Finally, transcriptome sequencing, which allowed the team to analyze gene expression how and when genes are activated across the genome enabled the researchers to learn more about how HPV is driving cervical cancer.
It has long been known that exposure to HPV is a primary risk factor for cervical cancer. Once an individual is exposed, the immune system often clears out the infection, but in cases in which the virus lingers, it can integrate itself into the human genome. This study looked at where, in the genome, HPV inserted itself and found that HPV integration sites were associated with higher levels of gene expression and were often amplified, resulting in many copies of those sections of the genome. This connection between HPV integration and gene expression suggests that the virus may be driving cancer by promoting and elevating the activity of mutated genes.
"Our findings further elucidate the key role HPV is playing in the development of cervical cancer, which in turn emphasizes the importance of combating the disease by vaccinating against HPV," Meyerson said.
In addition to the evidence supporting vaccination as a means of prevention, the researchers say the study bears important clinical implications for targeted therapeutics.
"In metastatic cervical cancer, more effective systemic therapy is urgently needed," Salvesen explained. "So far, our knowledge regarding genetic alterations as potential targets for therapeutics has been limited, and no targeted therapeutics are yet in routine clinical use. The present study in particular the findings related to ERBB2 thus represents a unique and comprehensive new tool to guide clinical trial design in the future."
"The outstanding findings of our successful collaborative international research is giving us, here in Mexico, very powerful arguments in favor of the benefit of speeding up the adoption of molecular
|Contact: Nicole Davis|
Broad Institute of MIT and Harvard