User:Rudrateja24/Oncogene

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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 regularly 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), at which time they are referred to as oncogenes.

There are numerous ways to activate (turn on) oncogenes in cells. Remember this:

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. Visit Gene Alterations and Cancer to learn more about epigenetic alterations.

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 a "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 dys regulate 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.

Oncogene as an prognostic markers in cancer therapy

Cancer patients are frequently stratified according to clinical parameters in order to tailor their cancer therapy. For example, the separation of patients with acute leukemia into those with lymphocytic leukemia and those with myelocytic leukemia is important, since the optimal treatment for each form is different. Even in a particular disease, the identification of patients with good and poor prognostic potential is helpful, since more aggressive therapy may be needed to achieve cures in the poor prognostic group. Oncogenes are prognostic markers 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 a shorter survival [1,2]. Thus current therapeutic efforts are concentrated on intensifying treatment in this poor prognostic group.