Virally-induced cancer

In 1969, Henry Harris, George Klein, and colleagues, reported that cancerous cells, which could produce tumours in animals, lost their tumorigenicity when they were fused with non-cancerous normal cells. The loss of tumorigenicity was then perpetuated from one generation to the next. This experiment was a landmark in cancer research. Many experiments that followed demonstrated that this condition applied to all kinds of cancers—virally induced, chemically induced, and spontaneous tumours—and to a variety of cell types—epithelial cells, fibroblasts, and lymphoc5rtes. 

Immunodeficiency has been associated with an increased incidence of viral-induced cancers, which tend to be more immunogenic than those that are chemically-induced. Cancers related to immunosuppression include leukemia and cancers of the skin (seen in transplant patients4) as well as Kaposi s sarcoma and EB V-associated B cell lymphomas (observed in HIV/AIDS patients). 

Gradual diminution of CD4+ T-lymphocytes from the peripheral blood is the most consistent feature observed in HIV infection. Because the majority of CD4+ cells are T-helper lymphocytes, removal leads to deficiency of cellular immunity, which depends on T-helper cells to initiate cytotoxic T-cell killing of virus-infected cells of cancer. The loss of immune surveillance leads to the appearance of virally induced tumors from unopposed clonal expansion of vitally transformed cells. Furthermore, depletion of cellular immunity leads to exaggerated viral, fungal, and protozoal infections. 

Another model often used in cancer research is the spontaneous or virally induced tumor. Mouse mammary tumorigenesis is characterized by the presence of preneoplastic hyperplastic alveolar nodules that arise from normal mammary gland cells to develop mammary adenocarcinomas (51) Female inbred C H/St mice infected with the" Bittner Milk Factor", a B-type ribonucleic tumor virus (52) or Murine Mammary Tumor Virus-S (MuMTV-S) develop mammary adenocarcinoma. Addition of 2 ug/ml of selenite in the drinking... 

ViraUy induced (exogenous) cancers (hepatocellular carcinoma hepatitis C virus-induced squamous cell carcinoma of the uterine cervix or oral cavity (HPV-induced) are preventable with vaccines-induced immunity. The exogenously enforced virally induced cancers are reacted to with the induction of strong host immune defense, whereas the endogenously induced cancers often receive support from the subverted host, a reaction that a cancer vaccine is expected to break and reverse [1994-2000]. Some cancer vaccines caused tumor enhancement. Many cancer vaccines failed [2001a]. It is not clear at all what purpose the new review Cancer Vaccines served [2001b]. 

Newer uses have appeared in the treatment of viral diseases including AIDS, alteration of the immune response, and cancer. The lithium salt of 7-linolenic acid (LiGLA) has a significant anticancer effect against certain cancers. The neurochemical basis for lithium action is difficult to define. Lithium carbonate induces a wide range of intra- and extracellular changes—most emphasis has been naturally on the similarities with Na/K/Ca/Mg ions. Lithium selectively interferes with the inositol lipid cycle, representing a unified hypothesis of action. The biochemistry, distribution, and cellular localization of lithium has been extensively documented. 

Ongoing clinical trials continue to assess the efficacy of recombinant interferon preparations in treating a variety of cancers. Some trials suggest that treatments are most effective when administered in the early stages of cancer development. rhIFN-as have also proven effective in the treatment of various viral conditions, most notably viral hepatitis. Hepatitis refers to an inflammation of the liver. It may be induced by toxic substances, immunological abnormalities, or by viruses (infectious hepatitis). The main viral causative agents are ... 

Cytotoxic T cells may play a role in inducing direct destruction of cancer cells, in particular those transformed by viral infection (and who express viral antigen on their surface). In vitro studies have shown that cytotoxic T-lymphocytes obtained from the blood of persons suffering from various cancer types are capable of destroying those cancer cells. 

Bcl-2 B cell lymphoma protein 2 (Bcl-2) is a family of proteins that regulate apoptosis (programmed cell death). Apoptosis is a necessary process whereby aged or damaged cells are replaced by new cells. Dysfunction of the apoptosis process results in disease inhibition of apoptosis results in cancer, autoimmune disorder, and viral infection, whereas increased apoptosis gives rise to neurodegenerative disorders, myelodysplastic syndromes, ischemic injury, and toxin-induced liver disease. 

Substances such as promoters that interfere with cell-to-cell communication allow cancer cells to proliferate wildly. But cell proliferation can be induced by other means as well. Toxicity or other types of injury to tissues can result in a proliferative response. So can certain natural and synthetic hormones, such as estrogens, cause proliferation of certain tissues, such as the breast. Chronic viral infections may cause cell killing and its consequence is cell proliferation. It appears that sustained chronic proliferation induced in any of these ways, either by agents foreign to the body or some, such as the estrogens, that are natural to it, can increase tumor growth. 

Interferons induce a wide range of biological effects. Generally, type I IFNs induce similar effects, which are distinct from the effects induced by IFN-y. The most pronounced effect of type I IFNs relates to their anti-viral activity, as well as their anti-proliferative effect on various cell types, including certain tumour cell types. Anti-tumour effects are likely due not only to a direct anti-proliferative effect on the tumour cells themselves but also due to the ability of type I IFNs to increase natural killer (NK) cell and T cytotoxic cell activity. These cells can recognize and destroy cancer cells. 

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