Cancer is one of the most life-threatening diseases around the world with increasing number of people suffering from cancer. Its number keep increasing rapidly pass over this decade and expected to increase in next decade. Recent study by WHO (World Health Organization) shown that the number of global cancer death is projected to increase 45% from 2007 to 2030 (from 7.9 million to 11.5 million deaths). Cancer is so malignant that most of people will do anything to kill cancer with intervention, surgery and chemotherapy. Chemotherapy has become the last option available to those who suffer cancer after having done intervention or surgical treatment. However, drug used to this therapy cause some negative side-effect to the patient. Until this bad impact of drug-related cancer can be substituted by the harmless one, scientist, doctors and pharmacist keep on researching the best possible drug to cure cancer.
The development of cancer-related drug have shown a great improvement over this decade. It’s started with the first discovery of arsenic dioxide as the chemotherapy agent and followed by the more harmless drug such as thalidomide and bendamustine. Now, the development of cancer-related drug has moved to a new perspective of healing with genome based medicine. Thanks to the discovery of the latest promising genomic cancer-related drug in 2010 by Jay Bradner and team. This research which is funded by Dana Farber Institute in joint with Harvard Medical School find a certain substance targeting genome triggering cancer. This substance is called JQ1, a cell-permeable small molecule that binds competitively to acetyl-lysine recognition motifs, or bromodomains. Bromodomain-containing proteins are of substantial biological interest, as components of transcription factor complexes and determinants of epigenetic memory which may turn the transcription of normal cells into cancerous.
This JQ1 molecule targets a specific bromodomain called BRD4 by displaces it from nuclear chromatin in cells in order to avoid getting transcripted and causing cancerous cells. Moreover, cancerous cells targeted by JQ1 was forgetting that it was cancer and becoming normal cells.
Clinical trial in mice has shown a massive dramatic changes. Mice infused by cancerous cell developed a large mass of tumour in its thigh. Treatment from this compound made the rapid growth of cancerous cell faded. With complete clinical trial in 4 mouse models, the mice that get the drug lived and ones that don’t get the drug rapidly perished. It is also shown that mouse models that the drug has a longer life than those which don’t. In addition, those mouse models not getting the drug grew a rapid mass of tumour while the ones getting the drug didn’t.
Another recent study has shown that JQ1 compound make the leukimia cell revert back to normal as well as happened in myeloma and fatty liver which revert to their normal condition. Eventhough this substance has not yet to be claimed undergone in human experiment, it has become a magnet towards other researchers."We're also excited to have found a pharmacological way to suppress Myc, which plays a role in many oncogenic pathways and is deregulated in most cancers," says Scott Lowe, Scientist at Cold Spring Harbor Laboratory (CSHL) . It is expected that the derivative compound of JQ1 will be discovered and create a stronger cancer-related drug in the future.
JQ1 is expected to be a powerful cancer drug in the near future. There are magnificent empiric prove shown by laboratorium and clinical trial, such as revert cancerous cells to normal and lengthen the life expectancy by making the rapid growth of tumur faded, which support it to be one of the biggest discovery in medicine.
Bibliography
1. Bardner, James, “Selective Inhibition of BET Bromodomain”, Dana Farber-Cancer Institute.
2. Cold Spring Harbor Laboratory, “Unconventional hunt for new cancer targets leads to a powerful drug candidate for leukemia”, Medical press.
3. Bardner, James. “TEDxBoston: Open-source Cancer Research”. Video taken from youtube at October 31th 2011 at 9.15 p.m.