Rosa Rubicondior: Malevolent Design - How ID Creationism 'Proves' Pancreatic Cancer is 'Intelligently Designed'

CSHL’s Krainer lab has discovered a key oncogenic circuit driving aggressive pancreatic ductal adenocarcinoma (PDAC) progression. Using human PDAC tumor organoids, seen here, the team developed a potential RNA splicing-based therapeutic that collapses the circuit.

Short-circuiting pancreatic cancer | Cold Spring Harbor Laboratory

These examples of what Discovery Institute fellows Michael J. Behe and William A. Dembski call “irreducible complexity” and “complex specified information” respectively — cited by them as evidence for an intelligent designer — are now being discovered with such monotonous regularity that it is astonishing they never appear in any of the Discovery Institute’s anti-evolution, anti-science propaganda.

The answer to that conundrum is, of course, that such examples are far more frequently found in parasites, pathogens, and idiopathic conditions such as cancer and autoimmune disease. No self-respecting religious fundamentalist is going to open that particular can of worms and appear to be promoting a manifestly malevolent god. It is far safer to remain silent and instead present cult followers with carefully curated examples of supposedly “beneficial” complexity, selected to appeal to their pre-existing biases.

Nevertheless, here is yet another example whose refusal to be addressed by creationists neatly illustrates the disingenuous nature of these alleged “proofs of intelligent design”. The news comes from a paper just published in the Cell Press journal, Molecular Cell, which shows how pancreatic cancer—specifically pancreatic ductal adenocarcinoma (PDAC)—depends on a complex regulatory circuit consisting of three key components.

The research, conducted by a team from Cold Spring Harbor Laboratory (CSHL) and led by former CSHL graduate student Alexander Kral, builds on earlier work by Professor Adrian Krainer, who discovered that the protein SRSF1 jump-starts PDAC. The new study shows that SRSF1 does not act alone, but forms one of three interdependent “pillars” in this malignant system—the other two being Aurora kinase A (AURKA) and the oncogene MYC. In laboratory experiments, disabling any one of these three components using RNA-based therapy collapsed the circuit, reduced tumour viability, and triggered programmed cell death.

In Michael Behe’s terms, reducing the complexity kills the system. In William Dembski’s terms, destroying the “complex specified genetic information” kills the cancer cells.

This leaves creationists who are honest enough to confront the evidence with a stark choice: either this is evidence that their intelligent designer deliberately designed pancreatic cancer, or Behe’s and Dembski’s long-trumpeted “proofs of intelligent design” are nothing of the sort. Some of the less scientifically literate will, predictably, invoke “The Fall”, thereby revealing once again that Intelligent Design creationism is not science at all. It is merely Bible-literalist religious fundamentalism dressed up in a laboratory coat — exactly what the Discovery Institute has been attempting to smuggle into US classrooms ever since the 1987 Supreme Court ruling in Edwards v. Aguillard made it clear that teaching creationism in public schools violates the Establishment Clause of the US First Amendment.

Creationist Claims vs Reality. Claim:
*“Irreducible complexity proves intelligent design.”
— advocated by Michael J. Behe

Reality:
Irreducibly complex systems are routinely found in pathological biological processes, including cancers, parasites, and pathogens. The pancreatic cancer regulatory circuit involving SRSF1, AURKA, and MYC is irreducibly complex in precisely Behe’s sense — yet its destruction halts disease and kills tumour cells. If irreducible complexity implies design, then cancer is designed.

Claim:
“Complex specified information cannot arise naturally.”
— asserted by William A. Dembski

Reality:
The cancer-promoting gene network described here contains complex, specific, functional genetic information. Disrupting that information destroys the system. Either such information can arise through natural evolutionary processes—or the “designer” intentionally engineered lethal disease. There is no third option.

Claim:
“Intelligent Design predicts beneficial, life-enhancing systems.”

Reality:
ID has no predictive power. It selectively highlights systems that appear beneficial while systematically ignoring equally complex systems that cause suffering and death. This is confirmation bias, not science.

Claim:
“Diseases result from ‘The Fall’, not design.”

Reality:
Invoking The Fall abandons science entirely and admits that Intelligent Design is merely theology in disguise. Scientific theories explain observations without recourse to supernatural events. Once theological excuses are introduced, ID ceases to be falsifiable and fails as a science.

Bottom line:
If the criteria of Intelligent Design are applied consistently, pancreatic cancer qualifies as a designed system. If that conclusion is rejected, then the criteria themselves are meaningless — and Intelligent Design collapses as a scientific claim.

The work of the CSHL team is explained for a lay readership in a CSHL news item.

Short-circuiting pancreatic cancer
Pancreatic ductal adenocarcinoma (PDAC) is the most lethal form of pancreas cancer. It’s also the most common form of the disease. Potential treatments typically target a key mutated oncogene called KRAS. In some cases, PDAC tumors with these mutations have resisted therapeutic efforts. However, combination therapies involving alternative drug targets may one day help clinicians overwhelm these defenses.

The Takeaway
The Krainer lab discovered a three-oncogene circuit that helps drive the aggressive progression of pancreatic ductal adenocarcinoma. Using antisense oligonucleotide technology, the team developed a potential RNA therapy. In lab tests, the new treatment broke the cancerous circuit, reduced tumor viability, and triggered a type of programmed cell death.

In 2023, Cold Spring Harbor Laboratory (CSHL) Professor Adrian Krainer’s lab discovered how the protein SRSF1 jumpstarts PDAC tumor development. Now, after revisiting data from that study, a team led by former CSHL graduate student Alexander Kral has found that SRSF1 doesn’t act alone. Instead, the protein is one of three pillars in a key circuit promoting aggressive PDAC progression.
Our theory was that some of the changes caused by increased levels of SRSF1 were playing a role in the accelerated tumor growth we were seeing. We homed in on a molecule we thought could be an important driver of this called Aurora kinase A (AURKA). We found it’s part of a complex regulatory circuit that includes not only AURKA and SRSF1, but another key oncogene called MYC.

Alexander J. Kral, lead author
Cold Spring Harbor Laboratory
Cold Spring Harbor, NY, USA.

In this circuit, SRSF1 regulates AURKA through a process called alternative splicing. This increases AURKA production, which allows it to stabilize and protect the MYC protein. MYC then increases SRSF1 levels, restarting the loop.

Bits and pieces of this circuit were known previously, but we didn’t have the full picture until now. Once we figured out alternative splicing of AURKA was involved, we could start looking into ways to disrupt it.

Professor Adrian R. Krainer, senior author
Cold Spring Harbor Laboratory
Cold Spring Harbor, NY, USA.

The team developed an antisense oligonucleotide (ASO) to alter the process. These molecules are a specialty of the Krainer lab. They previously developed an ASO called Spinraza, the first-ever FDA-approved treatment for spinal muscular atrophy. Based on their observations, the team hoped their new ASO could obstruct AURKA’s alternative splicing. Remarkably, in pancreatic cancer, the ASO didn’t just interfere. It collapsed the entire oncogenic circuit. This reduced tumor cells’ overall viability and triggered a programmed cell death called apoptosis.

It’s like killing three birds with one stone. SRSF1, AURKA, and MYC are all oncogenes contributing to PDAC progression. Just by targeting AURKA splicing with our ASO, we see the loss of these other two molecules as well./p>
Professor Adrian R. Krainer.

The Krainer lab is now working to refine their ASO. Potential clinical applications are still a long way off. However, Krainer says every clinical breakthrough begins with such basic research. That was true of Spinraza, which has saved thousands of lives. So, hopefully, it will be for the next lifesaving cancer treatment.

Publication:
Kral, Alexander J.; Jia, Lu; Sim, GeunYoung; Wan, Ledong; Ishigami, Yuma; Krainer, Adrian R.
Splice-switching ASOs targeting the AURKA 5′ UTR collapse an SRSF1-AURKA-MYC oncogenic circuit in pancreatic cancer
Molecular Cell (2026) 86(1) 60-77.e7, DOI: 0.1016/j.molcel.2025.12.004.

This work leaves Intelligent Design in an untenable position. The very criteria that Behe and Dembski have spent decades promoting as hallmarks of a designing intelligence—interdependent parts, tightly regulated circuits, and highly specific functional information—are now being documented most clearly in systems that cause profound harm. When the removal of a single component collapses a cancerous network and kills tumour cells, the appeal to “irreducible complexity” ceases to look like evidence of design and starts to look like a description of biological fragility shaped by evolutionary processes.

Creationists are therefore faced with a dilemma entirely of their own making. Either their intelligent designer deliberately engineered pancreatic cancer, complete with elegant regulatory feedback loops and lethal efficiency, or the concepts of irreducible complexity and complex specified information are not indicators of design at all. The routine retreat to theological explanations such as *“The Fall”* merely underscores the point: Intelligent Design cannot function as science because, when confronted with inconvenient evidence, it abandons testable explanations in favour of religious doctrine.

As studies like this continue to accumulate, the selective silence of the Intelligent Design movement becomes ever more conspicuous. The failure to engage with such findings is not an oversight, but a tacit admission that their central claims cannot survive contact with real biology. Far from rescuing creationism, modern molecular biology is steadily dismantling it—one complex, lethal, and entirely natural system at a time.

Advertisement

Amazon