Student Research at Duke

So I think it’s about time to describe what exactly I’ll be working on. When friends ask me what am I doing research on this summer, my simple reply is: cancer stem cells. But that’s not even scratching the surface, nor is it completely accurate. I will be working on the link between the Wnt signalling pathway and development of CML…but I am getting ahead of myself.

First, cancer stem cells. Other than embryonic stem cells and the morality question linked with it that everyone thinks of at the mention of “stem cells,” the adult body also contains stem cells to replace the cells that die. We’ve all learned about mitosis, the cell cycle, etc etc etc…but what’s interesting is that most of the cells in our bodies no longer have that function; it’s a property unique to the remaining stem cells we have. These unspecialized cells can give rise, or differentiate, to any number of specific cell. Cancers also have their equivalent of normal stem cells; these are cells that have self-renewal capabilities and can keep the tumor growing, even after radiation or chemotherapy, much like how our bodies can repair skin even after it’s been scraped. One direction of future therapy targets these cancer stem cells.

Since most cells do not self-renew, the mutated pre-cancer cell must first gain this ability for the cancer to develop. This is where the canonical Wnt signaling pathway comes in. In most basic terms, I like to think of a signaling pathway as a game of telephone between biomolecules, one with much greater accuracy in transferring the message. Specifically, when a Wnt protein binds to the cell surface, it induces a series of events that results in the accumulation of a different protein, beta-catenin in the cytoplasm. Beta-catenin is usually broken down in the cell, but when it accumulates, it translocates to the nucleus and acts as a transcription factor, turning on many gene not normally expressed. Some of them are necessary for self-renewal. This pathway has been implicated in a number of different cancers, such as colon cancer, but it has not been linked to leukemia.

It’s already known that the oncogene that induces the onset of chronic myeloid leukemia (CML) is called bcr-abl. In simplistic terms, part of the bcr gene and part of the abl gene (these are genes on different chromosomes) fuse together to form a mutant. It’s protein product, also called bcr-abl (but without the italics), is thought to do many things to promote unregulated cell proliferation. Previous studies from the lab show that CML does not develop as well in the absence of beta-catenin (remember, these are cells with inhibited Wnt signalling). I will be looking at protein levels of bcr-abl and beta-catenin to start figuring out why this occurs. This work is important because it opens up new potential drug targets for cancer therapy.

Okay maybe not, but most things do. In any case, I’m giving this blog one.

• The first seminar we attended for the Howard Hughes Research Fellows program was about science blogs that we would all need to keep. And we all thought we were home free after work. But instead of making this useless occupied webspace that I’d dread writing in, I want to approach it with a purpose in mind: a real account of all the activities occuring behind that incomprehensible science paper of which you only read the conclusion. Specifically, I hope (once Duke gets this science blog thing going) high school and other college students thinking about going in science/research will find my ramblings useful.
• Disclaimer: Anything I write in this blog, unless otherwise indicated, is my own views and opnions, and in no way reflects upon my lab or the University.