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Cancer resistance mechanism found
A newly identified mechanism that helps explain why some tumours are resistant to specific anti-cancer drugs could help improve patient care and drug design.

Chemotherapy drugs, such as Taxol and vincristine, are used to treat certain types of cancers, such as ovarian and breast adenocarcinomas, some types of lung cancer, leukaemias and lymphomas. But in some patients the effectiveness of these drugs is reduced.

Two teams of researchers now believe they have discovered why this is the case.

They found the loss of a tumour suppressing protein called FBW7 blocks degradation of a protein called MCL1, which normally causes old or damaged cells to die.

According to one of the studies, led by Dr Ingrid Wertz and Dr Vishva Dixit of Genentech in California and published in the journal Nature, this mechanism is normally activated during mitotic arrest - the process in which cell division is blocked.

Some chemotherapeutic drugs intiate mitotic arrest by attacking cellular structures called microtubules.

"Microtubules play many roles, including movement of things within a cell," says study co-author Professor David Huang of the Walter and Eliza Hall Institute of Medical Research in Melbourne.

"They play an essential role in cell division, because you have to move all the different bits of furniture around in a coordinated, orchestrated process before the cells divide."

Huang says anti-microtubule agents like Taxol and vincristine interfere with the action of the microtubules. This disrupts the ability of the cells to divide normally, which can arrest the growth of a cancer.

"The problem that we found is that some tumours harbour mutations in FBW7 or they have lost FBW7," he says.

"So although the microtubules are disrupted, the message for the cells to die is not being sent. This is exactly what you don't want in the context of cancer treatment."

Huang says the discovery of this mechanism may allow an improved understanding of why some patients respond less well to drugs than others.

"If they also happen to have mutations in FBW7, their tumours would probably respond poorly to agents like Taxol," he says.

"The second thing is that understanding why that occurs has helped us identify that the culprit in this case is really MCL1, because it's hanging around too long keeping the cells alive.

"So we hope to add to the activity of drugs like these by adding in an agent that would target MCL1. That would be the most obvious route to go."
Second study confirms findings

In a second paper published today in Nature,Dr Wenyi Wei of the Dana-Farber Harvard Cancer Centre and colleagues, looked at a related family of cell suicide proteins, known as BCL2.

They also found there was loss of the FBW7 tumour suppressor in various cancers, including breast and colon cancer, and that treating these patients with antitubulin or BCL2-targeted cancer drugs may also be of limited value.

They add, analysing levels of FBW7 and MCL1 could offer a simple molecular diagnostic test to identify which patients are likely to benefit from these therapies.

Huang says the two groups started with different angles and reached the same point by chance.

"That's very satisfying, because it means that what's been discovered is more likely to be important and we've been able to confirm each other's findings."

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