Cell kinetics of African cases of Burkitt Lymphoma

Iversen, Ulla; Iversen, Olav Hilmar; Bluming, Avrum Z.; Ziegler, John L.; Kyalwasi, Sebastian

doi:10.1016/0014-2964(72)90025-4

Cited by 53 publications

(18 citation statements)

References 6 publications

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“…Both actions could encourage expansion and frequency of EBV-positive B lymphocytes, and, therefore, increase the probability of disease development. BL tumour cells proliferate rapidly (estimated doubling time of 24 -48 h) [16], but also have high rates of apoptosis [17]. All neoplastic cells in EBV-associated BL tumours carry the virus in a latent (or occasionally integrated) state and the virus is usually clonal within BL.…”

Section: Epstein-barr Virus-associated Burkitt's Lymphomamentioning

confidence: 99%

The role of Epstein–Barr virus in cancer

Pattle

Farrell

2006

Expert Opinion on Biological Therapy

133

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Epstein-Barr virus (EBV), discovered > 40 years ago from a Burkitt's lymphoma biopsy, was the first virus to be directly associated with human cancer. EBV has two distinct life cycles in the human host; a lytic form of infection that produces new infectious virions, and a latent form of infection that allows the virus to persist in a dormant state for the lifetime of the host. EBV has evolved a life cycle that mimics the natural differentiation pathway of antigen-activated B cells, giving the virus access to its site of latent infection, the resting memory B cell. By steering infected cells through the various stages of lymphocyte differentiation, EBV is able to enter a cell type suitable for long-term latent persistence and periodic reactivation. However, its presence in various stages of B-cell development, and its ability to infect certain epithelial cells, can have pathogenic consequences, and can contribute to the development of a diverse group of lymphomas and carcinomas. The presence of EBV in the tumour cells of EBV-associated cancers might provide a basis for specific therapy. This article focuses on the contributions that the virus may play in different types of human cancer, particularly Burkitt's lymphoma, Hodgkin's lymphoma, lymphomas and lymphoproliferative diseases in the immunocompromised, and nasopharyngeal and gastric carcinoma.

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Section: Epstein-barr Virus-associated Burkitt's Lymphomamentioning

confidence: 99%

The role of Epstein–Barr virus in cancer

Pattle

Farrell

2006

Expert Opinion on Biological Therapy

133

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“…Risk for both eBL and sBL appears to be highest at ages 5-9 years and sBL rates are also elevated at the oldest ages. 4,6 Because BL is a rapidly growing tumor, doubling its cell mass approximately every 1-2 days, 7 the interval from trigger to diagnosis may be relatively short, so study of age-specific risk may provide etiologic information.…”

Section: Introductionmentioning

confidence: 99%

AIDS-related Burkitt lymphoma in the United States: what do age and CD4 lymphocyte patterns tell us about etiology and/or biology?

Guech-Ongey

Simard

Anderson

et al. 2010

Blood

113

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Trimodal or bimodal age-specific incidence rates for Burkitt lymphoma (BL) were observed in the United States general population, but the role of immunosuppression could not be excluded. Incidence rates, rate ratios, and 95% confidence intervals for BL and other non-Hodgkin lymphoma (NHL), by age and CD4 lymphocyte count categories, were estimated using Poisson regression models using data from the United States HIV/AIDS Cancer Match study . BL incidence was 22 cases per 100 000 person-years and 586 for non-BL NHL. Adjusted BL incidence rate ratio among males was 1.6؋ that among females and among non-Hispanic blacks, 0.4؋ that among non-Hispanic whites, but unrelated to HIV-transmission category. Non-BL NHL incidence increased from childhood to adulthood; in contrast, 2 age-specific incidence peaks during the pediatric and adult/geriatric years were observed for BL. Non-BL NHL incidence rose steadily with decreasing CD4 lymphocyte counts; in contrast, BL incidence IntroductionBurkitt lymphoma (BL) is an aggressive B-cell non-Hodgkin lymphoma (NHL) with 3 clinical variants: endemic (eBL), sporadic (sBL), and acquired immunodeficiency-associated BL (aBL). 1 These clinical variants, which are defined in part by where they occur geographically, are histologically indistinguishable 1 and their etiology is incompletely understood. 2 eBL occurs in children mostly as extranodal jaw or orbital masses in equatorial Africa and Papua New Guinea. 3 sBL occurs anywhere in the world at any age mostly with abdominal or nodal involvement. [4][5] Immunodeficiencyassociated BL is diagnosed in people with HIV, 1 among whom it is often the first indication of AIDS onset at least in the West. Risk for both eBL and sBL appears to be highest at ages 5-9 years and sBL rates are also elevated at the oldest ages. 4,6 Because BL is a rapidly growing tumor, doubling its cell mass approximately every 1-2 days, 7 the interval from trigger to diagnosis may be relatively short, so study of age-specific risk may provide etiologic information.In an assessment of age-specific risk for BL in the United States, using data from the National Cancer Institute Surveillance, Epidemiology, and End Results Program (1973-2005), 8 we observed 3 incidence peaks near ages 10, 40, and 70 years among males and 2 peaks near ages 10 and 70 years among females for both whites and blacks. However, the role of AIDS-related immunosuppression could not be excluded 9,10 because we were not able to separately analyze AIDS and non-AIDS BL. To address this limitation, we investigated age-specific BL incidence among persons with AIDS (PWA) in the United States Because age is a surrogate for cumulative exposure to deleterious infections a linear increase in risk for BL with age in PWA would suggest cumulative impact of deleterious infections given immunosuppression, whereas a nonlinear risk increase would suggest that age may be a surrogate for differences in the etiology or biology of BL diagnosed at different ages that occur independent of immunosuppression. 8 MethodsData...

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“…Thus, 2/3 of the cells produced in the region of the erythroblasts in the spleen would appear to be lost. Similar cell losses have been recognized for a long time in solid tumors, whether experimental or human Iversen et al, 1972). It is unfortunately not always possible to make a distinction between loss due to cellular differentiation and true cell death.…”

Section: Discussionmentioning

confidence: 95%