title: Intraoral squamous cell carcinoma in human immunodeficiency virus infection. A clinicopathologic study.
abstract: The purpose of this study was to characterize the clinical and histological features of intraoral squamous cell carcinoma in men who were seropositive for the human immunodeficiency virus and to evaluate viral cofactors (human papillomavirus, herpes simplex virus, Epstein-Barr virus), proliferative index (proliferating cell nuclear antigen), a factor associated with invasion (cathepsin D), and mutated tumor suppressor gene and proto-oncogene products (mutated p53, c-erbB-2). Four men who were seropositive for the human immunodeficiency virus and had acquired immunodeficiency syndrome presented with painful oral lesions of variable duration. Oral cancer risk factors included heavy tobacco use (four of four), heavy alcohol use (three of four), and previous radiotherapy (one of four). The lesions consisted of ulcers (two of four), a fungating mass (one of four), and papillary erythroplakia (one of four). Incisional biopsy specimens were obtained. High-stringency in situ hybridization was performed with DNA probes to the human papillomavirus (types 6/11; 16/18; 31/33/35) and Epstein-Barr virus: Immunocytochemical studies for the herpes simplex virus, proliferating cell nuclear antigen, cathepsin D, mutated p53, and c-erbB-2 were performed. Two lesions were moderately differentiated squamous cell carcinoma, one lesion was a basaloid squamous cell carcinoma, and one was carcinoma in situ. Stage of disease at diagnosis was II (one of four), III (two of four), and IV (one of four). Three cases were positive for the human papillomavirus, one case was positive for Epstein-Barr virus, and three cases were positive for the herpes simplex virus. C-erbB-2 was focally positive in one case, and mutated p53 was positive in a separate case.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Stomatology, University of Texas Health Science Center-Houston, USA.
authors.forename: C M
authors.initials: CM
authors.lastname: Flaitz
authors.forename: C M
authors.initials: CM
authors.lastname: Nichols
authors.forename: K
authors.initials: K
authors.lastname: Adler-Storthz
authors.forename: M J
authors.initials: MJ
authors.lastname: Hicks
mesh_terms: D000328:Adult; D000428:Alcohol Drinking / Q000009:adverse effects; D002278:Carcinoma in Situ / Q000209:etiology / Q000473:pathology / Q000821:virology; D002281:Carcinoma, Basosquamous / Q000209:etiology / Q000473:pathology / Q000821:virology; D002294:Carcinoma, Squamous Cell / Q000209:etiology* / Q000473:pathology / Q000821:virology; D015658:HIV Infections / Q000150:complications*; D004854:Herpesvirus 4, Human / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000209:etiology* / Q000473:pathology / Q000821:virology; D027383:Papillomaviridae / Q000302:isolation & purification; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D000090063:Proto-Oncogene Mas; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000032:analysis; D012307:Risk Factors; D018139:Simplexvirus / Q000302:isolation & purification; D012907:Smoking / Q000009:adverse effects; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D000090063:Proto-Oncogene Mas; D018719:Erb-b2 Receptor Tyrosine Kinases; D016159:Tumor Suppressor Protein p53; C000715470:MAS1 protein, human