A new paper in Molecular Cancer from Johns Hopkins Medicine describes yet another discovery that should be deeply uncomfortable for Intelligent Design creationists. The researchers found that the spread of pancreatic cancer is driven not chiefly by fresh mutations in DNA sequence, but by epigenetic reprogramming — changes in chromatin organisation and gene activity. In particular, they identified KLF5 as a major driver of metastatic growth, with higher expression in most metastatic lesions than in the matched primary tumours. The paper in Molecular Cancer shows that KLF5 promotes metastatic proliferation through epigenetic modifier genes including NCAPD2 and MTHFD1, helping switch on programmes involved in migration, plasticity and invasion. [1]
What makes this especially important is that epigenetics is not some magical extra layer of “specified information” inserted into life by a supernatural designer. Its roots are ancient. In bacteria, DNA methylation is a major form of epigenetic regulation, involved in gene expression, chromosome replication and DNA repair. In archaea, histone-based chromatin already exists in a form strikingly similar to that of eukaryotes, and studies show that chromatin architecture and its role in regulating gene expression long predate complex multicellular life. In other words, the basic machinery was already there in simpler organisms, doing ordinary cellular housekeeping long before animals and plants ever appeared. [2]
Multicellular organisms did not receive a brand-new control system from an intelligent agent; they inherited this ancient molecular toolkit and elaborated it. As multicellularity evolved, epigenetic regulation expanded and became central to cell differentiation, allowing cells with the same DNA to adopt different stable identities by opening some regions of the genome and closing others. Work on the transition from unicellular to multicellular states in Dictyostelium, for example, shows that chromatin reorganisation and histone modifications are closely tied to the shift into multicellularity, while evolutionary reviews note that epigenetic diversity expanded rapidly with multicellular life and that epigenetic marks are crucial in development and long-lived cell lineages. [3]
And that is exactly why this Johns Hopkins work is such bad news for ID creationists. The same ancient, repurposed system that multicellular organisms rely on for cell specialisation can also be subverted to drive one of the deadliest features of cancer: metastasis. That is what evolved systems do. They are modified from older parts, good enough to work, but never perfect and never immune to catastrophic failure. What this study reveals is not elegant, flawless engineering, but the vulnerability of a historically evolved regulatory system — one that natural selection adapted for development and tissue specialisation, but which disease can hijack with lethal consequences. That is entirely consistent with evolution, and profoundly at odds with the notion of a competent, benevolent designer. [1]




































