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An oncogene is a gene that has the potential to cause cancer. In tumor cells, these genes are often mutated, or Gene expression at high levels. Kimball's Biology Pages. "Oncogenes" Free full text
Most normal cells undergo a preprogrammed rapid cell death (apoptosis) if critical functions are altered and then malfunction. Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead. The Nobel Prize in Physiology or Medicine 2002. Illustrated presentation. Most oncogenes began as proto-oncogenes: normal genes involved in cell growth and proliferation or inhibition of apoptosis. If, through mutation, normal genes promoting cellular growth are up-regulated (gain-of-function mutation), they predispose the cell to cancer and are termed oncogenes. Usually, multiple oncogenes, along with mutated apoptotic or tumor suppressor genes, act in concert to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the encoded by oncogenes. The Nobel Prize in Physiology or Medicine 1989 to J. Michael Bishop and Harold E. Varmus for their discovery of "the cellular origin of retroviral oncogenes". Oncogenes are a physically and functionally diverse set of genes, and as a result, their protein products have pleiotropic effects on a variety of intricate regulatory cascades within the cell.
Genes known as proto-oncogenes are those that normally encourage cell growth and division in order to generate new cells or sustain the viability of pre-existing cells. When overexpressed, proto-oncogenes can be inadvertently activated (turned on), which changes them to oncogenes.
There are numerous ways to activate (turn on) oncogenes in cells:
Gene changes or mutations: A person's genetic "coding" may differ in a way that causes an oncogene to always be activated. These types of gene changes can develop spontaneously throughout the course of a person's life or they might be inherited from a parent when a transcription error occurs during cell division.
Cells can frequently switch genes on or off via epigenetic mechanisms rather than actual genetic alterations. Alternately, different chemical compounds that can be linked to genetic material (DNA or RNA) may have an impact on which genes are active. An oncogene may sporadically become activated due to these epigenetic modifications.
Chromosomal rearrangement: Every living creature has chromosomes, which are substantial strands of DNA that contain the genes for a cell. A chromosome's DNA sequence may alter each time a cell divides. This could cause a gene to be located near to a proto-oncogene that acts as an "on" switch, keeping it active even when it shouldn't. The cell can develop irregularly with the aid of this new oncogene.
Gene duplication: If one cell has more copies of a gene than another, that cell may produce too much of a certain protein.
The first human oncogene (HRAS), a crucial finding in the field of cancer research, was discovered more than 40 years ago, and since then, the number of novel pathogenic oncogenes has increased steadily. The discovery of specific small-molecule inhibitors that specifically target the different oncogenic proteins and a comprehensive mechanistic analysis of the ways in which oncogenes dysregulate physiological signaling to cause different cancer types and developmental syndromes are potential future advances in the field of cancer research. Investigating the quickly expanding field of oncogene molecular research, the goal of this special issue was to generate practical translational indicators that could be able to meet clinical needs.
Genes that are considered crucial for cancer can be divided into two categories based on whether the harmful mutations in them result in function loss or gain. Gain-of-function mutations of proto-oncogenes drive cells to proliferate when they shouldn't, while loss-of-function mutations of tumor suppressor genes free cells from inhibitions that typically serve to control their numbers. The ability of the mutant genes, known as oncogenes, to steer a specific line of test cells toward malignant proliferation can occasionally be used to identify these later mutations, which have a dominating effect.
Many of them were initially found to induce cancer in animals when they are introduced through viral vector infection, which carries genetic information from a prior host cell. Another method for identifying oncogenes is to look for genes that are activated by mutations in human cancer cells or by chromosomal translocations that may indicate the presence of a gene that is crucial for cancer.
Cancer patients are generally categorized according to clinical parameters in order to tailor their Cancer treatment. For example, the separation of patients with acute leukemia into those with lymphocytic leukemia and those with Myeloid leukemia is important, because the optimal treatment for each form is different. Even in a particular disease, the identification of patients with good and poor Prognosis potential is helpful, since more aggressive therapy may be needed to achieve a cure in the poor prognostic group. Oncogenes are Prognosis marker in certain human cancers. N-Myc amplification is an independent determinant in predicting a poor outcome in childhood neuroblastoma. Those children with amplification of N-myc, regardless of stage, will have shortened survival. Thus, therapeutic efforts are concentrated on intensifying treatment in this poor prognostic group.
Later on, the term "oncogene" was rediscovered in 1969 by National Cancer Institute scientists George Todaro and Robert Huebner.The Emperor of All Maladies, Siddhartha Mukherjee, 2011, p. 363
The first confirmed oncogene was discovered in 1970 and was termed SRC (pronounced "sarc" as it is short for sarcoma). SRC was first discovered as an oncogene in a chicken retrovirus. Experiments performed by Dr. G. Steve Martin of the University of California, Berkeley demonstrated that SRC was indeed the gene of the virus that acted as an oncogene upon infection. The first nucleotide sequence of v-Src was DNA sequencing in 1980 by A.P. Czernilofsky et al.
In 1976, Drs. , J. Michael Bishop and Harold E. Varmus of the University of California, San Francisco demonstrated that oncogenes were activated proto-oncogenes as is found in many organisms, including humans. Bishop and Varmus were awarded the Nobel Prize in Physiology or Medicine in 1989 for their discovery of the cellular origin of retroviral oncogenes. Nobel Prize in Physiology or Medicine for 1989 jointly to J. Michael Bishop and Harold E. Varmus for their discovery of "the cellular origin of retroviral oncogenes". Press Release.
Dr. Robert Weinberg is credited with discovering the first identified human oncogene in a human bladder cancer cell line. The molecular nature of the mutation leading to oncogenesis was subsequently isolated and characterized by the Spanish biochemist Mariano Barbacid and published in Nature in 1982. Dr. Barbacid spent the following months extending his research, eventually discovering that the oncogene was a mutated allele of HRAS and characterizing its activation mechanism.
The resultant protein encoded by an oncogene is termed oncoprotein. (2025). 9781416029731, Saunders. ISBN 9781416029731 Oncogenes play an important role in the regulation or synthesis of proteins linked to tumorigenic cell growth. Some oncoproteins are accepted and used as tumor markers.
The expression of oncogenes can be regulated by (miRNAs), small 21-25 nucleotides in length that control gene expression by downregulate them. Mutations in such microRNAs (known as ) can lead to activation of oncogenes. Antisense messenger RNAs could theoretically be used to block the effects of oncogenes.
Additional oncogenetic regulator properties include:
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