Digest №7: What Even Is Cancer?
Photo by National Cancer Institute / Unsplash

Digest №7: What Even Is Cancer?

2026, week 13: What is cancer? How does it develop? And what can that tell us about its treatment?


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Bless!

Isn't that a fascinating and I dare say quite important question? What even is cancer? We talk a lot about how to counteract the disease's many aberrations in order to give you a longer and more enjoyable life, but what is we're actually trying to heal?

I wager, that it'll help you significantly with the task ahead of you to intuitively understand what cancer is. After all, wrestlers, footballers, and hockey players don't go into a match with an opponent without first at least trying to understand their opponent by watching bygone footage. And whilst I may not be able to make cancer, its moods and habits entirely intuitive to you, I think I can get you far along that way. 

Fundamentally, the problem with cancer is two-fold: its cells don't behave as though they are part of the whole organism that is you, and it incites your others cells to behave in the cancer's interest instead of your own. But how does it ever come to this? How does a tiny cell, perfectly integrated into your organismal whole ever become so aberrant, that it begins killing you?

Let's start from the beginning – say, with a perfectly normal lung epithelium (inner lining of the lungs).

Throughout the lifetime of this epithelial tissue, it's inundated with whatever you choose to breathe in. If you smoke cigarettes, your entire body, but also your lung will experience higher levels of inflammation.1 The specific type of inflammation induced by smoking – interleukin-6 (IL-6) – is highly similar to that induced by asbestos, which causes pleural mesothelioma.2–3 Similar inflammatory patterns are also seen in ovarian, prostate, and breast cancers.4

Such inflammation is quite harmless, when it occurs transiently. It happens hundreds, if not thousands of times during our lifetime. You breathe in something toxic, you get infected with a cold virus, or you get pneumonia. There's nothing disastrous in particular about such inflammation.

Unless, it's a chronic thing. Unless, it never abates.

One of the first things such chronic IL-6 inflammation does is, that it suppresses immune surveillance of the affected tissues and constituent cells. Due to the constantly high load of IL-6 you immune systems tips over into a blind mend-and-repair mode of operation, where its capacity to kill of defective cells is highly diminished.

Now, this alone isn't much of an issue... Not until a few of your cells in such an affected tissue develop into such defective cells, ordinarily killed off by the immune system or even themselves. Now these beginning aberrant cells are allowed to survive and slowly accrue damage and alterations – both in their genetic information and their behaviour.

Say, they begin growing at a slightly too high rate. Say, they start dying at a slightly too low rate. That's not really something to worry about, right? Say, those rates of increasing growth and decreasing death continue to diverge.

Eventually, you'll be left with a small tumour – a mass of abnormally grown cells.

This tumour will very improbably be of any issue. It's too small, too localised, too pacifist. It doesn't really do anything than give you a weird cyst, that – sure – shouldn't be there, but also doesn't impact the function of the surrounding tissue. For that reason, such tumours are said to have good intentions (or rather be benign).

Say, you don't stop having chronic inflammation – due to smoking, asbestos, bad dietary choices, or any number of other toxic ingestions. Say, your immune system still doesn't get active in diminishing the size of this benign tumour. Say, the tumour grows to a size, where oxygen can no longer properly penetrate into its core.

We now get to a point, where the cells in the core will either die or adapt to a lifestyle with too little oxygen (hypoxic). This hypoxic lifestyle will lead the cell to forgo mitochondrial energy metabolism and instead rely on lactic acid fermentation, which can function without oxygen.5–6

Such an acidic fermentation metabolism will inevitably acidify the core of such a growing tumour. This acidity then significantly destabilises the genome of the cell through various means.7–8 This genomic instability in turn further handicaps the mitochondria, which locks these very early–stage cancer cells into a preference for lactic acid fermentation and simultaneously lowers their ability to kill themselves in a process of sacrificial cell suicide (apoptosis).9–11

Eventually, these cells, through a process of evolution will in a very real sense stop being your cells and rather be cell, which evolved from you, but can no longer be considered a true part of you.

And that is cancer.

It's a slow evolutionary process, relying on various factors coming together to allow the gradual evolution – first only in behaviour, later also majorly in genetics – of your cells into not your cells, i. e. into cancer cells.

When cancer has become fully ill-intentioned (malignant) and has advanced sufficiently, its cells have stopped being your cells and become an entirely different organism. They are no longer beholden to what serves you as an organism, for they are no longer part of you as an organism.

Cancer isn't a mass of 'rogue' cells, they're a mass of foreign cells, which evolved from rogue cells. They are no longer you. And that is why cancer is so difficult to deal with. Not impossible, mind you, but difficult.

I hope this has shed some light on what cancer truly is.

Swift healing and lasting health to you.

God bless, Merlin L. Marquard

P.S.: Should you ever need help, you know where to reach us.


References

  1. Elisia I, Lam V, Cho B, et al. The effect of smoking on chronic inflammation, immune function and blood cell composition. Sci Rep 2020;10:19480. doi:10.1038/s41598-020-76556-7
  2. Simeonova PP, Toriumi W, Kommineni C, et al. Molecular regulation of IL-6 activation by asbestos in lung epithelial cells: role of reactive oxygen species. J Immunol 1997;159:3921–8.
  3. Abdul Rahim SN, Ho GY, Coward JIG. The role of interleukin-6 in malignant mesothelioma. Transl Lung Cancer Res 2015;4:55–66. doi:10.3978/j.issn.2218-6751.2014.07.01
  4. Zaporowska-Stachowiak I, Springer M, Stachowiak K, et al. Interleukin-6 Family of Cytokines in Cancers. Journal of Interferon & Cytokine Research 2024;44:45–59. doi:10.1089/jir.2023.0103
  5. Alberts B, Johnson A, Lewis J, et al. Cell Chemistry and Bioenergetics. In: Molecular Biology of the Cell. New York, US: : Garland Science, Taylor & Francis Group, LLC 2015. 43–108.
  6. Alberts B, Johnson A, Lewis J, et al. Energy Conversion: Mitochondria and Chloroplasts. In: Molecular Biology of the Cell. New York, US: : Garland Science, Taylor & Francis Group, LLC 2015. 753–812.
  7. Dai C, Sun F, Zhu C, et al. Tumor Environmental Factors Glucose Deprivation and Lactic Acidosis Induce Mitotic Chromosomal Instability – An Implication in Aneuploid Human Tumors. PLOS ONE 2013;8:e63054. doi:10.1371/journal.pone.0063054
  8. Tan Z, Chu DZV, Chan YJA, et al. Mammalian Cells Undergo Endoreduplication in Response to Lactic Acidosis. Sci Rep 2018;8:2890. doi:10.1038/s41598-018-20186-7
  9. Amponsah PS, Bökenkamp J-E, Kurpa O, et al. Aneuploidy-induced proteostasis disruption impairs mitochondrial functions and mediates aggregation of mitochondrial precursor proteins through SQSTM1/p62. Nature Communications 2025;16:5328. doi:10.1038/s41467-025-60857-4
  10. Alberts B, Johnson A, Lewis J, et al. Cancer. In: Molecular Biology of the Cell. New York, US: : Garland Science, Taylor & Francis Group, LLC 2015. 1091–144.
  11. Alberts B, Johnson A, Lewis J, et al. Cell Death. In: Molecular Biology of the Cell. New York, US: : Garland Science, Taylor & Francis Group, LLC 2015. 1021–34.

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