Etiology of Hodgkin’s Disease by Freda E. Alexander (auth.), Ruth F. Jarrett (eds.)

By Freda E. Alexander (auth.), Ruth F. Jarrett (eds.)

This quantity studies the complaints of a NATO complicated Workshop held at Cameron condominium resort, Loch Lomond, Scotland, from may perhaps 2 - five, 1994. the foremost impetus for this workshop was once the realisation, during the last 7 years, that the Epstein-Barr virus is linked to a percentage of situations of Hodgkin's ailment and is probably going to play an aetiological position. there have been 4 major goals of the workshop: first, to debate the new findings relating to Epstein­ Barr virus and the aetiology of Hodgkin's illness; moment, to narrate those information to the epidemiology of Hodgkin's ailment; 3rd, to debate different power aetiological elements and eventually, to debate destiny instructions for learn into Hodgkin's sickness. best specialists within the box have contributed chapters to this quantity. there's a few overlap between chapters, relatively concerning Epstein-Barr virus, thereby permitting varied teams to specific perspectives on related issues. maybe, even if, the main impressive function of the workshop was once the shortcoming of controversy in regards to the function of Epstein-Barr virus in Hodgkin's ailment, an organization that used to be handled with nice scepticism before everything of the last decade. the 1st 3 chapters, through Alexander, Taylor et al., and Levine el al., speak about the epidemiology of Hodgkin's sickness with specific recognition to clustering and genetic susceptibility. those chapters symbolize the 1st try and compile epidemiological and molecular reviews in Hodgkin's disease.

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Jarrett, Plenum Press, New York, 1995 and colon cancer, general epidemiological studies often provide a clue as to where scientists should focus their attention. Geographical patterns and migrant studies have led us to focus on sunlight as a risk factor for melanoma and diet as a risk factor for breast cancer and colon cancer. , 1968; Gutensohn 1982; see other chapters). FAMILIAL HODGKIN'S DISEASE Regardless of how one examines the data, whether it be by age at onset, geographical variation, or histopathological subtype, the evidence continues to accumulate supporting MacMahon's hypothesis (MacMahon, 1966) that HD consists of more than one aetiological entity (see Alexander, this volume).

1974; Yao et al .. 1985). Etiology of Hodgkin's Disease Edited by R. Jarrett, Plenum Press, New York, 1995 33 ( EPITHELIAL TISSUES ( LYMPHOID TISSUES Fig. l: EBV infection in nonnal healthy virus carriers. Primary EBV infection occurs in the oropharynx and is mediated either through B-cells or epithelial cells. Following primary infection of B lymphocytes, a chronic virus carrier state is established in which the outgrowth ofEBV-infected Bcells is controlled by an EBV-specific cytotoxic T-cell response.

According to this hypothesis, virus infection of epithelial cells would be accidental and not relevant to virus persistence. The significance of HL as a model for virus replication in the immunocompetent host has probably been exaggerated. , 1984), but the significance of this observation for EBV shedding in chronic virus carriers is uncertain. Recently, EBV has been detected in a surprisingly large number of peripheral T-cell lymphomas, and EBV infection of non-neoplastic T-Iymphocytes has been demonstrated in certain conditions.

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