What Makes a Healthy Cell Turn Cancerous?

When someone receives a cancer diagnosis, one of the first questions that arises is: “How do healthy cells become cancer cells?” Understanding this fundamental process can help patients and their families comprehend what’s happening in the body.

At its core, healthy cells turn cancerous when they experience specific genetic changes that cause the cell to become immortal. Instead of undergoing regular cellular death (apoptosis), these transformed cells continue to live indefinitely, no longer carrying out their normal functions and often impeding other cells from performing theirs. While some cancers have genetic predispositions, more often the genetic changes that make a cell cancerous are triggered by external factors such as exposure to chemicals, radiation, or lifestyle choices.

This article explains the process of how cancer cells form, what makes normal cells become cancerous, and factors that influence this transformation.

All cells within the body have a purpose. Red blood cells bind to oxygen and deliver it to other cells in the body. Epithelial cells come together to produce skin that protects us from outside elements. Neurons enable thought and the sharing of information within the brain, followed by nerve impulses throughout the body.

Regardless of their purpose, different cells have different typical lifespans. However, some cells gain an unusual capability—immortality. Cells that have obtained immortality do not die, but they lose their basic functions in the process. Unfortunately, these cells can come from anywhere in the body and form the basis of cancer.

All cancer cells form tumors, or growths within the body, and they may form in any tissue. However, not all cells that result in cyst or tumor growths have true cancerous characteristics. They may impede normal function, but they do not threaten the function of surrounding tissues. Unfortunately, these cells can also progress and become cancerous, resulting in the spread of tumors that result in major disruptions to normal, healthy tissues. To eliminate the confusion and uncertainty, people need to know a few things about cancerous cells and how a healthy cell transforms into cancerous material.

Cancer is a broad term used to describe the condition that arises from a growth due to cancerous cells. Cancerous cells refer to cells that loose their preprogrammed apoptosis, or cellular death. When a single cell achieves this level of immortality, its subsequent cells, created through the process of mitosis (cell division) have the same quality. Over time, the cells continue to grow and divide, resulting in a tumor. According to the National Cancer Institute, this series of events disrupts the “orderly process,” and cancerous cells may influence nearby healthy cells to become cancerous as well.

Not all growths have the same characteristics of cancerous growths. In these cases, the tumor is known as benign, meaning it is not infiltrating into adjacent structures or tissues. Cancerous tumors, on the other hand, spread and invade nearby tissues. Not infrequently, cancerous cells may break free from the tumor and travel to distant places in the body. Malignancy refers to the capability of the cell to spread locally and distantly. When cancerous cells spreads to a different location and continue to grow it is referred to as a metastasis.

Cancer involves a genetic change to the cell that results in immortality. All cancers have a foundation within genetics. Their genetic structure becomes compromised and, depending on the severity of the mutation, the cell begins to perform unnecessary and even harmful functions. In fact, the average cancerous cell contains 60 or more mutations. This is a major hurdle in identifying exactly which change resulted in the development of cancer.

Genetic changes often affect proto-oncogenes, tumor suppressor genes, and genes that repair DNA. These three genes form the primary driving forces of cancer.

The first two genes are involved in cellular growth and division. DNA repair genes are those that would otherwise identify a cell with damaged nuclear material, such as DNA, repairing the cell. Unfortunately, mutations may occur within these genes, resulting in cancerous cells.

What specifically makes a cell cancerous at the genetic level? The transformation typically requires multiple mutations affecting how the cell functions. These mutations can impact:

1. Cell growth signals – causing cells to multiply uncontrollably
2. Growth inhibitors – removing natural brakes on cell division
3. Apoptosis (programmed cell death) – making cells immortal
4. DNA repair mechanisms – preventing the correction of further mutations
5. Angiogenesis – allowing tumors to create their own blood supply
6. Tissue invasion capability – enabling cancer to spread

Understanding how healthy cells become cancer cells helps explain why cancer treatments often target specific genetic pathways.

Carcinogens describe a host of chemicals that result in the genetic mutation of cellular tissues after exposure. Depending on the substance in question, a single exposure incident may be enough to result in a cancerous cell. Others take time to develop.

For instance, spending time in sunlight is necessary to enable the production of vitamin D in the skin. The radiation within sunlight serves as the catalyst for this change. But when exposure is repetitive and is matched with other genetic or systemic aberrations, it can result in mutations to cellular tissue which could become cancer.

The elements and natural materials, such as molds, bacteria and other pathogens, have the potential to drive genetic change within cells as well. In these cases, cancer arises from the repetitive demand for cellular replacement or proliferation. More cells increase the risk for a mutation, and the very cause of proliferation may contribute to mutation.

Consider the case of melanomas. Melanoma is a cancer of the melanocytes, cells within the skin that secret a UV-blocking substance, melanin. That substance is what gives people a tan and determines skin color. More melanin amounts to darker skin, providing additional protection against damaging sunlight.

Prolonged exposure will trigger melanocytes to divide, resulting in the release of more melanin to protect the body. Unfortunately, the same trigger that resulted in their buildup, also known as proliferation, may lead to mutation within the genetic structure of the cell. Since all cellular activities are the result of genetic coding, damage may lead to the inability to undergo apoptosis. As a result, a tumor begins to form, ending in this deadly form of skin cancer.

An individual’s lifestyle choices also affect the risk of mutations within cells.  The list of potentially cancerous lifestyle influences is extensive, and can affect more than 100 types of cancer, from prostate cancer to breast cancer.

For example, smoking, heavy alcohol consumption, failure to maintain a proper body mass index (BMI), sedentary lifestyles and poor nutrition increase risk for cancer. When it comes to smoking, the repeat exposure to the toxins within tobacco smoke may lead to mutation within tissues of the bronchioles, resulting in lung cancer.

Such lifestyle choices increase the chances of mutation within healthy cells. Unfortunately, cancer cells’ ability to invade virtually any body tissue means treatment must be specific to each person and the unique tumors and cancerous cells within the body.

Not all risk factors for cancer derive from lifestyle choices or routine activities. Instead, the biggest risk factor for cancer in general is age. In fact, the majority of cancer cases, 87 percent, are diagnosed in people over age 50, according to the American Cancer Society. Those in this age range are likely to have the longest exposure to all factors that affect the risk of a healthy cell becoming cancerous. In addition, their immune systems may diminish, resulting in a decreased ability to identify and destroy cancerous cells within the body.

Another uncontrollable factor exists—a person’s genetic structure as defined at the time of conception. Genetic anomalies may result in changes to the formation of proteins that would usually repair damaged cells. Damaged cells have the potential to become cancerous. If a parent possesses genes that do not prescribe the correct course of action, the parent may pass such genes along to children. While unknown genetic factors have traditionally been blamed for causing most cancers, more recently studies suggest that epigenetic factors, such as the various toxins and insults the body is in contact with, could be the source of most cancers.  Mitochondrial dysfunction disrupting the cellular milieu appears to predispose the cell to DNA and other damages, leading to an environment right for cancer. This is being studied in more detail.

Understanding how healthy cells become cancer cells is an important first step for patients and families navigating a cancer diagnosis. While healthcare providers cannot always identify the specific cause of an individual’s cancer, knowing the general mechanisms helps explain treatment approaches.

For those with a family history of cancer, genetic predisposition, or exposure to risk factors, working with oncology specialists who can create a personalized treatment plan is essential. Depending on your specific situation, treatments may include radiation therapy, chemotherapy, immunotherapy, targeted therapies, or integrated approaches.

Remember that cancer care is constantly evolving with new research into what makes cells cancerous leading to more effective treatments. Choose a cancer treatment center that offers comprehensive care tailored to your specific needs, such as Southeast Radiation Oncology Group (SERO). Connect with us by requesting a consultation online or calling 704-333-7376 today.