A cellular switch that can be turned off and on to slow down the growth of the aggressive malignant brain tumour has been discovered by scientists.
The findings show that the protein RIP1 acts as a mediator of brain tumor cell survival, either protecting or destroying cells.
Brain Tumor
Brain tumors are the abnormal growth of brain cells that may be benign or metastatic. Brain tumors account for about 2.4% of all the tumor diagnosesandare most challenging due to their critically delicate location.
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According to the researchers the protein, found in most glioblastomas, can be targeted to develop a drug treatment for these highly malignant brain tumors.
Senior author Dr. Amyn Habib, associate professor of neurology and neurotherapeutics at UT Southwestern Medical Center, said that their study identifies a new mechanism involving RIP1that regulates cell division and death in glioblastomas.
![Quiz on Brain]( "Quiz on Brain")
The human brain is exquisitely intrinsic and is the seat of all emotions. If you are curious about what makes you bad, sad, silly or glad this quiz on the brain will satiate you.
She said that for individuals with glioblastomas, this finding identified a target for the development of a drug treatment option that currently does not exist.
In the study, researchers used animal models to examine the interactions of the cell receptor EGFRvIII and RIP1. Both are used to activate NFkB, a family of proteins that is important to the growth of cancerous tumor cells. When RIP1 is switched off in the experimental model, NFkB and the signalling that promotes tumour growth is also inhibited. Furthermore, the findings show that RIP1 can be activated to divert cancer cells into a death mode so that they self-destruct.
The study has been published online in Cell Reports.
Source: ANI
Quiz on Brain
The human brain is exquisitely intrinsic and is the seat of all emotions. If you are curious about what makes you bad, sad, silly or glad this quiz on the brain will satiate you.
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She said that for individuals with glioblastomas, this finding identified a target for the development of a drug treatment option that currently does not exist.
In the study, researchers used animal models to examine the interactions of the cell receptor EGFRvIII and RIP1. Both are used to activate NFkB, a family of proteins that is important to the growth of cancerous tumor cells. When RIP1 is switched off in the experimental model, NFkB and the signalling that promotes tumour growth is also inhibited. Furthermore, the findings show that RIP1 can be activated to divert cancer cells into a death mode so that they self-destruct.
The study has been published online in Cell Reports.
Source: ANI
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