Cancer :: Cell skeleton may hold key to overcoming drug resistance in cancer

Researchers have uncovered a new way in which a cell protein protects cancer cellsfrom a wide range of chemotherapeutic drugs, identifying a possible target forimproving treatment outcomes for patients.

A team of scientists at Children’s Cancer Institute Australia for Medical Research (CCIA), ledby Associate Professor Maria Kavallaris, discovered that the bIII-tubulin component of thecell’s cytoskeleton could play an important role in resistance to a wide range of drugs used totreat lung, ovarian and breast cancers.

Advanced non-small cell lung carcinomas (NSCLC) account for more than 80 per cent oflung cancer cases. More than one million people are diagnosed with lung cancer every year,the most common cancer in the world and the leading cause of cancer deaths.Chemotherapy remains the most effective treatment option, involving a diverse range ofdrugs, often used in combination. However, the emergence of drug-resistant tumours inNSCLC means chemotherapy no longer holds the promise of a good outcome for manypatients.

Increased expression of bIII-tubulin has been linked to drug resistance in NSCLC, ovarianand breast cancers. In the latest Cancer Research publication, Associate ProfessorKavallaris and her team showed that blocking the expression of the bIII-tubulin gene inNSCLC cells led to an increase in their sensitivity to a range of chemotherapeutic drugs.

“Our results strongly suggest that the bIII-tubulin component is responsible for protectingNSCLC cells from the action of key chemotherapeutic drugs,” said Associate ProfessorKavallaris.

“This is the first scientific evidence for the broader implications of abnormal expression of thisprotein.

“We now have new insight into a mechanism of drug resistance in NSCLC which has notpreviously been reported. This has important implications for improving the targeting andtreatment of a number of cancers which are resistant to current chemotherapeutic drugs,”said Associate Professor Kavallaris.


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