Match your treatment to your cancer

Lina Happo

(Medical Xpress) -- New research has uncovered why certain cancers don’t respond to conventional chemotherapy, highlighting the need to match treatments to cancers better.

Cancer researcher Lina Happo and colleagues at the Walter and Eliza Hall Institute have identified three ‘cell death’ that are crucial for making anti-cancer drugs more effective at killing . The discovery could be the first step in developing new cancer treatments that target only cancer cells.

Most currently available chemotherapy drugs do not distinguish between normal and cancerous cells, Lina says. This means when using them that collateral damage to healthy cells—the origin of side effects—is unavoidable.

“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,” Lina says.

Programmed cell death, or apoptosis, removes unwanted or dangerous cells from our bodies, protecting us against cancer and autoimmune diseases. The process is regulated by a family of genes called Bcl-2.

“Many anti-cancer drugs act by damaging the DNA in tumour cells, causing the cells themselves to commit suicide. Until now we didn’t know which genes were essential for this process,” Lina says.

Working with colleagues from the institute’s Molecular Genetics of Cancer division, she was able to identify that three Bcl-2 genes – puma, noxa and bim – 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 cells continue to survive and the tumour continues to grow,” she said.

Abnormalities within the Bcl-2 gene family are common in many human cancers, Lina says, and can often be responsible for resistance to chemotherapy treatments.

Her discovery has the potential to improve treatment through the development of more efficient, targeted therapies for blood, breast and ovarian cancers.

“We hope to be able to reduce unwarranted toxicity, ultimately improving the quality of life for patients.”

Lina Happo is one of 16 early-career scientists unveiling their research to the public for the first time thanks to Fresh Science, a national program sponsored by the Australian Government. Her challenges included presenting her discoveries in verse at a Melbourne pub.

add to favorites email to friend print save as pdf

Related Stories

Researchers reveal PAX gene’s role in cancer

May 24, 2011

(Medical Xpress) -- University of Otago researchers have uncovered further evidence that PAX genes − members of a small family of genes that play important roles in embryonic development – also allow cancer cells ...

Missing Puma reveals cancer conundrum

Aug 01, 2010

Walter and Eliza Hall Institute researchers in Melbourne, Australia, have made a discovery that has upended scientists' understanding of programmed cell death and its role in tumour formation.

Picking cancer stem cells out of the crowd

Jun 15, 2011

(Medical Xpress) -- Stem cells receive a vast amount of research attention due to their abilities to differentiate, heal, and divide in perpetuity, properties that yield promise for regenerative medicine. In cancer stem cells, ...

New test for ovarian cancer patients

Nov 09, 2010

Scientists have developed a new test to select which patients with ovarian cancer will benefit from new drugs called PARP inhibitors, according to research presented at the National Cancer Research Institute ...

Cancer cells brought under control by scientists

Jan 13, 2011

Scientists at The University of Nottingham have brought cancer cells back under normal control -- by reactivating their cancer suppressor genes. The discovery could form a powerful new technology platform ...

Recommended for you

User comments