Colgate
students are sharing their experiences conducting research with faculty
members on campus and in the field. This post is by molecular biology
major Brandon Fiegoli, of Bedford, NY.
Every day, you hear about an infamous disease called
cancer. You are constantly reading about celebrities with breast cancer,
kidney cancer, and many more. You may even have friends or family
members fighting the disease. But what do you really know about cancer?
Where does it come from? Why does it occur and how does it harm us?
This semester, my research is under the direction of
Professor Engda Hagos,
and is aiming to answer some of these challenging questions. My project
is focusing on what causes cancer to manifest itself in a person’s
body. Rather than developing the disease in a day, cancer is the result
of several cellular processes that fail, causing the errors to build up.
The reason that regulation mechanisms fail to catch mutant cellular
division can be due to a number of variables and why these errors occur
is not yet fully understood.
In short, cancer is the uncontrolled replication of unhealthy cells
that proliferate at a rate faster than the body can destroy them. This
growth is regulated and monitored by the cell cycle. A cell’s growth
pathway has many points where it can be checked for normal functioning,
but it also has gaps in unregulated development where these checkpoint
mechanisms can malfunction.
I am working with the protein Kruppel-like factor 4 (KLF4). The
protein has been found to directly regulate the cell cycle from going
between the G1 phase, a segment when a cell’s internal structures are
growing, and S phase, when a cell’s DNA is duplicated. Previous research
and scholarship have found that when the protein KLF4 is not present,
this checkpoint malfunctions and uncontrolled cellular division occurs.
However, there is more than one pathway that prevents mutant cells
from duplicating and becoming malignant. Preliminary findings have shown
that KLF4 may potentially have a connection to another protein called
mTOR. In separate research, it has been determined that mTOR is known to
amplify the growth of tumors, giving mTOR the moniker “Tumor Enhancer.”
My research aims to find a connection between KLF4 and mTOR. Through
my initial findings, I have found that cells lacking the KLF4 protein
have increased levels of mTOR and, therefore, have an enhanced rate of
tumor formation. This semester I will continue to explore the
relationship between these proteins.
Cancer will not be beaten by me or my lab alone, but it is research
like this that is making strides to understand and beat this terrible
disease.
—Brandon Fiegoli ‘14
Let’s Keep Going!
