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An oncovirus or oncogenic virus is a virus that can cause cancer. [4] This term originated from studies of acutely transforming retroviruses in the 1950–60s, [ 5 ] when the term oncornaviruses was used to denote their RNA virus origin. [ 6 ]
Illustration of how a normal cell is converted to a cancer cell, when an oncogene becomes activated. An oncogene is a gene that has the potential to cause cancer. [1] In tumor cells, these genes are often mutated, or expressed at high levels. [2]
Viruses that are known to cause cancer such as HPV (cervical cancer), Hepatitis B (liver cancer), and EBV (a type of lymphoma), are all DNA viruses. It is thought that when the virus infects a cell, it inserts a part of its own DNA near the cell growth genes, causing cell division.
This discovery changed the current thinking about cancer from a model wherein cancer is caused by a foreign substance (a viral gene) to one where a gene that is normally present in the cell can cause cancer. It is believed that at one point an ancestral virus mistakenly incorporated the c-Src gene of its cellular host.
A virus that can cause cancer is called an oncovirus. These include human papillomavirus ( cervical carcinoma ), Epstein–Barr virus ( B-cell lymphoproliferative disease and nasopharyngeal carcinoma ), Kaposi's sarcoma herpesvirus ( Kaposi's sarcoma and primary effusion lymphomas ), hepatitis B and hepatitis C viruses ( hepatocellular ...
When a virus transforms a cell it often causes cancer by either altering the cells' existing genome or introducing additional genetic material which causes cells to uncontrollably replicate. [11] It is rarely considered that what causes so much harm also has the capability of reversing the process and slowing the cancer growth or even leading ...
Further research done later on by others showed that RSV was a type of retrovirus.It was found that the v-Src gene in RSV is required for the formation of cancer. [3]A function for Src tyrosine kinases in normal cell growth was first demonstrated with the binding of family member p56lck to the cytoplasmic tail of the CD4 and CD8 co-receptors on T-cells. [4]
The herpes simplex virus type 1 (HSV-1) mutant 1716 lacks both copies of the ICP34.5 gene, and as a result is no longer able to replicate in terminally differentiated and non-dividing cells but will infect and cause lysis very efficiently in cancer cells, and this has proved to be an effective tumour-targeting strategy.