A short news piece on cancer stem cell work caught my eye today:
According to the "stem cell theory", only a minute number of cells within each tumour can multiply enough to keep the tumour growing and spreading. The vast majority of the cells cannot do this so were viewed as passengers. The Melbourne researchers, however, found that many tumours are fuelled to grow by a substantial portion of the tumour cells - sometimes even the majority. "(This) suggests that the proportion of cells that can propagate tumours was previously grossly underestimated," the institute said. Determining whether most cells in a tumour, or only a rare population, can maintain its growth has important implications for therapy, they say.
Very true: we'll all be very lucky indeed if it turns out that a majority of cancers are sustained by small, distinct, characteristic populations of cells. Scientists are becoming very good at safely destroying distinct populations of cells, and any research at the extremely well-funded intersection of cancer and stem cell research will move rapidly.
I chased the news above back to the scientific paper in question:
The cancer stem cell hypothesis postulates that tumor growth is driven by a rare subpopulation of tumor cells. Much of the supporting evidence for this intriguing idea is derived from xenotransplantation experiments in which human leukemia cells are grown in immunocompromised mice. We show that, when lymphomas and leukemias of mouse origin are transplanted into histocompatible mice, a very high frequency (at least 1 in 10) of the tumor cells can seed tumor growth. We suggest that the low frequency of tumor-sustaining cells observed in xenotransplantation studies may reflect the limited ability of human tumor cells to adapt to growth in a foreign (mouse) milieu.
Determining whether the growth of various tumors is sustained by most of the tumor cells or by a rare subpopulation has important ramifications for the design of novel therapies. Therefore, the cancer stem cell hypothesis merits more rigorous tests. For human tumors, ultimately this will require transfer of tumor cells into mice installed with all the requisite human support cells.
Unfortunately, we're likely to see more of this sort of thing in the next couple of years; there are good reasons to believe that the cancer stem cell hypothesis will not hold for more than a few types of cancer.
Cancers are characterised by extremely rapid mutation and adaptation as the result of their fast growth and aggressive cell replication. This is one of the reasons cancers are so hard to treat with more brute force techniques such as radiation and chemotherapy - cancer cell populations very quickly evolve resistance to most of what can (reasonably) safely be tried as a therapy in this arena. There is no reason per se that this rapid mutation cannot include the mutation of normal cells into stem cells or stem-like states sufficiently empowered to support the cancer. It is possible that many combinations of a small number of mutations exist to produce cells sufficiently stem-like to support a cancer - and are therefore likely to be created in a rapidly mutating cancer.
We can hope, however. Sometimes we get lucky, and an age-related condition really does have narrow, distinctive roots waiting to be discovered. At the present blistering pace of research, I don't see uncertainty surrounding cancer stem cells continuing for many more years.