By: April Carson
After an extensive search, the scientists from the University of Pittsburgh School of Medicine have discovered that elusive missing element which explains how melanoma tumors determine their own fatality.
In a paper published in Science, researchers unveiled the molecular mechanisms behind melanoma growth and survival, offering oncologists crucial insight into how to better understand and treat this aggressive cancer. By identifying the specific genetic alterations that enable tumors to proliferate while avoiding their own destruction, they have laid the groundwork for potentially lifesaving treatments.
Using a combination of DNA sequencing and genomic analysis, the researchers were able to identify certain gene expression changes that occurred when melanoma cells went through programmed cell death (apoptosis). They also uncovered a surprisingly intricate web of signaling pathways which helped tumors turn off or dampen apoptosis, thereby boosting their own survivability.
Alder, an assistant professor in the Division of Pulmonary, Allergy, and Critical Care Medicine at Pitt’s School of Medicine proclaimed that they accomplished something which derived from fundamental research and was associated with occurrences happening to patients.
Telomeres, which protect the ends of our chromosomes and make sure that our DNA is not degraded, become shorter every time a cell replicates. If this process continues until they are too short for a cell to divide any further, it can cause serious diseases. Diseases caused by shortened telomeres often lead to premature aging and even death; conversely, if telomeres are longer than usual they may be linked with cancer risks. Therefore maintenance of an optimal length in the telomere is essential to keeping healthy cells functioning properly.
One such ailment that has been associated with telomere shortening is melanoma, an aggressive form of skin cancer. Recent research conducted on melanoma tumors revealed that the tumor cells actively manipulated their own mortality by lengthening their telomeres and becoming immortalized.
For decades, scientists have noted that melanoma tumors display unusually long telomeres when compared to other types of cancer.
Alder asserts that there is a distinct connection between telomere maintenance and melanoma. For any melanocyte to become cancerous, it first needs to conquer the challenge of achieving immortality. If successful in this pursuit, then it has nearly accomplished its goal of transforming into cancer.
The research team's findings showed that the melanoma cells used various strategies to achieve immortality. In some cases, they harnessed the same mechanisms used by normal skin cells in order to increase their telomere length.
Telomerase is a protein that can elongate telomeres, shield them from harm and avert cell death. Usually inactive in the majority of cells, certain cancer types such as melanoma are known to exploit mutations on the TERT gene—which activates this particular protein—allowing for cellular proliferation.
In other cases, the cancer cells managed to survive by down-regulating p53, a protein that normally prevents tumors from growing.
Astonishingly, 75% of melanoma tumors possess mutations in the TERT gene which activate protein production and telomerase activity. But when researchers mutated TERT in melanocytes, they couldn't replicate the extended telomeres identified in patients' tumors - indicating that only one factor was responsible for this development. It turns out that those promoter mutations were just half of what was necessary to produce observable outcomes. The other half was a chromatin remodeling gene called BRG1, which changes the structure of DNA molecules to allow for high levels of telomerase activity.
The discovery of this link between BRG1 and TERT-driven telomerase activity in melanoma tumors may open new doors for early detection and treatment. By understanding how these genes interact to cause tumor formation, scientists may be able to develop better therapies or even preventive measures, like screening tests.
As Alder's lab team scoured through cancer mutation databases, they identified an area in a telomere-binding protein known as TPP1 that repeatedly had mutations present in melanoma tumors. They hypothesized that this region was key to regulating telomerase activity and began to experiment on melanoma cells. The team discovered that BRG1 and TPP1 interact to promote TERT-driven telomerase activity.
This revolutionary discovery not only has transformed the way we comprehend melanoma, but it also carries a great potential to enhance treatments. Scientists have detected an exclusive telomere maintenance system that is unique to cancer cells, providing them with a new target for therapies. As telomeres are essential for the survival of cancer cells, by targeting its maintenance mechanism, scientists may be able to stop cancer progression and potentially increase mortality.
This study was published in the prestigious journal Nature, and has been featured in a number of scientific articles.
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April Carson is the daughter of Billy Carson. She received her bachelor's degree in Social Sciences from Jacksonville University, where she was also on the Women's Basketball team. She now has a successful clothing company that specializes in organic baby clothes and other items. Take a look at their most popular fall fashions on bossbabymav.com
To read more of April's blogs, check out her website! She publishes new blogs on a daily basis, including the most helpful mommy advice and baby care tips! Follow on IG @bossbabymav
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