| Literature DB >> 27698858 |
Therese Högfeldt1, Crystal Jaing2, Kevin Mc Loughlin3, James Thissen2, Shea Gardner3, Abeer A Bahnassy4, Baback Gharizadeh5, Joachim Lundahl6, Anders Österborg1, Anna Porwit1, Abdel-Rahman N Zekri7, Hussein M Khaled8, Håkan Mellstedt1, Ali Moshfegh1.
Abstract
Diffuse large B-cell lymphoma (DLBCL), the most common type of non-Hodgkin's lymphoma (NHL) in adults, accounts for approximately 30-40% of newly diagnosed lymphomas worldwide. Environmental factors, such as viruses and bacteria, may contribute to cancer development through chronic inflammation and the integration of oncogenes, and have previously been indicated in cervical cancer, hepatocellular carcinoma, gastric cancer and lymphoproliferative disorders. In the present study, the presence of microbial agents was analyzed in the lymphoma tissue of patients with activated B-cell like (ABC) DLBCL. The present study compared two groups of patients from geographically varied regions that possess a difference in the prevalence of viral and other microbial agents. The patient populations were from Sweden (a low endemic infectious disease region) and Egypt (a high endemic infectious disease region). A differential expression of several viruses in lymphoma tissues was noted when comparing Swedish and Egyptian patients. JC polyomavirus (JCV) was detected in Swedish and Egyptian patients and, uniquely, the complete hepatitis B virus (HBV) genome was detected only in Egyptian lymphoma patients. None of these viruses were detected in control lymph tissues from Sweden or Egypt. In total, 38% of the Egyptian patients were found to have HBV surface antigens (HBsAgs) in their serum; however, HBsAgs were not found in any of the Swedish patients. The percentage of serum HBsAgs in Egyptian patients with ABC DLBCL was significantly increased compared with the general Egyptian population (P<0.05). The present study may support a notion that viral agents, including JCV and HBV, may be involved in the tumorigenesis of DLBCL in regions of high infectious disease.Entities:
Keywords: gene array; hepatitis B virus; lymphoma and Hodgkin disease; molecular genetics; virus
Year: 2016 PMID: 27698858 PMCID: PMC5038175 DOI: 10.3892/ol.2016.5012
Source DB: PubMed Journal: Oncol Lett ISSN: 1792-1074 Impact factor: 2.967