Disease relevance of Vulvar Neoplasms

• Overexpression of wild-type p53 in lichen sclerosus adjacent to human papillomavirus-negative vulvar cancer [1].
• These findings underscore the heterogeneity of vulvar cancers with respect to loss of wild type p53 function either by interaction with the HPV E6 oncoprotein or somatic mutation of p53, and suggest that squamous hyperplasias do not serve as direct precursors of HPV-negative squamous carcinomas [2].
• One patient developed a squamous cell cancer of the anus under the midline block 54 months after the initial vulvar cancer and an additional patient developed transitional cell carcinoma of the ureter (outside the radiation field) 12 months after diagnosis [3].
• S-Phase fraction, p53, and HER-2/neu status as predictors of nodal metastasis in early vulvar cancer [4].
• Only 4 of 12 (33%) patients with vulvar cancer and 1 of 5 (20%) patients with vaginal cancer, usually those with more advanced disease, had elevated serum SCC levels at the time of diagnosis [5].

High impact information on Vulvar Neoplasms

• Somatic mutation of PTEN in vulvar cancer [6].
• The aim of the present study was to evaluate serum concentrations of vascular endothelial growth factor (VEGF) in patients with vulvar cancer and healthy female controls with respect to correlation of VEGF with clinicopathological parameters and impact on the patients' prognosis [7].
• Human papillomavirus E6 protein targets TP53 for degradation and by inference it has been assumed that human papillomavirus-negative vulvar cancer is dependent upon the acquisition of p53 somatic mutations and subsequent allelic loss [1].
• The 75% quantile of serum concentrations of SCC-Ag in patients with vulvar cancer was defined as cut-off level [8].
• Our aim was to evaluate the clinical usefulness of serum concentrations of squamous-cell carcinoma antigen (SCC-Ag) and tissue polypeptide antigen (TPA) in the follow-up of patients with vulvar cancer [9].

Chemical compound and disease context of Vulvar Neoplasms

• Technetium-99m-labelled colloid human albumin was administered perilesionally in 37 patients with invasive epidermoid vulvar cancer (T1-T2) and lymphoscintigraphy performed the day before surgery [10].
• METHODS AND MATERIALS: Thirty four patients were treated with iridium-192 (192Ir) brachytherapy for vulvar cancer between 1975 and 1993 at Centre Alexis Vautrin [11].
• 5-fluorouracil topical treatment of in situ vulvar cancer. A preliminary report [12].
• Effective chemotherapy consisting of bleomycin, vincristine, mitomycin C, and cisplatin (BOMP) for a patient with inoperable vulvar cancer [13].
• Pathologic evaluation of inguinal sentinel lymph nodes in vulvar cancer patients: a comparison of immunohistochemical staining versus ultrastaging with hematoxylin and eosin staining [14].

Biological context of Vulvar Neoplasms

• CYP2D6 genotype and the incidence of anal and vulvar cancer [15].
• We found that allelic variation within intron 4, but not ithin exon 7 of NOS3, influences the length of disease-free survival, but not the biological phenotype of vulvar cancer [16].
• To determine the relation of tumor behavior and patient survival in vulvar cancer in regard to p53 status, we retrospectively analyzed 38 paraffin-embedded specimens of primary vulvar cancer for genetic alterations of exons 5-8 of the p53 gene [17].
• Immunostaining of COX-2, expressed as values of COX-2 intensity density (COX-2 IDV) was performed on 57 metastatic TDL and 24 corresponding primary rumors from 14 cervical and 9 vulvar cancer patients admitted to the Department of Obstetrics and Gynecology, Catholic University of Rome [18].

Anatomical context of Vulvar Neoplasms

• OBJECTIVE: Primary surgical resection of locally advanced squamous cancer of the vulva may compromise the integrity of important midline structures such as the anus, clitoris, urethra, and vagina [19].

Gene context of Vulvar Neoplasms

• Although various studies showed a certain association between genes encoding the IL-1 family and human malignancies, no data with respect to vulvar cancer have been published to date [20].
• Although associated with impaired disease-free and overall survival, pre-treatment serum concentrations of VEGF are not an independent predictor of outcome in patients with vulvar cancer [21].
• In vulvar cancer COX-2 IDV in tumor cells from positive TDL were lower (median = 0.39, range 0.02-6.09) than those from primary tumors (median = 2.49, range 0.71-8.10) (p=0.04) [18].
• Immunohistochemically detected expression of CD44 isoforms containing variant exon v6 or v3 is correlated with a poor relapse-free and overall survival in FIGO stage I vulvar cancer patients [22].
• A proliferating cell nuclear antigen (Ki-67) expression was investigated in 73 cases of invasive vulvar cancer, to detect new diagnostic and prognostic factors [23].

Analytical, diagnostic and therapeutic context of Vulvar Neoplasms

• PURPOSE/OBJECTIVE: To report the long-term results of vulvectomy, node dissection, and postoperative nodal irradiation using a midline vulvar block in patients with node positive vulvar cancer [3].
• Glutathione S-transferase M1 genotypes and the risk of vulvar cancer: a population-based case-control study [24].
• METHODS: We used peripheral venous blood sampling, DNA extraction, and polymerase chain reaction (PCR) and pyrosequencing to genotype 68 women with vulvar cancer and 227 healthy Caucasian women for the presence of the intron 4 27-bp-repeat [NOS3*A] and exon 7 Glu298Asp polymorphisms [16].
• We investigated by immunohistochemistry the expression of COX-2 in normal vulvar tissue, non-neoplastic vulvar epithelial lesions, vulvar intraepithelial neoplasia (VIN) and invasive vulvar cancer (IVC) [25].
• In addition to use of the CO2 laser in gynecologic surgery for the treatment of pelvic, vaginal and vulvar neoplasms, it has been more recently applied to the treatment of infertility [26].

References