Your DNA is like a complex software code (the genetic code) that has the precise information required to run a machine — your body. Your genes, the specific lines of that code, instruct your body about how to maintain different cells, tissues, and organs. These lines issue precise instructions about when a particular cell should divide, grow, and eventually die, maintaining a proper balance in the body. But sometimes mutations and glitches can appear in the code that cause the breakdown of this tightly regulated normal process, resulting in uncontrolled cell division. Cancer, a condition where cells continue to divide without following instructions, develops as a result of this software malfunction. The genes that cause cancer are, indeed, an integral part of our genetic codes. Consequently, they can mutate at any point. As a result, these changes can eventually become one of the primary causes of cancer.
Cancer Causes – a glitch in the master code
Cancer results from the abnormal cell division of any type of cell in the body that eventually invades normal healthy cells and tissues and spreads throughout the body through a property called metastasis. Any type of body cell can defy instructions and start dividing uncontrollably, resulting in various cancer types. These tumors can be either benign tumor which are localized at only one part of the body, or malignant (malignancy), i.e., spread throughout the body to different organs.
Compared to normal cells, cancer cells require significantly less maintenance. They survive even in reduced growth factor conditions. They can break away and propagate more readily than normal cells because they are less adhesive. Moreover, cancer cells can outsmart immune surveillance and escape immune responses. The ability of cancer cells to switch off the DNA repair machinery, which typically corrects genetic flaws, is particularly concerning as it allows them to divide even when their DNA is flawed and damaged.
For a long time, cancer has been one of the leading causes of death worldwide, and its effects are only becoming worse. Globally, the disease reported nearly 20 million new cases in 2022 alone, resulting in 9.7 million deaths. According to concerning estimates, by 2040, there may be about 30 million new cases of this disease annually, and it may claim 15.3 million lives. This dramatic increase highlights the critical need for increased knowledge and research to address this escalating worldwide emergency.
The Role of Mutations in Causing Cancer
Mutations in DNA are basically like typos in the genetic code. These mutations are sudden changes in the nucleotide sequence, leading to the formation of faulty proteins. However, not every mutation in the DNA results in cancer. It all depends upon where, in the code, the typo occurs.
A mutation in unimportant genome regions won’t have a significant impact. But if the typo is in important genes, like oncogenes, tumor suppressor genes, or DNA repair genes that control the cell cycle, cancer will definitely grow. Such a mutation disrupts the rhythm of cell growth and death, leading to unregulated division of cells and, hence, one of the major cancer causes.
To understand this mechanism in detail, one must first get acquainted with the key genes involved in the process: protooncogenes and oncogenes (promoters of cell growth), tumor suppressor genes (inhibitors of cell growth), and DNA repair machinery (genetic-error fixers).
Protooncogenes and Oncogenes
Proto-oncogenes are essentially your normal genes that regulate cell growth and development. There are around 40 different types of proto-oncogenes present in your genome. Protooncogenes function akin to a green traffic light in a cell, providing a ‘GO’ signal that triggers cell division, which halts when the signal ceases. But what if the light remains stuck at green due to some glitch? What if the switch remains turned on indefinitely? The cells will keep on dividing without any check. Therefore, a protooncogene transforms into an oncogene when a mutation causes it to become overactive and increase its expression level.
Oncogenes are the mutated or overexpressed versions of normal genes that send out constant signals for increased cell division, growth, and survival tendency even when it is unnecessary.
A protooncogene can change into an oncogene through point mutation, gene duplication, or even chromosomal translocation. A point mutation is a change in a single nucleotide base pair. Protooncogenes typically exhibit dominant mutations, meaning that a single allele mutation is sufficient to transform them into oncogenes.
Table 1: Different Types of Oncogenes and their effects
| Oncogene Type | Example | Effect | Type of Cancer caused |
| Growth Factors and Growth Factor Receptors | PDGF | Excessive production leads to uncontrolled cell growth | Glioma and Chronic myelomonocytic leukemia |
| EGFR | Mutated receptors remain active even without any signal | Lung cancer | |
| ERBB2 | Over-Expressed receptors cause unregulated cell growth | Breast cancer | |
| Signal Transduction Proteins | RAS | Mutated RAS is permanently active and leads to amplified cell proliferation and survival | Pancreatic cancer Colorectal cancer and Lung cancer |
| RAF | Mutated RAF results in constant cell division | Melanoma, Colorectal cancer and Ovarian cancer | |
| Nuclear Transcription Factors | MYC | Overactive MYC enhances cell division and survival | Burkitt lymphoma |
| FOS and JUN | Increased cell proliferation and differentiation | Sarcoma , Lung cancer and Breast cancer | |
| Cell Cycle Regulators | Cyclin D1 | Promotes cell cycle progression through G1 phase | Breast cancer |
| CDK 4 | Unchecked cell cycle progression | Melanoma, Glioblastoma and Breast cancer |
The Tumor Suppressor Genes
Tumor suppressor genes, as their name suggests, prevent unregulated cell division and guard the genome. Whenever they find any problems or changes in the DNA, they call on the body’s DNA repair system to fix them. If the damage is too severe to fix, TSGs can trigger apoptosis, which means the cell dies on its own.
Similar to oncogenes, which act as GO signals, tumor suppressor genes act as warning lights that halt cell division until DNA repair machinery intervenes and repairs them. However, mutations can compromise the protective activities of these genes by making them inactive. Even a recessive mutation can inactivate a tumor suppressor gene.
TP53, also known as the guardian angel of the genome, and Retinoblastoma protein are major tumor suppressor genes. TP53 mutations are found in more than half of all human cancers, making it one of the most common genes changed in cancer. Loss of RB1 function can cause cancers like retinoblastoma and other cancers like lung and breast tumors.
Cancer Development: The Imbalance Between Growth and Control
The perfect equilibrium between growth and control of cell division maintains the harmony of our body. However, once mutated, the oncogenes become hyperactive while the tumor suppressor genes become inactive. Therefore, the cells continue to grow unrestricted, evading the DNA repair machinery, while the mutations continue to accumulate, ultimately leading to the formation of tumors. These tumors grow out and eventually metastasize, traveling freely into the body and causing destruction at different sites. So, even a single mutation at a critical site of the genome can start off a deadly chain reaction in your body.
Carcinogens
Carcinogen is a substance or exposure that has the tendency to mutate your DNA and eventually cause unregulated cell growth—cancer. If you were aware of the number of carcinogens you encounter every day, you might be too terrified to leave your house. However, if we look beyond a normal day, you will see how inevitable these subtle threats are.
Cancer Causes – Environment and Lifestyle Choices
You get up and go outside to soak up the sun rays, but those pleasant beams contain ultraviolet radiation, which is one of the strongest carcinogens known to man. Damage is already occurring to your skin cells while you’re enjoying the sun, creating the conditions for mutations that may eventually result in skin cancer.
It’s Saturday! You decide to meet your friends at your favorite place. You settle on ordering a hotdog with a side of fries and then wash it down with a cocktail. No harm in that, right? Despite its deliciousness, the hotdog contains processed meat, nitrates, and nitrites, all of which directly contribute to an elevated risk of colon cancer. Those fries? Cooking potatoes at high temperatures can form acrylamide, a well-known carcinogen. While alcohol may be enjoyable at the time, your liver converts it into acetaldehyde, which directly destroys your DNA and increases your risk of developing breast, liver, and oral cancers.
By the end, you light up a cigarette to feel better. However, each puff is a blend of over 70 recognized carcinogens, including formaldehyde, arsenic, and benzene. With every drag, the risk increases, increasing your chance of developing throat, lung, and other cancers.
While stuck in traffic on your way home, you inhale the contaminated air without giving it any thought. But the small particulate matter and vehicle exhaust linger in the air and go into your lungs. Prolonged exposure to air pollution, which you breathe in with each breath, is believed to cause lung cancer.
Within a few hours, you have unintentionally come upon a carcinogenic minefield. Air pollution, alcohol, cigarettes, processed foods, and sunlight all seem harmless on their own, but when combined, they create a deadly network of cancer hazards.
Cancer Causes – a Genetic Legacy?
Although your lifestyle and environment determine your cancer risk, 5–10% of cancers are hereditary. These inherited malignancies originate from mutated genes inherited from one generation to the next. Once you inherit these faulty genes, your risk of getting some malignancies rises dramatically.
Li–Fraumeni syndrome and the BRCA1 and BRCA2 genes are major examples. BRCA1 and BRCA2 genes are a significant part of the DNA repair machinery, and inherited mutated BRCA genes increase your chances of developing breast and prostate cancer to 72% and 12%, respectively. A mutated TP53 gene present from birth can cause Li Fraumeni syndrome.
Cancer Causes—Aging, the rusting of a machine
Aging is one of the major cancer causes and also one of the strongest risk factors. As we age, our cells undergo numerous cycles of growth, division, and repair, which increases the likelihood of mutations occurring. These mutations, while harmless in the beginning, keep on accumulating in the genome with each cell cycle, and as we age, we reach a point where these mutations can wreak havoc inside our body, ordering our cells to divide relentlessly. Our body’s defenses against cancer—tumor suppressors and DNA repair machinery—weaken with time. They can no longer detect DNA damage and repair it as we age, leading to mutation accumulation and eventually cancer.
Conclusion
Various triggers can cause cancer, which is the unregulated division of body cells. It may be environmental or lifestyle choices-induced, genetic, or an age factor. The complex interplay of various triggers that cause cancer raises a common question in our minds: can we truly prevent tumors? How can we monitor mutations? Can we track changes that are so minute and nuanced? Although cancer may not be completely preventable, we can significantly reduce our risk by making decisions that consider the various risk factors that we can control. We can prevent our exposure to carcinogens such as tobacco and alcohol, shield ourselves from UV rays with sun protection, monitor our diet, and engage in regular exercise. Although complete prevention may not be achievable, early detection and risk reduction can significantly impact the disease’s fight.
FAQs
What is Cancer?
Cancer results from the abnormal cell division of any types of cells in the body, that eventually invade normal healthy cells and tissues and spread throughout the body through a property called metastasis. Any type of body cell can defy instructions and start dividing uncontrollably, leading to various cancer types.
What are Oncogenes? Give Examples
Oncogene are the mutated or over-expressed versions of normal genes which send out constant signals for increased cell division, growth, and survival tendency even when it is unnecessary. Different types of mutations like point mutation i.e., change in a single nucleotide base pair, gene duplication, i.e., occurrence of multiple copies of protooncogenes or even chromosomal translocation can lead to the transformation of a protooncogene into oncogenes. Over expressed RAS, RAF, MYC, JUN and FOS are some examples of Oncogenes
Explain the various Cancer Causes related to environmental and lifestyle choices.
Cancer can be caused by environmental and lifestyle choices like UV exposure, eating processed foods, tobacco and alcohol consumption, inherited, and age-induced.
How can Mutations be a one of the Cancer Causes?
Mutations in critical genes like protooncogenes, tumor suppressor genes, and DNA repair machinery can lead to the overexpression of oncogenes; inactivation of tumor suppressors and DNA repair machinery can lead to cancer.
References
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- Proto-oncogenes to Oncogenes to Cancer | Learn Science at Scitable. (n.d.). https://www.nature.com/scitable/topicpage/proto-oncogenes-to-oncogenes-to-cancer-883/
- Cooper, G. M. (2000). The Development and Causes of Cancer. The Cell – NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK9963/
- The Genetics of Cancer. (2024, August 8). Cancer.gov. https://www.cancer.gov/about-cancer/causes-prevention/genetics
- Genetic Mutations | Types of Mutations. (n.d.). American Cancer Society. https://www.cancer.org/cancer/understanding-cancer/genes-and-cancer/gene-changes.html
- Oncogenes, Tumor Suppressor Genes, and DNA Repair Genes. (n.d.). American Cancer Society. https://www.cancer.org/cancer/understanding-cancer/genes-and-cancer/oncogenes-tumor-suppressor-genes.html
- Causes. (2017, September 12). Stanford Health Care. https://stanfordhealthcare.org/medical-conditions/cancer/cancer/cancer-causes.html
- Booth, S. (2022, August 11). Common Carcinogens You Should Know. WebMD. https://www.webmd.com/cancer/know-common-carcinogens
- Cancer. (2024, September 30). Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/12194-cancer
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So informative….. thankyou for sharing your thoughts 🫶✨