Friday, October 4, 2013

Dr. Michael Har-Noy Says Weakened Immunity is NOT the Reason Cancer Occurs



Dr. Michael Har-Noy of Immunovative Therapies, an Israeli biotech company founded in 2004, says that the idea that cancer occurs because of weakened immunity is erroneous and misguided. 

Dr. Michael Har-Noy explains that when a normal cell grows into a cancer cell, changes in the display of surface antigens give rise to tumor-associated antigens (TAAs) that could be detected by one’s immune system.  In 1909,Ehrlich first theorized  that a person’s own immunity protected them from cancer, an idea that was promoted in the 1950s by Lewis Thomas and later by Sir Macfarlane Burnet, who theorized that a patient’s immune cells had a “surveillance” system that identified and killed precancerous and cancerous cells.  Dr. Michael Har-Noy indicates that this hypothesis was based on the idea that cancer cells continually form in a person’s body and that their immune system must identify and kill cells that express surface TAAs

This hypothesis goes on to state that in instances where the patient’s immunity is compromised, the surveillance system is then disabled, and the cancer cells grow unchecked and clinical disease occurs. Dr. Michael Har-Noy says that this is the idea behind the notion that in cancer, the patient’s immune system is weakened, and that it must be reinforced to effectively attack the cancer cells.

Dr. Michael Har-Noy goes on to indicate that there is much evidence contradicting this theory. While a minority of the more unusual cancers develop in immune compromised patients, most malignant tumors arise in individuals with intact immunity.  Also, many tumors, especially epithelial cell cancers, have a significant number of inflammatory cells. This includes an array of leukocyte infiltrates consisting of neutrophils, macrophages, mast cells, eosinophils, often in the presence of lymphocytes. Dr. Michael Har-Noy points out that malignant tumors are usually profusely infiltrated with immune cells, which contradicts the hypothesis of deficient immune recognition of TAAs.

Additionally, many previous efforts to augment the immune response resulted in faster growth rather than slower growth of the cancer. For example, in mice, a newly formed cancer of combined mesenchymal and epithelial origin grows more quickly of it stimulates a response from the patient’s immune cells.  Dr. Michael Har-Noy indicates that cancers that stimulate a significant immune response will often, if left undisturbed, grow more quickly than those that do not trigger the patient’s immunity.  So, the notion that cancers are “invisible” to the patient’s immune cells and that the patient’s immune response needs to be enhanced appears to be wrong.

Dr. Michael Har-Noy concludes that the issue may be that the patient’s immune reaction to the cancer is the incorrect type of response.  Therefore, by attempting to augment an immune response that has already failed to protect the patient against malignancies, tumor propagation may be sped up rather than slowed.  This is likely the reason that most immune cancer therapies to date have been ineffective.

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