An Introduction to Cancer

Sahasra Pokkunuri
students x students
7 min readDec 7, 2020

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(Image by Depositphotos)

No, cancer isn’t a “death sentence.” No, eating sugar doesn’t exacerbate cancer in an individual. No, cancer isn’t contagious.

These might seem like obvious facts, but they’re actually common misconceptions associated with this condition. If cancer isn’t any of these, then what exactly is it?

What is Cancer?

Cancer refers to a series of conditions characterized by the abnormal growth and division of cells. Essentially, an individual with cancer will have poorly-functioning cells that multiply out of control, which leads to a series of symptoms. Although there are different types of cancer, these “symptoms” include nausea, vomiting, dizziness, stomach discomfort, and several more.

One of the most well-known characteristics of cancer is a tumor, which is the “combined” growth of these abnormal cells in a particular space. Tumors don’t normally express inflammation and can be either benign or malignant.

Benign Tumors

In a benign tumor, the “cancerous” cells (tumors aren’t necessarily an indication of cancer) will not invade nearby tissue or spread throughout the body. Although these masses don’t normally cause any lethal conditions, they can be dangerous if in proximity with any vessels or nerves. These tumors can be removed surgically and typically don’t return once they leave the affect individual’s body. If a benign tumor ends up returning, it’s typically in the same region.

A CT scan of a benign tumor in the brain.
This CT scan shows a benign tumor in the brain (Image by Science Photo Library).

Malignant Tumors

Malignant tumors are almost always cancerous, and these are the types of tumors that need special attention if untreated. With malignant tumors, the cells involved have the capability to invade nearby tissue and metastasize (when cancerous cells migrate from the initial tumor, also called the primary tumor, to other regions in the body). These tumors grow extremely fast, and thus require immediate treatment/removal.

For example, cancerous lung cells (both in NSCLC and SCLC) might metastasize and start growing in lymph nodes, the brain, bones, and even the liver! Clearly, metastasis is a terrible occurrence that typically occurs when a cancer is not immediately treated.

An instance of metastasis in the lungs in a patient with lung cancer (Image by Public Domain).

How and Where Does Cancer Start?

Unlike most other conditions, cancer can start anywhere in the body. Whether it be liver or prostate cancer, cancerous cells can start growing virtually anywhere and begin the many complications associated with this condition.

Cancer is both a genetic and environmental condition. In some cases, changes to genetic code in DNA might trigger a variety of different factors that lead to cancer. While these changes might be inherited from one’s parents, cancer can also be caused by “naturally-occurring” mistakes made when cells divide throughout a person’s lifetime. The “naturally-occurring” mutations that might occur throughout over an individual’s lifespan is heavily influenced by environmental factors.

External factors such as sunlight, radiation, and substances like tobacco smoke contribute extensively to the development of cancer in one’s body. In particular, these conditions influence the presence of highly-unstable free radicals in the body, which are responsible for much of the body’s damage to essential macromolecules.

How Free Radicals Work

Throughout our lives, we are frequently exposed to a variety of environmental factors, such as sunlight and radiation. Such conditions will cause molecules known as free radicals to enter the body, where the free radicals typically lack an electron and are thus highly unstable. Without control, free radicals can easily cause damage to critical macromolecules in the body, including DNA!

To combat this issue, the intake of antioxidants is super important. When these superheroes enter the body, they’re able to donate an electron to the free radical and thus generate stability. The harmonious balance between free radicals and antioxidants is what prevents your body from facing complete destruction.

When there’s an imbalance (otherwise known as oxidative stress), however, this will immediately become a problem. Without the antioxidant molecules to control the presence of free radicals, the latter will continue to inflict damage throughout the body and cause major consequences. When free radicals have the capability to damage DNA, this leads to a variety of issues pertaining to cancer.

How an antioxidant manages to stabilize a free radical (Image by Wikimedia Commons).

Specific Genes Involved in Cancer

In a majority of cancers, the genetic changes brought on by free radicals and other factors will affect 3 types of genes: tumor suppressor genes, proto-oncogenes, and DNA repair genes. These critical genes are otherwise called the “drivers” of cancer due to their impact on the functionality of cancerous cells.

Tumor Suppressor Genes

Tumor suppressor genes are classified as a group of genes that regulate the presence of “bad” or “damaged” cells. They are primarily responsible for slowing cell division, repairing DNA, and determining which cells are meant to perform apoptosis (programmed cell death). When cell regulation is being performed smoothly, tumor suppressor genes are always on. In the case of cancer, the situation is entirely different.

Epigenetic factors refer to any external condition that impacts genetic material in some way. With regards to tumor suppressor genes, these factors can control when a particular gene is turned on or off. Since tumor suppressor genes are responsible for regulating the cell cycle and ensuring damaged cells aren’t freely moving throughout the body, turning them off will cause drastic consequences. Cell regulation will immediately come to a halt, as there are no longer any genes determining which cells are unfit to continue developing. In addition, cancerous cells will be rampant through the body without this critical regulation, inevitably leading to cancer.

The most common example of a tumor suppressor gene is the TP53 gene, which creates the p53 protein. If you remember from high school biology, this protein is responsible for the regulation of the cell cycle by making sure a developing cell doesn’t have any damage throughout the process. Improperly-functioning p53 plays a huge factor in many types of cancers!

This is the extremely complicated molecular diagram of the p53 protein (Image by Getty Images).

Proto-Oncogenes

Unlike tumor suppressor genes, the responsibilities of proto-oncogenes is the exact opposite. While tumor suppressor genes regulate the production of cells, proto-oncogenes promote the development of a cell. Specific functions of a proto-oncogene include stimulating cell division, inhibiting apoptosis, and preventing cell differentiation (the process where one cell type changes to another).

An important thing to note is the difference between proto-oncogenes and oncogenes. Oncogenes are actually the mutated form of proto-oncogenes that leads to the development of cancer, whereas proto-oncogenes are considered “normal.” This mutation can be caused by point mutation, gene amplification, and chromosomal translocation.

A point mutation occurs when several nucleotides in a DNA sequence are added, removed, or even changed into completely different base pairs.

Gene amplification is characterized by the creation of multiple copies of a particular gene. This might lead to certain proto-oncogenes being over-expressed, thus resulting in cancer-like results.

In chromosomal translocation, part of or an entire gene might be relocated to another chromosome, which results in increased expression of the proto-oncogene.

Oncogenes are an over-expressed form of proto-oncogenes; this over-expression will result in heightened cell production and rapid cell division, one of the key turmoils associated with cancer.

An extremely common proto-oncogene is the Ras gene, which has the capability to produce intracellular signal-transduction proteins; these proteins are responsible for remaining as on/off switches during a cell’s growth. However, a mutation to the protein encoded by the Ras gene (which is typically caused by a point mutation in the Ras proto-oncogene itself) results in continuously relayed signals of cell growth, leading to cancer.

An image of the Ras protein encoded by the Ras gene (Image by Science Photo Library).

DNA Repair Genes

Lastly, DNA repair genes code for proteins that correct DNA after replication during the cell cycle. When mutated, there is a lack of proteins correcting the mistakes made during DNA replication. This results in developed cells with damaged DNA, which might lead them to develop abnormally and transform into a cancerous cell. This might continue for the creation of many more cells, which could form malignant tumors and thus cause many complications in the body.

An example of a DNA repair gene is BRCA1 and BRCA2, which are most commonly affected in both breast and ovarian cancer. When either one of these genes are mutated, cells in these particular areas will develop with improperly-developed DNA. This ultimately leads to the symptoms associated with cancer, especially malignant tumors with the capability to metastasize.

The structure of the protein encoded by the BRCA1 gene (Image by Adobe Stock).

Key Takeaways

  • Cancer is a condition where the abnormal growth/division of cells causes a number of complications, the most common of which are tumors.
  • Cancer can be caused by both genetic and environmental factors. While it’s possible for internal DNA damage to lead to symptoms of cancer, external conditions such as sunlight and radiation may also contribute to the development of cancer.
  • In particular, three types of genes (when mutated) are responsible for the severity of cancer: tumor suppressor genes, proto-oncogenes, and DNA repair genes.

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