Rosa Rubicondior: Malevolent Design - How Dembski's 'Complex Specified Information' Causes Acute Myeloid Leukemia

Malevolent Design

How Dembski's 'Complex Specified Information' Causes Acute Myeloid Leukemia

Rapid growth of blood cancer driven by a single genetic ‘hit’

William A. Dembski’s concept of complex specified information (CSI) remains ambiguous—arguably by design. His use of the word specified is particularly opaque: is he referring to information that produces outcomes he wishes his readers to believe are purposeful and intelligently designed by a particular deity, or is the term intended to encompass any genetic information that results in any outcome—beneficial, neutral, or harmful?

Taken at face value, and in the absence of a clear, testable definition, there appears to be no reason Dembski’s concept could not apply to information that is ultimately detrimental, either to the organism itself, or to another organism in the case of parasites or cancer. Why, for instance, should we conclude that the complex information in a gene enabling the expansion of the human brain and the enhancement of cognitive function was specified, but that the equally complex genetic information enabling a cell to become a malignant cancer, or allowing the Plasmodium falciparum parasite to evade anti-malarial drugs, was not also specified by the same intelligent designer?

Given that Dembski is a senior fellow of the Discovery Institute — an organisation notorious for its Wedge Strategy, which seeks to undermine public trust in science through disinformation and misrepresentation while promoting creationism under the guise of scientific legitimacy — it is unsurprising that complex specified information remains a nebulous and ill-defined term. The strategy’s aim has never been to engage in genuine scientific discourse or subject its claims to critical scrutiny, but rather to advance a religious agenda while avoiding the accountability that comes with reasoned analysis and empirical testing. A cynic might conclude that the leading ID advocates know their claim has no scientific basis but want their target audience to believe otherwise.

So, I invite Intelligent Design creationists to explain why the recent discovery of a gene that promotes the rapid early development of acute myeloid leukaemia should not be an example of Dembski's 'complex specified information' and so evidence that Dembski's intelligent designer designed acute myeloid leukaemia, or whether Dembski's term is deliberately vague so as to appeal to people looking for confirmation of existing bias.

What is Acute Myeloid Leukaemia?

Acute Myeloid Leukaemia (AML) is an aggressive form of blood cancer that originates in the bone marrow—the soft inner tissue of bones responsible for producing blood cells. In AML, the bone marrow produces abnormal white blood cells known as myeloblasts, which fail to mature properly and multiply uncontrollably. These immature cells crowd out healthy blood cells, leading to symptoms such as fatigue, frequent infections, easy bruising or bleeding, and anaemia.

AML progresses rapidly and typically requires prompt diagnosis and treatment. It can occur at any age but is more common in older adults. Treatment often involves intensive chemotherapy, targeted therapy, and sometimes stem cell transplantation.

From an evolutionary standpoint, the persistence of such harmful conditions is not surprising. Many cancers, including AML, tend to develop later in life—often after the typical reproductive age—so the mutations driving them are not strongly selected against by natural selection. Evolution operates without foresight; it selects traits that enhance reproductive success in a given environment, not those that guarantee long-term health. The accumulation of mutations over time, combined with the limitations of biological repair mechanisms, makes diseases like AML an expected consequence of an imperfect, evolved system — not the product of intelligent or benevolent design.

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The discovery was made by researchers from the Wellcome Sanger Institute and their collaborators led by Dr Jyoti Nangalia of Cambridge University, UK.

Rapid growth of blood cancer driven by a single genetic 'hit'
Researchers have explored the evolution of the genetic change that causes chronic myeloid leukaemia and show its ability to drive the disease.
A new study has unveiled when chronic myeloid leukaemia, a type of cancer that affects the blood and bone marrow, arises in life and how fast it grows. Researchers reveal explosive growth rates of cancerous cells years before diagnosis and variation in these rates of growth between patients. Such rapid growth rates had previously not been observed in most other cancers.

Researchers from the Wellcome Sanger Institute and their collaborators used whole genome sequencing to study when BCR::ABL1 – an abnormal fusion of the different genes called BCR and ABL1, which is known to cause chronic myeloid leukaemia. The team investigated when BCR::ABL1 first arises in a blood cell and how quickly these cells with this genetic change then multiply and expand to lead to a diagnosis of a type of leukaemia.

The research, published 9 April, 2025 in Nature, contributes to the scientific understanding of how strong this abnormal fusion gene is in its ability to drive cancer.

Chronic myeloid leukaemia (CML) is a cancer of the bone marrow and blood. CML is caused by a rearrangement of genetic material between two chromosomes. In those with CML, part of the ABL1 gene from chromosome 9 is fused with the BCR gene from chromosome 22. This creates an abnormal fusion gene called BCR::ABL1 on chromosome 22, also known as the Philadelphia chromosome.¹

However, despite its well-understood role in CML, little is known about the evolution of this fusion gene, the rate at which cells with BCR::ABL1 start to multiply, and how this contributes to disease progression.

In a new study, researchers from the Sanger Institute used DNA sequencing to analyse over 1,000 whole genomes of single blood cells from nine people with CML, ranging from 22 to 81 years of age² The researchers then used the genetic changes identified in these genomes to study how the cells were ancestrally related to one another. This is akin to creating family trees of cells – known as phylogenetic trees – which allowed the team to look back in the past to explore how the tumour cells grew over time and exactly when the abnormal fusion of the two genes occurred to start off the cancer growth.

The phylogenetic trees from CML patients showed that the BCR::ABL1 fusion gene typically appeared three to 14 years before diagnosis. Once this fusion occurred, the tumour clones – tumour cells that are genetically identical – grew very quickly, sometimes in excess of 100,000 per cent growth annually, suggesting the fusion gene has a uniquely strong ability to drive the disease. Interestingly, this rapid growth is substantially faster than the growth rates of other blood cancers and solid tumours, which tend to develop more slowly with multiple genetic changes accumulating over many decades. Not only was the rapid growth of the tumour compared to other cancers unusual, but that this growth was driven by just one single genetic variation, whereas most other cancers require multiple genetic changes to accumulate before the cancer arises.

The researchers also discovered that age impacts tumour growth rates, with younger patients showing much higher rates at which cancerous cells with the fusion gene multiply compared to older patients. The study also found that patients with faster-growing CML were less likely to respond well to tyrosine kinase inhibitors (TKIs) – the standard treatment for CML. With one in five patients not responding to TKIs,³ this study has implications for considering cancer cell growth rates in a clinical setting. However, the researchers note that further studies in larger patient cohorts are needed to validate this.

To investigate whether people could carry BCR::ABL1 without showing symptoms, the researchers also analysed sequencing data and health records from over 200,000 participants from the USA-based “All of Us” cohort.⁴ They showed that almost all individuals with BCR::ABL1 were later diagnosed with a blood disorder, and so they suggest that expansion of BCR::ABL1 clones without developing subsequent symptoms is unlikely.

Overall, the results show the uniquely strong ability of the BCR::ABL1 fusion gene to drive growth of cancerous cells in CML, and that variation in these growth rates between patients may be useful in the future clinical setting to better predict patient responses to treatment.

In a clinical setting, healthcare professionals will perform a reverse transcription polymerase chain reaction (RT-PCR) test, a type of blood test, to measure a patient’s response to CML treatment. However, they are not able to routinely see differences in the genetic cause of CML in patients at the DNA level, which we have been able to highlight in our study. Our findings also provide a rationale to look at the rate of cancer growth more closely in future studies in order to understand if we can use such information in a clinical setting.

Dr Aleksandra Kamizela, co-first author of the study
Lister Hospital, Stevenage
and soon Addenbrooke’s Hospital, Cambridge, UK.

What our study suggests is that chronic myeloid leukaemia is an outlier compared to other cancers – both solid tumours and other blood cancers. We have shown that chronic myeloid leukaemia cells undergo incredibly rapid growth within a few years to a decade before diagnosis, whereas for most cancers, the timeline from start to clinical presentation is several decades. This work paves the way to understanding how we might optimise treatment for those patients that currently respond poorly to treatment.

Dr Jyoti Nangalia, senior author
University of Cambridge, Cambridge, UK And Wellcome Sanger Institute, Cambridge, UK.

Publication
Aleksandra E Kamizela et al. (2025)
Timing and trajectory of BCR-ABL1 driven chronic myeloid leukaemia. Nature. DOI: 10.1038/s41586-025-08817-2

Abstract
Mutation of some genes drives uncontrolled cell proliferation and cancer. The Philadelphia chromosome in chronic myeloid leukaemia (CML) provided the very first such genetic link to cancer1,2. However, little is known about the trajectory to CML, the rate of BCR::ABL1 clonal expansion and how this affects disease. Using whole-genome sequencing of 1,013 haematopoietic colonies from nine patients with CML aged 22 to 81 years, we reconstruct phylogenetic trees of haematopoiesis. Intronic breaks in BCR and ABL1 were not always observed, and out-of-frame exonic breakpoints in BCR, requiring exon skipping to derive BCR::ABL1, were also noted. Apart from ASXL1 and RUNX1 mutations, extra myeloid gene mutations were mostly present in wild-type cells. We inferred explosive growth attributed to BCR::ABL1 commencing 3–14 years (confidence interval 2–16 years) before diagnosis, with annual growth rates exceeding 70,000% per year. Mutation accumulation was higher in BCR::ABL1 cells with shorter telomere lengths, reflecting their excessive cell divisions. Clonal expansion rates inversely correlated with the time to diagnosis. BCR::ABL1 in the general population mirrored CML incidence, and advanced and/or blast phase CML was characterized by subsequent genomic evolution. These data highlight the oncogenic potency of BCR::ABL1 fusion and contrast with the slow and sequential clonal trajectories of most cancers.

Main
Chronic myeloid leukaemia (CML) occupies a landmark position in the history of oncology research, marking the first instance in which a genetic anomaly was implicated in the development of cancer. The seminal discovery of the Philadelphia (Ph) chromosome in 1960 by Nowell and Hungerford¹ and BCR::ABL1 fusion gene in 1973 by Rowley², heralded the era of oncogenomics. Targeting BCR::ABL1 by means of tyrosine kinase inhibition (TKI) has since resulted in uniquely successful patient outcomes in CML, a result not replicated for most other cancers³.

Cancers emerge from the stepwise accumulation of key genetic mutations critical to cell growth and regulation⁴. Such mutations accumulate over an extended period, commencing decades before clinical presentation, for example, early in life whole-genome duplication in ovarian cancer and chromosome 3p loss in clear cell renal cell carcinoma^5,6. Cancer evolution may even commence in utero, as demonstrated for JAK2 mutations in adult-onset polycythaemia vera⁷. By contrast, cancer incidences in Japanese survivors of the atomic bombs showed a peak in CML within 10 years of radiation exposure, raising the possibility that BCR::ABL1 driven clonal expansion and the trajectory to CML are unlike that of adult malignancies studied so far⁸.

Somatic mutations accumulate in haematopoietic cells throughout life in a clock-like fashion^7,9. The resulting unique mutational profiles of individual cells can be harnessed to reconstruct phylogenetic trees that depict ancestral cellular relationships and evolutionary history. This approach has enabled precise quantification of clonal dynamics in both healthy haematopoiesis and haematological malignancy^7,9,10. Here, using genome-wide somatic mutations and phylogenetic inference, we characterize the fitness and trajectory of BCR::ABL1 driven clonal expansion and how these factors affect clinical features of CML.

Aleksandra E Kamizela et al. (2025)
Timing and trajectory of BCR-ABL1 driven chronic myeloid leukaemia. Nature. DOI: 10.1038/s41586-025-08817-2

Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Since this devastating disease can be readily explained by the utilitarian nature of evolution — which prioritises short-term reproductive success over long-term health and survival — it stands in stark contrast to the claims made by proponents of Intelligent Design, who must reject such science to preserve their position.

So, I repeat my challenge to advocates of Intelligent Design: if William A. Dembski's complex specified information is taken as evidence of an intelligent designer, then why should a complex gene that promotes the rapid early development of acute myeloid leukaemia not also be considered an example of such information? Does this not imply that the same designer must be credited with designing this deadly disease?

Or is Dembski’s term deliberately left vague in order to provide rhetorical cover for those seeking confirmation of pre-existing religious beliefs, rather than offering a coherent or testable scientific explanation?

Or is Dembski's complex specified information not the evidence for an intelligent designer he wants his audience to believe it is?

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