Our Body Continually Fighting Cancer Cells

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Humans are a remarkable amalgamation of countless cells, with the average person boasting an astounding 30 trillion cells, complemented by an additional 40 trillion bacteria thriving within our digestive tract. Although our bodies consist of trillions of cells, they do not always operate in perfect harmony to sustain our well-being. Within this intricate symphony of cellular activity, some cells seem determined to seize nutrients for themselves, often taking the form of mutated cells that defy regulation and continue to proliferate. These rogue cells, aptly known as cancer cells, persistently expand and endeavor to develop tumors. It's a continuous struggle within our bodies, with one cell or another occasionally going rogue. However, our bodies have evolved robust defense mechanisms to counteract such deviations.

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Cancers are regarded as abnormal growth of cells but if are to examine cancer properly, it describes over 200 diseases that differs from one another. People who suffer from different cancers experience different events and their chances of survival differ. A person suffering from prostrate cancer have a 98.6% chance of surviving the next five years but a person diagnosed with Diffuse Intrinsic Pontine Glioma has less than 1% chance of surviving the next 5 years. The same word cancer but different type. While different cancers have different characteristics, they all arise from a series of mutation which occurs as a result of changes in the DNA of cells.

Mutation is cells occur as a result of a few things including cell division because cell needs to reproduce and create new cells so as to be able to keep the body alive. The cell has to make its cells symmetrical (identical). Humans have 4 to 6 pieces of DNA in the form of chromosomes which span about 6 billion base pair which has to be replicated. A base pair is the fundamental unit of DNA. If the duplication of all the 6 base pair isn't correct, then there will be a mutation accidentally.

Asides division, mutation can also occur from external sources which includes exposure to UV light, radiation and chemicals. The UV light from the sun is partially absorbed by the DNA and when this occurs, it can lead to a distort in the shape of DNA and can lead to mutation. Our DNA also possesses ancient pieces of viruses and those wired fragment can cause mutation as they jump around the DNA.


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While all these can happen to our DNA, our DNA have found ways to repair themselves. This can be done via base excision repair, nucleotide excision repair, mismatch repair, and homologous recombination. Nucleotide Excision Repair helps to repair mutations caused by UV light where a protein notices a damaged DNA strand, then another protein removes the damaged DNA strand, then DNA polymerase adds the missing DNA strand to the DNA. With this the body helps to reduce the number of mutated DNA.

Additionally, the body employs programmed cell death, or apoptosis, as a strategy to reduce mutation risk. Genes like tp53 produce proteins like p53, which instruct cells to halt their growth until DNA is repaired. If the repair process fails, these proteins can induce cell death. Nevertheless, when these proteins malfunction, it can pave the way for cancer to develop.

In essence, our bodies are continually engaged in a complex dance to safeguard our genetic integrity, repair DNA mutations, and prevent the emergence of cancer. These intricate mechanisms exemplify the remarkable resilience and adaptability of the human body in its perpetual struggle against cellular abnormalities.



Reference



https://www.nationalgeographic.com/science/article/160111-microbiome-estimate-count-ratio-human-health-science
https://www.ncbi.nlm.nih.gov/books/NBK279410/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4991899/
https://www.ncbi.nlm.nih.gov/books/NBK20362/
https://www.ncbi.nlm.nih.gov/books/NBK560640/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5474181/
https://www.nature.com/scitable/topicpage/dna-damage-repair-mechanisms-for-maintaining-dna-344/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117903/
https://www.ncbi.nlm.nih.gov/books/NBK22268/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852800/

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