Cancer invented iPS cells

Yesterday I ran a Cancer Stem Cell meeting here at UC Davis School of Medicine.

We had some great speakers and over 150 participants including our outstanding keynote speaker, Dr. Jeremy Rich, Director of Stem Cell Research at the Cleveland Clinic.

One of the ideas percolating through the meeting was that during cancer development, there is a tremendous amount of plasticity.

Cancer is not a linear process that starts with a stem cell gone bad and proceeds through defined steps A-Z. It is more like chaos with a thread of evolution running through it.

It seems likely that at multiple steps during cancer formation that cells undergo changes that most accurately could be defined as reprogramming or dedifferentiation. In some cases cells that are not stem cells are reprogrammed back to a pluripotent-like state.

During this meeting the idea was proposed that in a certain sense, cancer really invented iPS cells.

While Dr. Yamanaka deservedly should get the Nobel Prize and he did indeed invent iPS cells, cancer has always been sneakily doing the same kind of thing.  All the iPS cell-associated genes used to make these amazing cells are one way or another cancer genes. While iPS cells only were invented 5 years ago, for thousands of years cancer has been using these same genes to kill millions of people each year.

Many if not most cancers co-opt pluripotency machinery because it gives their cells an advantage over other cells. They change identities into stem-like cells that can grow better, resist differentiation, and pull disappearing acts so that our immune systems cannot kill them. Cancer cells have been using these tricks in a deadly fashion. The good news is that through iPS cell and other stem cell research we can better understand cancer and cancer stem cells. In addition if we are smart enough we might be able to turn the stem-like properties of cancers against them, making them an Achilles Heal that we can target with new treatments.

1 Comment


  1. This is especially interesting in light of recent research that indicates autologous iPS cells can trigger a rejection response. If iPS cells are similar to cancer cells, it would be very interesting to know what is triggering, and how to enhance, the rejection response to autologous iPS cells.

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