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Yeast cells like these have helped scientists understand how cells divide. Credit: Flickr/CC BY 2.0

We’re up in Liverpool for the next 4 days reporting from the annual National Cancer Research Institute (NCRI) Cancer Conference.

You can follow updates live from the conference on Twitter by keeping an eye on #NCRI2016. And we’ll be blogging the highlights from an action-packed schedule of talks spanning research into cancer prevention, diagnosis, treatment and patient care.

Ahead of the conference’s opening day some of the research being presented has already hit the headlines.

Scientists in London have fished prostate cancer cells from blood samples that could indicate how likely the disease to spread, which the Mail Online and Express covered.

So, onto the day’s talks

Small cell lung cancer

Dr Charles Rudin, from the Memorial Sloan-Kettering Cancer Center in the US, kicked off the conference with brand new results from his team working on small cell lung cancer.

The DNA inside these cancer cells is “really, really messed up,” said Rudin. And his team is studying why, despite usually working to begin with, chemotherapy eventually stops working for most patients with this disease.

Crucially, some new (unpublished) research from Rudin’s lab may have an explanation for this – and a potential way to stop it.

By looking at patient samples, and growing these cells in the lab and in mice, the team found that a particular gene – called Schlafen11 – is switched off in these cells. The gene gets its name from the German verb ‘to sleep’, which seems apt in chemotherapy resistant cells where it’s being put to sleep.

Interestingly, the team found that in cells that chemotherapy kills, Schlafen11 is switched on.

And Rudin presented early results suggesting that Schlafen11 can be reawakened in chemotherapy resistant cells by blocking a different molecule, called EZH2.

The team’s work suggests that treating small cell lung cancer cells with EZH2 drugs and chemotherapy might stop cells becoming chemotherapy resistant. And it could make those that are resistant respond again.

A new treatment for this hard-to-treat cancer might sound like the stuff of dreams, but this work suggests the disease might be in for Rudin awakening.

What have yeast ever done for us?

Professor Iain Hagan, from the Cancer Research UK Manchester Institute, rounded off the afternoon with a question: “What have yeast ever done for us?”

If beer and baking wasn’t enough, yeast have also helped scientists understand cancer.

Over many decades researchers have turned to yeast as a simple way to watch cells grow and divide.

This, Hagan explained, has made it easy to spot when something’s going wrong.

“You can clearly see when the cell grows but doesn’t divide,” he said.

In fact, working with yeast landed two Cancer Research UK scientists – Paul Nurse and Tim Hunt – a Nobel Prize in 2001, which they shared with US researcher Leland Hartwell. And Hagan acknowledged the huge contribution Cancer Research UK has played in funding this type of research that is now leading to new drugs.

Scientists have been drawn to yeast because a lot that goes on inside yeast is shared by the cells in our own bodies. Especially when it comes to cell division.

Work with yeast has helped map out in meticulous detail each of the steps a cells takes as it divides – a series of processes called the cell cycle.

Crucially, many of these steps can be faulty in cancer cells. And the map has helped scientists navigate the way towards finding new cancer treatments that target key point safety checks during the cell cycle.

Several drugs have already come from this work, and Hagan hoped that there will be more on the horizon.

So as it turns out, we have more than just beer and bread to thank yeast for.

That’s it for today’s round up. Check back tomorrow for more of what’s hot at this year’s NCRI conference.

The Cancer Research UK news team

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