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• W2169648328 abstract "The practice of pediatric oncology is at once exhilarating, perplexing and frightening. On the one hand, medical science has advanced to the point where we can actually cure cancer in some cases; nothing could be more exhilarating. Using combinations of chemotherapy, radiation, and surgery, so-called ‘conventional’ therapy, we are able to achieve long-lasting cures for the vast majority of patients who are diagnosed with cancers such as childhood acute lymphoblastic leukemia, Wilms kidney tumor, Hodgkin’s disease, localized sarcomas, and low-risk neuroblastoma. Unfortunately, we have not been so successful with many other childhood cancers such as acute myeloblastic leukemia, metastatic sarcomas, and high-risk neuroblastoma (age >18 months, MYCN amplification, unfavorable histology and advanced stage of disease). What is perplexing is that in most cases these diseases do respond to conventional treatment, and most patients achieve remission – their disease is no longer detectable. In these cases the cancer usually returns without warning, any time, even years later. Patients and their families are constantly on edge, living in fear of relapse. Until recently, medical science has never been able to satisfactorily explain cancer relapse. How is it that we can kill more than 99% of cancer cells but not 100%? It has been assumed that a few cells are able to survive the treatment and re-grow. Did such cells pre-exist in the tumor, or did they develop resistance during the course of treatment? Either way, what is different about those few cells compared with all the others? If a few cancer cells can become resistant to treatment, why don’t all cancer cells become resistant? If treatment selects for resistant cells, how is it possible that some patients can be retreated and achieve a second remission, sometimes with the same drugs that were used originally? And finally, why is it that chemotherapy alone is usually not sufficient to cure solid tumors: patients also need good ‘local control’ using surgery and/or radiation at the site of any bulky disease. The answers to these questions may lie in the idea of cancer stem cells, which is a new, exciting and potentially far-reaching concept in cancer biology. Normal stem or progenitor cells are known to reside in most if not all normal organs, giving rise to the differentiated ‘bulk’ cells of the organ. In an analogous way, cancer stem cells are postulated to be the seeds that generate the tumor bulk, most of which is comprised of cells that are partially differentiated and no longer capable of forming tumors themselves. There has been considerable controversy regarding the origin and nature of such cancer stem cells, also known as tumor-initiating cells, and scientists now admit that referring to them as stem cells may be misleading as they do not necessarily exhibit properties of normal stem cells [1]. Regardless of the nomenclature, the fact that most leukemia cells are not tumorigenic and that a subpopulation of self-renewing, tumor-forming cells exists in leukemia is now well established. Mounting evidence suggests that cancer stem cells also lie at the heart of many solid tumors, including neuroblastoma. Identifying and killing these underlying culprit cells may be crucial to finding more effective treatments." @default.
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• W2169648328 date "2009-05-01" @default.
• W2169648328 modified "2023-10-18" @default.
• W2169648328 title "Targeting cancer cells with stem cell-like properties: the key to preventing recurrence in neuroblastoma?" @default.
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• W2169648328 doi "https://doi.org/10.2217/thy.09.14" @default.
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