Harvard researchers have created a molecule that can block an important element of the on-off switch in cancer genes, potentially opening a new front in cancer research.
The study, published recently in Nature online, is the first to report a successful inhibitor of bromodomains—a family of “reader” proteins that sit on the folded DNA and send signals to activate DNA replication.
Since cancer is caused by uncontrollable cell growth and division, targeting bromodomain readers can turn off the gene pathway, prevent DNA from making copies, and potentially arrest the growth of the cancerous cell, according to researchers at Harvard-affiliate Dana-Farber Cancer Institute.
“We’re using this molecule as a tool to manipulate the gene regulation pathway to find a cure for cancer,” said Jun Qi, one of the lead researchers.
The findings detail the structure and function of the new molecule, which the scientists dubbed JQ1, after Qi.
The new molecule has shown great promise in targeting BRD4, a bromodomain-containing molecule that plays a key role in initiating DNA transcription. The development will advance the search for a cure for a deadly and currently untreatable type of cancer called nuclear protein in testis midline carcinoma.
The results “underscore the broad utility and immediate therapeutic potential of a direct-acting inhibitor of human bromodomain proteins,” according to the paper.
Now that JQ1 has shown potential in arresting cancerous cell growth in mice and in-vitro experiments, the researchers are eager to move forward and test it in human clinical trials.
“Unfortunately, the last patient that we got cell lines from was in the last stage of cancer, so we [were not] able to do anything for him. But in the future, we hope to use the compound we’ve made to save lives,” Qi said.
According to Dipanjan Chowdhury, an assistant professor of radiation oncology at Harvard Medical School, the study draws light to a “relatively new theme in cancer research.”
“The big thing right now in cancer research is personalized medicine, as we move away from broad pharmaceutical treatments,” Chowdhury said. “This work is about finding molecules that selectively affect new players in cancer biology, and it definitely moves research in that direction.”
Researchers at Dana-Farber collaborated with researchers from four other institutes including Oxford University, Harvard-affiliate Children’s Hospital Boston, Harvard-affiliate Brigham and Women’s Hospital, and the University of Notre Dame.
—Staff writer Helen X. Yang can be reached at firstname.lastname@example.org.
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