Cancer Cells: How They Start and Characteristics

Cancer cells differ from normal cells in the body in many ways. Normal cells become cancerous when a series of mutations leads the cell to continue to grow and divide out of control, and, in a way, a cancer cell is a cell that has achieved a sort of immortality. Also unlike normal cells that remain in the region where they began, cancer cells have the ability to both invade nearby tissues and spread to distant regions of the body. We will look at the process that leads to the development of a cancer cell, some of the ways in which cancer cells differ from normal cells, and why the body may not recognize cancer cells and destroy them as it does other "foreign" cells.

Diagram of cancer cells / Stock Photo©vitanovski


There are as many types of cancer cells as there are types of cancer. Of the hundred-plus types of cancer, most are named for the type of cancer cells in which it began. Carcinomas are cancers that arise in epithelial cells that line bodily cavities. Sarcomas are cancers that arise in mesenchymal cells in bones, muscles, blood vessels, and other tissues. Leukemias, lymphomas, and myeloma are "blood-related cancers" that are arise from the bone marrow (leukemias and multiple myelomas) or the lymphoid tissues (lymphomas)  and  "fed" by nutrients in the bloodstream and lymph fluid such that they don't need to form tumors. Just as cancers may behave differently from one another, not all cancer cells behave the same way.

How Do They Start?

Cancer cells appear through a series of genetic and epigenetic changes. Some of these changes may be either inherited or more often, caused by carcinogens (cancer-causing substances) in our environment. In general, solid tumors, contain multiple mutations. Interestingly, the metastatic process that is the main culprit for the high mortality of advanced cancers is thought to be caused mostly by epigenetic changes as no specific genetic alterations have been found in metastases. It also helps explain a genetic predisposition to cancer. A genetic predisposition does not mean you will get cancer, but, simplistically, if a few mutations are already in place, it will likely take fewer acquired mutations for a cell to become cancerous.

The process of normal cells becoming cancer often goes through stages in which the cell becomes progressively more abnormal appearing. These stages may include hyperplasia, dysplasia, and finally cancer. You may also hear this described as differentiation. Early on a cell may look much like normal cells of that organ or tissue, but as progression occurs, the cell becomes increasingly undifferentiated. This is, in fact, why sometimes the original source of cancer cannot be determined.

What Makes Them Divide and Grow

A cancer cell can have thousands of mutations, but only a certain number of these genetic changes in cancer cells cause cancer to divide and grow. Mutations which result in the growth of the cancer cells are referred to as "driver mutations," whereas other mutations are considered "passenger mutations." Normal genes called proto-oncogens can become "oncogenes" when mutated and code for proteins that drive the growth of cancer, and give cancer its immortality. Tumor suppressor genes, in contrast, are genes within the cell which tell cells to slow down and stop growing, repair damaged DNA, or tell cells when to die.

Most cancer cells have mutations in both oncogenes and tumor suppressor genes which lead to their behavior.

Cancer Cells vs. Normal Cells

There are many important differences between cancer cells and normal cells. Some of these include:

  • Growth: Normal cells grow as a part of growth and development such as during childhood, or to repair injured tissue. Cancer cells continue to grow (reproduce) even when further cells are not needed. Cancer cells also fail to listen to signals that tell them to stop growing or commit cell suicide (apoptosis) when the cells become old or damaged.
  • Ability to invade nearby tissues: Normal cells respond to signals from other cells which tell them they have reached a boundary. Cancer cells do not respond to these signals and extend into nearby tissues often with finger-like projections. This is one reason why it is difficult at times to surgically remove a cancerous tumor. The word cancer, in fact, is derived from the Greek word carcinos for crab, referring to these claw-like extensions into neighboring tissues.
  • Ability to spread (metastasize) to other regions of the body: Normal cells make substances called adhesion molecules that cause them to stick to nearby cells. Some cancer cells, lacking the stickiness caused by these adhesion molecules, can break free and float to other regions of the body. They may travel to nearby tissue, or through the bloodstream and lymphatic system to areas of the body far from the original cancer cell—for example, a lung cancer cell may travel (metastasize) to the lymph nodes, brain, liver, or the bones.
  • Immortality: Most normal cells, like humans, have a limited lifespan. When they reach a certain age, they die. Cancer cells, in contrast, have developed a way to “defy” death. On the end of our chromosomes is a structure known as a telomere. Every time a cell divides, its telomeres become shorter. When the telomeres become short enough, the cells die. Cancer cells have figured out a way to restore their telomeres so that they don’t continue to shorten as the cell divides, thus, in a way, making them immortal.

The ability to invade and metastasize is very important in differentiating a cancer cell from a normal healthy cell, but there are many other important distinctions as well.

Cancer Cell
  • May keep growing

  • May invade nearby tissues

  • May spread to other regions of the body

  • Can be immortal

Normal Cell
  • Grows when needed

  • Stays within tissue boundaries

  • Sticks to nearby cells

  • Has defined lifespan

Why Doesn’t the Body Recognize Cancer Cells as Abnormal and Destroy Them?

A good question is, "Why don’t our bodies recognize and remove cancer cells as they would, say a bacteria or virus?" The answer is that most cancer cells are indeed detected and removed by our immune systems. Cells in our immune cells called natural killer cells have the job of finding cells that have become abnormal so that they can be removed by other cells in our immune system. Cancer cells remain alive either by evading detection (they disguise themselves in different ways) or by inactivating the immune cells that come to the scene.

The ability of the immune system to recognize and eliminate cancer cells is thought to be responsible for the uncommon but well-documented phenomena of some cancers going away without treatment of (the spontaneous remission of cancer.) This process also lies at the crux of the new field of cancer treatment known as immunotherapy.

Cancer Cells Keep Changing

Once a cancer has formed, the cells don't remain the same, but rather continued mutations may occur. This, in fact, is why resistance develops to chemotherapy and targeted therapy drugs in time. The cancer cell develops a mutation that allows it to bypass the damaging effects of these treatments.

That cancer cells change is very important in treatment. For example, a breast cancer that is estrogen-receptor positive may be estrogen-receptor negative when it recurs or spreads. It also helps explain whey cancer cells in different parts of a tumor may be different. This is referred to as "heterogenicity" and is important in diagnosis and treatment as well.

How Do Cancer Cells Differ From Precancerous Cells?

Precancerous cells may look abnormal and similar to cancer cells but are distinguished from cancer cells by their behavior. Unlike cancer cells, precancerous cells do not have the ability to spread (metastasize) to other regions of the body.

An often confusing condition is that of carcinoma-in-situ (CIS.) Carcinoma in situ consists of cells with the abnormal changes found in cancer cells, but since they have not spread beyond their original location (or technically, have not gone beyond something called the basement membrane,) they are not technically cancer. Since CIS can turn into cancer, it is usually treated as early cancer.

Final Thoughts

An analogy to describe cancer cells has been that of a car. The growth of the cells can be pictured as a car that has the accelerator stuck down. At the same time, the brakes don’t work (the cells doesn’t respond to tumor suppressor proteins.)

We can take this analogy a step further. The invasion of cancer cells can be viewed as a car breaking through a gate into a gated community. Normal cells respond to signals from neighboring cells that say “this is my boundary, stay out.” Cancer cells are antisocial in other ways as well. As they “gang” up with other cancer cells, all of which are becoming more immature in their actions over time (due to rapid division), they spread out and invade other communities as well.

But just as crime hasn’t overridden the United States, there are many police officers (checkpoints) that keep the majority of cells in the body in line.

It is actually very difficult for a normal cell to become a cancer cell. It has to be abnormal in ways that facilitate growth, inhibit repair and death, ignore signals from neighbors, and achieve a form of immortality. This is why cancer isn’t caused by a single mutation, but rather by a series of mutations. But considering that a billion cells in our bodies divide every day, something is bound to go wrong and mutations occur once in a while. And they do, for an estimated 1.6 million people in the United States each year.

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  1. Cancer. US National Library of Medicine. 2017.

  2. What does it mean to have a genetic predisposition to a disease?. National Library of Medicine. 2020.

  3. Hyperplasia. NCI Dictionary of Cancer Terms.

  4. Changes in genes. American Cancer Society. 2014.

  5. What is Cancer?. National Cancer Institute. 2015.

  6. Kim E, Kim JY, Smith MA, Haura EB, Anderson ARA. Cell signaling heterogeneity is modulated by both cell-intrinsic and -extrinsic mechanisms: An integrated approach to understanding targeted therapy. PLoS Biol. 2018;16(3):e2002930.  doi:10.1371/journal.pbio.2002930

  7. Overview of Cancer. Johns Hopkins Medicine.

  8. Adjiri A. Tracing the path of cancer initiation: the AA protein-based model for cancer genesis. BMC Cancer. 2018;18(1):831.  doi:10.1186/s12885-018-4739-1

  9. Marcus A, Gowen BG, Thompson TW, et al. Recognition of tumors by the innate immune system and natural killer cells. Adv Immunol. 2014;122:91-128.  doi:10.1016/B978-0-12-800267-4.00003-1

  10. Peters GJ. Cancer drug resistance: a new perspective. CDR. 2018;1:1-5.  doi:10.20517/cdr.2018.03

  11. Treatment Options for Testicular Cancer, by Type and Stage. American Cancer Society. 2019.

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