This year’s Origins of Cancer symposium explores cancer evolution, from genetics to selection pressure
By Guillermo Flores and Leslie Wyman
Van Andel Institute Graduate School Ph.D. students and organizers of the 2019 Origins of Cancer symposium
Why have we not yet cured cancer?
As scientists, we get this question a lot.
After all, we read about new discoveries every day in scientific journals and in the news. Moreover, we know that cancer is largely a genetic disease. Scientists have already sequenced the entire human genome; it should be as easy as finding the differences between tumor cells and healthy cells and then just fixing the problems, right? Or perhaps we could exploit these differences to come up with an effective, individual treatment strategy for each patient — the pinnacle of true, personalized therapy.
Yet despite these advances and humanity’s collective efforts, cancer persists.
Worse still, cancer sometimes appears to be cured only to return with a vengeance. Countless hours of work from some of the world’s brightest minds, incalculable amounts of money, innumerable tragic stories of those touched by cancer and an ever-increasing awareness have certainly yielded positive results.
Yet, cancer persists.
That brings us back to the question — why haven’t we cured cancer?
To find the answer, we have to recognize one crucial fact — cancer evolves. It does so in a fashion not so different from what Charles Darwin described 150 years ago in his groundbreaking book On the Origin of Species. Cancer is subject to natural selection just like organisms and viruses. Unfortunately, when it comes to survival of the fittest, cancer cells use natural selection to become hardier and tougher to treat.
If we want to finally cure cancer, we need to understand how and why it evolves. That’s the focus of this year’s Origins of Cancer, a one-day scientific symposium that will be held July 26 at Van Andel Institute.
Scientists have begun to unravel questions into how complex genetic machinery orchestrates natural selection on a cellular level and how those processes contribute to human health and disease. Intense research is underway to understand the mechanisms of how cancer begins, changes with time and becomes resistant to therapy. The 2019 Origins of Cancer will explore these topics, specifically:
- How we can use genomics to understand the genetics of cancer to appreciate what has to happen to turn a healthy cell into a cancerous one. (Speakers: David Wheeler and Dr. Catherine Cottrell)
- The actual mechanisms that lead to the accumulation of mutations that lead to the initiation of tumorigenesis. (Catherine O’Brien and Dr. Ludmil Alexandrov)
- How the selection pressure of our current therapies leads to relapse and progression of cancer. (Marcelo Aldaz and Dr. Jean Wang)
We are also honored to host Prof. Charles Swanton as our keynote speaker. Prof. Swanton combines laboratory research at the Francis Crick Institute with clinical duties at University College London Cancer Institute. His research focuses on how tumors evolve over space and time. Prof. Swanton has helped to define the branched evolutionary histories of solid tumors, processes that drive cancer cell-to-cell variation in the form of new cancer mutations or chromosomal instabilities, and the impact of such cancer diversity on effective immune surveillance and clinical outcome.
Origins of Cancer will be held at the Institute July 26. For more information and to register, visit originsofcancer.org.
Variation: In genetics, variation refers to DNA differences between individuals. Even identical twins have slight differences in their DNA. There is typically significant variation between healthy cells and cancer cells.
Inheritance: Before a person is born, the DNA from each biological parent is first shuffled in the sperm and egg. During fertilization, two sets of shuffled DNA are combined. All this adds up to increased variation. Cancer cells often mutate. By dividing, new cancer cells can inherit these mutations.
Selection: Often referred to as “survival of the fittest,” selection is the mechanism by which evolution occurs. If a gene increases the chance for an individual to survive it will become more common in a population over time because individuals with that gene are more likely to survive and pass it down to their offspring. Conversely, if a gene decreases the chance for an individual to survive, it will become less common because it is less likely to be passed on to future generations.
The environment plays a big part by applying what is referred to as a “pressure.” If the stakes of living and dying are raised, there is an increased pressure and selection becomes more powerful. For example, if there is a gene that makes a cancer cell resistant to chemotherapy, it may be just as common as any other gene until chemotherapy is applied. Once the pressure of chemotherapy is present the gene becomes much more important for survival and “selects” for these resistant cells to survive. Alas, this is commonly the basis of tumor recurrence and relapse.