World Cancer Day - in a world where everything can now lead to cancer

World Cancer Day - in a world where everything can now lead to cancer
05 Feb 2018

1 in 2 people in the UK born after 1960 will be diagnosed with some form of cancer during their lifetime. 1 Although 42% of cancer cases each year are considered to be preventable, cancer still causes more than 1 in 4 of all deaths in the UK.1

Despite major leaps in detection and treatment, cancer is clearly still a huge health issue. So what causes cancer, and what impact does a 21st-century lifestyle have on it?

How does cancer start?

Cancers are either benign – sometimes leading to morbidities, but rarely death – or malignant. Malignant tumours are what we often refer to when we talk about cancer, and it is the secondary tumours caused by metastases which cause the vast majority of cancer-related deaths.

Neoplasia: the abnormal growth of tissue resulting in the production of a tumour.2

The development of a neoplasm is a very slow, protracted event requiring the mutation of just a single parent cell’s genetic make-up which leads to the loss of function in a tumour suppressor gene and gain of function in an oncogene. These genetic mutations are caused by the uptake of carcinogenic material into a cell where they alter the cells’ DNA and the genes expressed. This alteration in gene expression initiates the uncontrolled cell growth that eventually leads to neoplasia.

Tumour initiation: the process by which normal cells are changed to enable them to form tumours.

Examples of tumour initiators include:

  1. Environmental factors: mutagens which we come into contact with in our everyday environment. They can be found in the foods we eat and the chemicals we are exposed to, e.g. asbestos and environmental pollutants, as well as drugs.2, 3, 4
  2. Viruses: such as the human papilloma virus, which have the capability to insert their own genes into a host’s DNA and stimulate proliferation. They also have the capacity to alter the body’s immune response to viruses and prevent programmed cell death, a process put in place by the body to safeguard against mutated or damaged cells.5
  3. Genetic defects: inhibited tumour suppressor genes which result in a loss of function. These defects are usually present from birth.

90–95% of these initiators have their roots in the environment and our choice of lifestyle, meaning only 5–10% of all cancer cases can be attributed to genetic defects.3

In addition to tumour initiators, there are other factors called promoters which contribute to the probability of developing cancer.

Examples of promoters include:

  1. Wounds, inflammatory injuries that lead to a chemical change,
  2. Sunlight radiation, excessive exposure to UV,
  3. Chemicals, such as cigarette smoke and alcohol,
  4. Environmental pollutants, and
  5. Infectious agents such as the hepatitis viruses.

Promoters cannot initiate tumour development; they increase the likelihood that a particular carcinogen will cause cancer and the rate at which the tumour develops. They do this by triggering an inflammatory response which up-regulates the production of inflammatory cytokines that lead to increased proliferation and prostaglandin production.

For example, one of these inflammatory cytokines is NF-κB, a family of transcription factors central to the induction of inflammation in neoplasia.6 Its activation has been encountered in most types of cancers, 3 and has been linked with chemo- and radio-resistance. Its suppression has been shown to inhibit tumour proliferation through the up-regulation of transcription factors associated with programmed cell death.2    

As a result of the up-regulation of NF-κB within a cell, the cell gains a proliferative advantage and can carry out an indeterminate number of divisions. It becomes immortalized.

This transformation comes as a result of continued exposure to mutagenic initiators, leading to an accumulation of mutations over time that causes the epithelial cell morphology to change.

The tumour at this stage is still benign.

The shift from benign to malignant

Once these epithelial cells transition to become mesenchymal cells, they gain the ability to enter the bloodstream, spread around the body and invade other tissues.

This transition is the marker for the development of a malignant tumour and it is at this point, when the transformed cells invade other tissues of the body, that the first metastatic event occurs and the tumour becomes cancer.5

In summary, it is the harmful substances we either choose to come into contact with, or are part of our everyday lives in the 21st century that augment our risk of developing cancer. Our genetics really play a very small part. If we want to reduce these risks we need to pay attention to the foods we eat, the habits we keep and the environment in which we choose to live.

February 4th is World Cancer Day; reduce your risks, do something about the way in which you choose to live today.

 

References

  1. Cancer Risk Statistics. Cancer Research UK. Available from: http://www.cancerresearchuk.org/health-professional/cancer-statistics [Accessed January 2018].
  2. Definition of Neoplasia. Collins English Dictionary. Harper Collins Publishers. Available from: https://www.collinsdictionary.com/dictionary/english/neoplasia [Accessed January 2018].
  3. Bray F and and Møller B. Predicting the Future Burden of Cancer. Nat Rev Cancer. 2006;6(1):63–74.
  4. Anand, P, et al. Cancer is a Preventable Disease that Requires Major Lifestyle Changes. Pharm Res. 2008; 25(9): 2097–2116.
  5. Elmore S. Apoptosis: A Review of Programmed Cell Death.Toxicol Pathol. 2007;35(4):495–516.
  6. Rakoff-Nahoum S. Why Cancer and Inflammation?Yale J Biol Med. 2006;79(3-4): 123–130.
  7. Micalizzi, DS, et al. Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression. J Mammary Gland Biol Neoplasia. 2010 Jun;15(2):117–34.

 

April Rosson
Senior Account Executive

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