Table of ContentsView AllTable of ContentsBasic DifferencesHow Do Cells Become Cancerous?Technical DifferencesDifferences Among Cancer Cells
Table of ContentsView All
View All
Table of Contents
Basic Differences
How Do Cells Become Cancerous?
Technical Differences
Differences Among Cancer Cells
Cancercells are different from normal cells in how they grow, how they look, and what they do in the body. Even though cancer is common, there are actually many steps that a normal cell has to go through to become a cancerous cell.
This article will explain how cancer cells and normal, healthy cells are different. It covers the basic differences between cancer cells and normal cells, like how they grow and communicate. It also goes a bit deeper, covering technical differences between normal cells and cancer cells, including how they invade tissue in the body and “hide” from cancer treatments.
© Verywell, 2017.
How Common Is Cancer?
Basic Differences Between Cancer Cells and Normal Cells
There are many differences between cancer cells and normal cells in noncancerous (benign) or cancerous (malignant) tumors.
The major differences between normal cells and cancer cells relate to growth, communication, cell repair and death, “stickiness” and spread, appearance, maturation, evasion of the immune system, function and blood supply.
It’s these differences that account for how cancerous tumors grow and respond differently to their surroundings than benign tumors.
Growth
Normal cells stop growing (reproducing) when enough cells are present. For example, if cells are being produced to repair a cut in the skin, new cells are no longer produced when there are enough cells present to fill the hole (when the repair work is done).
In contrast, cancer cells don’t stop growing when there are enough cells present. Cancer cells reproduce rapidly before they have had a chance to mature. This continued replication often results in a tumor (a cluster of cancer cells) being formed.
Each gene in the body carries a blueprint that codes for a different protein. Some of these proteins are growth factors—chemicals that tell cells to grow and divide.
2:08Click Play to Learn About the Start and Characteristics of Cancer Cells
2:08
Click Play to Learn About the Start and Characteristics of Cancer Cells
How Do Oncogenes Cause Cancer?
Communication
Cell Repair and Cell Death (Homeostasis)
Homeostasis is the body’s way of ensuring all its processes are working properly. Homeostasis is one area where normal cells and cancer cells are very different.
To maintain homeostasis, normal cells are either repaired or die (undergoapoptosis) when they are damaged or get old. Cancer cells are either not repaired or do not undergo apoptosis.
For example, one protein called p53 has the job of checking to see if a cell is too damaged to repair, and if so, advise the cell to kill itself. If this protein p53 is abnormal or inactive (for example, from a mutation in thep53 gene), then old or damaged cells are allowed to reproduce.
The p53 gene is one type of tumor suppressor gene that code for proteins that suppress the growth of cells.
What Are Tumor Suppressor Genes?
Stickiness
Spread
Normal cells stay in the area of the body where they belong. For example, lung cells remain in the lungs. Some cancer cells may lack the adhesion molecules that cause stickiness, and are able to detach and travel via the bloodstream and lymphatic system to other regions of the body—they have the ability to spread (metastasize).
Once they arrive in a new region (such aslymph nodes, the lungs, the liver, or the bones) they begin to grow, often forming tumors far removed from the original tumor.
How Cancer Spreads
Appearance
Under a microscope, normal cells and cancer cells may look quite different. In contrast to normal cells, cancer cells often exhibit much more variability in cell size—some are larger than normal and some are smaller than normal.
In addition, cancer cells often have an abnormal shape—both the cell and thenucleus(the “brain” of the cell.) The nucleus appears both larger and darker than normal cells.
The reason for the darkness is that the nucleus of cancer cells contains excess DNA. Up close, cancer cells often have an abnormal number ofchromosomesthat are arranged in a disorganized fashion.
Maturation
Normal cells mature. Cancer cells, because they grow rapidly and divide before cells are fully mature, remain immature. Doctors use the termundifferentiatedto describe immature cells (in contrast to differentiated to describe more mature cells.)
Another way to explain this is to view cancer cells as cells that don’t “grow up” and specialize to adult cells. The degree of maturation of cells corresponds to the grade of cancer. Cancers are graded on a scale from 1 to 3 with 3 being the most aggressive.
Evasion of the Immune System
When normal cells become damaged, the immune system (via cells calledlymphocytes) identifies and removes them.
Function
Normal cells perform the function they are meant to perform, whereas cancer cells may not be functional.
For example, normalwhite blood cellshelp fight off infections. Inleukemia, the number of white blood cells may be very high, but since the cancerous white blood cells are not functioning as they should, people can be more at risk for infection even with an elevated white blood cell count.
The same can be true of substances produced. For example, normal thyroid cells produce thyroid hormones. Cancerous thyroid cells (thyroid cancer) may not produce thyroid hormone. In this case, the body may lack enough thyroid hormone (hypothyroidism) despite an increased amount of thyroid tissue.
Blood Supply
Cancer cells undergo angiogenesis even when growth is not necessary. One type of cancer treatment involves the use of angiogenesis inhibitors—medications that block angiogenesis in the body in an effort to keep tumors from growing.
Why Do Cells Turn Into Cancer?
There are proteins in the body that regulate cell growth. YourDNAcarries genes that are the blueprint for proteins produced in the body.
Some of these proteins are growth factors—chemicals that tell cells to divide and grow. Other proteins work to stop (suppress) growth.
It takes a combination of abnormalities to make a cancerous cell happen, rather than a single mutation or protein abnormality. It’s actually very difficult for a normal cell to become cancerous, which may seem surprising considering that one in three people will develop cancer in their lifetime.
Cancer Growth and Angiogenesis
A Deeper Dive Into the Technical Differences
This list contains further differences between healthy cells and cancer cells.
Evading Growth Suppressors
Mutations that result in any of these tumor suppressor genes being inactivated allow cancer cells to grow unchecked.
Invasiveness
What Is Invasive Ductal Carcinoma?
Energy Source
Normal cells get most of their energy (in the form of a molecule called ATP) through a process called the Krebs cycle, and only a small amount of their energy through a different process calledglycolysis.
Many types of cancer cells produce their energy through glycolysisdespite the presence of oxygen(Warburg phenomenon). Thus, the reasoning behind hyperbaric oxygen therapy is flawed. Sometimes hyperbaric oxygen may induce cancer growth.
Mortality/Immortality
Normal cells are mortal, that is, they have a lifespan. Cells aren’t designed to live forever, and just like the humans they are present in, cells grow old. Researchers are beginning to look at something calledtelomeres, structures that hold DNA together at the end of the chromosomes, for their role in cancer.
One of the limitations to growth in normal cells is the length of the telomeres. Every time a cell divides, the telomeres get shorter. When the telomeres become too short, a cell can no longer divide and the cell dies.
Cancer cells have figured out a way to renew telomeres so that they can continue to divide. An enzyme called telomerase works to lengthen the telomeres so that the cell can divide indefinitely—essentially becoming immortal.
Ability to “Hide”
Many people wonder why cancer can recur years, and sometimes decades after it appears to be gone (especially with tumors such asestrogen receptor-positive breast cancers). There are several theories about why cancers may recur.
In general, it’s thought that there is a hierarchy of cancer cells, with some cells (cancer stem cells) having the ability to resist treatment and lie dormant. This is an active area of research, and extremely important.
Why Does Cancer Come Back?
Genomic Instability
Normal cells have normal DNA and a normal number of chromosomes. Cancer cells often have an abnormal number of chromosomes and the DNA becomes increasingly abnormal as it develops a multitude of mutations.
Some of these are driver mutations, meaning they drive the transformation of the cell to be cancerous. Many of the mutations are passenger mutations, meaning they don’t have a direct function for the cancer cell.
For some cancers, determining which driver mutations are present (throughgenetic testing) allows providers to use targeted medications that specifically target cancer growth.
The development of targeted therapies such as EGFR inhibitors for cancers withEGFR mutationsis one of the more rapidly growing and progressing areas of cancer treatment.
Malignant and Benign Tumors: Key Differences
Can Cancer Cells Differ From Other Cancer Cells?
Given the many differences between cancer cells and normal cells, you might be wondering if there are differences between cancer cells themselves. That there may be a hierarchy of cancer cells—some having different functions than others—is the basis of discussions looking at cancer stem cells as discussed above.
We currently treat all the cancer cells in a tumor as being identical, but it’s likely that in the future, treatments will take some of the differences in cancer cells in an individual tumor into account.
Summary
Some of the differences between normal cells and cancer cells are well known, whereas others have only been recently discovered and are less well understood.
Many people become frustrated, wondering why we haven’t yet found a way to stop all cancers in their tracks. Understanding the many changes a cell undergoes in the process of becoming a cancer cell can help explain some of the complexity. There is not one step, but rather many, that are currently being addressed in different ways.
For researchers, understanding how cancer cells function differently from normal cells lays the foundation for developing treatments designed to rid the body of cancer cells without damaging normal cells.
In addition, cancer isn’t a single disease, but rather hundreds of different diseases. And even two cancers that are the same with regard to type and stage, can behave very differently. If there were 200 people with the same type and stage of cancer in a room, they would have 200 different cancers from a molecular standpoint.
How Many Types of Cancer Are There?
A Word From Verywell
As more is learned about what makes a cancer cell a cancer cell, more insight into how to stop that cell from reproducing—and perhaps even making the transition to becoming a cancer cell in the first place—is gained.
Progress is already being made in that arena, as targeted therapies are being developed which discriminate between cancer cells and normal cells in their mechanism.
Research on immunotherapy is just as exciting, as experts are finding ways to “stimulate” the immune system to do what it already know how to do—find and eliminate invaders.
Figuring out the ways in which cancer cells “disguise” themselves and hide has resulted in better treatments, and uncommonly, complete remissions, for some people with the most advanced solid tumors.
10 SourcesVerywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Mercadante AA, Kasi A.Genetics, Cancer Cell Cycle Phases.Vanneman M, Dranoff G.Combining immunotherapy and targeted therapies in cancer treatment.Nat Rev Cancer. 2012;12(4):237-51. doi:10.1038/nrc3237Chandran R, Hakki M, Spurgeon S.Infections in Leukemia. In: Azevedo L, editor.Sepsis: An Ongoing and Significant Challenge. IntechOpen; 2012. doi:10.5772/50193Carter Y, Sippel RS, Chen H.Hypothyroidism after a cancer diagnosis: etiology, diagnosis, complications, and management.Oncologist. 2014;19(1):34-43. doi:10.1634/theoncologist.2013-0237Alexandrov LB, Ju YS, Haase K, et al.Mutational signatures associated with tobacco smoking in human cancer.Science. 2016;354(6312):618-622. doi:10.1126/science.aag0299National Cancer Institute.Cancer-causing substances in the environment.American Cancer Society.Lifetime risk of developing or dying from cancer.Moen I, Stuhr LE.Hyperbaric oxygen therapy and cancer–a review.Target Oncol.2012;7(4):233-42. doi:10.1007/s11523-012-0233-xArtandi SE, Depinho RA.Telomeres and telomerase in cancer.Carcinogenesis. 2010;31(1):9-18. doi:10.1093/carcin/bgp268Wheeler DL, Dunn EF, Harari PM.Understanding resistance to EGFR inhibitors-impact on future treatment strategies.Nat Rev Clin Oncol.2010;7(9):493-507. doi:10.1038/nrclinonc.2010.97Additional ReadingDeBaradinis, R. et al.The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.Cell Metabolism. 2008;7(1):11-20.National Cancer Institute.SEER Training Module. Cell Biology of Cancer.National Cancer Institute.What is Cancer?Nio, K., Yamashita, T., and S. Kaneko.The Evolving Concept of Liver Cancer Stem Cells.Molecular Cancer. 2017;16(1):4.
10 Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Mercadante AA, Kasi A.Genetics, Cancer Cell Cycle Phases.Vanneman M, Dranoff G.Combining immunotherapy and targeted therapies in cancer treatment.Nat Rev Cancer. 2012;12(4):237-51. doi:10.1038/nrc3237Chandran R, Hakki M, Spurgeon S.Infections in Leukemia. In: Azevedo L, editor.Sepsis: An Ongoing and Significant Challenge. IntechOpen; 2012. doi:10.5772/50193Carter Y, Sippel RS, Chen H.Hypothyroidism after a cancer diagnosis: etiology, diagnosis, complications, and management.Oncologist. 2014;19(1):34-43. doi:10.1634/theoncologist.2013-0237Alexandrov LB, Ju YS, Haase K, et al.Mutational signatures associated with tobacco smoking in human cancer.Science. 2016;354(6312):618-622. doi:10.1126/science.aag0299National Cancer Institute.Cancer-causing substances in the environment.American Cancer Society.Lifetime risk of developing or dying from cancer.Moen I, Stuhr LE.Hyperbaric oxygen therapy and cancer–a review.Target Oncol.2012;7(4):233-42. doi:10.1007/s11523-012-0233-xArtandi SE, Depinho RA.Telomeres and telomerase in cancer.Carcinogenesis. 2010;31(1):9-18. doi:10.1093/carcin/bgp268Wheeler DL, Dunn EF, Harari PM.Understanding resistance to EGFR inhibitors-impact on future treatment strategies.Nat Rev Clin Oncol.2010;7(9):493-507. doi:10.1038/nrclinonc.2010.97Additional ReadingDeBaradinis, R. et al.The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.Cell Metabolism. 2008;7(1):11-20.National Cancer Institute.SEER Training Module. Cell Biology of Cancer.National Cancer Institute.What is Cancer?Nio, K., Yamashita, T., and S. Kaneko.The Evolving Concept of Liver Cancer Stem Cells.Molecular Cancer. 2017;16(1):4.
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
Mercadante AA, Kasi A.Genetics, Cancer Cell Cycle Phases.Vanneman M, Dranoff G.Combining immunotherapy and targeted therapies in cancer treatment.Nat Rev Cancer. 2012;12(4):237-51. doi:10.1038/nrc3237Chandran R, Hakki M, Spurgeon S.Infections in Leukemia. In: Azevedo L, editor.Sepsis: An Ongoing and Significant Challenge. IntechOpen; 2012. doi:10.5772/50193Carter Y, Sippel RS, Chen H.Hypothyroidism after a cancer diagnosis: etiology, diagnosis, complications, and management.Oncologist. 2014;19(1):34-43. doi:10.1634/theoncologist.2013-0237Alexandrov LB, Ju YS, Haase K, et al.Mutational signatures associated with tobacco smoking in human cancer.Science. 2016;354(6312):618-622. doi:10.1126/science.aag0299National Cancer Institute.Cancer-causing substances in the environment.American Cancer Society.Lifetime risk of developing or dying from cancer.Moen I, Stuhr LE.Hyperbaric oxygen therapy and cancer–a review.Target Oncol.2012;7(4):233-42. doi:10.1007/s11523-012-0233-xArtandi SE, Depinho RA.Telomeres and telomerase in cancer.Carcinogenesis. 2010;31(1):9-18. doi:10.1093/carcin/bgp268Wheeler DL, Dunn EF, Harari PM.Understanding resistance to EGFR inhibitors-impact on future treatment strategies.Nat Rev Clin Oncol.2010;7(9):493-507. doi:10.1038/nrclinonc.2010.97
Mercadante AA, Kasi A.Genetics, Cancer Cell Cycle Phases.
Vanneman M, Dranoff G.Combining immunotherapy and targeted therapies in cancer treatment.Nat Rev Cancer. 2012;12(4):237-51. doi:10.1038/nrc3237
Chandran R, Hakki M, Spurgeon S.Infections in Leukemia. In: Azevedo L, editor.Sepsis: An Ongoing and Significant Challenge. IntechOpen; 2012. doi:10.5772/50193
Carter Y, Sippel RS, Chen H.Hypothyroidism after a cancer diagnosis: etiology, diagnosis, complications, and management.Oncologist. 2014;19(1):34-43. doi:10.1634/theoncologist.2013-0237
Alexandrov LB, Ju YS, Haase K, et al.Mutational signatures associated with tobacco smoking in human cancer.Science. 2016;354(6312):618-622. doi:10.1126/science.aag0299
National Cancer Institute.Cancer-causing substances in the environment.
American Cancer Society.Lifetime risk of developing or dying from cancer.
Moen I, Stuhr LE.Hyperbaric oxygen therapy and cancer–a review.Target Oncol.2012;7(4):233-42. doi:10.1007/s11523-012-0233-x
Artandi SE, Depinho RA.Telomeres and telomerase in cancer.Carcinogenesis. 2010;31(1):9-18. doi:10.1093/carcin/bgp268
Wheeler DL, Dunn EF, Harari PM.Understanding resistance to EGFR inhibitors-impact on future treatment strategies.Nat Rev Clin Oncol.2010;7(9):493-507. doi:10.1038/nrclinonc.2010.97
DeBaradinis, R. et al.The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.Cell Metabolism. 2008;7(1):11-20.National Cancer Institute.SEER Training Module. Cell Biology of Cancer.National Cancer Institute.What is Cancer?Nio, K., Yamashita, T., and S. Kaneko.The Evolving Concept of Liver Cancer Stem Cells.Molecular Cancer. 2017;16(1):4.
DeBaradinis, R. et al.The biology of cancer: metabolic reprogramming fuels cell growth and proliferation.Cell Metabolism. 2008;7(1):11-20.
National Cancer Institute.SEER Training Module. Cell Biology of Cancer.
National Cancer Institute.What is Cancer?
Nio, K., Yamashita, T., and S. Kaneko.The Evolving Concept of Liver Cancer Stem Cells.Molecular Cancer. 2017;16(1):4.
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