Rosa Rubicondior: Malevolent Designer News - How Cancer is Cleverly Designed to Trick Our Immune System

Mitochondrial transfer and metabolic reprogramming of the tumor microenvironment aid cancer immune evasion.

How Cancer Cells Trick the Immune System by Altering Mitochondria - Okayama University

There is an ongoing arms race between medical science and cancer - and guess whose side creationism's intelligent designer appears to be on.

Yep, it's the same intelligent designer who designed cancers in the first place by creating an error-prone DNA replication mechanism that goes wrong, as does the error-correction mechanism it designed to try to rectify its faulty design with an added layer of complexity. And one of the results of it going wrong is cancer.

One of the more hopeful treatments for cancer was a tailor-made immunotherapy in which specific antibodies to the cancer cells were used to attack the cancer and treat it like a parasitic pathogen, by training the immune system to recognise the cancer and attack and destroy it.

But, true to form, creationism's divine malevolence has hit back by designing a response by cancer cells to attack by cells of the immune system.

We can be sure this is the work of creationism's intelligent designer because William A Dembski, the Discovery Institute's flunky and pseudoscientist in residence, tells us that any genetic sequence that produces a function must have been given 'specified information' in the form of the DNA that codes for that specific protein because, so he claims, specified information is too complex to have evolved.

Can you explain how immunotherapy is used to treat cancer, please. Certainly! Immunotherapy is a type of cancer treatment that harnesses the body's immune system to recognize, attack, and destroy cancer cells. It works by either boosting the immune system’s natural defences or by modifying it to better target cancer cells. There are several main types of immunotherapy used in cancer treatment:

Checkpoint Inhibitors (Immune Checkpoint Blockade)

The immune system has "checkpoints" that prevent it from attacking normal cells. Some cancers exploit these checkpoints to evade detection.
Checkpoint inhibitors (e.g., PD-1, PD-L1, and CTLA-4 inhibitors) block these checkpoints, allowing the immune system to attack cancer cells.
Examples: Pembrolizumab (Keytruda), Nivolumab (Opdivo), Ipilimumab (Yervoy).

CAR-T Cell Therapy (Chimeric Antigen Receptor T-Cell Therapy)

A patient’s T cells are extracted, genetically modified to target specific cancer antigens, and then reinfused into the body.
Mostly used for blood cancers like leukaemia and lymphoma.
Examples: Axicabtagene ciloleucel (Yescarta), Tisagenlecleucel (Kymriah).

Cancer Vaccines

Stimulate the immune system to recognize and attack cancer cells.
Examples: Sipuleucel-T (Provenge) for prostate cancer, HPV vaccine (which prevents HPV-related cancers).

Monoclonal Antibodies (mAbs)

Lab-made proteins that target specific antigens on cancer cells, marking them for destruction by the immune system.
Some also deliver toxins directly to cancer cells.
Examples: Rituximab (Rituxan) for lymphoma, Trastuzumab (Herceptin) for breast cancer.

Cytokine Therapy

Uses immune system signalling proteins like interleukins (IL-2) and interferons (IFN-α) to enhance the immune response against cancer.
Example: Aldesleukin (IL-2) for kidney cancer and melanoma.

Oncolytic Virus Therapy

Uses genetically modified viruses to infect and destroy cancer cells while stimulating an immune response.
Example: Talimogene laherparepvec (T-VEC) for melanoma.

Advantages of Immunotherapy

Can be highly effective, especially in cancers that resist traditional treatments.
Provides long-term immune memory, reducing the risk of recurrence.
Often has fewer side effects than chemotherapy or radiation.
Challenges and Limitations

Not all cancers respond to immunotherapy.
Can cause immune-related side effects (e.g., inflammation, autoimmune-like reactions).
Expensive and not always widely available.
Immunotherapy has revolutionized cancer treatment, offering hope for many patients with previously untreatable cancers. Let me know if you want details on a specific type!

And Michael J Behe's biologically nonsensical notion of 'devolution' due to 'genetic entropy' from some assumed created perfection, following 'The Fall', can be ruled out if for no other reason than that it assumes there was ever a perfect cancer!

The trick cancers use to evade the immune response depends on the cancer cells inserting their faulty mitochondria into the immune cells where they displace the T-cells own mitochondria, because they bring with them a method for preventing the T-cells mechanism for destroying faulty mitochondria. Ingenious, eh?

How this works is the subject of an open access research paper in Nature by researchers led by Professor Yosuke Togashi from Okayama University, Japan. The research is explained in an Okayama University press release:

How Cancer Cells Trick the Immune System by Altering Mitochondria
Researchers discover mitochondrial transfer between cancer cells and immune cells as a key immune evasion strategy
The immune system plays a key role in detecting and destroying cancer cells. Cancer immunotherapy works by programming immune cells to recognize and eliminate cancer cells. However, many cancers can escape immune surveillance through various mechanisms, resulting in resistance to treatment. This highlights the need to better understand the molecular processes that enable immune evasion.

The tumor microenvironment (TME)—the space surrounding a tumor—plays a critical role in interactions between cancer and immune cells. Cancer cells can reshape the TME to their advantage, weakening tumor-infiltrating lymphocytes (TILs), the immune cells that attack tumor. Mitochondria, also known as the ‘powerhouse of the cell,’ are small organelles that produce energy for various cellular processes. They play a significant role in the metabolic reprogramming of cancer cells and TILs. However, precise mechanisms underlying mitochondrial dysfunction and its impact on the TME are poorly understood.

To address this knowledge gap, a team of researchers led by Professor Yosuke Togashi from Okayama University, Japan, has uncovered novel insights into mitochondrial dysfunction in cancer immune evasion. Working alongside Tatsuya Nishi and Tomofumi Watanabe from Okayama University, as well as Hideki Ikeda, Katsushige Kawase, and Masahito Kawazu from the Chiba Cancer Center Research Institute, the team identified mitochondrial transfer as a key mechanism of immune evasion. This study was published online in Nature on January 22, 2025.
We have discovered mitochondrial transfer as one of the key mechanisms of immune evasion. Our research adds a new dimension to the understanding of how tumors resist immune responses, potentially leading to the development of more comprehensive and tailored approaches in treating different cancers.

Professor Yosuke Togashi, corresponding author.
Division of Cell Therapy
Chiba Cancer Center Research Institute, Chiba, Japan
And Department of Tumor Microenvironment
Faculty of Medicine, Dentistry and Pharmaceutical Sciences
Okayama University, Okayama, Japan.

Mitochondria carry their own DNA (mtDNA), which encodes proteins crucial for energy production and transfer. However, mtDNA is prone to damage, and mutations in mtDNA can promote tumor growth and metastasis. In this study, the researchers examined TILs from patients with cancer and found that they contained the same mtDNA mutations as the cancer cells. Further analysis revealed that these mutations were linked to abnormal mitochondrial structures and dysfunction in TILs.

Using a fluorescent marker, the researchers tracked mitochondrial movement between cancer cells and T cells. They found that mitochondria were transferred via direct cell-to-cell connections called tunneling nanotubes, as well as through extracellular vesicles. Once inside T cells, the cancer-derived mitochondria gradually replaced the original T cell mitochondria, leading to a state called ‘homoplasmy,’ where all mtDNA copies in the cell are identical.

Normally, damaged mitochondria in TILs are removed through a process called mitophagy. However, mitochondria transferred from cancer cells appeared to resist this degradation. The researchers discovered that mitophagy-inhibiting factors were co-transferred with the mitochondria, preventing their breakdown. As a result, TILs experienced mitochondrial dysfunction, leading to reduced cell division, metabolic changes, increased oxidative stress, and impaired immune response. In mouse models, these dysfunctional TILs also showed resistance to immune checkpoint inhibitors, a type of immunotherapy.

By identifying mitochondrial transfer as a novel immune evasion mechanism, this study opens new possibilities for improving cancer treatment. Blocking mitochondrial transfer could enhance immunotherapy response, particularly in patients with treatment-resistant cancers.

Cancer therapies often involve high costs and significant side effects, particularly when they are ineffective. Enhancing the success of immunotherapy by inhibiting mitochondrial transfer could reduce the burden of cancer and improve patient outcomes.

Existing cancer treatments are not universally effective, and there is a pressing need for new therapies that can overcome resistance mechanisms. Developing drugs that inhibit mitochondrial transfer between cancer cells and immune cells may enhance the efficacy of immunotherapies, thereby providing personalized treatment options for patients with cancers that are resistant to current therapies.

Professor Yosuke Togashi.

This discovery offers exciting new insights into cancer biology and could pave the way for more effective therapies in the future.

Publication:
Ikeda, H., Kawase, K., Nishi, T. et al.
Immune evasion through mitochondrial transfer in the tumour microenvironment.
Nature 638, 225–236 (2025). https://doi.org/10.1038/s41586-024-08439-0

Abstract
Cancer cells in the tumour microenvironment use various mechanisms to evade the immune system, particularly T cell attack¹. For example, metabolic reprogramming in the tumour microenvironment and mitochondrial dysfunction in tumour-infiltrating lymphocytes (TILs) impair antitumour immune responses^2,3,4. However, detailed mechanisms of such processes remain unclear. Here we analyse clinical specimens and identify mitochondrial DNA (mtDNA) mutations in TILs that are shared with cancer cells. Moreover, mitochondria with mtDNA mutations from cancer cells are able to transfer to TILs. Typically, mitochondria in TILs readily undergo mitophagy through reactive oxygen species. However, mitochondria transferred from cancer cells do not undergo mitophagy, which we find is due to mitophagy-inhibitory molecules. These molecules attach to mitochondria and together are transferred to TILs, which results in homoplasmic replacement. T cells that acquire mtDNA mutations from cancer cells exhibit metabolic abnormalities and senescence, with defects in effector functions and memory formation. This in turn leads to impaired antitumour immunity both in vitro and in vivo. Accordingly, the presence of an mtDNA mutation in tumour tissue is a poor prognostic factor for immune checkpoint inhibitors in patients with melanoma or non-small-cell lung cancer. These findings reveal a previously unknown mechanism of cancer immune evasion through mitochondrial transfer and can contribute to the development of future cancer immunotherapies.

Ikeda, H., Kawase, K., Nishi, T. et al.
Immune evasion through mitochondrial transfer in the tumour microenvironment.
Nature 638, 225–236 (2025). https://doi.org/10.1038/s41586-024-08439-0

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)

Cancers are not organisms in the classic sense of evolutionary biology, but the basic principles of an evolutionary process still apply in that a cancer tumour is a population of cells in which DNA replication has gone haywire, so mutations are frequent. In a hostile, selective environment, those with mutations that make it possible for them to survive and replicate will come to dominate the tumour, and, even if reduced to a few cells, like a bacteria becoming antibiotic resistant, a whole new colony of resistance cancer cells can reestablish the tumour, by an evolutionary process.

But of course, creationists must discount that explanation, especially in view of William A. Dembski's dogma of 'specified complexity' implying an intelligence to do the specifying, and in his latest evolved version of his notion, supplying a new insertion of 'specified information' into the genome.

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