My Fred Hutch Experience
When I first saw Fred Hutch’s VECR internship program, I originally thought it was going to be a very serious and formal environment with lectures, but fortunately VECR wasn’t that. VECR was a very friendly but professional environment and had presentations that explained the way that cancer and different cells operated in an easy to understand format. One of the fun experiences that will stick with me forever was the “Imposter Syndrome” presentation.
There are a few definitions for imposter syndrome, the true definition of imposter syndrome is a collection of feelings of inadequacy that persist despite evident success. I feel like it’s a confusing definition of Imposter syndrome and Alicia Morales of Fred Hutch’s presentation of imposter syndrome included an easy to understand definition. The example was about a student that got straight-A’s on tests but then gets a single “B” on their test, the student seems to go into a sort of blind panic questioning and insulting their own intelligence over the single “B”, when in reality it wasn’t that big of a deal. This presentation really resonated with me because before the presentation, we had to take a survey that related to imposter syndrome and I was surprised on how many of the answers related to imposter syndrome I answered with either a “often” or a “very often”. It truly shocked me.
Figure 1 The group discussing the ways to help with Imposter syndrome
Another cool part of Fred Hutch was seeing all of the innovations and advances that the Fred Hutch researchers are making. One of those innovations was studying a disease in Tasmanian Devils to almost extinction called the devil facial tumor disease (or dft or short). The disease was a tumor that jumped from host to host then evolved to slow down. The Fred Hutch researchers were trying to see if the tumor regression in the Tasmanian Devils could also apply to human tumors.
This study is very important because it could be beneficial for cancer in humans or quite possibly the cure for cancer itself or at least a new kind of treatment to slow down tumor growth. I wasn’t able to get the question out in time for the due date but my question for the researchers was “I would’ve glossed over the mutation of the RASL11A because it was a part of the protein function and a regulatory mutation, what caught your eye when examining this mutation?” The reason for choosing this study is because I’ve always been interested in cancer on how the treatments worked.
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