February 7, 2020 | David F. Coppedge

Cancer Is Devolution

A major consortium examined 2,658 cancer genomes and found evolution going downward, not upward.

Nature this week published a special issue about cancer. Scientists from around the world studied genomes of tumors and learned a lot about mutations and how they lead to cancer. The Editorial is entitled, “The era of massive cancer sequencing projects has reached a turning point.”

This week, Nature is publishing a suite of papers that sheds new light on the genetic causes of cancer. The results show how far our understanding of cancer has come — and how far we still have to go.

See also the summary on Medical Xpress, “Massive genome study unlocks secrets of how cancers form,” and “A close-up look at mutated DNA in cancer cells” by MDC. Another summary from the Ontario Institute for Cancer Research, “Unprecedented exploration generates most comprehensive map of cancer genomes to date,” was published by Medical Xpress.

The human body fights incipient cancers every day, and has many intelligent defenses against damaging mutations, but sometimes it cannot stay ahead of aggressive tumors or mutational meltdown. An article at EMBL Science says that mutations leading to tumors can occur decades before cancer develops. Another article quips, “If cancer were easy, every cell would do it” (Santa Fe Institute). The point is that the body tries to defend itself against cancer continually.

The opening article in Nature, “Pan-cancer analysis of whole genomes,” tells about the project:

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4–5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete.

Almost everyone knows someone who has cancer, and understands the grief and anxiety that comes with a cancer diagnosis. Fortunately, cancer deaths have been on the decline over the last 20 years. But much remains unknown. For those interested in this major development in cancer research, here are links to the papers, which are all Open Access to the public:

Rheinbay et al, “Analyses of non-coding somatic drivers in 2,658 cancer whole genomes” (Nature).

Li et al., “Patterns of somatic structural variation in human cancer genomes” (Nature).

Alexandrov et al., “The repertoire of mutational signatures in human cancer” (Nature).

PCAWG Core Group, “Genomic basis for RNA alterations in cancer” (Nature).

Sieverling et al., “Genomic footprints of activated telomere maintenance mechanisms in cancer” (Nature).

Reyna et al., “Pathway and network analysis of more than 2500 whole cancer genomes” (Nature).

Some of the papers appealed to evolutionary theory to try to understand cancer:

Gerstung et al., “The evolutionary history of 2,658 cancers” (Nature).

Rubanova et al., “Reconstructing evolutionary trajectories of mutation signature activities in cancer using TrackSig” (Nature).

Cieselik and Chinnaiyan, for instance, used the e-word evolution ten times in their Nature News & Views article about the special issue, along with assorted Darwinian terms.

The idea that cancer develops through an evolutionary process was first presented in 1976. Since then, cancer evolution has been characterized in terms of random mutations and natural selection. A cancer cell harbouring a mutation that confers high fitness proliferates rapidly, becoming the most prominent cell clone in the population. This phenomenon, called a clonal sweep, occurs in recurring cycles during cancer growth.

Assuredly, the Stuff Happens Law operates in cancer, just like it does everywhere in the universe. Employing Darwinism in the explanation of cancer, however, is hardly useful, since it kills its host with all its metastatic offspring. Do out-of-control shipworms have higher fitness when they all go down with the ship? Darwin will never get humans to evolve from bacteria that way.

The article from the Santa Fe Institute referenced earlier appeals to Darwinian evolution, too, comparing cancer to a thief that gets the keys. Most thieves, however, operate by design, not by the Stuff Happens Law. The scientists admit,

Many mechanisms seem to have evolved to prevent cancer — from immune system control, cell death, limits on cell proliferation, to tissue architecture,” the authors write. “Our model only studies the reduced chance for invasion.”

“Cancer is incredibly complex,” Lachmann says, “and our [evolutionary] model is relatively simple.”

Simplistic is a more appropriate description. In our uniform experience, mechanisms that control things do not evolve; they are designed. That’s especially true of “incredibly complex” mechanisms like the immune system.

Please, scientists, proceed quickly on cancer research to help the millions who are suffering. Just keep Charlie out of it, OK?

Published March 1, 2019

Recommended Resource: Get Michael Behe’s third book Darwin Devolves for an explanation of “devolution” – why evolution is always downward, because mutations break existing genes; they do not create new genes. A broken gene can work for awhile, but hardly represents progress. A car without seats can get better gas mileage (if you want to call that “fitness”) but it cannot explain the origin of seats in the first place.

Watch the trailer for a new five-part film series, “Secrets of the Cell,” featuring Michael Behe, arriving in time for Darwin Day (Feb 12th).

 

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