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Pathology and genetics of tumours of the lung , pleura, thymus and heart

Nasopharyngeal carcinoma (NPC) has a unique and complex etiology that is not completely understood. Although NPC is rare in most populations, it is a leading form of cancer in a few well-defined populations, including natives of southern China, Southeast Asia, the Arctic, and the Middle East/North Africa. The distinctive racial/ethnic and geographic distribution of NPC worldwide suggests that both environmental factors and genetic traits contribute to its development. This review aims to summarize the current knowledge regarding the epidemiology of NPC and to propose new avenues of research that could help illuminate the causes and ultimately the prevention of this remarkable disease. Well-established risk factors for NPC include elevated antibody titers against the Epstein-Barr virus, consumption of salt-preserved fish, a family history of NPC, and certain human leukocyte antigen class I genotypes. Consumption of other preserved foods, tobacco smoking, and a history of chronic respiratory tract conditions may be associated with elevated NPC risk, whereas consumption of fresh fruits and vegetables and other human leukocyte antigen genotypes may be associated with decreased risk. Evidence for a causal role of various inhalants, herbal medicines, and occupational exposures is inconsistent. Other than dietary modification, no concrete preventive measures for NPC exist. Given the unresolved gaps in understanding of NPC, there is a clear need for large-scale, population-based molecular epidemiologic studies to elucidate how environmental, viral, and genetic factors interact in both the development and the prevention of this disease.

https://cebp.aacrjournals.org/content/cebp/15/10/1765.full.pdf

The enigmatic epidemiology of nasopharyngeal carcinoma.

Infections may be responsible for over 15% of all malignancies worldwide. Important mechanisms by which infectious agents may induce carcinogenesis include the production of chronic inflammation, the transformation of cells by insertion of oncogenes and inhibition of tumour suppressors, and the induction of immunosuppression. Common characteristics shared by infectious agents linked to malignancies are that they are persistent in the host, often highly prevalent in the host population and induce cancer after a long latency. The associations between a selection of infectious agents and malignancies are covered in detail.

https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2796.2000.00742.x

Infections as a major preventable cause of human cancer

Position du probleme : La surveillance de la tendance de l'incidence et de la mortalite par cancers est essentielle a la recherche en cancerologie et a la planification en sante publique. Les registres de cancer francais ne couvrent pas l'ensemble du territoire et ne procurent pas un echantillon representatif de l'ensemble de la population. Notre etude a pour objectif d'estimer la tendance de l'incidence et de la mortalite, au niveau national et sur la plus longue periode possible. Materiel et methode : Les donnees d'incidence et de mortalite ont ete collectees sur la periode 1978-1997. Vingt-sept sites de cancer ont ete retenus ; pour chaque site, les taux d'incidence et de mortalite par sexe et par âge ont ete estimes pour chaque annee de 1978 a 2000. Les donnees d'incidence et de mortalite observees dans les populations couvertes par un registre ont ete modelisees par un modele âge-cohorte. Une estimation du rapport incidence/mortalite a ete obtenue a partir de cette modelisation et appliquee a des taux de mortalite predits par un modele âge-cohorte issu des donnees de mortalite de l'ensemble de la France. Les personnes-annees d'observation ont ete calculees par cohorte de naissance a partir des donnees du recensement de la population. Resultats : L'incidence du cancer a augmente de 63 % au cours de la periode d'etude, passant de 170 000 nouveaux cas en 1980 a 278 000 nouveaux cas en 2000. Cette croissance est due au changement demographique mais aussi a l'augmentation du risque de cancer qui est estimee a 35 % durant la meme periode. Pour les hommes, ce changement est largement explique par l'augmentation de l'incidence du cancer de la prostate. Pour les femmes, cette evolution est dominee par l'accroissement continu de l'incidence du cancer du sein. Des augmentations importantes ont aussi ete observees pour le lymphome malin non hodgkinien, le melanome de la peau et le cancer de la thyroide pour les deux sexes, pour le cancer du poumon dans la population feminine. La mortalite par cancer a augmente de 20 %, passant de 125 000 deces en 1980 a 150 000 deces en 2000. Cette augmentation est moindre que celle predite par les changements demographiques et correspond en fait a une diminution du risque de deces estimee a environ 8 %, diminution legerement plus importante chez les femmes que chez les hommes. La baisse de la mortalite est associee a une baisse de l'incidence pour les cancers de l'estomac pour les deux sexes, pour les cancers lies a l'alcool chez l'homme et pour les cancers du col de l'uterus chez la femme. Conclusion : Entre 1980 et 2000, cette etude montre un large changement, a la fois qualitatif et quantitatif du poids que represente le cancer en France. La diminution des expositions, un diagnostic plus precoce et les progres therapeutiques expliquent en partie cette situation, mais d'une facon generale la distribution des cancers tend vers une distribution avec moins de cancers agressifs. Une divergence frappante est observee entre les tendances de l'incidence et les tendances de la mortalite pour un grand nombre de cancers. Le cancer de la prostate partage avec le cancer du sein le meme type d'evolution, avec un accroissement severe de son incidence et une stabilite de sa mortalite. Ceci indique d'importants changements dans les pratiques medicales qui necessitent des analyses supplementaires.

Cancer incidence and mortality in France over the period 1978-2000

A number of men with malignant lymphoma of the histiocytic type and previous exposure to phenoxy acids or chlorophenols were observed and reported in 1979. A matched case-control study has therefore been performed with cases of malignant lymphoma (Hodgkin's disease and non-Hodgkin lymphoma). This study included 169 cases and 338 controls. The results indicate that exposure to phenoxy acids, chlorophenols, and organic solvents may be a causative factor in malignant lymphoma. Combined exposure of these chemicals seemed to increase the risk. Exposure to various other agents was not obviously different in cases and in controls.

Malignant lymphoma and exposure to chemicals, especially organic solvents, chlorophenols and phenoxy acids: a case-control study.

[Epidemiology of Hodgkin's disease].

During the period of three years (1972–1974), serum samples from 60 patients (children and adolescents) with lympho-hematopoietic system diseases were examined for antibodies to all four human herpesviruses. Among these were 26 active Hodgkin's disease (AHD) patients and 6 HD patients with a minimum five years' remission. Simultaneously matched controls (age, sex) of AHD patients were examined. Antibody levels against the viral capsid antigen of Epstein-Barr virus (EBV/VCA) in AHD patients were significantly higher, with overrepresentation of higher titres (≥1:160), than in matched controls. The lowest EBV/VCA antibody titres were in the leukemia-non-Hodgkin's lymphoma patients. We could not prove any significant relationship between cytomegalovirus or herpes simplex virus type 1 antibody titres and AHD or any other disease of lymphohematopoietic system. The varicella-zoster virus antibody titres in AHD patients were significantly higher than in matched controls. No significant differences in antibodies against EBV/VCA and the other human herpesviruses between the evolution and remission period of AHD patients could be detected. No differences in EBV/VCA antibody titres were observed between the healthy school-children aged 10 to 15 years who were and who were not in contact with a HD patient.

Hrodek O

Papers

[Epidemiology of Hodgkin's disease].

Herpesvirus group antibodies in children with Hodgkin's disease.