Miss Happo has identified three ‘cell suicide’ genes that are crucial for the effective treatment of some cancer cells by chemotherapy. The discovery could lead to more targeted and effective therapies for cancers such as breast, blood and ovarian cancers, and has the potential to improve cancer prognosis and treatment outcomes.
Miss Happo and colleagues from the institute’s Molecular Genetics of Cancer division identified three ‘cell suicide’ genes – puma, noxa and bim – responsible for instructing cancer cells to die following treatment with conventional anti-cancer drugs.
“Many anti-cancer drugs act by damaging the DNA in tumour cells, causing them to destroy themselves by programmed cell death, or apoptosis. But until now we didn’t know exactly which ‘cell suicide’ genes controlled this process,” Miss Happo said.
“Understanding which of these ‘cell suicide’ genes are required for successful drug response will allow medical researchers to identify how conventional cancer therapies work, and also why they sometimes fail.”
Miss Happo said the studies, using a pre-clinical model of a type of blood cancer called lymphoma, helped the team to discover how chemotherapy drugs acted to kill cancer cells through apoptosis.
“We found that the ‘cell suicide’ genes puma, noxa and bim work together to instruct the cancer cell to die once its DNA has been damaged. 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.”
Programmed cell death is regulated by a family of genes called the Bcl-2 family. The genes are responsible for removing unwanted or dangerous cells from our bodies, protecting us against cancer development and autoimmune diseases. Anti-cancer therapies that target genes in the programmed cell death pathway are the focus of many cancer researchers. A promising new class of drugs called BH3 mimetics, which targets genes in the Bcl-2 family, is currently under development.
Miss Happo said abnormalities within the Bcl-2 gene family were common in many human cancers, and are often the cause of resistance to chemotherapy treatments. Most currently available conventional chemotherapy drugs do not distinguish between cancer cells and normal cells, which means that collateral damage to healthy cells is unavoidable.
“These findings are vital to the development of more efficient, targeted therapies for cancer, which will reduce unwarranted toxicity, ultimately improving the quality of life for patients,” she said.
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