Meanwhile,
Australian scientists discover new way:
Australian researchers have discovered a promising new strategy for removing the growth of aggressive cancer. Consequently, difficult to treat by targeting a specialized molecular process called “minor episse”. Therefore,
Published in Embo reportsThe study shows that the blocking of minor splicing can considerably slow down the tumor growth of liver cancer. However, lungs and stomachs, while leaving largely unharmed healthy cells. Furthermore,
Research on animal models. For example, human cells, from Australian Medical Research Institute Wehi, demonstrates the potential of this strategy to target cancers caused by mutations in carcinogenic common genes. In addition,
At a glance – Australian scientists discover new way
- New research shows that the targeting of minor splicing considerably reduces the tumor growth of liver cancers. For example, lungs and gastric. Consequently,
- The strategy is australian scientists discover new way particularly effective for cancers driven by Kras mutations. Meanwhile, which are among the most common genetic changes found in cancer. Nevertheless,
- The study demonstrates the therapeutic potential of the inhibition of minor splicing through various models of cancer. Therefore,
Why the minor splicing is important – Australian scientists discover new way
Splicing is how cells transform the long splands of RNA into shorter parts called Messenger RNA. However, which provide the model for protein production. Nevertheless,
While major splicing achieves 99.5% of this work, minor splicing is an essential process for the remaining 0.05% of genes, affecting around 700 of the 20,000 human genome genes. Therefore,
The new research reveals that the minor splicing blocking causes the accumulation of DNA damage to cancer cells. In addition, activates a key tumor suppressor that leads to cell death. Therefore, Remarkably, healthy cells are not widely affected. Consequently,
Although australian scientists discover new way it affects only a small subset of genes. Therefore, minor splicing is crucial for the correct expression of genes that stimulate the growth and division of cells-which makes it a potential Achilles heel for cancer cells.
Above all. many of these genes are generally diverted by cancers driven by KRAS mutations, which are among the most frequent genetic changes found in solid tumors.
The Chief Professor of the Wehi Laboratory. Joan Heath, said that scientists had long known that Kras has been at the heart of many aggressive cancers, but has struggled to transform this knowledge into largely effective treatments.
Kras mutations are available in a variety of flavors. which makes them extremely difficult to treat, so even with decades of scientific efforts, there has been only limited progress.
But our approach is different. Instead of trying to target specific mutations which can only apply australian scientists discover new way to a subset of patients. we disturb a fundamental process on which these fast growing cancers rely.
This research offers a new way of solving a problem that has long been resisting conventional approaches. with the potential to help a much wider group of patients. »»
Professor Joan Heath, Wehi
A striking result reveals a path to new treatments
Using models of zebra and mice fish, as well as cancer cells of the human lung, research led by Wehi is the first to demonstrate the impact of minor splicing inhibition in in vivo models of solid tumors.
The study revealed that the reduction in the activity of a protein coded by the RNPC3 gene – an essential component of the minor splicing machine – considerably slows tumor growth in liver. lungs and stomach cancers.
“Half by half the australian scientists discover new way quantity of this protein, we were able to considerably reduce the tumor load,” said Dr. Karen Doggett, the first author of the study.
“It is a striking result, especially given the resilience of these cancers. »»
The study also revealed that the minor splicing disturbance triggers the tumor suppressor’s route P53. a critical defense mechanism in the fight against body cancer.
Nicknamed the “genome guardian”. the protein P53 responds to DNA damage by blocking cell division, by initiating DNA repair or the triggering of cell death. This well -known route is frequently transferred or disabled in many cancers, allowing these cells to develop without control.
“The minor splicing blocking leads to DNA damage. activates this critical defensive response, which means that cancers with a functional P53 route are probably particularly vulnerable to this strategy,” said Dr. Doggett.
“This opens the door to treatments that could australian scientists discover new way be both more effective. less toxic, offering hope for patients with aggressive cancers that currently have limited options. »»
Medicines discovery collaboration
To search for compounds that could inhibit minor splicing. the research team turned to the National Drug Discovery Center, the headquarters of which is in Wehi, with a screen of more than 270,000 drugs of the medicine type identifying several promising strokes.
“We have validated minor splicing as a convincing therapeutic target – the challenge is now to develop a drug compound that can inhibit it safely. effectively,” said Professor Heath.
Research is based on Wehi’s in -depth expertise in the discovery of genes. cancer biology, presenting the power of collaboration in several laboratories and technologies.
“One of the forces in this study is the extent of the models. types of tumors that we have used,” said Professor Heath.
australian scientists discover new way
“We have not just tested a type of cancer or used an analysis method. This diversity in our approach gives us the confidence that our strategy could be relevant through many forms of cancer. and not only in a close whole of conditions. »»
Research was supported by the National Health. Medical Research Council of Australia (NHMRC), the Ludwig Institute for Cancer Research and the National Institute of Neurological Disorders and Cerebral Vascular Accidents.
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