Cancer—a word that shakes you to the core, a feeling quite similar to the plot twists we in the Scream movie franchise, yet this one lingers. But what exactly is this murderous villain lurking around in our cells? Cancer is a multifaceted, global disease, one that’s so sneaky and evasive that our body’s protective services fail to eradicate it from our cells. Once cancer invades the cellular parts, it multiplies uncontrollably at a chaotic pace leading to the growth and spread of abnormal cells, throwing the entire system and functioning of the body out of tune.
Our body has over 36 trillion cells, all performing extremely specific functions through their particular roles. These cells are constantly growing, dividing, specialising and dying through a process called the cell cycle. A cell spends most of its life in interphase consisting of the G1, S, and G2 phases.
The G1 phase is where the cell primarily focuses on growth and preparing for the processes necessary for division, the cell also synthesizes various proteins and organelles, increasing in size to ensure that it has the resources required to continue the process. Afterwards, the cell progresses to the S phase, where DNA replication occurs. The "S" stands for DNA synthesis, as its responsible for duplicating the cell's genetic material precisely to ensure that each daughter cell will receive a complete and accurate set of chromosomes. After DNA replication is complete, the cell enters the G2 phase. This stage serves as a second checkpoint to ensure that everything is in order before the cell divides. During G2, the cell continues to grow and begins to organize and condense the newly replicated genetic material so that the proper segregation of chromosomes occurs later. Once it leaves interphase, it undergoes mitosis, a type of nuclear division. The cell undergoes cytokinesis, the final step of cell division, where the cytoplasm is divided, and two genetically identical daughter cells which then enter their own interphase and start a new round in the cell cycle.
The cell cycle is controlled by a series of checkpoints, which are regulated by proteins called cyclins and enzymes known as cyclin-dependent kinases (CDKs). These proteins ensure that cells only proceed to the next phase of the cycle when they see the cell has accurately regulated its DNA and segregated properly. If errors are detected, such as DNA damage, the cell cycle is paused to allow for repair. However, if the damage is too severe, the cell may undergo apoptosis, a form of programmed cell death, to prevent the propagation of damaged DNA.
Genes Involved
This regulation of the cell cycle is controlled by proto-oncogenes, tumour suppressor genes, and DNA repair genes. Proto-oncogenes promote cell division and survival, ensuring that cells divide when necessary. However, when a proto-oncogene is mutated or overexpressed, it can be activated to become an oncogene, driving the cell to divide uncontrollably. Activation can occur through gene variants where changes in the genetic code can cause an oncogene to be permanently turned on. These mutations can either be inherited or arise spontaneously during a person’s life due to errors in DNA replication. Gene duplication can lead to the production of excessive amounts of a particular protein which will lead to abnormal cell growth and the development of cancer. Epigenetic changes also activate the oncogene inadvertently by involving the addition of chemical groups to DNA or RNA, without altering the DNA sequence itself can possibly change gene activity. Moreover, chromosome rearrangements during cell division can result in the relocation of regulatory genes next to proto-oncogenes, causing continuous activation of these oncogenes.
Tumour suppressor genes act as the brakes on cell division.
They help prevent cells from dividing too quickly or in an uncontrolled manner.
If a tumour suppressor gene is inactivated or lost due to a mutation, the
brakes on cell division are released, allowing the cell to proliferate
unchecked, causing certain types of cancer. For example, when the TP53 gene, a
tumour suppressor gene, functions properly, it acts as a guardian of our cells,
preventing them from growing out of control. However, inherited mutations in
the TP53 gene can lead to a condition known as Li-Fraumeni syndrome. Families
affected by this syndrome have a higher risk of developing various types of cancer
because every cell in their body carries this altered TP53 gene. Moreover, changes
in the TP53 gene aren't just limited to those with inherited syndromes. In
fact, TP53 mutations are commonly found in cancer cells of individuals who
don't have a hereditary predisposition. These changes occur during a person's
lifetime and can give cancer cells a dangerous growth advantage. However, since
these mutations are acquired and confined to the cancer cells, they aren't
passed on to future generations.
DNA repair genes fix mistakes in the DNA, or else cause them
to die in the process called apoptosis. Changes in these genes cause more
mistakes and the cell to grow out of control. Just like other gene alterations,
changes in DNA repair genes like BRCA1 and BRCA2 can be inherited from a parent
or can develop during a person’s lifetime. Women who inherit a harmful mutation
in one of these genes face a higher risk of breast and ovarian cancer. However,
it's not just about inherited mutations—these gene changes can also occur in tumour
cells of people who didn’t inherit the mutations as develop over time,
contributing to the cancer's growth.
In conclusion, cancer is a disease cause by the uncontrolled growth of abnormal cells in the body which occurs when genes and systems involved within the cell cycle malfunction. Understanding these mutations as a global audience allow us to research and understand further to improve our chances of preventing, diagnosing, treating, and eventually winning the battle against cancer!
American Cancer Society (2022). Oncogenes, Tumor Suppressor Genes, and DNA Repair Genes. [online] www.cancer.org. Available at: https://www.cancer.org/cancer/understanding-cancer/genes-and-cancer/oncogenes-tumor-suppressor-genes.html#:~:text=Proto%2Doncogenes%20are%20genes%20that.
Britannica (2019). mitosis | Definition, Stages, Diagram, & Facts. In: Encyclopædia Britannica. [online] Available at: https://www.britannica.com/science/mitosis.
Brody, L. (2020). Cell Cycle. [online] National Human Genome Research Institute. Available at: https://www.genome.gov/genetics-glossary/Cell-Cycle.
Cooke, E. (2023). How many cells are in the human body? New study provides an answer. [online] livescience.com. Available at: https://www.livescience.com/health/anatomy/how-many-cells-are-in-the-human-body-new-study-provides-an-answer#:~:text=According%20to%20a%20new%20analysis.
Łukasik, P., Załuski, M. and Gutowska, I. (2021). Cyclin-Dependent Kinases (CDK) and Their Role in Diseases Development–Review. International Journal of Molecular Sciences, [online] 22(6), p.2935. doi:https://doi.org/10.3390/ijms22062935.

This comment has been removed by the author.
ReplyDeleteNice information
ReplyDeleteReally good information
ReplyDeleteGot to know something new and you explained it beautifully, appreciate the efforts.
ReplyDeleteNice information
ReplyDeleteWell done and keep it up! It looks professional!
ReplyDeleteIt can be very helpful for many patients to know where to look for help, especially if they lack funds. Providing information on resources for staying near hospitals, funding for checkups and therapy, and alternative therapies that are helping people can be invaluable. A blog dedicated to these topics could be very beneficial.