Cancer Stem Cells More Complex Than Previously Thought

Studies into cancer stem cells and how they might be targeted for cancer treatment have been fervent over the past ten years. Indeed, there is a lot of evidence that suggests these unique cancer cells may lead to significant breakthroughs in treatment. However, as more and more research is being put into stem cells, researchers are discovering that the path to successful drug development may be more complex than initially thought.

Like healthy stem cells, cancer stem cells serve as progenitors (at least that’s the theory). As progenitors, these cells are responsible for re-growing tumor cells following cancer-killing treatments such as chemotherapy. Clearly, finding drugs or treatments that diminish the effects of these stem cells could help improve cancer survival rates.

In the past, researchers believed that all cancers followed a cancer stem cell model. This model suggests that such cells initiate the growth of cancer tumors. However, such a belief is changing as more research suggests a number of different cell types may instigate tumor growth.

While early cancers linked to stem cell tumor growth – such as acute myeloid leukemia and other blood cancers – continue to show a string linkage, there have been mixed research results for other types of cancer. As Dr. Jean Wang of the University of Toronto explains, “most of the markers we have right now are still very rough.” While many of these markers suggest stem cell growth in such cancers as brain, breast, colon and pancreatic cancer, there is enough variation in studies to result in skepticism among some experts. In fact, according to Dr. Barbara Vonderhaar of the NCI Center for Cancer Research, “We still don’t have definitive proof that cancer stem cells exist.”

As such, the initial goal for cancer stem cell research is to clearly validate their presence and importance in tumor growth. Until this happens, it will be extremely difficult (and possibility even futile) to attempt to create cancer drugs that target these progenitors.

Source:

http://www.cancer.gov/ncicancerbulletin/072710/page4