Abstract
This review explores similarities between lymphocytes and cancer cells, and proposes a new model for the genesis of human cancer. We suggest that the development of cancer requires infection(s) during which antigenic determinants from pathogens mimicking self-antigens are co-presented to the immune system, leading to breaking T cell tolerance. Some level of autoimmunity is normal and necessary for effective pathogen eradication. However, autoreactive T cells must be eliminated by apoptosis when the immune response is terminated. Apoptosis can be deficient in the event of a weakened immune system, the causes of which are multifactorial. Some autoreactive T cells suffer genomic damage in this process, but manage to survive. The resulting cancer stem cell still retains some functions of an inflammatory T cell, so it seeks out sites of inflammation inside the body. Due to its defective constitutive production of inflammatory cytokines and other growth factors, a stroma is built at the site of inflammation similar to the temporary stroma built during wound healing. The cancer cells grow inside this stroma, forming a tumor that provides their vascular supply and protects them from cellular immune response.As cancer stem cells have plasticity comparable to normal stem cells, interactions with surrounding normal tissues cause them to give rise to all the various types of cancers, resembling differentiated tissue types. Metastases form at an advanced stage of the disease, with the proliferation of sites of inflammation inside the body following a similar mechanism. Immunosuppressive cancer therapies inadvertently re-invigorate pathogenic microorganisms and parasitic infections common to cancer, leading to a vicious circle of infection, autoimmunity and malignancy that ultimately dooms cancer patients. Based on this new understanding, we recommend a systemic approach to the development of cancer therapies that supports rather than antagonizes the immune system.
Highlights
Understanding the pathomechanism of cancer is of primary interest in medical research
In a previous paper [14] we have shown that specific dietary deficiencies mimic the effects of chemical or radiation damage to DNA, which we propose plays an important role in human carcinogenesis and tumorigenesis
Antigen-presenting cells activate T and B cells in response to molecular patterns expressed on the surfaces of pathogenic microorganisms
Summary
Understanding the pathomechanism of cancer is of primary interest in medical research. IL-10, the most potent Th2 polarizing cytokine, suppresses the tumoricidal activity of macrophages [202], blocks presentation of tumor antigens to professional APCs [203,204,205], and inhibits tumor-specific cytotoxic T cells [206] In cancers both cellular and humoral immune response may be depressed, as in the absence of IL-4 production IL-10 secretion alone cannot induce a Th2-type response. It was reported that gastric atrophy and pernicious anemia carries a risk for gastric carcinoma 18 times that of the population average [224] It appears that a variety of infections may induce autoimmune serological features without overt autoimmune disease or organ involvement [225]; this condition http://www.molecular-cancer.com/content/5/1/6 may progress to clinical autoimmune disease and malignancy if impaired T cell function prevails. Cancer cells continue to act like T cells performing their immune-regulating functions
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