Lymphoma, red meat, and poultry Cancer Causes Control. 2012 Oct;23(10):1681-92. doi: 10.1007/s10552-012-0047-2. Epub 2012 Aug 14. Meat intake and risk of non-Hodgkin lymphoma. Aschebrook-Kilfoy B1, Ollberding NJ, Kolar C, Lawson TA, Smith SM, Weisenburger DD, Chiu BC. We conducted a population-based, case-control study to test the hypothesis that consumption of meat and meat-related mutagens increases the risk of non-Hodgkin lymphoma (NHL), and whether the associations are modified by N-acetyltransferase (NAT) 1 and 2. Participants (336 cases and 460 controls) completed a 117-item food frequency questionnaire. The risk of NHL was associated with a higher intake of red meat (OR = 1.5; CI, 1.1-2.2), total fat (OR = 1.4; CI, 1.0-2.1), and oleic acid (OR = 1.5; CI, 1.0-2.2). NHL risk was also associated with a higher intake of very well-done pork (OR = 2.5; 95 % CI, 1.4-4.3) and the meat-related mutagen MeIQx (OR = 1.6; 95 % CI, 1.1-2.3). Analyses of the major NHL histologic subtypes showed a positive association between diffuse large B cell lymphoma (DLBCL) and higher intake of red meat (OR = 2.1; 95 % CI, 1.1-3.9) and the association was largely due to meat-related mutagens as a positive association was observed for higher intakes of both MeIQx (OR = 2.4; 95 % CI, 1.2-4.6) and DiMeIQx (OR = 1.9; 95 % CI, 1.0-3.5). Although the OR for follicular lymphoma (FL) was also increased with a higher red meat intake (OR = 1.9; 95 % CI, 1.1-3.3), the association appeared to be due to increased oleic acid (OR = 1.7; 95 % CI: 0.9-3.1). We found no evidence that polymorphisms in NAT1 or NAT2 modify the association between NHL and meat-related mutagens. Our results provide further evidence that red meat consumption is associated with an increase in NHL risk, and new evidence that the specific components of meat, namely fat and meat-related mutagens, may be impacting NHL subtype risk differently. PMID: 22890783 [PubMed - indexed for MEDLINE] PLoS One. 2014 Jun 19;9(6):e100004. doi: 10.1371/journal.pone.0100004. eCollection 2014. Cell cycle modulation by Mareks disease virus: the tegument protein VP22 triggers S-phase arrest and DNA damage in proliferating cells. Trapp-Fragnet L1, Bencherit D1, Chabanne-Vautherot D1, Le Vern Y2, Remy S1, Boutet-Robinet E3, Mirey G3, Vautherot JF1, Denesvre C1. Abstract Mareks disease is one of the most common viral diseases of poultry affecting chicken flocks worldwide. The disease is caused by an alphaherpesvirus, the Mareks disease virus (MDV), and is characterized by the rapid onset of multifocal aggressive T-cell lymphoma in the chicken host. Although several viral oncogenes have been identified, the detailed mechanisms underlying MDV-induced lymphomagenesis are still poorly understood. Many viruses modulate cell cycle progression to enhance their replication and persistence in the host cell, in the case of some oncogenic viruses ultimately leading to cellular transformation and oncogenesis. In the present study, we found that MDV, like other viruses, is able to subvert the cell cycle progression by triggering the proliferation of low proliferating chicken cells and a subsequent delay of the cell cycle progression into S-phase. We further identified the tegument protein VP22 (pUL49) as a major MDV-encoded cell cycle regulator, as its vector-driven overexpression in cells lead to a dramatic cell cycle arrest in S-phase. This striking functional feature of VP22 appears to depend on its ability to associate with histones in the nucleus. Finally, we established that VP22 expression triggers the induction of massive and severe DNA damages in cells, which might cause the observed intra S-phase arrest. Taken together, our results provide the first evidence for a hitherto unknown function of the VP22 tegument protein in herpesviral reprogramming of the cell cycle of the host cell and its potential implication in the generation of DNA damages. PMID: 24945933 [PubMed - in process] PMCID: PMC4063868
Posted on: Mon, 29 Sep 2014 17:43:22 +0000
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