Abstract
With the political, social and financial drives for cancer research, many advances have been made in the treatment of many different cancer types. For example, given the increase in awareness, early detection, and treatment of breast and prostate cancers, we have seen substantial increases in survival rates. Unfortunately there are some realms of cancer that have not seen these substantial advancements, largely due to their rapid progression and the inability to specifically target therapy.The hypothesis that cancers arise from a small population of cells, called cancer stem cells (CSCs), is gaining more popularity amongst researchers. There are, however, still many skeptics who bring into question the validity of this theory. Many skeptics believe that there is not a specific subset of cells that originate with these characteristics, but that they develop certain features over time making them more resistant to conventional therapy. It is theorized that many of the relapses occurring after remission are due to our inability to destroy the self-renewing CSCs. This central idea, that CSCs are biologically different from all other cancer cells, has directed research towards the development of therapy to target CSCs directly. The major dilemma in targeting therapy in myeloproliferative disorders, malignancies of the central nervous system or malignancies in general, is the inability to target CSCs as opposed to normal stem cells. However, with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs, it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers.
Highlights
When discussing potential targets for the treatment of cancer today, the conversation will generally lean towards targeted therapy of cancer stem cells (CSCs)
Research seemed to focus on isolating CSCs by specific identifying markers but the research has seemed to shift towards identifying the way in which these stem cells behave that make them different from bulk tumor cells
Results of this study indicated that after 6 hours of incubation with daunorubicin plus cyclosporine, the sensitivity of the K562/ADM strain approached that of the daunorubicin sensitive K562 strain of AML cells [40]
Summary
When discussing potential targets for the treatment of cancer today, the conversation will generally lean towards targeted therapy of cancer stem cells (CSCs). It has been found that BCRP is the key player in drug efflux in AML leukemic cells as opposed to P-gP which is common in many other biological systems [3] Identification of this subpopulation is an important discovery in terms of narrowing the search for a viable target, it only gives information that LSCs are derived from a subpopulation of immature bone marrow cells. It did provide researchers with a definition of CSCs for AML.
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