May 21, 2015 | by Tami Dennis
Cancer may not be the disease many people think it is.
Normally, cancer is considered to be a disease in which cells multiply at an extremely high, and unusual, rate – increasing the likelihood of genetic mutations. But increasingly, leading researchers at City of Hope and elsewhere are contending that cancer is, in large part, a disease of cell movement and so-called seeding.
If you’re looking for a culprit, they say, look to cancer cells’ microenvironment. That environment – with its fostering of cell accumulation and growth – likely encourages tumors to form. By looking at cancer in this revolutionary way, they hope to develop new and better treatments for a disease that continues to take far too high a toll.
In a presentation at the Arnold and Mabel Beckman Center for Cancer Immunotherapeutics & Tumor Immunology, Norton presented evidence that cancer is, in large part, a disease of cell movement and so-called seeding. The lecture, part of the Comprehensive Cancer Center Seminar Series, was titled “Cancer as a Disease of Migration and Colonization.”
Norton explained his view in more simple terms during a Memorial Sloan Kettering talk last year. “Nobody ever died of breast cancer cells. Cells don’t kill you. Cells are only a problem if they form tumors,” Norton said.
Some City of Hope researchers not only agree, they’ve been investigating the potential treatment avenues inherent within this line of thinking. One of those researchers – and Norton’s host for the event – is Peter P. Lee, M.D., the Billy and Audrey L. Wilder Professor in Cancer Immunotherapeutics and chair of the Department of Cancer Immunotherapeutics and Tumor Immunology at City of Hope.
While many researchers focus on attacking cancer cells themselves, Lee aims to target the cancer cells as well as their “co-conspirators” – support cells within the tissue stroma and tumor microenvironment.
In order to survive, cancer cells recruit and manipulate these support cells, and as a result, a patient’s immune system is destroyed. Lee is currently studying these “co-conspirator” cells to broaden his understanding of their interactions. By gaining a better understanding of the ways these co-conspirators help feed cancer cells, he may be able to develop therapeutics that target both malignant cells and their supporting cells – thereby restoring and enhancing the immune function in patients with breast cancer.
More effective therapeutics is a goal that everyone can support.
Here is an abstract of Norton’s presentation.
Cancer is commonly thought of as a disease of hyperproliferation. Indeed, there is a logical basis for this since masses (tumors) must contain a large number of cells, which had to have arisen by mitosis, and on microscopic examination most cancers demonstrate a concentration of cancer cells. Nevertheless, there is a growing body of evidence that increased ("hyper") proliferation alone cannot explain malignancy, at least in the sense of causing disease, e.g., organ dysfunction. Moreover, cancer cells themselves rarely cause disease unless they contribute to the formation of invasive tumors, which are mixtures of cells of various types, often predominantly host tissues that are presumed to be normal. Furthermore, the most destructive of these tumors are not found in the organ of origin of the cancer, but rather in distant, noncontiguous organs. Hence, a more consistent model is that cancer is a disease in which aberrant cell migration is the prime defect, with recruitment of supportive stroma and an abnormal accumulation of cells – from both mitosis and aggregation – secondary phenomena. There are no a priori reasons why such a cellular microenvironment might not contain genetic or functional polymorphisms that promote the growth of the cancer cells, or even mutations representing forme fruste malignancies. Such a model would explain many enigmas in cancer medicine and might provide for the discovery of novel therapeutic targets.**
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