Researchers discover new drug targets for fatal brain cancer

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London: With the help of a mouse model, a team of researchers has now discovered more than 200 genes with novel and known roles in glioblastoma – the most aggressive type of brain cancer that promises new drug targets.
Researchers and colleagues at the Hospital of Welcome Sanger Institute, Edenbrook, for the first time showed a new mouse model that mutated well-known cancer genes, introduced EGFR glioblastoma, and with a selection of more than 200 other genes Works. Drive Cancer
The results, published today in Genome Biology, present the first mouse model of its kind, available to the research community to pursue new treatments for this deadly form of brain cancer.
Glioblastoma is an aggressive form of brain cancer. It is treated with chemotherapy or radiotherapy followed by surgery, however, glioblastoma cells can treat and return tumors. The prognosis is poor – the average patient survives 12–18 months after diagnosis.
New, targeted therapies and immunotherapy are currently being developed to help patients with glioblastoma. It is still not known exactly why glioblastoma begins to grow.
In a new study, researchers and colleagues at the Welcome Sanger Institute created a new mouse model with glioblastoma to investigate which genes were implicated in cancer.
The model showed that the well-known cancer gene, EGFR (epidermal growth factor receptor) can only initiate brain tumors to develop in mice, resulting in tumors that were highly representative of human glioblastoma.
Is a former author of Welcome Sanger Institute and now of Edenbrook Hospital and University of Cambridge. Dr. Emraan Noorani said: “We have created a new mouse model to study the malignant human brain cancer, globoblastoma. For the first time., We showed that the familiar cancer gene, EGFR, is capable of introducing glioblastoma and we have identified new driver genes. , Whose therapeutic targeting capabilities deserve further exploration. ”
To find out which genes help EGFR in eradicating cancer, the team used the Piggybeck transposon technique – a small segment of DNA inserted into different parts of the genome to present mutations. It was detected more than 200 known and novel mutations in tumor suppression genes working with EGFR to drive the development of brain tumors, many of which introduce new drug targets.
The team compared the results of human genome sequences from glioblastoma patients and uncovered several genetic mutations found in both humans and mice. Human genomic data contain multiple mutations implicated in glioblastoma, without any clear indication that specific mutations lead to cancer. With the new mouse model, the team was able to narrow down which mutations drive glioblastoma, which will focus on future drug development.
Professor Alan Bradley, former director of the Wellcome Sanger Institute, and now professor in the Department of Medicine, University of Cambridge, chief scientific officer of Kayamb, said: “Patients with glioblastoma need immediate new, targeted therapies. Unfortunately, glioblastoma tumors are excessive Resistant to treatments targeting specific molecules, as there are many other genetic drivers that can advance cancer. This new mouse model translates findings from new potential therapies tested in clinical trials on mice Provides missing link for.

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