Our knowledge of carcinogenesis has tremendously improved through decades of research. However, till date the therapeutic refractoriness and tumor dormancy that leads to cancer recurrence after therapy presents formidable obstacles through severely limiting the successful treatment outcomes for majority of cancers. Significant advances made recently in the cancer stem cell (CSC) biology field have provided new insights into cancer biology that are radically changing both our understanding of carcinogenesis and cancer treatment. The cancer stem cell hypothesis provides an attractive cellular mechanism to account for the therapeutic refractoriness and dormant behavior exhibited by many of these tumors. Direct evidence for the CSC hypothesis has recently emerged through their identification and isolation in diverse tumor types. These tumor types appeared to be hierarchically organized and sustained by a distinct fraction of self-renewing and tumor-initiating CSCs. Such illustration of the CSC paradigm in diverse tumor types necessitates reassessment and improvisation of the current therapeutic strategies originally developed against the homogenous tumor mass; now to specifically target the CSC population. Preliminary findings in the field indicate that such specific targeting of CSCs may be possible.
KeywordsAcute Myeloid Leukemia Cancer Stem Cell Cancer Stem Cell Marker Cancer Stem Cell Population Cancer Stem Cell Hypothesis
Cancer stem cells
Normal stem cells, HSCs, Hematopoetic stem cells
Label retaining cells
Epithelial to mesenchymal transition
Non-obese diabetic/severe combined immunodeficient
We thank Dr. G.C. Mishra, Director, National Center for Cell Science (Pune, India) for encouragement and support. We thank Dr. Santosh Honavar and team for providing clinical samples for Retinoblastoma work. We also acknowledge the Association for Research in Vision and Ophthalmology, the copyright holder of Figs. 15.3 and 15.4 for permitting use of these figures