Cancer stem cells FOR EXPERTS
A breakthrough discovery
Timeline of CSCs
In a 2003 breakthrough discovery, Dr. Michael Clarke, Dr. Max Wicha, and colleagues (University of Michigan, USA) discovered that a small number of cells within a tumor — the cancer stem cells — were responsible for fueling the growth and spread of solid tumors. At this time, Dr. John Dick (University of Toronto), that has pioneered the concept of cancer stem cells in leukemia (1997), was saying:
“If the tumor is a dandelion, cancer stem cells are its evil roots.”
Since, our understanding of cancer has been transformed by exploring clonal diversity, cell plasticity, drug resistance, and causation within an evolutionary framework. It is now well accepted that neoplasms change over time through an evolutionary process at the cell level, driven by genetic and epigenetic alterations, and especially under sustained treatment. This evolution explains the processes of tumor progression and therapeutic resistance. While tumor cell heterogeneity composes a complex ecosystem, cancer stem cells (CSCs) seem to orchestrate the evolutionary selection in cancer. Dr. Owen Witte of the UCLA Broad Stem Cell Center was clear about what these results mean for cancer research:
People can stop arguing…Now they can say, “OK, the cells are here. We now need to know how to treat them.” (L.A. Times, 2012)
Indeed, a direct consequence for these breakthroughs is the pivotal role of CSCs in leading clinical evolution. It has been clearly established a positive association between CSCs burden and disease progression or therapeutic failure. Thus, developing CSC-targeting therapies is of major interest. This is clearly a paradigm shift for the future development of new anti-cancer therapies. As highlighted by Dr. John Dick:
“Data show that gene sequencing of tumors to find the spectrum of their mutations is definitely not the whole story when it comes to determining which therapies will be most effective”.
The cancer researcher community has to decipher the underlying mechanisms regulating stemness properties. While CSC self-renewal capability offers to tumors a unique capacity to promote cancer recurrence, it may also unveil therapeutic opportunities to control tumor progression through clinically relevant methods targeting CSC dynamics.
In this context, The SUNRiSE Network will be a unique opportunity to foster interactions and partnerships between university researchers, clinicians, and pharmaceutical companies. It will give strong impetus to development of new research project on cancer stem cells.