Lessons from cancer risk in animals

 

Think for a moment about a young girl, four years old, diagnosed with acute lymphoblastic leukaemia (ALL). This is not so unusual, and in fact, ALL is the most commonly diagnosed childhood cancer. However, only two years earlier, this young girl was also diagnosed with a grade II glioma in her brain, treated by surgical resection with no chemotherapy or radiation exposure. Moreover, her father and her father’s brother both recently died of aggressive glioblastoma multiforme (GBM) brain tumours. This young girl and her family have Li-Fraumeni Syndrome, an inherited defect in one of the TP53 genes leading to a nearly 100% lifetime risk of cancer1.

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“Big Bang” cancer growth

In the second of our guest blog posts, Dr Andrea Sottoriva describes how a comparison between the expanding universe and the growth of cancers led him to formulate his “Big Bang” theory of tumour growth – a model with novel treatment implications.

Image from Physicsworld.com

Image from Physicsworld.com

In 1929 Edward Hubble, sitting at the top of Mount Wilson, observed that stars and galaxies are moving away from each other. He reasoned that, if stars are continuously moving apart, they must have been closer together at earlier times, to the point that at the very beginning the entire cosmos would have been compressed into a tiny space. This led to the hypothesis that our universe could have originated from a cosmic explosion, “the Big Bang”. But where are the remnants of such an enormous blast? Surely such a phenomenon must have left its mark in today’s universe? In fact, it did. Radio astronomers, Arno Penzias and Robert Wilson, detected the Cosmic Microwave Background radiation in 1964. This is the glow of the Big Bang explosion, it permeates the whole universe at an almost uniform -270 degrees Celsius.

So, what does all of this have to do with cancer? Tumours are large collections of cancer cells that grow out of control and invade healthy tissue, thus becoming life-threatening. Like the universe, cancers expand from something tiny, a single tiny cell. By sequencing the DNA of tumours we discovered that each cancer is unique to a single patient, in the same way that the universe is unique, as far as we can tell.

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Cancer Evolution – It’s in the Blood!

In the first of our guest blog posts, Dr. Marco Gerlinger highlights some of the remarkable developments being made in ctDNA analysis, a powerful new technology with the potential to transform tumour predictions and treatment outcomes.

Photo credit: Csutkaa via Foter.com / CC BY-NC-SA

Photo credit: Csutkaa via Foter.com / CC BY-NC-SA

Cancer cells are masters in adapting to changing environments. This allows them to colonise other organs, to form metastases and also to acquire drug resistance. Darwinian evolution is thought to be a key driver of this adaptability. Randomly acquired mutations encode for novel phenotypes and some of these phenotypes may allow individual cells to survive changes in the environment1.

This adaptability is a key reason for the high rates of mortality from metastatic cancers. Treating a cancer that cannot evolve would probably be an easy task – maybe as straightforward as eradicating a bacterial infection with antibiotics. Thus, there is great need to understand how and why cancers readily evolve and to use this information to design more effective treatment approaches for ever-changing cancers.
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