According to the U.S. Centers for Disease Control and Prevention (CDC), colorectal cancer is the “second leading cancer killer in the United States.” The National Cancer Institute (NIH)’s Surveillance, Epidemiology, and End Results Program (SEER) says there were 1,317,247 Americans living with
colorectal cancer in the country in 2014. The group estimates that 135,430 new cases of the cancerwould be diagnosed this year, while there would be about 50,260 deaths as a result of the cancer.
As with most cancers, the reason for cancer’s growth is unknown, although there are several risk factors involved that can increase a person’s chances of contracting the disease. Experts are continually trying to find means to combat cancer. This includes finding out why it occurs in the first place, and why some people are susceptible to it.
In line with this, the American Cancer Society expounds that other researches are ongoing to create early detection tests and develop a colorectal cancer vaccine that is designed to fight the cancer more effectively. These aren’t the only research that are being conducted to beat colorectal cancer, however.
In fact, Case Western Reserve University School of Medicine researchers came out with a
groundbreaking study, first published in Nature Communications. The researchers noticed a pattern that certain gene enhancers activate gene mutations that are known to increase a person’s risk of getting colorectal cancer. These enhancer elements are “short sections of DNA that function as switches to control genes.” Essentially, these enhancers would activate chromosomes related to the progression of colorectal cancer, further facilitating its spread and growth. “Our data suggest that the survival of colon cancer cells often depends on the expression of genes associated with common enhancer changes,” explains Peter Scacheri, PhD, senior author of the study. Scacheri is also an associate professor of genetics and genome sciences at the Case Western Reserve University School of Medicine. His team noted how gene mutations known to increase colon cancer risks are “hotspots” for enhancer activity, signifying that there is a significant activity on these genes. When the enhancer activates a gene, other proteins would flock to the site which can lead to the development of tumors and speed up cancer growth.
The study is revolutionary particularly in terms of how it can crack open the enigma of effective
cancer treatments. The study can be pivotal in the development of medication with the hope that the enhancers can be switched off so that cancer would not grow. “Identifying common
enhancer changes helps us pinpoint a specific set of genes that are consistently switched on during transformation of normal cells to cancer cells,” says Scacheri. By inhibiting these enhancers from activating, they could potentially hinder the cancer from growing.
Our next step is to determine exactly how the common enhancers form in colon cancer, and
whether we can target their destruction as a strategy to kill tumor cells without harming normal
cells,” says Scacheri. If his team succeeds, then they would be a step closer to finding out how to
cure colorectal cancer, and how to minimize its risk so that there would be fewer cases annually.
