Telomeres shown as white caps on the ends of the chromosome arms.
Pitt scientists discovered a key genetic step in melanoma’s race to live forever | University of Pittsburgh
Examples from nature in which, if creationist arguments for the existence of an intelligent designer are applied consistently, that designer can only be regarded as a malevolent entity intent on increasing suffering in the world, continue to accumulate. And the more examples there are, the more creationists need to ignore their own arguments, abandon any pretence that creationism is a genuine alternative science, and retreat instead into the fundamentalist biblical myths of 'The Fall' and 'Original Sin'. The evidence remains the same; only the interpretation is twisted to preserve the preferred narrative.
The latest such example concerns the genetics behind one of malignant melanoma's most dangerous properties: its ability to evade the normal cellular limit on repeated division. This had long been a missing piece in understanding how melanoma cells avoid the ordinary route to cellular senescence and continue to proliferate. Like Michael J. Behe's and William A. Dembski's supposed 'evidence' for intelligent design, it depends on a set of interacting components being in place and on genetic changes producing just the right molecular effect — precisely the kind of arrangement the Discovery Institute insists cannot arise by natural processes because, in its caricature of biology, evolution is merely 'random chance'. That claim, of course, ignores the elementary biological fact that natural selection makes evolution very much a non-random process.
The discovery,
published in Science in November 2022 by Pattra Chun-on, Jonathan K. Alder and colleagues, concerns telomeres — the protective caps at the ends of chromosomes. In most normal somatic cells, telomeres gradually shorten with repeated cell division until the cell can no longer divide. This is one of the body's safeguards against uncontrolled proliferation. Cancer cells, however, often find ways to bypass this limit, and melanoma has long been known for having unusually long telomeres, even compared with many other cancers. What had not been fully understood was how melanoma achieved this.
The answer involves telomerase, the enzyme complex that lengthens telomeres. In most normal adult cells, telomerase activity is switched off or kept very low. Many melanomas carry mutations in the promoter region of
TERT, the gene that encodes the catalytic component of telomerase, and these mutations increase telomerase activity. But that turned out to be only part of the story. When researchers introduced
TERT promoter mutations into melanocytes, they did not reproduce the exceptionally long telomeres seen in melanoma tumours.
The missing component was TPP1, a member of the shelterin complex that helps regulate telomeres. The researchers found that mutations in the promoter region of
ACD, the gene that encodes TPP1, can increase TPP1 production. When these TPP1-promoter mutations occur together with
TERT promoter mutations, the two changes cooperate to produce the long telomeres characteristic of melanoma. In other words, melanoma's ability to evade normal cellular mortality depends on a coordinated interaction between altered telomerase activity and altered telomere regulation.
So, in intelligent-design creationist terms, we have a system requiring interacting molecular components, each specified by genetic changes in ordinary cellular genes, and each contributing to a result that benefits the cancer cell at the expense of the patient. If the same kind of molecular cooperation in a harmless or useful organism is to be paraded as evidence of design, then consistency demands the same conclusion here. Melanoma, on that argument, would be another product of the same intelligent designer — one whose ingenuity is directed towards helping cancer cells escape the body's normal restraints.
Of course, the scientifically honest conclusion is not that melanoma was designed, malevolently or otherwise. It is that cancer exploits the same evolved molecular machinery that normal cells use, and that mutations filtered by selection within the tumour can favour cells that divide faster, survive longer and outcompete their neighbours. The creationist problem is that the very mechanisms they claim as evidence for their designer are just as plainly at work in disease, parasitism and suffering.