| Autor: |
Koukourakis IM; Radiation Oncology Unit, 1st Department of Radiology, Aretaieion Hospital, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 11528 Athens, Greece., Platoni K; Medical Physics Unit, 2nd Department of Radiology, Attikon University Hospital, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 12462 Athens, Greece., Kouloulias V; Radiation Oncology Unit, 2nd Department of Radiology, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 12462 Athens, Greece., Arelaki S; Translational Functional Cancer Genomics, National Center for Tumor Diseases, German Cancer Research Center, 69120 Heidelberg, Germany., Zygogianni A; Radiation Oncology Unit, 1st Department of Radiology, Aretaieion Hospital, School of Medicine, National and Kapodistrian University of Athens (NKUOA), 11528 Athens, Greece. |
| Abstrakt: |
Stem cells differentiate into mature organ/tissue-specific cells at a steady pace under normal conditions, but their growth can be accelerated during the process of tissue healing or in the context of certain diseases. It is postulated that the proliferation and growth of carcinomas are sustained by the presence of a vital cellular compartment resembling stem cells residing in normal tissues: 'stem-like cancer cells' or cancer stem cells (CSCs). Mutations in prostate stem cells can lead to the formation of prostate cancer. Prostate CSCs (PCSCs) have been identified and partially characterized. These express surface markers include CD44, CD133, integrin α2β1, and pluripotency factors like OCT4, NANOG, and SOX2. Several signaling pathways are also over-activated, including Notch, PTEN/Akt/PI3K, RAS-RAF-MEK-ERK and HH. Moreover, PCSCs appear to induce resistance to radiotherapy and chemotherapy, while their presence has been linked to aggressive cancer behavior and higher relapse rates. The development of treatment policies to target PCSCs in tumors is appealing as radiotherapy and chemotherapy, through cancer cell killing, trigger tumor repopulation via activated stem cells. Thus, blocking this reactive stem cell mobilization may facilitate a positive outcome through cytotoxic treatment. |
