RESUMO
Obesity is a chronic metabolic condition affecting up to 40% of the adult population. Gynecologic neoplasms, such as those involving the breasts, uteri, and ovaries, are all associated with obesity, but data on whether weight loss could reduce cancer incidence, recurrence or mortality are still scarce. This article focuses on review the association between obesity and gynecologic cancer incidence and prognosis.
Assuntos
Neoplasias da Mama , Neoplasias dos Genitais Femininos , Adulto , Feminino , Neoplasias dos Genitais Femininos/epidemiologia , Neoplasias dos Genitais Femininos/etiologia , Humanos , Incidência , Obesidade/complicações , Obesidade/epidemiologia , Prognóstico , Redução de PesoRESUMO
2-Methoxyestradiol (2ME) is an endogenous metabolite of 17ß-estradiol. Once thought of as a mere degradation product, 2ME has gained attention as an important component of reproductive physiology and as a therapeutic agent in reproductive pathologies such as preeclampsia, endometriosis, infertility, and cancer. In this review, we discuss the involvement of 2ME in reproductive pathophysiology and summarize its known mechanisms of action: microtubule disruption, inhibition of angiogenesis and stimulation of apoptosis. Currently, the clinical uses of 2ME as a single agent are limited due to its poor water solubility and thus low bioavailability; however, 2ME analogs and derivatives have been recently developed and tested as cancer treatments. Despite some isolated success stories and ongoing research, 2ME derivatives have not yet provided the expected results. The adjuvant use of 2ME derivatives with chemotherapeutic agents is hindered by their intrinsic toxicity confounding the unwanted secondary effects of chemotherapy. However, due to the well-tested tolerance of the body to high doses of native 2ME, it may the combination of native 2ME with conventional treatments that will offer novel clinically relevant regimens for cancer and other reproductive disorders.
Assuntos
Estradiol/análogos & derivados , Doenças dos Genitais Femininos/tratamento farmacológico , Doenças dos Genitais Femininos/etiologia , 2-Metoxiestradiol , Animais , Ensaios Clínicos como Assunto , Quimioterapia Combinada , Estradiol/metabolismo , Estradiol/farmacologia , Estradiol/uso terapêutico , Estrogênios/metabolismo , Feminino , Doenças dos Genitais Femininos/patologia , Neoplasias dos Genitais Femininos/tratamento farmacológico , Neoplasias dos Genitais Femininos/etiologia , Humanos , Resultado do TratamentoRESUMO
The interrelation between cancer and ageing in women is emphasized, on its increased incidence, in their molecular background, into the particular biological characteristics of the different tumors and the effects of ageing in the affected women.
Assuntos
Envelhecimento/fisiologia , Carcinoma/etiologia , Neoplasias dos Genitais Femininos/etiologia , Fatores Etários , Idoso , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/etiologia , Carcinoma/diagnóstico , Carcinoma/genética , Feminino , Neoplasias dos Genitais Femininos/diagnóstico , Neoplasias dos Genitais Femininos/genética , Humanos , Prognóstico , Fatores de RiscoRESUMO
Se destaca la relación entre el cáncer y el envejecimiento en la mujer, en su aumentada incidencia, en los diferentes aspectos moleculares que la sustentan y las características biológicas propias de los distintos carcinomas y aquellas vinculadas al avance de la edad en la mujer huésped.
The interrelation between cancer and ageing in women is emphasized. on its increased incidence. in their molecular background, into the particular biological characteristics of the different tumors and the effects of ageing in the affected women.
Assuntos
Humanos , Feminino , Idoso , Envelhecimento/fisiologia , Carcinoma/etiologia , Neoplasias dos Genitais Femininos/etiologia , Fatores Etários , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/etiologia , Carcinoma/diagnóstico , Carcinoma/genética , Neoplasias dos Genitais Femininos/diagnóstico , Neoplasias dos Genitais Femininos/genética , Prognóstico , Fatores de RiscoRESUMO
Se destaca la relación entre el cáncer y el envejecimiento en la mujer, en su aumentada incidencia, en los diferentes aspectos moleculares que la sustentan y las características biológicas propias de los distintos carcinomas y aquellas vinculadas al avance de la edad en la mujer huésped.(AU)
The interrelation between cancer and ageing in women is emphasized. on its increased incidence. in their molecular background, into the particular biological characteristics of the different tumors and the effects of ageing in the affected women.(AU)
Assuntos
Humanos , Feminino , Idoso , Neoplasias dos Genitais Femininos/etiologia , Envelhecimento/fisiologia , Carcinoma/etiologia , Neoplasias dos Genitais Femininos/diagnóstico , Neoplasias dos Genitais Femininos/genética , Carcinoma/diagnóstico , Carcinoma/genética , Fatores de Risco , Fatores Etários , Neoplasias da Mama/diagnóstico , Neoplasias da Mama/etiologia , PrognósticoAssuntos
Adolescente , Adulto , Feminino , Condiloma Acuminado/diagnóstico , Condiloma Acuminado/etiologia , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Femininos/patologia , Papillomaviridae , Infecções Tumorais por Vírus/patologia , Neoplasias do Colo do Útero/patologia , ArgentinaAssuntos
Adolescente , Adulto , Feminino , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Femininos/patologia , Neoplasias do Colo do Útero/patologia , Infecções Tumorais por Vírus/patologia , Condiloma Acuminado/etiologia , Condiloma Acuminado/diagnóstico , Papillomaviridae , ArgentinaRESUMO
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.
Assuntos
Humanos , Masculino , Feminino , Oncogenes/genética , Papillomaviridae/genética , Condiloma Acuminado/genética , Regulação para Baixo , Genes Virais/genética , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Masculinos/etiologia , Regulação Viral da Expressão Gênica , Transcrição Gênica/genéticaRESUMO
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.
Assuntos
Condiloma Acuminado/genética , Regulação Viral da Expressão Gênica , Papillomaviridae/genética , Regulação para Baixo , Feminino , Genes Virais/genética , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Masculinos/etiologia , Humanos , Masculino , Oncogenes/genética , Transcrição GênicaRESUMO
Activated cellular oncogenes (myc and ras, for example) and inactivated anti-oncogenes (p53 or Rb) participate in multistep carcinogenesis. In addition, some high risk human papillomaviruses (HPV) are also involved in uterine cervix carcinomas. Typification of HPV is important for clinical diagnosis. Unravelling the complexities of the immune system and understanding the biochemistry and molecular genetics of cellular oncogenes and tumor viruses have opened up new possibilities for vaccination.
Assuntos
Cocarcinogênese , Doenças dos Genitais Femininos/complicações , Doenças dos Genitais Femininos/virologia , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Femininos/prevenção & controle , Papillomaviridae/genética , Papillomaviridae/imunologia , Infecções por Papillomavirus/genética , Infecções por Papillomavirus/prevenção & controle , Vacinas contra Papillomavirus , Infecções Tumorais por Vírus/genética , Infecções Tumorais por Vírus/prevenção & controle , Vacinas Virais/uso terapêutico , Feminino , Neoplasias dos Genitais Femininos/diagnóstico , Humanos , Infecções por Papillomavirus/complicações , Infecções Tumorais por Vírus/complicações , Neoplasias do Colo do Útero/diagnóstico , Neoplasias do Colo do Útero/etiologia , Neoplasias do Colo do Útero/terapiaRESUMO
Activated cellular oncogenes (myc and ras, for example) and inactivated anti-oncogenes (p53 or Rb) participate in multistep carcinogenesis. In addition, some high risk human papillomaviruses (HPV) are also involved in uterine cervix carcinomas. Typification of HPV is important for clinical diagnosis. Unravelling the complexities of the immune system and understanding the biochemistry and molecular genetics of cellular oncogenes and tumor viruses have opened up new possibilities for vaccination
Assuntos
Carcinoma/diagnóstico , Neoplasias dos Genitais Femininos/diagnóstico , Neoplasias dos Genitais Femininos/etiologia , Neoplasias/diagnóstico , Papillomaviridae/fisiologia , Útero/fisiopatologiaRESUMO
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.
Assuntos
Humanos , Masculino , Feminino , Papillomaviridae/fisiologia , Infecções Tumorais por Vírus , Genes Supressores de Tumor/fisiologia , Papillomaviridae/genética , Genes Supressores de Tumor/genética , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Masculinos/etiologia , Supressão Genética/fisiologiaRESUMO
La búsqueda, detección y control del virus del papiloma humano (VPH) ha llamado la atención de los investigadores por comprobarse su participación directa como cofactor en la génesis de lesiones premalignas y malignas en los órganos genitales. Es por esto que se realiza la presente revisión bibliográfica, en donde tratamos de motivar a los médicos ginecólogos para que establezcan un protocolo de manejo en la consulta externa. De tal manera que sea posible, reducir los altos índices de morbimortalidad femenina generada por este padecimiento que a la fecha continúa siendo la primera causa de mortalidad por cáncer en México.
Assuntos
Humanos , Feminino , Adulto , Biologia Celular , Colposcopia , Neoplasias dos Genitais Femininos/etiologia , Papillomaviridae/patogenicidadeRESUMO
El virus del papiloma humano (VPH) ha sido inmplicado como agente etiológico del cáncer genital. Los tipos 6 y 11 se asocian con condilomas y displasias leves, mientras que los tipo 16, 18 y 35 con displasias severas y carcinomas intraepiteliales e invasores; el tipo16 es el más fecuentemente relacionado con el NIC, se ha informado que el tipo 18 es un factor de rápida transformación entre NICI y carcinomas invasores. Se describen brevemente las técnicas del Southerm Blot e hidrización in situ para tipificar los grupos del VPH. Los resultados obtenidos con este último método en nuestro laboratorio confirma lo publicado recientemente
Assuntos
Humanos , Feminino , Papiloma/complicações , Papiloma/diagnóstico , Papiloma/fisiopatologia , Neoplasias dos Genitais Femininos/complicações , Neoplasias dos Genitais Femininos/diagnóstico , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Femininos/fisiopatologiaRESUMO
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 of HPV in non-genital and genital warts, laryngeal papillomas, and their possible roles in several malignancies.
Assuntos
Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Masculinos/etiologia , Neoplasias Laríngeas/etiologia , Papiloma/etiologia , Verrugas/etiologia , Condiloma Acuminado/etiologia , Feminino , Humanos , Masculino , Papillomaviridae , Fatores de Risco , Verrugas/patologiaRESUMO
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