Scientists have identified three ‘cell death’ genes which they claim are crucial for anti-cancer drugs to work effectively,a discovery that could pave the way for better treatments for various cancers.
Programmed cell death,or apoptosis,removes unwanted or dangerous cells from human bodies,thus protecting against cancer and autoimmune diseases. The process is regulated by a family of genes called Bcl-2.
Now,a team at Walter and Eliza Hall Institute,led by Lina Happo,has identified three Bcl-2 genes,puma,noxa and bim which tell cancer cells to commit suicide following treatment with conventional chemotherapy drugs.
In our studies we found that puma,noxa and bim work together to instruct the cancer cell to die,once its DNA has been damaged by chemotherapy drugs. But if certain combinations of these genes are missing or not functioning,the anti-cancer therapies are unable to work effectively,so the cancer cells continue to survive and the tumour continues to grow, Happo said.
According to the scientists,most chemotherapy drugs do not distinguish between normal and cancerous cells. This means when using them that collateral damage to healthy cells the origin of side effects is unavoidable.
Many anti-cancer drugs act by damaging DNA in tumour cells,causing cells themselves to commit suicide. Until now we didn’t know which genes were essential for this process. By understanding which of the three genes we identified are required for successful drug responses,medical researchers should be able to work out how conventional cancer therapies work,and why they sometimes fail, she said.
Abnormalities within the Bcl-2 gene family are common in many human cancers and can often be responsible for resistance to chemotherapy treatments. We hope to be able to reduce unwarranted toxicity,ultimately improving the quality of life for patients, she said.
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