Associate Professor at University of Colorado at Boulder
Ph.D.: University of California, Berkeley, 1985
Postdoctoral Fellow: University of Washington,
Awards:
Howard Hughes Medical Institute Investigator
Searle Scholar, 1993-1996
Merck Fellow, 1988-1991
Background:
“When Natalie Ahn was a postdoctoral student from 1988 to 1990 in the laboratory of Edwin Krebs at the University of Washington in Seattle, she was one of a group of scientists who discovered a signal transduction pathway (the mitogen activated protein or MAP kinase pathway) growth factors. Her approach was painstaking, requiring more than 10,000 assays. She also found an enzyme called MAP kinase kinase, which adds a phosphate to the enzyme MAP kinase to make it active.
Today, as a chemistry professor at the University of Colorado at Boulder, Ahn continues researching the subtleties of the MAP kinase and other signaling pathways, and their possible role in cancer. She also studies the fundamental chemical behavior of proteins.”
Source: Howard Hughs Medical Institute
Dr. Ahn, I as a Melanoma stage IV Patient/ Survivor applauded you and your colleagues on the research that you are doing for the Melanoma Cause.
Do you see some day that there will be genomic testing at the clinical level in the near future? Is the Molecular diagnostics keeping up with the research?
My type of Melanoma was the Nodular, which must be a mutation in the BRAF and or NRAS. Would doing the CTLA-4 therapy and then IL-2 correct those mutations? Or is it a temporarily response?
Any insight would be greatly appreciated.
To answer your last question first:
Mutations in B-Raf and N-Ras have been shown to cluster at specific nucleotides. This strongly suggests that there is a cellular mechanism which targets these sites in each gene. However, you are probably right, that anti-CTLA4 and IL2 are working by enhancing immune surveillance of your melanoma.
Therefore, I think it is unlikely that these therapies would reverse the mutations in cells which harbor them. On the other hand, it seems possible that immune therapy might somehow select for a subpopulation of melanoma cells within the heterogeneous tumors which lack mutations in B-Raf or N-Ras, so that after extended treatment, the cells with mutations die and cells without mutations expand. This could lead to an apparent switch in cell population within the tumors.
To answer your first two questions:
Yes, I believe that genomic testing will be feasible to predict disease susceptibility as well as treatment routes. This is already being used for some cancers. For example, markers such as estrogen receptor, progesterone receptor, or HER2 are already being used to predict responsiveness to different therapies for breast cancer. Such markers are less well developed for melanoma, but I think it is a matter of time and effort to discover and characterize them. One aim of my research is to develop new technologies for profiling proteins and chemical modifications of proteins, in hopes of identifying protein markers that can be used to diagnose melanomas and predict responsiveness to different therapies.
With respect to molecular diagnostics:
I think that there are many powerful technologies for molecular diagnostics -- such as gene chips which are used to survey transcripts. But other diagnostic technologies, e.g. for surveying proteins, are still immature. Also difficult is developing good laboratory medicine assays that can be performed with high accuracy and sensitivity. There are many blood markers that can be used to diagnose diseases, but a serious bottleneck is in the assays for quantifying these markers. So new technologies in laboratory medicine remains an important goal for the future.
I am also studying how B-Raf causes melanoma metastasis, and why targeted therapeutics which inhibit this pathway work in cells outside the body, but fail to work in patients. I believe that by studying mechanisms for resistance to these drugs, we might understand what else is needed in order to trigger melanomas to respond to these compounds. This would provide alternative therapies to melanoma patients, especially the many who fail to respond to current therapies.
Thank you for contacting me. I wish you the very best for your
treatment, and hope that your disease continues to remain stable for
many years to come.
Sincerely yours,
Natalie Ahn
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