Assuntos
Neoplasias da Mama/diagnóstico , Autoexame de Mama , Detecção Precoce de Câncer , Mamografia , Guias de Prática Clínica como Assunto , Adulto , Comitês Consultivos , Idoso , Neoplasias da Mama/diagnóstico por imagem , Neoplasias da Mama/genética , Neoplasias da Mama/mortalidade , Análise Custo-Benefício , Detecção Precoce de Câncer/métodos , Feminino , Humanos , Imageamento Tridimensional , Pessoa de Meia-Idade , UltrassonografiaRESUMO
The cutaneous beta human papillomavirus (beta HPV) types appear to be involved in skin carcinogenesis. However, only a few beta HPVs have been investigated so far. Here, we compared the properties of E6 and E7 oncoproteins from six uncharacterized beta HPVs (14, 22, 23, 24, 36, 49). Only HPV49 E6 and E7 immortalized primary human keratinocytes and efficiently deregulated the p53 and pRb pathways. Furthermore, HPV49 E6, similarly to E6 from the oncogenic HPV16, promoted p53 degradation.
Assuntos
Betapapillomavirus/fisiologia , Transformação Celular Viral , Proteínas Oncogênicas Virais/metabolismo , Proteínas E7 de Papillomavirus/metabolismo , Infecções por Papillomavirus/virologia , Betapapillomavirus/genética , Células Cultivadas , Humanos , Queratinócitos/virologia , Proteínas Oncogênicas Virais/genética , Proteínas E7 de Papillomavirus/genética , Infecções por Papillomavirus/genética , Infecções por Papillomavirus/metabolismo , Transdução de Sinais , Proteína Supressora de Tumor p53/genética , Proteína Supressora de Tumor p53/metabolismoAssuntos
Benzeno/toxicidade , Carcinogênese/induzido quimicamente , Carcinógenos Ambientais/toxicidade , Neoplasias Hematológicas/induzido quimicamente , Leucemia Mieloide Aguda/induzido quimicamente , Animais , Benzeno/administração & dosagem , Testes de Carcinogenicidade , Consenso , Modelos Animais de Doenças , Feminino , França , Neoplasias Hematológicas/epidemiologia , Neoplasias Hematológicas/fisiopatologia , Humanos , Incidência , Internacionalidade , Leucemia Mieloide Aguda/fisiopatologia , Masculino , Exposição Ocupacional/efeitos adversos , Distribuição Aleatória , Ratos , Medição de Risco , Taxa de SobrevidaAssuntos
Carcinógenos Ambientais/efeitos adversos , Molibdênio/efeitos adversos , Neoplasias/induzido quimicamente , Exposição Ocupacional/efeitos adversos , Saúde Ocupacional , Óxidos/efeitos adversos , Compostos de Estanho/efeitos adversos , Soldagem , Animais , Carcinógenos Ambientais/classificação , Humanos , Molibdênio/classificação , Neoplasias/diagnóstico , Neoplasias/epidemiologia , Óxidos/classificação , Medição de Risco , Compostos de Estanho/classificaçãoRESUMO
Beta-papillomaviruses (beta-HPV) have been linked to the development of skin cancer in humans. Because both E6 and E7 proteins from beta-HPV have been involved in the potential carcinogenicity of these viruses, we investigated their role on UVB-induced apoptosis in HaCaT cell line. HaCaT cells have been transduced with both E6/E7 using a retroviral system and treated with PRIMA-1. Apoptosis was assessed by flow cytometry to measure mitochondrial membrane potential and DNA fragmentation. HaCat keratinocytes transduced with both E6 and E7 genes of seven beta-HPV types (HPV5, HPV8, HPV14, HPV24, HPV36, HPV38 and HPV49) did not demonstrate any inhibition of UVB-induced apoptosis, even after p53 reactivation through PRIMA-1. Our data suggest that the expression of E6 and E7 exert different modulatory effects on UVB-induced apoptosis according to beta-HPV types and to the cellular genetic context.
Assuntos
Apoptose/efeitos da radiação , Betapapillomavirus/patogenicidade , Queratinócitos/efeitos da radiação , Queratinócitos/virologia , Proteínas Oncogênicas Virais/fisiologia , Raios Ultravioleta/efeitos adversos , Apoptose/efeitos dos fármacos , Compostos Aza/farmacologia , Betapapillomavirus/fisiologia , Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia , Linhagem Celular , Cocarcinogênese , Humanos , Queratinócitos/patologia , Neoplasias Cutâneas/etiologia , Proteína Supressora de Tumor p53/genética , Proteína Supressora de Tumor p53/fisiologiaAssuntos
Ácido 2,4-Diclorofenoxiacético/toxicidade , Carcinógenos/toxicidade , Transformação Celular Neoplásica/induzido quimicamente , DDT/toxicidade , Hexaclorocicloexano/toxicidade , Imunossupressores/toxicidade , Inseticidas/toxicidade , Neoplasias/induzido quimicamente , Animais , Transformação Celular Neoplásica/imunologia , Transformação Celular Neoplásica/metabolismo , Humanos , Neoplasias/metabolismo , Estresse Oxidativo , Medição de Risco , Testes de ToxicidadeRESUMO
Cholangiocarcinoma is relatively rare, but high incidence rates have been reported in Eastern Asia, especially in Thailand. The etiology of this cancer of the bile ducts appears to be mostly due to specific infectious agents. In 2009, infections with the liver flukes, Clonorchis sinensis or Opistorchis viverrini, were both classified as carcinogenic to humans by the International Agency for Research on Cancer for cholangiocarcinoma. In addition, a possible association between chronic infection with hepatitis B and C viruses and cholangiocarcinoma was also noted. The meta-analysis of published literature revealed the summary relative risks of infection with liver fluke (both Opistorchis viverrini and Clonorchis sinensis), hepatitis B virus, and hepatitis C virus to be 4.8 (95% confidence interval [95% CI]: 2.8-8.4), 2.6 (95% CI: 1.5-4.6), and 1.8 (95% CI: 1.4-2.4), respectively - liver fluke infection being the strongest risk factor for cholangiocarcinoma. Countries where human liver fluke infection is endemic include China, Korea, Vietnam, Laos, and Cambodia. The number of infected persons with Clonorchis sinensis in China has been estimated at 12.5 million with considerable variations among different regions. A significant regional variation in Opistorchis viverrini prevalence was also noted in Thailand (average 9.6% or 6 million people). The implementation of a more intensive preventive and therapeutic program for liver fluke infection may reduce incidence rates of cholangiocarcinoma in endemic areas. Recently, advances have been made in the diagnosis and management of cholangiocarcinoma. Although progress on cholangiocarcinoma prevention and treatment has been steady, more studies related to classification and risk factors will be helpful to develop an advanced strategy to cure and prevent cholangiocarcinoma.
Assuntos
Neoplasias dos Ductos Biliares/etiologia , Ductos Biliares Intra-Hepáticos , Colangiocarcinoma/etiologia , Clonorquíase/complicações , Opistorquíase/complicações , Neoplasias dos Ductos Biliares/epidemiologia , Colangiocarcinoma/epidemiologia , Ásia Oriental , Humanos , Fatores de RiscoAssuntos
Amiantos Anfibólicos/efeitos adversos , Compostos Inorgânicos de Carbono/efeitos adversos , Transformação Celular Neoplásica/induzido quimicamente , Nanotubos de Carbono/efeitos adversos , Neoplasias/induzido quimicamente , Compostos de Silício/efeitos adversos , Materiais Biocompatíveis/efeitos adversos , Transformação Celular Neoplásica/patologia , Humanos , Neoplasias/patologiaAssuntos
Caprilatos/efeitos adversos , Carcinogênese/induzido quimicamente , Fluorocarbonos/efeitos adversos , Cloreto de Metileno/efeitos adversos , Propano/análogos & derivados , Tiofenos/efeitos adversos , Caprilatos/química , Carcinógenos/toxicidade , Educação , Fluorocarbonos/química , Humanos , Cooperação Internacional , Cloreto de Metileno/química , Exposição Ocupacional/efeitos adversos , Saúde Ocupacional , Propano/efeitos adversos , Propano/química , Medição de Risco , Tiofenos/químicaRESUMO
The Monographs produced by the International Agency for Research on Cancer (IARC) apply rigorous procedures for the scientific review and evaluation of carcinogenic hazards by independent experts. The Preamble to the IARC Monographs, which outlines these procedures, was updated in 2019, following recommendations of a 2018 expert advisory group. This article presents the key features of the updated Preamble, a major milestone that will enable IARC to take advantage of recent scientific and procedural advances made during the 12 years since the last Preamble amendments. The updated Preamble formalizes important developments already being pioneered in the Monographs program. These developments were taken forward in a clarified and strengthened process for identifying, reviewing, evaluating, and integrating evidence to identify causes of human cancer. The advancements adopted include the strengthening of systematic review methodologies; greater emphasis on mechanistic evidence, based on key characteristics of carcinogens; greater consideration of quality and informativeness in the critical evaluation of epidemiological studies, including their exposure assessment methods; improved harmonization of evaluation criteria for the different evidence streams; and a single-step process of integrating evidence on cancer in humans, cancer in experimental animals, and mechanisms for reaching overall evaluations. In all, the updated Preamble underpins a stronger and more transparent method for the identification of carcinogenic hazards, the essential first step in cancer prevention.