TY - JOUR
T1 - Pathogenesis of virus-associated human cancers
T2 - Epstein-Barr virus and hepatitis B virus as two examples
AU - Chang, Kung Chao
AU - Chang, Yao
AU - Wang, Lily Hui Ching
AU - Tsai, Hung Wen
AU - Huang, Wenya
AU - Su, Ih Jen
N1 - Funding Information:
This program project receives support from the National Health Research Institutes , the Excellence Center Project from Department of Education (to National Cheng Kung University), and National Science Council, Taiwan .
PY - 2014/9
Y1 - 2014/9
N2 - Virus-associated human cancers may exhibit two characteristic histopathologic features: (1) the inflammation-rich background as observed in Epstein-Barr virus-associated Hodgkin lymphoma (HL) and nasopharyngeal carcinoma (NPC); and (2) the characteristic nuclear morphology such as the Reed-Sternberg cells in HL. Besides, the hepatocytes of chronic hepatitis B virus (HBV) infection frequently exhibit characteristic ground glass hepatocytes, a phenomenon associated with endoplasmic reticulum stress response induced by the overloaded or malfolded HBV surface antigens. In this review, we explore specifically the pathogenesis of Epstein-Barr virus-associated HL and NPC, and HBV-associated hepatocellular carcinoma based on the observed histopathologic features. We propose that the retention of viral proteins induces inflammation, endoplasmic reticulum stress, and genomic instability in HL, NPC, and hepatocellular carcinoma, whereby the viral oncoproteins may play additional transactivational roles to induce host genes for transformation, invasion, and metastasis. Therapeutic implications based on the pathogenesis of virus-associated cancers are discussed.
AB - Virus-associated human cancers may exhibit two characteristic histopathologic features: (1) the inflammation-rich background as observed in Epstein-Barr virus-associated Hodgkin lymphoma (HL) and nasopharyngeal carcinoma (NPC); and (2) the characteristic nuclear morphology such as the Reed-Sternberg cells in HL. Besides, the hepatocytes of chronic hepatitis B virus (HBV) infection frequently exhibit characteristic ground glass hepatocytes, a phenomenon associated with endoplasmic reticulum stress response induced by the overloaded or malfolded HBV surface antigens. In this review, we explore specifically the pathogenesis of Epstein-Barr virus-associated HL and NPC, and HBV-associated hepatocellular carcinoma based on the observed histopathologic features. We propose that the retention of viral proteins induces inflammation, endoplasmic reticulum stress, and genomic instability in HL, NPC, and hepatocellular carcinoma, whereby the viral oncoproteins may play additional transactivational roles to induce host genes for transformation, invasion, and metastasis. Therapeutic implications based on the pathogenesis of virus-associated cancers are discussed.
UR - http://www.scopus.com/inward/record.url?scp=84905573604&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84905573604&partnerID=8YFLogxK
U2 - 10.1016/j.jfma.2013.09.001
DO - 10.1016/j.jfma.2013.09.001
M3 - Review article
C2 - 24095032
AN - SCOPUS:84905573604
SN - 0929-6646
VL - 113
SP - 581
EP - 590
JO - Journal of the Formosan Medical Association
JF - Journal of the Formosan Medical Association
IS - 9
ER -