BACKGROUND: Until few years ago, all neoplastic cells within a tumour were suggested to have tumorigenic capacity, but recent evidences hint to the possibility that such feature is confined to a subset of Cancer Initiating Cells (CICs), also called Cancer Stem Cells (CSCs). These cells are the reservoir of the heterogeneous populations of differentiated cancer cells constituting the tumour bulk. Mechanisms shared with somatic stem cells, such as quiescence, self-renewal ability, asymmetric division and multidrug resistance, allow to these cells to drive tumour growth and to evade conventional therapy. OBJECTIVE: Here, we give a brief overview on the origin of CICs, the mechanisms involved in chemoresistance and therapeutic implications. CONCLUSION: Current cancer treatments, based on the assumption that tumour cell population responds homogeneously, have been developed to eradicate proliferating cells. The new model of tumorigenesis entails significant therapeutic implications, in fact if a small fraction of CICs survives conventional therapy it may lead to recurrence after month or years of apparent remission. Selective targeting of CICs could eliminate the tumour from the root, overcoming the emergence of clones capable of evading traditional therapy and increasing overall disease free survival.
BACKGROUND: Until few years ago, all neoplastic cells within a tumour were suggested to have tumorigenic capacity, but recent evidences hint to the possibility that such feature is confined to a subset of Cancer Initiating Cells (CICs), also called Cancer Stem Cells (CSCs). These cells are the reservoir of the heterogeneous populations of differentiated cancer cells constituting the tumour bulk. Mechanisms shared with somatic stem cells, such as quiescence, self-renewal ability, asymmetric division and multidrug resistance, allow to these cells to drive tumour growth and to evade conventional therapy. OBJECTIVE: Here, we give a brief overview on the origin of CICs, the mechanisms involved in chemoresistance and therapeutic implications. CONCLUSION: Current cancer treatments, based on the assumption that tumour cell population responds homogeneously, have been developed to eradicate proliferating cells. The new model of tumorigenesis entails significant therapeutic implications, in fact if a small fraction of CICs survives conventional therapy it may lead to recurrence after month or years of apparent remission. Selective targeting of CICs could eliminate the tumour from the root, overcoming the emergence of clones capable of evading traditional therapy and increasing overall disease free survival.
Authors: Alexey A Leontovich; Shuya Zhang; Cosima Quatraro; Ianko Iankov; Pier Francesco Veroux; Mario W Gambino; Amy Degnim; James McCubrey; James Ingle; Evanthia Galanis; Antonino B D'Assoro Journal: Int J Oncol Date: 2012-03-19 Impact factor: 5.650
Authors: Kevin Leder; Ken Pitter; Quincey LaPlant; Dolores Hambardzumyan; Brian D Ross; Timothy A Chan; Eric C Holland; Franziska Michor Journal: Cell Date: 2014-01-30 Impact factor: 41.582
Authors: Theresa L Whiteside; Deborah L Griffin; Joanna Stanson; William Gooding; David McKenna; Darin Sumstad; Diane Kadidlo; Adrian Gee; April Durett; Robert Lindblad; Deborah Wood; David Styers Journal: Cytotherapy Date: 2010-08-26 Impact factor: 5.414
Authors: Nicholas J Giacalone; Robert B Den; Rosana Eisenberg; Heidi Chen; Sandra J Olson; Pierre P Massion; David P Carbone; Bo Lu Journal: Future Oncol Date: 2013-05 Impact factor: 3.404