The Darwin Cancer Blog
Led by Professor Mel Greaves, this blog provides a forum for the discussion of how an evolutionary perspective is changing thinking about cancer. This blog was formerly hosted by the British Journal of Cancer before moving to the ICR's website in May 2018.
When normal is the favoured type
Before we discuss cancer, let’s consider other sets of nasty characters – criminals, Nazis and terrorists. We know that the best way to limit crime is to create neighbourhoods that provide opportunities for education and jobs – a healthy infrastructure disfavours the criminal phenotype.
How cancer outsmarts multicellularity
The transition from unicellularity to multicellularity was one of the most significant advances in the evolution of life on Earth. This allowed adaptation to a wide range of new ecological niches, rapidly accelerating the pace of evolution and creating an explosion of diversity across the plant, animal and fungal kingdoms.
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Which cancers are most survivable and why?
Cancer is not a death sentence; there is a great deal of difference between a prostate and a pancreatic cancer diagnosis, and even differences between subtypes of cancer within any particular organ.
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Do mutations cause cancer? (or the dog that did not bark)
Evolution is change over time, and it is well-accepted that cancers evolve through the stepwise accumulation of somatic mutations. Logically, mutations ‘cause’ cancer, and therefore, simplistically, the key to preventing cancer could be to avoid mutations.
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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.
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Ways of escape
Cancers are life threatening because they migrate within the body, spreading far from their point of origin. This process – metastasis – hijacks tissues and compromises their critical functions.
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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.
Convergence in tumour evolution: singing the same tune
Cancer clone evolution, just like evolutionary speciation, is characterised by an extraordinary diversity of descendants derived from a common ancestor. Yet, paradoxically, some evolutionary trajectories are convergent on a common phenotype.
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Cancer versus immunological diversity
We are seeing a renaissance of optimism about immunotherapy for cancer – after many years of disappointment. Patients with advanced and clinically intransigent lung cancers and melanomas, treated in early clinical trials with antibodies to immune checkpoint inhibitors PD-1 and CTLA-4, have been surviving longer than would previously have been expected.
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.
Predicting evolutionary futures
One of the striking achievements of cancer genomics and its allied bioinformatics has been to construct phylogenetic trees depicting the trajectories of sub-clones in cancers and their ancestral relationships. It’s like taking a peek back in time at the origin and prior evolutionary history of the malignancy.
‘Drivers’ and ‘Passengers’: who’s in charge?
Genome sequencing has revealed that a plethora of gene mutations can co-exist in individual cancers: thousands in some cases. Based on Darwinian theory, we assume that whilst most are irrelevant, buried in the background is a modest number of mutations (perhaps counted in single figures) that are functionally active in a way that contributes to cancer clonal development.
NCRI 2015 – Evolutionary tales in leukaemia
This post is a synopsis of the lecture I gave at the National Cancer Research Institute (NCRI) conference in Liverpool on the 2nd November 2015 – minus some anecdotes about mentors and colleagues – you needed to be there to hear those.
How many mutations does it take?
For some time before we had the benefit of cancer genomics, it was generally believed that for a cancer to disseminate and become potentially lethal, it would have had to accrue several mutations that, collectively, would provide a kind of ‘full house’ for malignancy.
Background: Darwin’s branching tree of evolutionary phylogeny
Since the turn of this century, cancer genomics has strongly endorsed the Darwinian view of cancer biology. Interrogation of the genomes of single cancer cells and multi-regional small biopsies of tumours have allowed us to construct evolutionary histories, or phylogenies, of cancer clones.
Background: The principles of evolutionary natural selection in cancer
Charles Darwin had it right, despite knowing nothing of genetics or the basis of inheritable variation.
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Background: What has evolution got to do with cancer?
What exactly is cancer? Can we capture its biological essence in a few words or a phrase? For the ancient Greeks, it was a manifestation of black bile, or constitutional melancholy.
Time for a new perspective on cancer?