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Oncogene

Oncogene

An oncogene is a special type of gene that is capable of transforming host cells and triggering carcinogenesis. The name is derived from the Greek onkos, meaning bulk, or mass, because of the ability to cause tumor growth. Oncogenes were first discovered in retroviruses (viruses containing the enzyme reverse transcriptase, and RNA , rather than DNA ) that were found to cause cancer in many animals (e.g., feline leukemia virus, simian sarcoma virus). Although this is a relatively common mechanism of oncogenesis in animals, very few oncogene-carrying viruses have been identified in man. The ones that are known include the papilloma virus HPV16 that is associated with cervical cancer, HTLV-1 and HTLV-2 associated with T-cell leukemia, and HIV-1 associated with Kaposi sarcoma.

Studies of humans led to the discovery of related genes called proto-oncogenes that exist naturally in the human genome. These genes have DNA sequences that are similar to oncogenes, but under normal conditions, the proto-oncogenes do not cause cancer. However, specific mutations in these genes can transform them to an oncogenic form that may lead to carcinogenesis. So, in humans, there are two unique ways in which oncogenesis occurs, by true viral infection and by mutation of proto-oncogenes that already exist in human cells.

See also Molecular biology and molecular genetics; Oncogenetic research; Viral genetics; Viral vectors in gene therapy; Virology; Virus replication; Viruses and responses to viral infection

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oncogene

oncogene A dominant mutant allele of a cellular gene (a proto-oncogene) that disrupts cell growth and division and is capable of transforming a normal cell into a cancerous cell. Proto-oncogenes typically encode proteins involved in positive control of the cell division cycle, such as growth factor receptors, signal transduction proteins, and transcription factors. Mutations in these genes tend to relax control mechanisms and accelerate cell division, leading to the cell proliferation that is characteristic of cancer. Some oncogenic mutations cause inhibition of programmed cell death (apoptosis), so that cancerous cells are less likely to be destroyed by the body's defences. Certain oncogenes of vertebrates are derived from viruses (see oncogenic). Compare tumour-suppressor gene.

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oncogenic

oncogenic Describing a chemical, organism, or environmental factor that causes the development of cancer. Some viruses are oncogenic to vertebrates, notably the retroviruses (including the Rous sarcoma virus of chickens), and some are suspected of being oncogenic (e.g. some of the adenoviruses and papovaviruses). Many of these viruses contain genes (known as oncogenes) that are responsible for the transformation of a normal host cell into a cancerous cell. See also growth factor.

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oncogene

oncogene (onk-oh-jeen) n. a gene in viruses and mammalian cells that can cause cancer; it results from the mutation of a normal gene and is capable of both initiation and continuation of malignant transformation of normal cells. Oncogenes probably produce peptides (growth factors) regulating cell division that, under certain conditions, become uncontrolled and may transform a normal cell to a malignant state.

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oncogene

oncogene Gene that, by inducing a cell to divide abnormally, contributes to the development of cancer. Oncogenes arise from gene mutations (proto-oncogenes), which are present in all normal cells and in some viruses. See also genetics

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oncogenic

oncogenic (onk-oh-jen-ik) adj. describing a substance, organism, or environment that is known to be a causal factor in the production of a tumour. Some viruses are oncogenic. See also carcinogen.

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oncogene

on·co·gene / ˈängkəˌjēn/ • n. Med. a gene that in certain circumstances can transform a cell into a tumor cell.

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oncogene

oncogene A gene that has the ability to cause eukaryotic cells to grow in an unregulated fashion, like that of a cancerous tumour. compare APOPTOSIS.

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oncogenic

oncogenic Capable of causing the formation of tumours.

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oncogenic

oncogenic Capable of causing the formation of tumours.

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Oncogene

Oncogene

Definition

In a cell with normal control regulation (non-cancerous), genes produce proteins that provide regulated cell division. Cancer is the disease caused by cells that have lost their ability to control their regulation. The abnormal proteins allowing the non-regulated cancerous state are produced by genes known as oncogenes. The normal gene from which the oncogene evolved is called a protooncogene.

Description

History

The word oncogene comes from the Greek term oncos, which means tumor. Oncogenes were originally discovered in certain types of animal viruses that were capable of inducing tumors in the animals they infected. These viral oncogenes, called v-onc, were later found in human tumors, although most human cancers do not appear to be caused by viruses. Since their original discovery, hundreds of oncogenes have been found, but only a small number of them are known to affect humans. Although different oncogenes have different functions, they are all somehow involved in the process of transformation (change) of normal cells to cancerous cells.

The transformation of normal cells into cancerous cells

The process by which normal cells are transformed into cancerous cells is a complex, multi-step process involving a breakdown in the normal cell cycle. Normally, a somatic cell goes through a growth cycle in which it produces new cells. The two main stages of this cycle are interphase (genetic material in the cell duplicates) and mitosis (the cell divides to produce two other identical cells). The process of cell division is necessary for the growth of tissues and organs of the body and for the replacement of damaged cells. Normal cells have a limited life span and only go through the cell cycle a limited number of times.

Different cell types are produced by the regulation of which genes in a given cell are allowed to be expressed. One way cancer is caused, is by de-regulation of those genes related to control of the cell cycle; the development of oncogenes. If the oncogene is present in a skin cell, the patient will have skin cancer; in a breast cell, breast cancer will result, and so on.

Cells that loose control of their cell cycle and replicate out of control are called cancer cells. Cancer cells undergo many cell divisions often at a quicker rate than normal cells and do not have a limited life span. This allows them to eventually overwhelm the body with a large number of abnormal cells and eventually affect the functioning of the normal cells.

A cell becomes cancerous only after changes occur in a number of genes that are involved in the regulation of its cell cycle. A change in a regulatory gene can cause it to stop producing a normal regulatory protein or can produce an abnormal protein which does not regulate the cell in a normal manner. When changes occur in one regulatory gene this often causes changes in other regulatory genes. Cancers in different types of cells can be caused by changes in different types of regulatory genes.

Proto-oncogenes and tumor-suppressor genes are the two most common genes involved in regulating the cell cycle. Proto-oncogenes and tumor-suppressor genes have different functions in the cell cycle. Tumor-suppressor genes produce proteins that are involved in prevention of uncontrolled cell growth and division. Since two of each type of gene are inherited two of each type of tumor-suppressor gene are inherited. Both tumor suppressor genes of a pair need to be changed in order for the protein produced to stop functioning as a tumor suppressor. Mutated tumor-suppressor genes therefore act in an autosomal recessive manner.

Proto-oncogenes produce proteins that are largely involved in stimulating the growth and division of cells in a controlled manner. Each proto-oncogene produces a different protein that has a unique role in regulating the cell cycles of particular types of cells. We inherit two of each type of proto-oncogene. A change in only one protooncogene of a pair converts it into an oncogene. The oncogene produces an abnormal protein, which is somehow involved in stimulating uncontrolled cell growth. An oncogene acts in an autosomal dominant manner since only one proto-oncogene of a pair needs to be changed in the formation of an oncogene.

Classes of proto-oncogene

There are five major classes of proto-oncogene/oncogenes: (1) growth factors, (2) growth factor receptors, (3) signal transducers (4) transcription factors, and (5) programmed cell death regulators.

GROWTH FACTORS Some proto-oncogenes produce proteins, called growth factors, which indirectly stimulate growth of the cell by activating receptors on the surface of the cell. Different growth factors activate different receptors, found on different cells of the body. Mutations in growth factor proto-oncogene result in oncogenes that promote uncontrolled growth in cells for which they have a receptor. For example, platelet-derived growth factor (PDGF) is a proto-oncogene that helps to promote wound healing by stimulating the growth of cells around a wound. PDGF can be mutated into an oncogene called vsis (PDGFB) which is often present in connective-tissue tumors.

GROWTH FACTOR RECEPTORS Growth factor receptors are found on the surface of cells and are activated by growth factors. Growth factors send signals to the center of the cell (nucleus) and stimulate cells that are at rest to enter the cell cycle. Different cells have different growth factors receptors. Mutations in a proto-oncogene that are growth factor receptors can result in oncogenes that produce receptors that do not require growth factors to stimulate cell growth. Overstimulation of cells to enter the cell cycle can result and promote uncontrolled cell growth. Most proto-oncogene growth factor receptors are called tyrosine kinases and are very involved in controlling cell shape and growth. One example of a tyrosine kinase is called GDFNR. The RET (rearranged during transfection) oncogene is a mutated form of GDFNR and is commonly found in cancerous thyroid cells.

SIGNAL TRANSDUCERS Signal transducers are proteins that relay cell cycle stimulation signals, from growth factor receptors to proteins in the nucleus of the cell. The transfer of signals to the nucleus is a stepwise process that involves a large number of proto-oncogenes and is often called the signal transduction cascade. Mutations in proto-oncogene involved in this cascade can cause unregulated activity, which can result in abnormal cell proliferation. Signal transducer oncogenes are the largest class of oncogenes. The RAS family is a group of 50 related signal transducer oncogenes that are found in approximately 20% of tumors.

TRANSCRIPTION FACTORS Transcription factors are proteins found in the nucleus of the cell which ultimately receive the signals from the growth factor receptors. Transcription factors directly control the expression of genes that are involved in the growth and proliferation of cells. Transcription factors produced by oncogenes typically do not require growth factor receptor stimulation and thus can result in uncontrolled cell proliferation. Transcription factor proto-oncogenes are often changed into oncogenes by chromosomal translocations in leukemias, lymphomas, and solid tumors. C-myc is a common transcription factor oncogene that results from a chromosomal translocation and is often found in leukemias and lymphomas.

PROGRAMMED CELL DEATH REGULATORS Normal cells have a predetermined life span and different genes regulate their growth and death. Cells that have been damaged or have an abnormal cell cycle may develop into cancer cells. Usually these cells are destroyed through a process called programmed cell death (apoptosis). Cells that have developed into cancer cells, however, do not undergo apoptosis. Mutated proto-oncogenes may inhibit the death of abnormal cells, which can lead to the formation and spread of cancer. The bcl-2 oncogene, for example, inhibits cell death in cancerous cells of the immune system.

Mechanisms of transformation of proto-oncogene into oncogenes

It is not known in most cases what triggers a particular proto-oncogene to change into an oncogene. There appear to be environmental triggers such as exposure to toxic chemicals. There also appear to be genetic triggers since changes in other genes in a particular cell can trigger changes in proto-oncogenes.

The mechanisms through which proto-oncogenes are changed into oncogenes are, however, better understood. Proto-oncogenes are transformed into oncogenes through: 1) mutation 2) chromosomal translocation, and 3) gene amplification.

A tiny change, called a mutation, in a proto-oncogene can convert it into an oncogene. The mutation results in an oncogene that produces a protein with an abnormal structure. These mutations often make the protein resistant to regulation and cause uncontrolled and continuous activity of the protein. The RAS family of oncogenes, found in approximately 20% of tumors, are examples of oncogenes caused by mutations.

Chromosomal translocations, which result from errors in mitosis, have also been implicated in the transformation of proto-oncogenes into oncogenes. Chromosomal translocations result in the transfer of a proto-oncogene from its normal location on a chromosome to a different location on another chromosome. Sometimes this translocation results in the transfer of a proto-oncogene next to a gene involved in the immune system. This results in an oncogene that is controlled by the immune system gene and as a result becomes deregulated. One example of this mechanism is the transfer of the c-myc proto-oncogene from its normal location on chromosome 8 to a location near an immune system gene on chromosome 14. This translocation results in the deregulation of c-myc and is involved in the development of Burkitt's lymphoma. The translocated c-myc protooncogene is found in the cancer cells of approximately 85% of people with Burkitt's lymphoma.

In other cases, the translocation results in the fusion of a proto-oncogene with another gene. The resulting oncogene produces an unregulated protein that is involved in stimulating uncontrolled cell proliferation. The first discovered fusion oncogene resulted from a Philadelphia chromosome translocation. This type of translocation is found in the leukemia cells of greater than 95% of patients with a chronic form of leukemia. The Philadelphia chromosome translocation results in the fusion of the c-abl proto-oncogene, normally found on chromosome 9 to the bcr gene found on chromosome 22. The fused gene produces an unregulated transcription factor protein that has a different structure than the normal protein. It is not known how this protein contributes to the formation of cancer cells.

Some oncogenes result when multiple copies of a proto-oncogene are created (gene amplification). Gene amplification often results in hundreds of copies of a gene, which results in increased production of proteins and increased cell growth. Multiple copies of proto-oncogenes are found in many tumors. Sometimes amplified genes form separate chromosomes called double minute chromosomes and sometimes they are found within normal chromosomes.

Inherited oncogenes

In most cases, oncogenes result from changes in proto-oncogenes in select somatic cells and are not passed on to future generations. People with an inherited oncogene, however, do exist. They possess one changed proto-oncogene (oncogene) and one unchanged protooncogene in all of their somatic cells. The somatic cells have two of each chromosome and therefore two of each gene since one of each type of chromosome is inherited from the mother in the egg cell and one of each is inherited from the father in the sperm cell. The egg and sperm cells have undergone a number of divisions in their cell cycle and therefore only contain one of each type of chromosome and one of each type of gene. A person with an inherited oncogene has a changed proto-oncogene in approximately 50% of their egg or sperm cells and an unchanged proto-oncogene in the other 50% of their egg or sperm cells and therefore has a 50% chance of passing this oncogene on to their children.

A person only has to inherit a change in one protooncogene of a pair to have an increased risk of cancer. This is called autosomal dominant inheritance . Not all people with an inherited oncogene develop cancer, since mutations in other genes that regulate the cell cycle need to occur in a cell for it to be transformed into a cancerous cell. The presence of an oncogene in a cell does, however, make it more likely that changes will occur in other regulatory genes. The degree of cancer risk depends on the type of oncogene inherited as well as other genetic factors and environmental exposures. The type of cancers that are likely to develop depend on the type of oncogene that has been inherited.

Multiple endocrine neoplasia type II (MENII) is one example of a condition caused by an inherited oncogene. People with MENII have usually inherited the RET oncogene. They have approximately a 70% chance of developing thyroid cancer, a 50% chance of developing a tumor of the adrenal glands (pheochromocytoma) and about a 5-10% chance of developing symptomatic parathyroid disease.

Oncogenes as targets for cancer treatment

The discovery of oncogenes approximately 20 years ago has played an important role in developing an understanding of cancer. Oncogenes promise to play an even greater role in the development of improved cancer therapies since oncogenes may be important targets for drugs that are used for the treatment of cancer. The goal of these therapies is to selectively destroy cancer cells while leaving normal cells intact. Many anti-cancer therapies currently under development are designed to interfere with oncogenic signal transducer proteins, which relay the signals involved in triggering the abnormal growth of tumor cells. Other therapies hope to trigger specific oncogenes to cause programmed cell death in cancer cells. Whatever the mechanism by which they operate, it is hoped that these experimental therapies will offer a great improvement over current cancer treatments.

Resources

BOOKS

Park, Morag. "Oncogenes." In The Genetic Basis of Human Cancer, edited by Bert Vogelstein and Kenneth Kinzler. New York: McGraw-Hill, 1998, pp. 205-228.

PERIODICALS

Stass, S. A., and J. Mixson. "Oncogenes and tumor suppressor genes: therapeutic implications." Clinical Cancer Research 3 (12 Pt 2) (December 1997): 2687-2695.

"What you need to know about Cancer." Scientific America (September 1996).

Wong, Todd. "Oncogenes." Anticancer Research 6(A) (Nov-Dec 1999): 4729-4726.

WEBSITES

Aharchi, Joseph. "Cell division–Overview." Western Illinois University. Biology 150. <http://www.wiu.edu/users/mfja/cell1.htm>. (1998).

"The genetics of cancer–an overview." (February 17, 1999). Robert H. Lurie Comprehensive Cancer Center of Northwestern University. <http://www.cancergenetics.org/gncavrvu.htm>.

Kimball, John. "Oncogenes." Kimball's Biology Pages. (March 22, 2000). <http://www.ultranet.com/~jkimball/BiologyPages/O/Oncogenes.html>.

Schichman, Stephen, and Carlo Croce. "Oncogenes." (1999) Cancer Medicine.<http://www.cancernetwork.com/CanMed/Ch005/005-0.htm>.

Lisa Maria Andres, MS, CGC

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Oncogene

Oncogene

Definition

In a cell with normal control regulation (non-cancerous), genes produce proteins that provide regulated cell division. Cancer is the disease caused by cells that have lost their ability to control their regulation. The abnormal proteins allowing the non-regulated cancerous state are produced by genes known as oncogenes. The normal gene from which the oncogene evolved is called a proto-oncogene.

Description

History

The word oncogene comes from the Greek term oncos, which means tumor. Oncogenes were originally discovered in certain types of animal viruses that were capable of inducing tumors in the animals they infected. These viral oncogenes, called v-onc, were later found in human tumors, although most human cancers do not appear to be caused by viruses. Since their original discovery, hundreds of oncogenes have been found but only a small number of them are known to affect humans. Although different oncogenes have different functions, they are all somehow involved in the process of transformation (change) of normal cells to cancerous cells.

The transformation of normal cells into cancerous cells

The process by which normal cells are transformed into cancerous cells is a complex, multi-step process involving a breakdown in the normal cell cycle. Normally, a somatic cell goes through a growth cycle in which it produces new cells. The two main stages of this cycle are interphase (genetic material in the cell duplicates) and mitosis (the cell divides to produce two other identical cells). The process of cell division is necessary for the growth of tissues and organs of the body and for the replacement of damaged cells. Normal cells have a limited life span and only go through the cell cycle a limited number of times.

Different cell types are produced by the regulation of which genes in a given cell are allowed to be expressed. One way cancer is caused, is by de-regulation of those genes related to control of the cell cycle; the development of oncogenes. If the oncogene is present in a skin cell, the patient will have skin cancer; in a breast cell, breast cancer will result, and so on.

Cells that loose control of their cell cycle and replicate out of control are called cancer cells. Cancer cells undergo many cell divisions often at a quicker rate than normal cells and do not have a limited life span. This allows them to eventually overwhelm the body with a large number of abnormal cells and eventually affect the functioning of the normal cells.

A cell becomes cancerous only after changes occur in a number of genes that are involved in the regulation of its cell cycle. A change in a regulatory gene can cause it to stop producing a normal regulatory protein or can produce an abnormal protein that does not regulate the cell in a normal manner. When changes occur in one regulatory gene this often causes changes in other regulatory genes. Cancers in different types of cells can be caused by changes in different types of regulatory genes.

Proto-oncogenes and tumor-suppressor genes are the two most common genes involved in regulating the cell cycle. Proto-oncogenes and tumor-suppressor genes have different functions in the cell cycle. Tumor-suppressor genes produce proteins that are involved in prevention of uncontrolled cell growth and division. Since two of each type of gene are inherited, two of each type of tumor-suppressor gene are also inherited. Both tumor suppressor genes of a pair need to be changed in order for the protein produced to stop functioning as a tumor suppressor. Mutated tumor-suppressor genes therefore act in an autosomal recessive manner.

Proto-oncogenes produce proteins that are largely involved in stimulating the growth and division of cells in a controlled manner. Each proto-oncogene produces a different protein that has a unique role in regulating the cell cycles of particular types of cells. We inherit two of each type of proto-oncogene. A change in only one proto-oncogene of a pair converts it into an oncogene. The oncogene produces an abnormal protein, which is somehow involved in stimulating uncontrolled cell growth. An oncogene acts in an autosomal dominant manner since only one proto-oncogene of a pair needs to be changed in the formation of an oncogene.

Classes of proto-oncogene

There are five major classes of proto-oncogene/oncogenes: (1) growth factors, (2) growth factor receptors, (3) signal transducers (4) transcription factors, and (5) programmed cell death regulators.

GROWTH FACTORS Some proto-oncogenes produce proteins, called growth factors, which indirectly stimulate growth of the cell by activating receptors on the surface of the cell. Different growth factors activate different receptors, found on different cells of the body. Mutations in growth factor proto-oncogene result in oncogenes that promote uncontrolled growth in cells for which they have a receptor. For example, platelet-derived growth factor (PDGF) is a proto-oncogene that helps to promote wound healing by stimulating the growth of cells around a wound. PDGF can be mutated into an oncogene called v-sis (PDGFB) which is often present in connective-tissue tumors.

GROWTH FACTOR RECEPTORS Growth factor receptors are found on the surface of cells and are activated by growth factors. Growth factors send signals to the center of the cell (nucleus) and stimulate cells that are at rest to enter the cell cycle. Different cells have different growth factors receptors. Mutations in a proto-oncogene that are growth factor receptors can result in oncogenes that produce receptors that do not require growth factors to stimulate cell growth. Overstimulation of cells to enter the cell cycle can result and promote uncontrolled cell growth. Most proto-oncogene growth factor receptors are called tyrosine kinases and are very involved in controlling cell shape and growth. One example of a tyrosine kinase is called GDFNR. The RET (rearranged during transfection) oncogene is a mutated form of GDFNR and is commonly found in cancerous thyroid cells.

SIGNAL TRANSDUCERS Signal transducers are proteins that relay cell cycle stimulation signals, from growth factor receptors to proteins in the nucleus of the cell. The transfer of signals to the nucleus is a stepwise process that involves a large number of proto-oncogenes and is often called the signal transduction cascade. Mutations in proto-oncogene involved in this cascade can cause unregulated activity, which can result in abnormal cell proliferation. Signal transducer oncogenes are the largest class of oncogenes. The RAS family is a group of 50 related signal transducer oncogenes that are found in approximately 20% of tumors.

TRANSCRIPTION FACTORS Transcription factors are proteins found in the nucleus of the cell which ultimately receive the signals from the growth factor receptors. Transcription factors directly control the expression of genes that are involved in the growth and proliferation of cells. Transcription factors produced by oncogenes typically do not require growth factor receptor stimulation and thus can result in uncontrolled cell proliferation. Transcription factor proto-oncogenes are often changed into oncogenes by chromosomal translocations in leukemias, lymphomas, and solid tumors. C-myc is a common transcription factor oncogene that results from a chromosomal translocation and is often found in leukemias and lymphomas.

PROGRAMMED CELL DEATH REGULATORS Normal cells have a predetermined life span and different genes regulate their growth and death. Cells that have been damaged or have an abnormal cell cycle may develop into cancer cells. Usually these cells are destroyed through a process called programmed cell death (apoptosis). Cells that have developed into cancer cells, however, do not undergo apoptosis. Mutated proto-oncogenes may inhibit the death of abnormal cells, which can lead to the formation and spread of cancer. The bcl-2 oncogene, for example, inhibits cell death in cancerous cells of the immune system.

Mechanisms of transformation of proto-oncogene into oncogenes

It is not known in most cases what triggers a particular proto-oncogene to change into an oncogene. There appear to be environmental triggers such as exposure to toxic chemicals. There also appear to be genetic triggers since changes in other genes in a particular cell can trigger changes in proto-oncogenes.

The mechanisms through which proto-oncogenes are changed into oncogenes are, however, better understood. Proto-oncogenes are transformed into oncogenes through: 1) mutation 2) chromosomal translocation, and 3) gene amplification.

A tiny change, called a mutation, in a proto-oncogene can convert it into an oncogene. The mutation results in an oncogene that produces a protein with an abnormal structure. These mutations often make the protein resistant to regulation and cause uncontrolled and continuous activity of the protein. The RAS family of oncogenes, found in approximately 20% of tumors, are examples of oncogenes caused by mutations.

Chromosomal translocations, which result from errors in mitosis, have also been implicated in the transformation of proto-oncogene into oncogenes. Chromosomal translocations result in the transfer of a proto-oncogene from its normal location on a chromosome to a different location on another chromosome. Sometimes this translocation results in the transfer of a proto-oncogene next to a gene involved in the immune system. This results in an oncogene that is controlled by the immune system gene and as a result becomes deregulated. One example of this mechanism is the transfer of the c-myc proto-oncogene from its normal location on chromosome 8 to a location near an immune system gene on chromosome 14. This translocation results in the deregulation of c-myc and is involved in the development of Burkitt's lymphoma. The translocated c-myc proto-oncogene is found in the cancer cells of approximately 85% of people with Burkitt's lymphoma.

In other cases, the translocation results in the fusion of a proto-oncogene with another gene. The resulting oncogene produces an unregulated protein that is involved in stimulating uncontrolled cell proliferation. The first discovered fusion oncogene resulted from a Philadelphia chromosome translocation. This type of translocation is found in the leukemia cells of greater than 95% of patients with a chronic form of leukemia. The Philadelphia chromosome translocation results in the fusion of the c-abl proto-oncogene, normally found on chromosome 9 to the bcr gene found on chromosome 22. The fused gene produces an unregulated transcription factor protein that has a different structure than the normal protein. It is not known how this protein contributes to the formation of cancer cells.

Some oncogenes result when multiple copies of a proto-oncogene are created (gene amplification). Gene amplification often results in hundreds of copies of a gene, which results in increased production of proteins and increased cell growth. Multiple copies of proto-oncogenes are found in many tumors. Sometimes amplified genes form separate chromosomes called double minute chromosomes and sometimes they are found within normal chromosomes.

Inherited oncogenes

In most cases, oncogenes result from changes in proto-oncogenes in select somatic cells and are not passed on to future generations. People with an inherited oncogene, however, do exist. They possess one changed proto-oncogene (oncogene) and one unchanged proto-oncogene in all of their somatic cells. The somatic cells have two of each chromosome and therefore two of each gene since one of each type of chromosome is inherited from the mother in the egg cell and one of each is inherited from the father in the sperm cell. The egg and sperm cells have undergone a number of divisions in their cell cycle and therefore only contain one of each type of chromosome and one of each type of gene. A person with an inherited oncogene has a changed proto-oncogene in approximately 50% of their egg or sperm cells and an unchanged proto-oncogene in the other 50% of their egg or sperm cells and therefore has a 50% chance of passing this oncogene on to their children.

A person only has to inherit a change in one proto-oncogene of a pair to have an increased risk of cancer. This is called autosomal dominant inheritance . Not all people with an inherited oncogene develop cancer, since mutations in other genes that regulate the cell cycle need to occur in a cell for it to be transformed into a cancerous cell. The presence of an oncogene in a cell does, however, make it more likely that changes will occur in other regulatory genes. The degree of cancer risk depends on the type of oncogene inherited as well as other genetic factors and environmental exposures. The type of cancers that are likely to develop depend on the type of oncogene that has been inherited.

Multiple endocrine neoplasia type II (MENII) is one example of a condition caused by an inherited oncogene. People with MENII have usually inherited the RET oncogene. They have approximately a 70% chance of developing thyroid cancer, a 50% chance of developing a tumor of the adrenal glands (pheochromocytoma) and about a 5-10% chance of developing symptomatic para-thyroid disease.

Oncogenes as targets for cancer treatment

The discovery of oncogenes approximately 20 years ago has played an important role in developing an understanding of cancer. Oncogenes promise to play an even greater role in development of improved cancer therapies since oncogenes may be important targets for drugs that are used for the treatment of cancer. The goal of these therapies is to selectively destroy cancer cells while leaving normal cells intact. Many anti-cancer therapies currently under development are designed to interfere with oncogenic signal transducer proteins which relay the signals involved in triggering the abnormal growth of tumor cells. Other therapies hope to trigger specific oncogenes to cause programmed cell death in cancer cells. Whatever the mechanism by which they operate, it is hoped that these experimental therapies will offer a great improvement over current cancer treatments.

Resources

BOOKS

Park, Morag. "Oncogenes." In The Genetic Basis of Human Cancer, edited by Bert Vogelstein and Kenneth Kinzler. New York: McGraw-Hill, 1998, pp. 205-228.

PERIODICALS

Stass, S. A., and J. Mixson. "Oncogenes and tumor suppressor genes: therapeutic implications." Clinical Cancer Research 3 (12 Pt 2) (December 1997): 2687-2695.

"What you need to know about Cancer." Scientific America (September 1996).

Wong, Todd. "Oncogenes." Anticancer Research 6(A) (Nov-Dec 1999): 4729-4726.

WEBSITES

Aharchi, Joseph. "Cell division–Overview." Western Illinois University. Biology 150. <http://www.wiu.edu/users/mfja/cell1.htm>. (1998).

"The genetics of cancer–an overview." (February 17, 1999). Robert H. Lurie Comprehensive Cancer Center of Northwestern University. <http://www.cancergenetics.org/gncavrvu.htm>.

Kimball, John. "Oncogenes." Kimball's Biology Pages. (March 22, 2000). <http://www.ultranet.com/~jkimball/BiologyPages/O/Oncogenes.html>.

Schichman, Stephen, and Carlo Croce. "Oncogenes." (1999) Cancer Medicine. <http://www.cancernetwork.com/CanMed/Ch005/005-0.htm>.

Lisa Maria Andres, MS, CGC

Cite this article
Pick a style below, and copy the text for your bibliography.

  • MLA
  • Chicago
  • APA

"Oncogene." Gale Encyclopedia of Genetic Disorders. . Encyclopedia.com. 19 Aug. 2018 <http://www.encyclopedia.com>.

"Oncogene." Gale Encyclopedia of Genetic Disorders. . Encyclopedia.com. (August 19, 2018). http://www.encyclopedia.com/science/encyclopedias-almanacs-transcripts-and-maps/oncogene-0

"Oncogene." Gale Encyclopedia of Genetic Disorders. . Retrieved August 19, 2018 from Encyclopedia.com: http://www.encyclopedia.com/science/encyclopedias-almanacs-transcripts-and-maps/oncogene-0

Learn more about citation styles

Citation styles

Encyclopedia.com gives you the ability to cite reference entries and articles according to common styles from the Modern Language Association (MLA), The Chicago Manual of Style, and the American Psychological Association (APA).

Within the “Cite this article” tool, pick a style to see how all available information looks when formatted according to that style. Then, copy and paste the text into your bibliography or works cited list.

Because each style has its own formatting nuances that evolve over time and not all information is available for every reference entry or article, Encyclopedia.com cannot guarantee each citation it generates. Therefore, it’s best to use Encyclopedia.com citations as a starting point before checking the style against your school or publication’s requirements and the most-recent information available at these sites:

Modern Language Association

http://www.mla.org/style

The Chicago Manual of Style

http://www.chicagomanualofstyle.org/tools_citationguide.html

American Psychological Association

http://apastyle.apa.org/

Notes:
  • Most online reference entries and articles do not have page numbers. Therefore, that information is unavailable for most Encyclopedia.com content. However, the date of retrieval is often important. Refer to each style’s convention regarding the best way to format page numbers and retrieval dates.
  • In addition to the MLA, Chicago, and APA styles, your school, university, publication, or institution may have its own requirements for citations. Therefore, be sure to refer to those guidelines when editing your bibliography or works cited list.