Why You Probably Don’t Need to Worry About Getting Cancer

By Dov Michaeli, MD, PhD | Published 2/5/2021 50

Middle-aged woman worried about getting cancer

Cancer phobia is a morbid dread of getting cancer that can lead to multiple medical evaluaitons to no avail. (Photo source: Adobe Stock Photos)

Some people continuously worry about getting cancer. In fact, a population-based survey found that although a third of respondents never worried about getting cancer, more than half worried occasionally and 6% worried often.[1]

When the persistent fear of cancer rises to the level of an overt phobia it is known as cancer phobia or carcinophobia. It may lead to repeated medical examinations that fail to reveal a malignancy. Despite this, people with this condition are unable to be reassured about their clean bill of health for any length of time. This article will explore why most of us probably don’t need to worry about getting cancer.

Luckily, as the survey demonstrated, most of us are not overtly phobic about cancer, even though it may be lurking deep in our subconscious. Why is it not an active fear for the bulk of the population? It is likely because in people without any signs of cancer, it is not perceived as an imminent threat. We are hard-wired to fear clear and present dangers. Risks and threats far into the future don’t get as much priority in our constellation of daily fears.

Examples of this from our daily life abound. For example, research has demonstrated that most people are not willing to take urgent action on climate change if it is presented as a distant threat.[2] But if portrayed as proximal in time and place, more people are willing to act with urgency.

This may seem unrelated to worrying about cancer, but the underlying neurobiological mechanism is the same. We’ll explore that later in this post.

So, should we worry more about getting cancer?

George Klein (1925-2016) was Professor Emeritus at the Microbiology and Tumor Biology Center at the Karolinska Institute in Stockholm, Sweden when he published a fascinating article in The Scientist. The article makes the point that approximately one in three people will be struck by cancer in their lifetime.[3] But, the other side of that coin is that two out of three people remain unaffected. Even the majority of heavy smokers who bombard their lungs with carcinogens and tumor promoters over many years remain cancer-free.

A systematic review revealed that prostate cancer’s incidental findings at autopsy ranged from <5% in men under age 30 to almost 60% by age 70.[4] A not-insignificant percentage of these cancers, when localized and low risk, do not progress to overt cancer during the person’s lifetime. This has led to a recommendation option of active surveillance as opposed to treatment.[5]

It is also known that circulating tumor cells (CTCs) are present in many cancer patients. However, only a portion of these cells will enter and persist in distant parts of the body.[6] These are known as disseminated tumor cells or DTCs. An only a fraction of them develop into secondary tumors (metastases).

  • What keeps these micro-cancers in check?

They are kept in check by a mix of the following elements:

In other words, when it comes to getting or not getting cancer, the glass is more than half-full.

So, should we just relax and not worry? Actually, that’s not a productive question to ask. A more interesting one, that may actually produce interesting answers is:

What makes most people resistant to cancer?

What causes cancer?

As the Cancer Society of Finland succinctly states [9]:

“Cancer is caused by accumulated damage to genes. Such changes may be due to chance or to exposure to a cancer causing substance.” 

Risks related to developing cancer

There are a number of ways this damage can occur including, but not limited to this list:

      • Lifestyle factors that expose us to carcinogens, including
        • tobacco smoke
        • alcohol
        • UV radiation in sunlight
        • food factors, such as nitrites
      • Occupational exposures, such as  
        • asbestos
        • tar and pitch
        • polynuclear hydrocarbons
        • some metal compounds
        • certain plastic compounds
      • Infections with certain viruses or bacteria (Helicobacter pylori, hepatitis B, or Epstein-Barr)
      • Radiation exposure
      • Some drugs, in particular,
        • medications that weaken the immune system
        • anticancer drugs
        • certain hormones
      • Genetic predisposition (for example, Lynch Syndrome [10])
      • Factors not yet identified

We know that colon cancer, breast cancer, and prostate cancer, develop through progressive stages of mutations that ultimately cause cell division to spin out of control and proliferate wildly.

Related content:
Have Breast Implants? Should You Be Worried About Cancer
A Lump or Bump on the Eyelid. Beware It Could Be Skin Cancer

Is cancer resistance simply the absence of mutations?

You might be wondering at this point if not getting cancer is merely the absence of harmful mutations? If that were the case, then is not getting cancer simply a matter of luck? To answer this question, let me paraphrase Albert Einstein’s quip about quantum mechanics, evolution doesn’t play dice. It increases its odds with natural selection.

It turns out that mutations, harmful or otherwise, occur all the time in all of us. With a few exceptions related to certain genetic or pathological conditions, most of the rest of us possess several well-known anti-cancer mechanisms.

The body’s anti-cancer mechanisms

In a classic paper published in PNAS, George Klein identified five kinds of anti-cancer mechanisms [11]:

1. Immunologic

The first type of resistance Klein describes is immunological. For example, researchers have compared the antibody responses of the squirrel monkey and the marmoset when infected with Herpesvirus saimiri. Marmosets, but not the squirrel monkeys, develop rapidly growing lymphomas after exposure to the virus. Of note, the virus is endogenous to squirrel monkeys, but marmosets never encounter it. 

The researchers found a striking difference in the timing of each animal’s antibody response. In the tumor-resistant squirrel monkeys, the antibodies rose to a high level just three days after the infection. However, in the marmosets, the response took three weeks, too late to stop the virus-driven lymphoma.

The dynamics of the antibody response suggest that squirrel monkeys had pre-existing memory T cells against the virus. Whereas the marmosets had to develop them first before a full-blown antibody response could be mounted, a process that takes about three weeks.

2. Genetic

The second mechanism Klein describes is genetic. Our cells are constantly subjected to DNA damage. And, there are individual variations in the efficiency of the repair mechanisms.

Although, in the vast majority, these mechanisms are capable of repairing the damage quickly, some are not. An example is a DNA repair deficiency disorder called xeroderma pigmentosum [12]. Individuals with this deficiency are highly sensitive to ultraviolet light. Even with careful protection, they develop multiple skin cancers due to their genetic deficiency.

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3. Epigenetic

According to a review of cancer epigenetics, the term refers to the “study of heritable changes in gene expression without alterations in DNA sequences.” [13] Unlike changes in the genome itself, epigenetic changes are reversible. Some key epigenetic processes include the following:

        • changes in DNA methylation,
        • chromatin modifications,
        • alterations of nucleosome positioning
        • changes in non-coding RNA profiles.

These alterations can lead to altered gene function as well as a neoplastic transformation of cells.

The next two mechanisms are, for some reason, my favorites.

4. Apoptosis or cell death

As part of an intracellular defense, a cell can trigger apoptosis (cell death) if it detects extensive DNA damage. This prevents the cell from reproducing and spreading the damage. It is the ultimate altruism on the cellular level.

In some individuals, this mechanism fails. For example, The cellular protein P53 is a tumor suppressor. When it is mutated, it increases the risk of inheriting Li-Fraumeni syndrome [14], a rare disease in which patients develop multiple cancers starting from childhood.

5. Factors in the tissue’s microenvironment

The last mechanism of defense against tumors resides in the microenvironment in which tissues are embedded. Here is a striking example. The naked mole-rat (NMR) and the blind mole rat (BMR), live up to 20 and 30 years, respectively, and never develop cancer. How do they pull off this trick?

The naked mole rat

The naked mole-rat (NMR) displays exceptional longevity, with a maximum lifespan exceeding 30 years [15]. This is the longest reported lifespan for a rodent species. It is especially striking considering its small body mass. In comparison, a similarly sized house mouse has a maximum lifespan of 4 years. In addition to their longevity, naked mole-rats show an unusual resistance to cancer.

The NMR is a social species that live in highly organized matriarchal societies. It has to force its way through narrow and often sinuous underground tunnels. The connective tissue in its skin contains a high-molecular-weight form of hyaluronic acid (HA) that makes the animal’s skin malleable. The corresponding HA in mice and humans has less than one-fifth of the molecular weight.

The heavy form of HA that occurs in the NMR is not only beneficial for the animal’s locomotion. It also prevents the transformation of normal cells in cell culture into cancer cells. Only after it has been removed can the NMR’s cells be transformed into cancer cells. The NMR cells also display an extreme sensitivity to contact inhibition. The cells stop dividing when barely touching each other.

The blind mole rat

Several species of the blind mole rats (Spalax judaei and Spalax golani) are common in Israel and surrounding countries. BMRs are small subterranean rodents. They are distinguished by their adaptations to life underground, remarkable longevity (with a maximum documented lifespan of 21 years. They also show remarkable resistance to cancer.

In tissue culture, when overproliferation starts taking place after several cell divisions, BMR cells began secreting interferon ß. [16] This triggers a massive cell suicide response (a.k.a. apoptosis). The Masada phenomenon is apparently alive and well in this Middle Eastern species.

In case you conclude that it is subterranean living or the small size that protects these animals from getting cancer, think again—the blue whale is cancer-resistant as well.  So, we don’t have to live underground or go back to the ocean where our very distant ancestors came from.

The bottom line is that most of us don’t need to worry about getting cancer

Rather, we can take a deep breath and relax because two-thirds of us will never develop cancer for all of the reasons described in this article.

As for the other third, don’t despair. New diagnostics and therapeutics for cancer are being developed at a rapid rate. That doesn’t mean all cancers are curable yet. But I, for one, am putting my faith in human ingenuity to one day make cancer much less feared than it is today.


  1. Murphy P, Marlow L, Wailer J, et al. What is it about a cancer diagnosis that would worry people? A population-based survey of adults in England, BMC Cancer, 2018 Jan 24. https://pubmed.ncbi.nlm.nih.gov/29361912/
  2. Brügger A,  Morton T,  Dessai S. Hand in Hand: Public Endorsement of Climate Change Mitigation and Adaptation, PLOS One, 2015 Apr 29,  https://doi.org/10.1371/journal.pone.0124843
  3. Klein G. Resisting Cancer, The Scientist, 2015 Apr 1, https://www.the-scientist.com/features/resisting-cancer-35711
  4. Bell K, Del Mar C, Wright G, et al. Prevalence of Incidental Prostate Cancer: A Systematic Review of Autopsy Studies, Int. J. Cancer, 2015 Oct 1, https://pubmed.ncbi.nlm.nih.gov/25821151/
  5. Garisto J, Klotz L. Active Surveillance of Prostate Cancer: How to Do It Right, Oncology (Williston Park), 2017 May 15, https://pubmed.ncbi.nlm.nih.gov/28512731/
  6. Dasgupta A, Lim A, Ghajar C. Circulating and Disseminated Tumor Cells: Initiators or Harbingers of Metastases? J Mol Oncol, 2017 Jan 9, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423226/
  7. Gonzalez H, Hagerling C, Werb Z. Roles of the Immune System in Cancer: from Tumor Initiation to Metastatic Progression, Genes Dev 2018 Oct. 1, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6169832/
  8. National Foundation for Cancer Research. What is Angiogenesis? Accessed 1/24/21. https://www.nfcr.org/research-programs/research-focus-areas/angiogenesis
  9. Cancer Society of Finland. All About Cancer: Facts About Cancer, Accessed 2021 Jan 24, https://www.allaboutcancer.fi/facts-about-cancer/what-causes-cancer/#d8f54e89
  10. Cancer.Net Editorial Board. Lynch Syndrome, Cancer.Net, 2020 Jan. https://www.cancer.net/cancer-types/lynch-syndrome. Accessed Jan 24, 2021
  11. Klein G. Towards a Genetics of Cancer Resistance. PNAS, 2009 Jan. 20, https://www.pnas.org/content/pnas/106/3/859.full.pdf?sid=f73133d0-35bf-4d9b-a3eb-a3fac2ba089f 
  12. MedlinePlus. Xeroderma Pigmentosa, National Library of Medicine, Accessed 1/24,2021, https://www.pnas.org/content/pnas/106/3/859.full.pdf?sid=f73133d0-35bf-4d9b-a3eb-a3fac2ba089f
  13. Kanwal R, Gupta K, Gupta S. Cancer Epigenetics: An Introduction, Methods Biol, 2015, 1238:3-25, https://pubmed.ncbi.nlm.nih.gov/25421652/
  14. Medline Plus. Li Fraumeni Syndrome. National Library of Medicine, Accessed 1/24/2021, https://medlineplus.gov/genetics/condition/li-fraumeni-syndrome/
  15. Tian X, Azapurua J, Hines C, et al. High-molecular-mass Hyaluronan Mediates Cancer Resistance in the Naked Mole Rate, Nature, 2013 June 19, https://www.nature.com/articles/nature12234
  16. Gorbunova V, Hinea C, Tian X, et al. Cancer resistance in the blind mole rat is mediated by concerted necrotic cell death mechanism, PNAS 2012 Nov 12, https://www.pnas.org/content/pnas/109/47/19392.full.pdf

First published 5/3/15. Updated 3/25/18. Major revision 11/9/19. Updated 1/24/21. Updated 2/5/21.

Dov Michaeli, MD, PhD

Dov Michaeli, M.D., Ph.D. (now retired) was a professor and basic science researcher at the University of California San Francisco. In addition to his clinical and research responsibilities, he also taught biochemistry to first-year medical students for many years.

During this time he was also the Editor of Lange Medical Publications, a company that developed and produced medical texts that were widely used by health professionals around the world.

He loves to write about the brain and human behavior as well as translate knowledge and complicated basic science concepts into entertainment for the rest of us.

He eventually left academia to enter the world of biotech. He served as the Chief Medical Officer of biotech companies, including Aphton Corporation. He also founded and served as the CEO of Madah Medica, an early-stage biotech company that developed products to improve post-surgical pain control.

Now that he is retired, he enjoys working out for two hours every day. He also follows the stock market, travels the world, and, of course, writes for TDWI.


  • You likely don’t need to worry about getting cancer because 2/3 of us will remain cancer-free during our lifetimes. Science explains why.

  • You ain’t gonna live forever so don’t worry about all the crap pumped out by the media. Enjoy life.

  • I’m a hypochondriac and this article really helped my anxiety and calmed me down. Very well said and supported throughout. Thank you so much 😁

  • This was a good article. I freak out over the C word.. every pain, bump or bruise and my mind goes straight there. Medicine is big $$ so dont trust them so im into preventative as much as possible.. though i respect their place as needed. Most know nothing about nutrition and supplements (i like to think more are waking up to this) but Big Pharmas running the show.. dont mean to offend but we all know it..
    I wish all great health! :)

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