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The tumor stem cell hypothesis


So far, little is known about why only some, but not all cells of a tumor acquire the ability to migrate through tissue barriers and spread to distant organs. In recent years, evidence has shown that only the so-called Cancer Stem Cells (CSCs) are responsible for the growth and spread of a tumor. In 1855, the physician Rudolf Virchow established the "Embryonic-Rest" hypothesis of tumor formation, based on his observations of histological similarities between tumor tissue and embryonic tissue. The pathologist Julius Cohnheim, a student of Virchow, extended this theory in 1875. Cohnheim postulated that human tumors arise from stem cells that are left during embryonic development and persist in the tissues. This theory was further developed to the tumor stem cell theory. The origin of such CSCs is still unclear but they may arise from mutated progenitor cells, that are in a transitional stage between stem and differentiated cell and develop self-renewal potential. On the other hand, CSCs may be derived from differentiated tumor cells, that converted back into stem cells. It is believed that CSCs exist in many tumor types and contribute to chemo- and radiotherapy resistance, because stem cells are very resistant. Likewise, it is assumed that tumor stem cells cause re-growth of the tumor despite initially successful therapy and trigger metastasis in secondary organs. It is believed that some residual CSCs remain after surgical removal of the tumor over long periods in a dormant state in the body and grow into tumors even years after a curative surgical removal of the primary tumor, which then causes relapse. In pancreatic cancer and also in other tumors of the gastrointestinal tract, there are proven markers for CSCs. The aim of our group is to examine the CSC properties of pancreatic cancer to establish new and improved treatment options that attack not only the differentiated tumor cells but also the CSCs.