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Neoplasia da cabeça e pescoço versus neoplasia do pulmão : uma análise comparativa
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Resumo(s)
O cancro da cabeça e pescoço (CCP) é a sexta causa de cancro mais comum, com cerca de 650000 novos casos e 350000 mortes por ano, a nível mundial. Já o cancro do pulmão (CP) é a neoplasia com maior taxa de incidência anual no mundo, com 2.09 milhões de novos casos, sendo também a mais mortal. Ambos têm como principal fator de risco o fumo do tabaco, que percorre todo o trato respiratório criando um campo de lesão contínuo. Nesta revisão tentar-se-á perceber se isso significa que partilham outras caraterísticas, a nível epidemiológico, genético e molecular e quais as implicações que essas diferenças/semelhanças poderão ter para o doente.
A ação carcinogénica do tabaco parece ser muito semelhante nas duas neoplasias. Envolve mecanismos de stress oxidativo, formação de adutos de ADN, alterações epigenéticas e ativação de vias de proliferação celular. Os genes mais frequentemente alterados são o KRAS, CDKN2A, TP53, PIK3CA e RB.
Estudos demonstram que o perfil de expressão genética em células citologicamente normais do epitélio dos brônquios pode distinguir, com alta sensibilidade e especificidade, fumadores com e sem CP. Uma alternativa menos invasiva seria utilizar as células do epitélio oral/nasal, onde se encontraram as mesmas alterações identificadas nos brônquios.
Um dos principais fatores de risco do CCP orofaríngeo é o HPV. Os seus efeitos a nível do CP têm despertado grande curiosidade. Um estudo concluiu que o tecido pulmonar tumoral era 4x mais provável de ser HPV-positivo que o tecido pulmonar normal, sugerindo uma ligação entre infeção por HPV e CP.
Indivíduos com CCP têm um risco mais elevado de desenvolver uma neoplasia síncrona, uma segunda neoplasia primária ou metástases no pulmão.
Head and neck cancer (HNC) is the sixth most common cause of cancer, with about 650000 new cases and 350000 deaths per year, worldwide. Lung cancer (LC) has the highest incidence rate in the world and is the most mortal one. Both have cigarette smoke has the main risk factor, that goes through the airway and creates a continuous lesion field. In this review we’ll try to understand if that means they share other features, such as epidemiology trends, genetic and molecular alterations and what could be the implications of these similarities/disparities to the patient. The carcinogenic action of tobacco seems to be very similar in both cancers. It involves oxidative stress, formation of DNA adducts, epigenetics changes and activation of cellular proliferation pathways. The genes most commonly altered are KRAS, CDKN2A, TP53, PIK3CA and RB. Studies show that the profile of genetic changes in cytological normal cells in the bronchi’s epithelium can distinguish, with high sensitivity and specificity, smokers with and without lung cancer. A less invasive alternative would be using oral/nasal epithelium, where were found the same alterations identified in the bronchi. One of the main risk factors for oropharyngeal HNC is HPV. Its effects on the lung have been of great interest and curiosity. A study showed that cancerous lung tissue was 4 times more likely to be HPV-positive than normal lung tissue, suggesting a link between HPV infection and LP. Subjects with HNC have a higher risk of developing a synchronous cancer, a second primary cancer or metastasis in the lung.
Head and neck cancer (HNC) is the sixth most common cause of cancer, with about 650000 new cases and 350000 deaths per year, worldwide. Lung cancer (LC) has the highest incidence rate in the world and is the most mortal one. Both have cigarette smoke has the main risk factor, that goes through the airway and creates a continuous lesion field. In this review we’ll try to understand if that means they share other features, such as epidemiology trends, genetic and molecular alterations and what could be the implications of these similarities/disparities to the patient. The carcinogenic action of tobacco seems to be very similar in both cancers. It involves oxidative stress, formation of DNA adducts, epigenetics changes and activation of cellular proliferation pathways. The genes most commonly altered are KRAS, CDKN2A, TP53, PIK3CA and RB. Studies show that the profile of genetic changes in cytological normal cells in the bronchi’s epithelium can distinguish, with high sensitivity and specificity, smokers with and without lung cancer. A less invasive alternative would be using oral/nasal epithelium, where were found the same alterations identified in the bronchi. One of the main risk factors for oropharyngeal HNC is HPV. Its effects on the lung have been of great interest and curiosity. A study showed that cancerous lung tissue was 4 times more likely to be HPV-positive than normal lung tissue, suggesting a link between HPV infection and LP. Subjects with HNC have a higher risk of developing a synchronous cancer, a second primary cancer or metastasis in the lung.
Descrição
Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2019
Palavras-chave
Cancro da cabeça e pescoço Cancro do pulmão Epidemiologia Tabaco Vírus do papiloma humano (VPH)