ABSTRACT
OBJECTIVE: To analyze how scrotal neoplasias have been managed during the past decade and to question possible factors or professions associated to its presence. MATERIALS AND METHODS: We retrospectively evaluated every case reported from 1995 to 2005 at our hospital. We described the clinical scenario, complementary exams, treatments and outcomes. We also tried to verify if there was any risk, predisposing factors or professions that would explain the cancer origin. RESULTS: Six cases were reviewed. Out of these, three patients were truck drivers. Five of them showed restricted lesions without inguinal lymph nodes enlargement. Histologically, six patients presented squamous carcinoma, with two of them having the verrucous type. The median age of patients was 52 years old (31 to 89). The five patients who are still alive had their lesions completely removed with safety margin and primary closure. CONCLUSIONS: We have noticed that the scrotal carcinoma behavior is similar to that of the penis, where removal of the lesion and study of the regional lymph nodes help to increase the patient survival rate. The outstanding fact was that three out of six patients were truck drivers, raising the hypothesis that such profession, maybe due to the contact or attrition with the diesel exhaust expelled by the engine or to sexual promiscuity, would imply in a larger risk of developing this rare neoplasia.
Subject(s)
Adult , Aged, 80 and over , Humans , Male , Middle Aged , Automobile Driving , Carcinoma, Squamous Cell/pathology , Genital Neoplasms, Male/pathology , Motor Vehicles , Occupational Diseases/pathology , Scrotum/pathology , Carcinoma, Squamous Cell/etiology , Carcinoma, Squamous Cell/surgery , Genital Neoplasms, Male/etiology , Genital Neoplasms, Male/surgery , Inhalation Exposure/adverse effects , Occupational Diseases/etiology , Retrospective Studies , Risk Factors , Sexual Behavior , Scrotum/surgery , Vehicle EmissionsABSTRACT
Los papilomavirus humano (PVH) infectan epitelios estratificados queratinizados con una alta especificidad y están asociados con la aparición y persistencia de neoplasias benignas y malignas. Los elementos que dirigen la expresión genética de estos virus se localizan en una región no codificadora conocida como región larga de control (RLC). Al inicio del ciclo viral, una combinación particular de factores celulares que interactúan con la RLC promueven la transcripción temprana de los oncogenes virales E6 y E7. Estos favorecen la división celular interrumpiendo los mecanismos regulatorios celulares: E6 se une a la proteína supresora de tumor p35 y E7 se une a p105RB. La continuidad en la transcripción temprana conlleva al aumento gradual de las proteínas virales E1 y E2. La proteína E2 impide la transcripción temprana y confiere especificidad de unión a E1, la cual promueve la replicación viral. El cese paulatino de la transcripción de los oncogenes virales a través de la represión por E2, libre la regulación del crecimiento celular mediada por p53 y p105RB, permitiendo que la diferenciación celular progrese. Es entonces cuando el promotor tardío funciona para la producción de las proteínas de la cápside viral L1 y L2, permitiendo la maduración de viriones en los estratos superiores del epitelio. La disrupción del gen E2 durante un evento de integración del genoma viral, impide la progreción del ciclo vira y la entrada del programa de diferenciación de la célula epitelial, sosteniendo el estado transformado producido por E6 y E7
Human papillomavirus (HPV) specifically infect stratified epithelial cells, causing benign and malignant neoplasia. Several elements directing this virus' genetic expression are present in a non-coding region called LCR. HPV infection starts in the basal cells of stratified epithelia, where a particular combination of cellular factors interacting with the LCR starts the transcription of the viral E6 and E7 oncogenes. The E6 and E7 genes alter the cell cycle because they interact and inactivate tumor suppressor proteins: E6 binds and degrades protein p53 and E7 associates with p105RB. E1 and E2 are the next synthesized proteins. E2 blocks the early transcription and permits E1 specific binding to the viral origin of replication located within the lcr, initiating the viral genome replication. Following the course of viral infection, the E2-induced E6 and E7 down-regulation releases p53 and p105RB proteins, and the differentiation process can continue. Then, a putative late promoter can activate the capsid genes L1 and L2. At this step, mature virions can be detected in the upper layers of the epithelium. Disruption in E2 gene transcription is usually associated to genital malignant neoplasia. In the absence of E2, E6 and E7 remain constitutively expressed, sustaining the immortality of the infected cell and blocking the epithelial differentiation program.
Subject(s)
Humans , Male , Female , Oncogenes/genetics , Papillomaviridae/genetics , Condylomata Acuminata/genetics , Down-Regulation , Genes, Viral/genetics , Genital Neoplasms, Female/etiology , Genital Neoplasms, Male/etiology , Gene Expression Regulation, Viral , Transcription, Genetic/geneticsABSTRACT
Os tumores de testiculo representam uma forma rara de neoplasia no sexo masculino. No periodo de 12 anos, foram atendidos 234 individuos portadores de tumor germinativo do testiculo, e destes, 173 foram seguidos no periodo pos-operatorio. Do total analisado, 137 eram seminomas que responderam satisfatoriamente ao tratamento e com sobrevida de 96 por cento em 3 anos, e 38 tumores nao-seminomatosos, cuja taxa de sobrevida foi de 84 por cento , no mesmo periodo. Dois pacientes apresentaram tumores em ambos os testiculos, de forma assincronica. O acompanhamento pos-operatorio medio foi de 36 meses
Subject(s)
Humans , Genital Neoplasms, Male/diagnosis , Genital Neoplasms, Male/etiology , Genital Neoplasms, Male/surgery , Genital Neoplasms, Male/therapyABSTRACT
Los virus del papiloma humano de tipo 16 y 18 está asociados al desarrollo de cáncer ano-genital. La actividad transformante de estos virus depende de la expresión de los oncogenes virales E6 y E7. Estos dos genes son necesarios y suficientes para la transformación de ketatinocitos humanos. Esta actividad transformante involucra la interacción de estos oncogenes con genes supresores de tumores. El oncogen E7 se une al gen supresor de tumors retinoblastoma (Rb) impidiendo que actúe en forma normal. Por otro lado; el oncogen E6 se asocia al gen supresores de tumores p53 estimulando su degradación. De esta forma los oncogens virales al inactivar funcionalmente genes que controlan negativamente proliferación celular conducen a la transformación.
Subject(s)
Humans , Male , Female , Papillomaviridae/physiology , Tumor Virus Infections , Genes, Tumor Suppressor/physiology , Papillomaviridae/genetics , Genes, Tumor Suppressor/genetics , Genital Neoplasms, Female/etiology , Genital Neoplasms, Male/etiology , Suppression, Genetic/physiologyABSTRACT
The human papillomavirus (HPV) belongs to a small group of viruses which are known to cause tumors in humans. not only do they cause benign papillomas, but they are also implicated in the pathogenesis of some malignancies. For this reason, it is important for both the practicing physicians and students to know about recent advances in the study of these viruses. The following is a review of the etiologic role HPV in non-genital and genital warts, laryngeal papillomas, and their possible roles in several malignancies