Creationism's intelligent designer creating cancer.
AI-generated image (ChatGPT 5.2).
ID advocates should be thrilled to learn that a team of researchers from Technische Universität Dresden (TUD), Germany, together with colleagues from Charles University, Prague, Czechia, have discovered a perfect example of what Discovery Institute fellows William A. Dembski and Michael J. Behe claim is proof of intelligent design—namely complex specified information and irreducible complexity. The team have just published their findings, open access, in Nature Communications.
There is one slight problem, however: this supposed ‘proof of intelligent design’ turns out to be one of the mechanisms that makes cancer so effective at increasing pain and suffering — and at killing people.
This presents creationists with a theological conundrum. Either there is more than one intelligent designer, which comes close to—or even crosses—the line into blasphemy, or the intelligent designer is actively and knowingly creating a cause of pain and suffering, and is therefore not the omnibenevolent deity portrayed in the Bible.
The stark alternative to these theologically insurmountable problems is equally problematic for ID creationism: admitting that their ‘proof of intelligent design’ is nothing of the sort, and is better explained as the result of a natural process in which no intelligence was involved—thereby absolving their god of any culpability.
The TUD-led team discovered that the protein MCL1 not only inhibits programmed cell death, or apoptosis, but also plays a central role in tumour metabolism. Normal, non-cancerous cells will usually self-destruct if their DNA becomes corrupted beyond repair, but when this process fails, a tumour can develop through the proliferation of cells carrying damaged DNA. In cancers, this self-destruct mechanism is suppressed by MCL1.
The team also found that MCL1 is not only responsible for preventing apoptosis, but also dysregulates cellular energy metabolism. In other words, a single factor ensures both cancer cell survival and the functioning of key metabolic and signalling pathways for the benefit of the tumour.
In Michael J. Behe’s terms, all the components of this survival mechanism must be present for the cancer to persist; and in William A. Dembski’s terms, the genetic information coding for MCL1 must constitute highly specified complex information.
Background^ Apoptosis and Cancer Metabolism.The work of the TUD-led team is explained in lay terms in a TUD news article.Apoptosis: the cell’s self-destruct mechanism
Diagram of intrinsic and extrinsic pathways of apoptosis. (A) In the intrinsic pathway, the proapoptotic BH3-only family members activate Bax or Bak, leading to mitochrondrial outer membrane permeabilization, which drives formation of the apoptosome, activation of the executioner caspases, 3 and 7, and subsequent apoptosis. The proapoptotic BH3-only proteins are inhibited via interactions with the anti-apoptotic Bcl-2 family of proteins. (B) In the extrinsic pathway, ligands such as Fas, tumor necrosis factor (TNF), or tumor necrosis factor-related apoptosis-inducing (TRAIL) ligand bind to death receptors. This results in the recruitment of Fas-associated death domain protein (FADD) and activation of caspase 8. Caspase 8 directly activates caspase 3 and 7. The two pathways interact via caspase 8-mediated cleavage of Bid.source: Ho, Jacqueline, 2014
Apoptosis is programmed cell death—a tightly regulated process that allows damaged, infected, or unnecessary cells to destroy themselves in an orderly way. It is essential for normal development, tissue maintenance, and cancer prevention.
When a cell detects severe DNA damage, metabolic failure, or other irreparable faults, it activates internal signalling pathways that dismantle the cell from within. This prevents defective cells from continuing to divide and protects the organism as a whole. Proteins of the BCL-2 family act as key regulators of this process, either promoting or blocking cell death depending on circumstances.
Cancer arises when this safety mechanism fails. Cells that should self-destruct instead survive, accumulate further mutations, and begin dividing uncontrollably.
Cancer metabolism: fuelling uncontrolled growth
Cancer cells do not behave metabolically like normal cells. To support rapid and continuous division, they rewire their energy production and nutrient use. Even when oxygen is available, many cancers favour inefficient pathways that prioritise the production of raw materials for growth rather than maximising energy efficiency—a phenomenon known as metabolic reprogramming.
This altered metabolism supports:
- rapid cell division
- resistance to cellular stress
- survival in hostile, low-oxygen environments
Crucially, cancer metabolism and resistance to apoptosis are closely linked. Proteins that prevent cell death often also help redirect energy production and cellular resources to favour tumour survival.
Why this matters
Cancer is not caused by a single failure, but by the breakdown of multiple protective systems that normally keep cells in check. Mechanisms that suppress apoptosis and enhance metabolic resilience give tumours a powerful survival advantage—but one that arises naturally through mutation and selection at the cellular level, not from foresight or intent.
Dresden research group uncovers new key mechanism in cancer cells
A study by the Mildred Scheel Early Career Center group led by Dr. Mohamed Elgendy at the TUD Faculty of Medicine provides fundamental insights into cancer biology. Published in the renowned journal Nature Communications, the study shows for the first time that the protein MCL1 not only inhibits programmed cell death, but also plays a central role in tumor metabolism.
The researchers have succeeded in tracing two classic hallmarks of cancer – the evasion of apoptosis (a form of programmed cell death) and the dysregulation of energy metabolism – back to a common molecular mechanism.
The study focuses on the protein MCL1, which is strongly overexpressed in many tumor types and has previously been considered primarily an anti-apoptotic factor of the Bcl-2 protein family. The Dresden researchers now show that MCL1 directly influences the central metabolic regulator mTOR and thus controls the bioenergetics of cancer cells. This is the first time that MCL1 has been described as an active regulator of central signaling and metabolic pathways.
Our findings show that MCL1 is much more than just a survival factor for tumor cells. The protein actively intervenes in key metabolic and growth signaling pathways, thereby linking two fundamental cancer mechanisms.
Dr. Mohamed Elgendy, senior author
Institute for Clinical Chemistry and Laboratory Medicine
University Hospital and Faculty of Medicine
Technische Universität Dresden
Dresden, Germany.
Mechanistically, the team identified a direct functional link between MCL1 and the mTORC1 complex in various cancer models. This newly discovered signaling pathway fundamentally expands the current understanding of the role of MCL1 and opens up new therapeutic perspectives.
In addition to genetic analyses, the study also investigated the effect of MCL1 inhibitors, which are currently undergoing clinical development as promising new cancer therapeutics. The study showed that these agents also inhibit mTOR signaling. This finding is of high clinical relevance, as mTOR inhibitors are already routinely used in cancer therapy.
Another particularly significant finding is the resolution of a previously unsolved problem: several clinical trials with MCL1 inhibitors had to be discontinued due to severe cardiotoxic side effects. The Dresden researchers identified an underlying molecular mechanism for the first time and, based on this, developed a dietary approach that can significantly reduce cardiac toxicity. This protective effect was confirmed in an innovative humanized mouse model.
This work represents a significant advance in our understanding of the molecular basis of cancer. This high-ranking publication with enormous clinical potential once again demonstrates that the targeted support of outstanding young scientists, as carried out at the Mildred Scheel Center for Young Scientists, is a prerequisite for innovations and the cancer therapy of tomorrow.
Professor Esther Troost, not an author of the paper.
Dean of the Carl Gustav Carus Faculty of Medicine
Technische Universität Dresden
Dresden, Germany.
This outstanding research work exemplifies how excellent basic research can create direct benefits for our cancer patients. Particularly significant from a clinical perspective is the solution to the cardiotoxicity problem of MCL1 inhibitors. The identification of the underlying mechanism and the development of a dietary protective approach can now pave the way for safer therapies.
Professor Uwe Platzbecker, not an author of the paper.
Chief Medical Officer
University Hospital and Faculty of Medicine
Technische Universität Dresden
Dresden, Germany.
The study is the result of interdisciplinary collaboration between various research groups and institutions. Dr. Mohamed Elgendy's working group in Dresden acted as the lead partner and was supported by experts from national and international partner institutes in Czechia, Austria, and Italy.
The importance of the work was also recognized by the editors of the journal Nature Communications: The publication was selected as one of the outstanding research papers on cancer on the “Editors' Highlights” website, which presents the 50 best currently published studies in this field.
Background
Dr. Mohamed Elgendy has been leading a research group on cancer metabolism at the Mildred Scheel Early Career Center in Dresden since 2019. His research focuses on molecular and cell biology methods, genome editing, and the analysis of tumor metabolism in cell and mouse models. Dr. Elgendy coordinates the METRICs project within the framework of ERA-NET (European Research Area Networks) and is also funded by an ERC Starting Grant from the European Research Council.
Since 2018, the Mildred Scheel Early Career Center has been supporting the career development of research physicians and scientists in the field of cancer research in Dresden and at four other university locations with funding from German Cancer Aid (DKH).
Publication:
What this research ultimately exposes is the intellectual cul-de-sac into which Intelligent Design has driven creationism. By insisting that complexity and interdependence are reliable indicators of conscious design, ID advocates have handed science a weapon that cuts both ways. When those same features turn up in diseases that maim, torment, and kill, the claim quietly becomes catastrophic for their theology.
Cancer does not merely fail by design standards; it succeeds spectacularly. It hijacks regulatory networks, exploits metabolic pathways, and deploys tightly coordinated molecular systems that would be praised as masterful engineering if they were doing something benign. If such systems genuinely require foresight and intent, then the designer responsible is either morally indifferent or actively malicious.
Faced with this, creationists are left with no viable escape route. To maintain belief in a benevolent, intelligent creator, they must abandon the very criteria they promoted as decisive evidence of design. Yet if they retreat from those criteria, Intelligent Design collapses into an empty assertion, offering no explanatory power beyond what evolutionary biology already provides—only without the evidence.
The uncomfortable reality is that biology looks exactly as one would expect if it were shaped by blind processes: effective but inefficient, powerful but dangerous, capable of astonishing innovation and horrific failure alike. Intelligent Design did not rescue creationism from science; it merely ensured that, when science advanced, creationism would be crushed under the weight of its own arguments.
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