Prostate cancer analysis yields interesting insight into existence of two distinct processes as potential therapeutic targets.
Researchers have used clinical data from prostate cancer patients to identify two new gene mutations. Previously considered redundant, these mutations have been introduced in mice to map their distinct effects on the development and progress of prostate cancer.
Cancer is the second most prominent cause of human mortality after cardiovascular diseases. In a bid to find a cure, genomic studies into understanding cancer have become a central focus of cancer research.
The complexity and variability in mutational drivers of cancer have made it hard for researchers to derive a ‘cure-all’ solution for a single type of …show more content…
In 2018, the disease is expected to cause 3,500 deaths in Australian males alone. It comes as no surprise then that the disease has driven a great deal of clinical analysis from patients. Researchers have used these analyses to spur important genomic studies into the cancer’s early development and progression.
The ‘gas and brake’ drive
Normal cell division is primarily controlled by a ‘gas and brake’ mechanism. Some molecular processes work as the ‘gas’ that accelerates cell division as needed. Other processes act as a ‘brake’ to prevent excessive cell division and growth, which can inevitably lead to cancerous cells if left unchecked. These antagonistic processes work to balance each other out and subsequently, contribute to a healthy, normal functioning cellular environment.
Mutations in even a single gene that participates in this ‘gas and brake’ system, may lead to cancer.
The PTEN gene has been identified as a tumour suppressor; it contributes to the ‘brake’ mechanism. Mutations in PTEN essentially cause a ‘brake failure’, resulting in uncontrollable cell division which leads to eventual tumour formation and cancer development in different organs, including the ovaries and the …show more content…
They have set out to observe these two mutations separately in different sets of mice. Their preliminary results indicate that while the ‘brake’ mutation remains the more aggressive driver of prostate cancer, the ‘gas' mutation does drive tumour formation independently. Even more interestingly, while the mutated genes cause hyper-activation of the same process (cellular division), they affect different biological pathways to achieve this common goal. “The two mutations appear to be anything but redundant. This is good news! It opens up the exciting potential to uncover previously inaccessible drug targets for prostate cancer treatment”, concludes Dr. Goode, the team leader on this
Researchers have used clinical data from prostate cancer patients to identify two new gene mutations. Previously considered redundant, these mutations have been introduced in mice to map their distinct effects on the development and progress of prostate cancer.
Cancer is the second most prominent cause of human mortality after cardiovascular diseases. In a bid to find a cure, genomic studies into understanding cancer have become a central focus of cancer research.
The complexity and variability in mutational drivers of cancer have made it hard for researchers to derive a ‘cure-all’ solution for a single type of …show more content…
In 2018, the disease is expected to cause 3,500 deaths in Australian males alone. It comes as no surprise then that the disease has driven a great deal of clinical analysis from patients. Researchers have used these analyses to spur important genomic studies into the cancer’s early development and progression.
The ‘gas and brake’ drive
Normal cell division is primarily controlled by a ‘gas and brake’ mechanism. Some molecular processes work as the ‘gas’ that accelerates cell division as needed. Other processes act as a ‘brake’ to prevent excessive cell division and growth, which can inevitably lead to cancerous cells if left unchecked. These antagonistic processes work to balance each other out and subsequently, contribute to a healthy, normal functioning cellular environment.
Mutations in even a single gene that participates in this ‘gas and brake’ system, may lead to cancer.
The PTEN gene has been identified as a tumour suppressor; it contributes to the ‘brake’ mechanism. Mutations in PTEN essentially cause a ‘brake failure’, resulting in uncontrollable cell division which leads to eventual tumour formation and cancer development in different organs, including the ovaries and the …show more content…
They have set out to observe these two mutations separately in different sets of mice. Their preliminary results indicate that while the ‘brake’ mutation remains the more aggressive driver of prostate cancer, the ‘gas' mutation does drive tumour formation independently. Even more interestingly, while the mutated genes cause hyper-activation of the same process (cellular division), they affect different biological pathways to achieve this common goal. “The two mutations appear to be anything but redundant. This is good news! It opens up the exciting potential to uncover previously inaccessible drug targets for prostate cancer treatment”, concludes Dr. Goode, the team leader on this