The molecular and genetic basis of urologic cancer
Despite the advances in medicine and research, cancer still remains to be a significant cause of morbidity and mortality. Cancer is not a single disease, but a plethora of different subtypes with its own complexity and behavior.
In the Philippines, cancer ranks as the third most common cause of death after heart disease and stroke. It is believed that in the near future, cancer will overtake them and become the leading cause of death. Genitourinary ( GU) or urologic cancers may not be as common or deadly compared to either lung or breast cancer; still a lot of Filipinos suffer from these diseases.
GU malignancies include kidney, prostate, urinary bladder, testicular and penile cancers. Significant advances and successes have been made in the diagnosis and treatment of testicular cancers but less success is seen in more common GU cancers like prostate, kidney and bladder. More studies are needed before we can replicate our success in testicular cancers to the other GU cancers.
The discovery of the DNA structure by Watson and Crick in 1953 is the backbone in our current understanding of cancer. It resulted in the expansion of the field of molecular biology and opened other fields like molecular genetics and biochemistry. This provided insights at the molecular level of the behavior of cancer cells.
How these cancer cells disrupt the molecular signaling pathways that control balance or homeostasis have been known and elucidated.
According to Hanahan and Winberg in 2000, there are several steps to make a normal cell become a malignant one and that it would take several years to complete. Cancer cells need to acquire at least nine key attributes for the change to happen. These are ( 1) mutation and genetic instability, ( 2) autonomous growth, ( 3) independence to both internal and external antiproliferative signals, ( 4) resistance to cell death, ( 5) infinite cell multiplication potential, ( 6) angiogenesis or the ability to form new blood vessels, ( 7) locally invasive behavior, ( 8) evasion of the immune system, and finally ( 9) either metastasis or the ability to spread and invade distant tissues or organs.
The first attribute, mutation and gene instability, is central to cancer development. Before cancer can develop, significant mutations in DNA that lead to changes in expression should happen and these changes increase the potential for tumor initiation, progression and metastasis.
Genomic alterations or gene mutation is an example of DNA mutation. Tumor suppressor genes are part of the DNA that is crucial for DNA repair and cell cycle regulation. So mutations that inhibit tumor suppressor genes to function normally can thereby promote unregulated cell cycle proliferation.
Another gene mutation is the over expression of oncogenes. Oncogenes are genes that encode for proteins that can transform normal cells to cancer cells. This over expression also leads to continuous cell proliferation. Mutation and gene instability is just the tip of the iceberg and our knowledge and understanding on cancers are continuously expanded with new discoveries. The other eight attributes are as equally important, as they are associated with cancer invasiveness and spread. Each of these attributes becomes a target for research and drug development in the hope that one day we may not only understand but also cure all people with cancers.
To help increase the knowledge on the molecular and genetic basis of urologic cancer, the Institute of Urology of St. Luke’s Medical Center- Global City will hold its 5th postgraduate course entitled “Where it All Starts: The Molecular and Genetic Basis of Urologic Cancer” on Oct. 14, 2016 8 a. m.- 5 p. m. at the Henry Sy, Sr. Auditorium, 5th floor, St. Luke’s- Global City. Both foreign and local speakers were invited to speak on a variety of topics on urologic malignancies during this event.