Oncogene
[2][4][5][6] 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.
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.
Alternately, different chemical compounds that can be linked to genetic material (DNA or RNA) may have an impact on which genes are active.
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.
[10] 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.
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.
[12] The theory of oncogenes was foreshadowed by the German biologist Theodor Boveri in his 1914 book Zur Frage der Entstehung Maligner Tumoren (Concerning the Origin of Malignant Tumors) in which he predicted the existence of oncogenes (Teilungsfoerdernde Chromosomen) that become amplified (im permanenten Übergewicht) during tumor development.
[13] Later on, the term "oncogene" was rediscovered in 1969 by National Cancer Institute scientists George Todaro and Robert Huebner.
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.
Dominique Stéhelin [fr], 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.
[20] 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.
