Background Of Lichen Sclerosus Research Articles

Identification of potential prognostic biomarkers in vulval squamous cell carcinoma based on human papillomavirus infection Status-Analysis of GSE183454

This study aimed to elucidate the differences in vulval squamous cell carcinomas (VSCC) based on the HPV infection status. The sequencing data GSE183454 which contains 23 VSCC samples based on its HPV infection status was obtained from the Gene Expression Omnibus (GEO) database. We comprehensively dissected the differences of genomic and tumour microenvironment (TME) immune cell infiltration landscapes between HPV + and HPV- VSCC. The potential molecular mechanisms of prognostic genes were explored by functional enrichment analysis. Five novel key molecules (SYCP2, SMC1B, RNF212, MAJIN and C14orf39) with significantly up-regulated expression in HPV + VSCC were identified while protein-protein interaction (PPI) networks were created upon Cytoscape software. Additionally, VSCC with up-regulated expression of these key molecules exhibited a significantly decreased TME immune cell infiltration. SYCP2 is overexpressed in HPV + VSCC and could be a candidate therapy target for further research. IMPACT STATEMENT What is already known on this subject? VSCC are characterised by two aetiological pathways. The former occurs in the background of lichen sclerosus, while the latter is related to HPV infection. VSCC most commonly arises from the non-HPV related pathway portends worse prognosis than VSCC derived from HPV infection. What do the results of this study add? Five key molecules are identified and significantly up-regulated in HPV + VSCC. In which, SYCP2 is overexpressed in HPV + VSCC and exhibited a significantly decreased TME immune cell infiltration. SYCP2 constant expression could be a potential biomarker of neoplasms associated with HPV and could be a candidate therapy target in VSCC especially HPV + VSCC for further research. What are the implications of these findings for clinical practice and/or further research? SYCP2 could be a candidate therapy target in VSCC especially with HPV + for further research.

Pseudoepitheliomatous keratotic and micaceous balanitis: a series of eight cases.

Pseudoepitheliomatous keratotic and micaceous balanitis (PEKMB) is a clinicopathological entity characterized clinically by micaceous scale on the glans, and histologically by acanthosis, hyperkeratosis and pseudoepitheliomatous hyperplasia. We present a series of eight cases of this rare condition, the first series of more than two cases to be reported. To determine the clinical and histological characteristics of cases of PEKMB, and evaluate treatments used and clinical course. This monocentric case series was conducted at the University College London Hospitals tertiary male genital dermatology clinic between April 2018 and August 2020. Eight patients with PEKMB were evaluated. Data were collected on demographics, clinical presentation, histological features, presence of human papilloma virus (HPV), history of lichen sclerosus, treatment of PEKMB and subsequent response, and presence or development of squamous cell carcinoma (SCC) or penile intraepithelial neoplasia (PeIN) during follow-up. Eight Caucasian males presented with clinical and histological evidence of PEKMB. Seven had a background of lichen sclerosus; two had failed treatment with superpotent topical steroids and four had symptoms for three or more years prior to circumcision. There was no clinical or histological relationship with HPV infection, and p16 staining was negative. HPV PCR, performed in two cases, was negative. Basal atypia, insufficient to amount to PeIN, was present in six patients. One patient progressed to PeIN during follow-up, and no patient progressed to invasive malignancy. Five patients were treated successfully with glans resurfacing and split skin graft reconstruction. Our observations demonstrate that PEKMB represents a form of chronic, undiagnosed or misdiagnosed, inadequately treated or treatment refractory, unstable lichen sclerosus. The significant potential for squamous carcinogenesis (differentiated PeIN and verrucous carcinoma) can be mitigated by timely diagnosis and treatment. Glans resurfacing and split skin graft reconstruction appears to be a successful treatment modality in patients with refractory disease.

070 (When) should we biopsy a vulvar naevus in a child or adolescent?

Objective: Decision-making regarding pigmented genital lesions in childhood or adolescence may be difficult. These are ‘special-site’ nevi1 and generally have a benign clinical course even when seeming clinically worrisome or showing disconcerting histological signs of atypia or dysplasia [ [1] Ahn C.S. Guerra A. Sangüeza O.P. Melanocytic nevi of special sites. Am J Dermatopathol. 2016; 38: 867-878 Crossref PubMed Scopus (15) Google Scholar ], especially when the naevus is in a background of vulvar lichen sclerosus (VLS) in a juvenile [ 2 Pinto A. McLaren S.H. Poppas D.P. Magro C.M. Genital melanocytic nevus arising in a background of lichen sclerosus in a 7-year-old female: The diagnostic pitfall with malignant Melanoma. A literature review. Am J Dermatopathol. 2012; 34: 838-843 Crossref PubMed Scopus (17) Google Scholar , 3 La Spina M. Meli M.C. De Pasquale R. Perrotta R.E. Lanzafame F. Caltabiano R. et al. Vulvar Melanoma Associated with Lichen Sclerosus in a Child: Case Report and Literature Review. Pediatr Dermatol. 2016; 33: E190-E194 Crossref PubMed Scopus (17) Google Scholar ]. The clinician would like to rule out malignant melanoma. Few case studies of vulvar melanoma in juveniles have been published, and those cases reported were generally found with concomitant VLS, making histopathological analysis complex [ 2 Pinto A. McLaren S.H. Poppas D.P. Magro C.M. Genital melanocytic nevus arising in a background of lichen sclerosus in a 7-year-old female: The diagnostic pitfall with malignant Melanoma. A literature review. Am J Dermatopathol. 2012; 34: 838-843 Crossref PubMed Scopus (17) Google Scholar , 3 La Spina M. Meli M.C. De Pasquale R. Perrotta R.E. Lanzafame F. Caltabiano R. et al. Vulvar Melanoma Associated with Lichen Sclerosus in a Child: Case Report and Literature Review. Pediatr Dermatol. 2016; 33: E190-E194 Crossref PubMed Scopus (17) Google Scholar , 4 Schaffer J.V. Orlow S.J. Melanocytic proliferations in the setting of vulvar lichen sclerosus: diagnostic considerations. Pediatr Dermatol. 2005; 22 (author reply 8–9): 276-278 Crossref PubMed Scopus (13) Google Scholar ]. Studying the prevalence of malignant melanocytic vulvar lesions in juveniles could support clinicians when deciding whether or not to biopsy.

Management of Advanced Squamous Cell Carcinoma of the Vulva.

Simple SummaryVulvar cancer is a rare gynaecological malignancy that has an increasing incidence, particularly in younger women. Early vulvar cancer can be treated and cured with surgical excision. Approximately 30% of women present with advanced disease, which requires treatment either with mutilating surgery or a combination of chemotherapy and radiotherapy, which is an effective treatment but has many side effects. Current research is focused on new less morbid approaches to treatment, in which drugs that target various steps on the biological pathway from pre-cancer to cancer are used, with the aim of preventing the growth of vulvar cancers. This review is an update of the current management of women with advanced vulvar cancer.Vulvar cancer is a rare gynaecological malignancy, accounting for 2–5% of cancers of the female genital tract. Squamous cell carcinoma is the most frequently occurring subtype and, historically, has been a disease of older post-menopausal women, occurring with a background of lichen sclerosus and other epithelial conditions of the vulvar skin that may be associated with well-differentiated vulvar intra-epithelial neoplasia (dVIN). An increase in human papillomavirus (HPV) infections worldwide has led to an increase in vulvar squamous carcinomas in younger women, resulting from HPV-associated high-grade vulvar squamous intra-epithelial lesions (vHSIL). Surgical resection is the gold standard for the treatment of vulvar cancer. However, as approximately 30% of patients present with locally advanced disease, which is either irresectable or will require radical surgical resection, possibly with a stoma, there has been a need to investigate alternative forms of treatment such as chemoradiation and targeted therapies, which may minimise the psychosexual morbidity of radical surgery. This review aims to provide an update on management strategies for women with advanced vulvar cancer. It is hoped that investigation of the molecular biologies of the two different pathways to vulvar squamous cell carcinoma (HPV-associated and non-HPV-associated) will lead to the development of targeted therapeutic agents.

Somatic Mutation Profiling in Premalignant Lesions of Vulvar Squamous Cell Carcinoma.

Vulvar squamous cell carcinoma (VSCC) originates from the progression of either a high-grade squamous intraepithelial lesion (HSIL) or differentiated-type vulvar intraepithelial neoplasia (dVIN), often in a background of lichen sclerosus (LS). The mechanisms leading to the progression of these premalignant lesions to VSCC are elusive. This study aims to identify pathogenic mutations implicated in VSCC development. Using next-generation sequencing, 38 HSIL, 19 dVIN, 20 LS, of which 10 were solitary lesions and 10 with adjacent VSCC, and 10 VSCC adjacent to LS, were screened for hotspot mutations in 50 genes covered by the Ion AmpliSeq Cancer Hotspot Panel v2 Kit (Thermo Fisher Scientific). Pathogenic mutations of TP53 were the most common genetic alterations identified in 53% and 24% of dVIN and HSIL cases, respectively, followed by CDKN2A (p16) mutated in 42% and 0% of dVIN and HSIL, respectively. Seven (70%) and three (30%) of 10 cases of VSCC associated with LS carried TP53 and CDKN2A mutations, respectively, whereas neither solitary LS nor LS associated with VSCC cases harbored mutations in these genes. It appears that TP53 mutations are early events during VSCC carcinogenesis, being present in both HSIL and dVIN lesions. Our preliminary data do not support a genetic background for the notion of LS as the VSCC premalignant lesion.

Under expression of the Sonic Hedgehog receptor, Patched1 (PTCH1), is associated with an increased risk of local recurrence in squamous cell carcinoma of the vulva arising on a background of Lichen Sclerosus

ObjectiveDysregulation of the Hedgehog (Hh) pathway has been described in a variety of cancers, including cervical cancer, a disease which shares a common aetiology with vulval squamous cell carcinoma (VSCC). Here, we investigate a large number of primary VSCC cases for evidence of Hedgehog pathway activation and examine the implications of pathway activity on clinical outcomes in a cohort of patients with primary VSCC.MethodsArchival histology blocks containing VSCC and histologically normal adjacent epithelium were retrieved from a cohort of 91 patients who underwent treatment for primary VSCC. Immunohistochemistry staining was undertaken to assess for the expression of key Hh pathway components (SHH, PTCH1, GLI1). A competing risks statistical model was used to evaluate the implications of the levels of key Hh pathway components on clinical outcomes.ResultsWe show that 92% of primary VSCC cases over-expressed one or more components of the Hh signalling pathway when compared to the adjacent normal epithelium. While expression of SHH and GLI1 did not correlate with any clinicopathological criteria, over- or under-expression of PTCH1 was associated with a reduced or increased risk of developing a local disease recurrence, respectively. In VSCC arising on a background of Lichen Sclerosus, the risk of local recurrence was potentiated in cases where PTCH1 was under-expressed.ConclusionsOur findings reveal, for the first time, that the Hh pathway is activated in VSCC and that PTCH1 expression can be used as a biomarker to stratify patients and inform clinicians of the risk of their local recurrence, particularly in cases of VSCC associated with LS.

Vulvar cancer: Two pathways with different localization and prognosis

BackgroundTwo etiologic pathways for vulvar squamous cell carcinoma (SCC) are described: in a background of lichen sclerosus and/or differentiated vulvar intraepithelial neoplasia and related to high-risk human papillomavirus (HPV) infection with high grade squamous intraepithelial lesion (HSIL) as precursor. The aim was to compare the predilection site and survival of HPV-related to non HPV-related vulvar SCCs. MethodsData of patients treated for primary vulvar SCC at the Radboudumc between March 1988 and January 2015 were analyzed. All histological specimens were tested for HPV with the SPF10/DEIA/LiPA25 system assay and p16INK4a staining was performed using CINtec® histology kit. Vulvar SCCs were considered HPV-related in case of either >25% p16INK4a expression and HPV positivity or >25% p16INK4a expression and HSIL next to the tumor without HPV positivity. Tumor localization, disease specific survival (DSS), disease free survival (DFS) and overall survival (OS) of patients with HPV-related and non HPV-related vulvar SCC were compared. ResultsIn total 318 patients were included: 55 (17%) had HPV-related (Group 1) and 263 (83%) had non HPV-related vulvar SCC (Group 2). Tumors in Group 1 were significantly more often located at the perineum compared to Group 2, 30% and 14%, respectively (p=0.001). The DSS, DFS and OS were significantly better in HPV-related than in non HPV-related vulvar SCC patients. ConclusionHPV-related vulvar SCCs are more frequently located at the perineum and have a favorable prognosis compared to non HPV-related vulvar SCCs. Both localization and HPV-relation could explain this favorable prognosis. HPV-related vulvar SCC seems to be a separate entity.

Assessment of CK17 as a Marker for the Diagnosis of Differentiated Vulvar Intraepithelial Neoplasia.

Differentiated vulvar intraepithelial neoplasia (dVIN), precursor of vulvar squamous cell carcinoma, is human papilloma virus independent and often found in a background of lichen sclerosus (LS) and lichen simplex chronicus (LSC). Subtle histologic findings make the diagnosis of dVIN difficult, and, although the use of p53 and Ki-67 has been of some value, there is a need for a better immunohistochemical marker. Cytokeratin 17 (CK17), a cytoskeletal intermediate filament protein, has previously been used in the diagnosis of anogenital lesions. Here we evaluated CK17 in dVIN in comparison with LS, LSC, and usual VIN (uVIN/HSIL). Twenty-nine cases of dVIN, 9 cases of uVIN, 8 cases of LS, and 7 of LSC were evaluated using CK17, Ki-67, and p53. All 29 dVIN cases displayed immunoreactivity for CK17, with 27 (93%) showing intermediate to strong and diffuse reactivity. No cases of uVIN displayed diffuse CK17 expression, whereas 63% of LS and 29% of LSC displayed intermediate to strong diffuse immunoreactivity, confined to the upper half of the epithelium. P53 and Ki-67 expression was present in varying degrees in all types of lesions, displaying limited discriminatory power for dVIN. Our findings suggest that CK17, although not specific for dVIN, when combined with histologic findings, Ki-67, and p53 immunohistochemistry, can be a marker of vulvar dysplasia and serve as an adjunct in the diagnosis of dVIN. Specifically, in small biopsies, the presence of diffuse suprabasal or full thickness expression strongly favors a diagnosis of dVIN over LSC, whereas focal and/or superficial expression supports a diagnosis of LSC.

Spindle Cell Carcinoma of the Vulva

Spindle cell or sarcomatoid squamous cell carcinoma is an uncommon variant of squamous cell carcinoma of the vulva (SCCV) with only 12 well-documented cases reported to date. Morphologically tumors may be biphasic or monophasic, and uncommonly include heterologous elements. Only 1 reported vulval tumor has previously been investigated for human papillomavirus DNA content. We describe 4 women with spindle cell (sarcomatoid) SCCV, 3 of which occurred de novo and 1 followed radiotherapy for previous SCCV. The tumors in all 4 women arose in a background of lichen sclerosus, and 3 were associated with vulval intraepithelial neoplasia differentiated (simplex) type. All tumors were negative for human papillomavirus DNA on polymerase chain reaction analysis. One case is the second reported with malignant heterologous elements described in the vulva. These tumors seem to be more aggressive than conventional SCCV.

Two major pathways of penile carcinogenesis: HPV-induced penile cancers overexpress p16ink4a, HPV-negative cancers associated with dermatoses express p53, but lack p16ink4a overexpression

Penile squamous cell carcinomas (SCC) arise either through transforming infections with human papillomavirus (HPV) or independent of HPV, often in the background of lichen sclerosus (LS) and lichen planus (LP). Despite impact on therapy and prognosis, etiologic stratifications are missing in most histological diagnoses and publications about penile cancers/precursors. Classification of penile lesions into HPV-induced or HPV-negative via immunohistochemical demonstration of p16(ink4a) overexpression, a surrogate marker for transforming HPV-high-risk infections, and p53 expression in the absence of p16(ink4a) overexpression. Archival formalin-fixed material of 123 invasive penile cancers and 43 pre-invasive lesions was evaluated for the presence of LS, LP, 28 HPV genotypes, and expression of p53 and p16(ink4a). Seventy-two of 123 SCCs and 33 of 43 pre-invasive lesions showed p16(ink4a) overexpression independent of HPV-HR genotypes involved; 66 of 72 SCCs and 29 of 43 precursor lesions revealed a single HPV-high-risk-genotype (HPV-HR16 in 76% followed by HPV33, HPV31, HPV45, HPV18, HPV56); 5 of 72 SCCs and 4 of 43 precursor lesions revealed multiple HPV-HR-genotypes. One SCC revealed HPV-LR and HR-DNA. Fifty-one of 123 SCCs and 10 precursor lesions were p16(ink4a) negative, but showed nuclear p53 expression in tumor cells and basal keratinocytes. Forty-nine of 51 SCCs and 10 of 10 precursor lesions lacked HPV DNA. Two of 51 SCCs contained HPV18 and HPV45 DNA, respectively, but p16(ink4a) negativity classified them as non-HPV-induced. Twenty-seven of 51 SCCs showed peritumoral LS, 13 of 51 SCCs showed peritumoral LP, and 11 SCCs revealed no peritumoral tissue. Histologically, HPV-negative precursors showed hyperkeratotic, verrucous, atrophic, and basaloid differentiation. This was a retrospective study. p16(ink4a) overexpression identifies HPV-HR-induced penile carcinogenesis independent of HPV-HR genotype. p53 expression along with p16(ink4a) negativity identifies HPV-negative cancers. Correct etiologic classification of penile lesions during diagnostic work-up allows optimal therapy decisions.

Unique case of dual gynecological malignancies co-existing with an uncommon thyroid lymphoma

Synchronous primaries are uncommon in medical literature but pose many diagnostic and therapeutic challenges which require a multi-disciplinary approach. A 64-year-old female was presented with a vulva lesion and bilateral inguinal lymphadenopathy. She was also noted to have a palpable abdominal growth and an enlarged neck mass. Blood evaluation yielded elevated CA-125 and thyroid stimulating hormone levels. All other tests were unremarkable. Computed tomography of the neck showed a large thyroid mass with bilateral lobe involvement and abdominal scanning showed a large cystic lesion causing right hydronephrosis and hydroureter. She was diagnosed with a primary vulva squamous carcinoma in a background of lichen sclerosus which was managed surgically. The patient also underwent laparotomy and was found to have a borderline ovarian malignancy. A neck biopsy yielded a thyroid lymphoma which was treated with chemotherapy. Prophylactic radiation to the groin was performed after multi-disciplinary consult. There was an excellent clinical response to the treatment. This is the first report of concurrent vulva and ovarian pathology associated with a hematologic malignancy. Specific immunologic and genetic abnormalities have not yet been identified in literature which may link these supposedly random occurrences. However, the immune dysregulation associated with lichen sclerosus and its role in the pathogenesis of vulva squamous carcinoma is of interest in the background of a co-existing hematological malignancy, and an inherent compromised immune response. In addition, ongoing genetic research may yet elucidate a common link between these synchronous primaries.

Genital Melanocytic Nevus Arising in a Background of Lichen Sclerosus in a 7-Year-Old Female

Genital melanocytic nevus represents a distinct form of melanocytic proliferation, which can exhibit significant atypia, both clinically and histologically. In a background of lichen sclerosus (LS), the histologic changes could be misconstrued as indicative of malignant melanoma. We present herein a case of the atypical genital nevus of childhood complicated by LS, and a review of the literature is performed. Tissue was available for routine light microscopy and immunohistochemical evaluation to assess the expression of soluble adenylyl cyclase. Fluorescent in situ hybridization studies were conducted to assess for abnormalities in Myb1, CCND1, RREB1 and CEP6. The specimen showed an atypical compound melanocytic proliferation arising in a background of LS. The lesion exhibited significant architectural atypia based on the high-density confluent nature of the junctional melanocytic proliferation with epidermal effacement, rare areas of pagetoid ascent, and the heavily pigmented epithelioid quality of the melanocytes. Fluorescent in situ hybridization studies were normal. The soluble adenylyl cyclase antibody preparation demonstrated a benign nevus-like pattern. The lesion was felt to represent an atypical genital melanocytic nevus, which can resemble a partially regressed melanoma in a background of LS. It is very important for the pathologist to be aware of this entity to avoid misdiagnosis.

Differentiated (Simplex) Vulvar Intraepithelial Neoplasia: A Case Report and Review of the Literature

Differentiated (simplex) vulvar intraepithelial neoplasia (VIN) is an uncommon variant of VIN characterized by highly differentiated morphology, making it a potential diagnostic pitfall. It may arise in the background of lichen sclerosus, and unlike most VIN, is not causally associated with human papilloma virus infection. It occurs in an older demographic and is thought to be the precursor of aggressive, invasive vulvar squamous cell carcinoma. For this reason, the timely and accurate diagnosis of this unusual lesion is crucial. The clinical and histologic features of a case of a 70-year-old woman with newly diagnosed differentiated (simplex) VIN arising in a background of long-standing lichen sclerosus is reported, and the historic aspects, current terminology, and diagnostic criteria of differentiated (simplex) VIN are reviewed.

Two Distinct Pathways to Development of Squamous Cell Carcinoma of the Vulva

Squamous cell carcinoma (SCC) accounts for approximately 95% of the malignant tumors of the vaginal vulva and is mostly found in elderly women. The future numbers of patients with vulvar SCC is expected to rise, mainly because of the proportional increase in the average age of the general population. Two different pathways for vulvar SCC have been put forth. The first pathway is triggered by infection with a high-risk-type Human Papillomavirus (HPV). Integration of the HPV DNA into the host genome leads to the development of a typical vulvar intraepithelial neoplasia (VIN), accompanied with overexpression of p14ARF and p16INK4A. This lesion subsequently forms a warty- or basaloid-type SCC. The HPV vaccine is a promising new tool for prevention of this HPV related SCC of the vulva. The second pathway is HPV-independent. Keratinizing SCC develops within a background of lichen sclerosus (LS) through a differentiated VIN. It has a different set of genetic alterations than those in the first pathway, including p53 mutations, allelic imbalances (AI), and microsatellite instability (MSI). Further clinical and basic research is still required to understand and prevent vulvar SCC. Capsule. Two pathway for pathogenesis of squamous cell carcinoma of the value are reviewed.

17. Is differentiated VIN a cancer precursor in women with vulval lichen sclerosus?

Introduction Approximately 60% of squamous cell carcinomas of the vulva (SCCV) arise in a background of lichen sclerosus (LS), and 30% in HPV-related ‘undifferentiated’ VIN. The pathogenesis of cancer arising in LS is unclear, occurring in less than 5% of women. In some women, an additional histological finding of differentiated VIN (DVIN, HPV negative) may be recognised in the skin adjacent to an invasive tumour, only rarely prior to invasion. Aim To evaluate the histology of vulval biopsies or excised specimens in women with LS who developed invasive cancer at least 6 months later. Methods The clinical records and histology of 206 women presenting to the Auckland Regional Gynaecological Cancer Unit (National Women’s Hospital) between 1990 and 2007 with SCCV were reviewed retrospectively. Results Invasive SCCV was found in a background of LS in 103 women (50%). Sixteen of these women (16%) had had a biopsy at least 6 months before presenting with their index vulval tumour. In 9 cases (56%) DVIN was demonstrated on biopsy, and in 7 cases LS alone. A second group of 17 women previously treated for SCCV presented with 26 subsequent ‘new’ cancers at least 6 months following complete excision of the earlier tumour. Review of the histology of the 26 tumours revealed incompletely excised DVIN in 12 (46%). Conclusions This study has demonstrated DVIN in previous biopsies or excised specimens in a significant proportion of women in whom invasive carcinoma has developed in a background of LS. These findings suggest DVIN is a cancer precursor in women with vulval LS.

Vulvar squamous cell carcinoma

Vulvar squamous cell carcinomas account for 90% of all vulvar cancers and originate following two different pathways. Approximately 20% of all vulvar squamous cell carcinomas are caused by an infection with high-risk human papillomavirus. It has been hypothesized that most of these vulvar cancers may be prevented by the recently introduced human papillomavirus 16/18 vaccines. However, the majority of vulvar cancers develop in a background of lichen sclerosus and differentiated vulvar intraepithelial neoplasia, of which the exact oncogenesis is unknown. Surgery is the cornerstone of therapy and has evolved from a radical vulvectomy with en bloc bilateral inguinofemoral lymphadenectomy to a less radical approach. In this review, this evolution is described, with the sentinel node procedure as the most recent development. In addition, attention is paid to prognostic factors and recurrence patterns.

Analysis of lymphocytic infiltrate does not help in prediction of vulvar squamous cell carcinoma arising in a background of lichen sclerosus

International Journal of Gynecology & ObstetricsVolume 100, Issue 2 p. 190-191 Brief communications Analysis of lymphocytic infiltrate does not help in prediction of vulvar squamous cell carcinoma arising in a background of lichen sclerosus M.R. Raspollini, Corresponding Author M.R. Raspollini [email protected] Department of Human Pathology and Oncology, School of Medicine, University of Florence, Florence, ItalyCorresponding author. Department of Human Pathology and Oncology, University of Florence, School of Medicine, Viale G.B. Morgagni, 85, 50134 Florence, Italy. Tel.: +39 055 4478110; fax: +39 055 4379868.Search for more papers by this authorG. Asirelli, G. Asirelli Department of Human Pathology and Oncology, School of Medicine, University of Florence, Florence, ItalySearch for more papers by this authorG.L. Taddei, G.L. Taddei Department of Human Pathology and Oncology, School of Medicine, University of Florence, Florence, ItalySearch for more papers by this author M.R. Raspollini, Corresponding Author M.R. Raspollini [email protected] Department of Human Pathology and Oncology, School of Medicine, University of Florence, Florence, ItalyCorresponding author. Department of Human Pathology and Oncology, University of Florence, School of Medicine, Viale G.B. Morgagni, 85, 50134 Florence, Italy. Tel.: +39 055 4478110; fax: +39 055 4379868.Search for more papers by this authorG. Asirelli, G. Asirelli Department of Human Pathology and Oncology, School of Medicine, University of Florence, Florence, ItalySearch for more papers by this authorG.L. Taddei, G.L. Taddei Department of Human Pathology and Oncology, School of Medicine, University of Florence, Florence, ItalySearch for more papers by this author First published: 27 September 2007 https://doi.org/10.1016/j.ijgo.2007.07.019Citations: 3Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume100, Issue2February 2008Pages 190-191 RelatedInformation

The association of squamous cell carcinoma of the vulva and lichen sclerosus: implications for management and follow up

Summary All cases of biopsy proven squamous cell carcinoma (SCC) of the vulva and of lichen sclerosus (LS) presenting to a district general hospital between 1984 and 1993 were studied. Twenty-eight cases of squamous cell carcinoma of the vulva were identified from histological specimens. Histological evidence of LS was found in 28.5% and clinical LS in 57%. There was poor correlation between clinical and histological findings when SCC arose on a background of LS. A second study of all cases of histological LS over the same period showed the incidence of SCC in vulval LS to be 7%.