Differences Oncogenes and Tumor Suppressor Genes how Cancer Starts

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For a cell to become cancerous, it generally must have both defective proto-oncogenes (also known as oncogenes) and defective tumor suppressor genes.

The terms oncogene and tumor-suppressor gene each represent a category of genes, rather than name a specific gene. Both categories contribute to the transformation of a normal cell into a cancerous cell. They differ from each other in two ways – how they are inherited and how they function. The information presented in this article summarizes and explains current research results as of October 24, 2010. Cancer research is making great strides, so this information could become partially obsolete at any time in the future.

Background Information

To understand the differences between oncogenes and tumor suppressor genes you need to know some genetics vocabulary and facts.You also need some basic information about cancers.

A gene is the section of the DNA molecule that codes for one specific protein. That protein can be part of the body’s structure, or it can be an enzyme that determines a chemical reaction in the body.

There are two versions of each gene in cells - except for gametes (eggs and sperm). Each version is called an allele. A person inherits one allele from his mother and one from his father. Often the alleles are identical, but other times they are different. Either situation can be normal for some genes and abnormal for others.

Each cell has many kinds of proteins that each play a different role in the cell cycle.

There are many kinds of cancer. Breast cancer and skin cancer are two examples. You probably know that the breasts and the skin are both organs of the body, but each of these organs has more than one type of tissue. Any single tissue consists of normal cells that are all alike. The most basic difference between one type of  breast cancer and another is the kind of tissue where the cancer starts – the cell type that becomes abnormal.

When a gene is not normal, that means that the process of DNA replication went wrong somewhere. That can happen when eggs and sperm are produced in the bodies of the parents. It can also happen during the cell cycle of the offspring.

What an Oncogene Is

A proto-oncogene is a normal gene that codes for a protein that plays a role in cellular division. There are many proto-oncogenes that each plays a different role in cellular division. That’s because the process has several steps and sub-steps. (An analogy is getting ready for your day. There are several steps to starting your day - getting-out of bed, going to the bathroom, showering, dressing, eating breakfast. These are the steps. Getting out of bed – the first step, has sub-steps. One sub-step would be sitting-up, another would be bending your knees, etc.)

The main thing all proto-oncogenes have in common is that they each produces a protein that must be present in order for the cell division process to start. The second thing they have in common is that each must respond to a tumor-suppressor protein when it signals for the cell division to stop.

A proto-oncogene that has mutated – has become abnormal – is  called an oncogene. An oncogene does not respond to the “stop-signal” given by the tumor-suppressor protein.

Each allele for the proto-oncogene must produce a molecule of the protein that starts the cell division. If one allele has mutated to become an oncogene, the protein it makes will be abnormal. That molecule will repeatedly signal for cell-division to occur. There are no “brakes” to stop the process. The result is a tumor that continues to grow without some kind of cancer treatment. Obviously if both alleles are mutant the cancer will be more aggressive.

What a Tumor-Suppression Gene Is

A tumor-suppressor gene codes for a protein that acts as a “stop” signal for the cell division process. The protein must be normal to signal for the process to stop. A mutant gene for a tumor-suppressor protein will result in an abnormal protein – one that can’t do its job. For a tumor to form, both alleles of this gene must be abnormal. If one is normal and the other abnormal, the normal one will produce the normal protein which will stop the cell division process. That will not result in a tumor.


An oncogene allele will result in cancer, even though its partner allele is a proto-oncogene (a normal one). Cell division will keep happening, because one of the proteins – the one from the mutant allele does not “know how” to stop. It is as though it is blind to the “stop” signal of the tumor -suppressor protein. If both alleles are mutant, of course, the tumor will grow faster.

A mutant tumor-suppressor allele will result in a protein that will not work, but that matters little if the partner allele is normal. The normal one will produce the tumor-suppressant protein that stops the cell division. A tumor will form only if both alleles are mutant, because then no effective protein will form. The “stop” signal won’t occur.

Two mutant tumor-suppressor genes inevitable result in a tumor, because there will be no response to a “stop” signal, since no signal occurs.

One mutant tumor-suppressor gene alone will not result in a tumor. The normal gene does its job correctly.

One oncogene results in a tumor, regardless of the stop signals.

Two oncogenes result in a faster growing tumor.


The primary differences between oncogenes and tumor-suppressor genes are in the roles they play and how destructive a single mutation within them is. Oncogenes "turn-on" run-away cell division, which results in a tumor. Tumor-suppressor genes "turn-off" cell division so that it never runs wild, unless the tumor-suppressor alleles are both mutant. In that case the resultant proteins don't work, the stop signal does not work, and a tumor results. It is rare for both tumor-suppressor alleles to be mutant. Therefore, most cancers occur because of a synergistic effect of a mutant tumor-suppressor allele and an oncogene allele.

For more information about oncogenes and tumor suppressor genes check the following web sites: (site owned by the national cancer institute)


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