted an independent prognostic factor for recurrence. In addition, a dense intraepithelial CD141 cell infiltration was associated with high numbers of intraepithelial CD41 Tregs and low numbers of stromal CD81TIM31 T cells. Patients with low numbers of intraepithelial CD141 cells and high numbers of stromal CD81TIM31 cells showed the best recurrence-free survival. These data clearly show the importance of the local immune response in HPV-induced vulvar neoplasia and may be of help in predicting the prognosis of patients or their response to immunotherapy.Usual-type vulvar intraepithelial neoplasia (uVIN) lesions are caused by a persistent high-risk human papilloma virus (HPV) infection (mainly HPV 16) and are characterized by high recurrences, a low spontaneous regression rate of 1.5% and a malignant potential of 3-4% in treated patients. [1][2][3] Treatment of uVIN lesions is indispensable since 80% of patients suffer from symptoms as pruritis and pain. 2-4 Conventional treatment consistent of potential disfiguring surgical interventions is associated with psychosexual problems and is increasingly replaced by either standardized immunotherapy with imiquimod or immunotherapy in experimental setting by therapeutic vaccination or photodynamic therapy, with promising clinical successes. [2][3][4][5][6][7][8] The incidence of hrHPV-induced dysplasia is increased in immunocompromised patients highlighting the essential role of the immune system in viral clearance. 9,10 Spontaneous regression of HPV is associated with systemic HPV-specific CD41 and CD81 immune responses, however in most of the patients with uVIN these T cell responses are either weak or absent. 11,12 In addition, the local innate immune cell environment is known to influence innate and adaptive immune responses in tumors. 13,14 Monocytes are innate immune cells which can differentiate into dendritic cells (DCs) or macrophages in response to local factors. 13 DCs process and present antigens to T cells, stimulate cytotoxicity of NK cells and initiate the adaptive immune response. 15 Studies of the microenvironment in uVIN revealed that ...

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