Title: Infection, Stem Cells and Cancer Signals
Volume: 12
Issue: 2
Author(s): S. Sell
Affiliation:
Keywords:
Cancer stem cells, infection, cancer etiology, cancer signaling, viral oncogenes, mouse polyoma virus, mouse mammary tumor virus, human papilloma virus, cervical cancer, Cytoplasmic Epstein Barr virus infection, Burkitt lymphoma, osteomyelitis, cytokines, Clonorchis sinensis, cholaniocarci-noma, mammary tumor viruses, Epstein-Barr Virus, Helicobacter pylori, cancer posits, black bile theory, Rous sarcoma virus, embryonic theory, leukemias, lytic infection, MPyV virus, basal cell breast carcinomas, multifo-cal preneoplastic, ductal carcinoma, human mammary tumor virus [HMTV], glycogen, cervical intraepithelial neoplasia, or CIN, Papanicolaou smear, aflatoxin, hepatitis, hepati-tis B virus, hepatitis C virus, protein kinases, Wnt-catenin cell, ductal progenitor cell, hepatocyte, apoptotic, hepatocellular carcinoma, diethylnitrosamine, chronic myeloid leu-kemia (CML), Philadelphia chromosome, Epstein-Barr Nuclear Antigen, staphylococcal, squamous cell carcinoma, metaplasia, cancerization, gastric cancer, gastric stem cells, cholangiofibromas
Abstract: The association of cancer with preceding parasitic infections has been observed for over 200 years. Some such cancers arise from infection of tissue stem cells by viruses with insertion of viral oncogenes into the host DNA (mouse polyoma virus, mouse mammary tumor virus). In other cases the virus does not insert its DNA into the host cells, but rather commandeers the metabolism of the infected cells, so that the cells continue to proliferate and do not differentiate (human papilloma virus and cervical cancer). Cytoplasmic Epstein Barr virus infection is associated with a specific gene translocation (Ig/c-myc) that activates proliferation of affected cells (Burkitt lymphoma). In chronic osteomyelitis an inflammatory reaction to the infection appears to act through production of inflammatory cytokines and oxygen radical formation to induce epithelial cancers. Infection with Helicobacter pylori leads to epigenetic changes in methylation and infection by a parasite. Clonorchis sinensis also acts as a promoter of cancer of the bile ducts of the liver (cholaniocarcinoma). The common thread among these diverse pathways is that the infections act to alter tissue stem cell signaling with continued proliferation of tumor transit amplifying cells.
