Affiliation:
1. Department of Genetic Engineering, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, India
Abstract
Over the years, many scientists and doctors have been treating the deadly cancer disease but cannot find a permanent treatment for this disease. Also, sometimes it becomes tough to understand the mechanisms and causes of cancer as it is a very complex disease that involves many biological processes. Due to the redundancy in our biological system, cancer progression becomes very easy, thus making it difficult to cure. To find the root cause of this disease, we should know what genetic alterations are causing cancer progress and who is participating in these alterations, like proteins, signaling pathways, or genes. Cancer is caused due to various reasons; it can be due to genetics but primarily due to carcinogens, causing mutations in the genes, thereby making them an oncogene. The Proto-oncogenes are those genes that usually assist the growth of tumor cells. The alteration, mutation, or increased copy number of a particular gene may turn into a proto-oncogene, which could end up completely activated or turned on. Many Tumor-causing alterations or mutations related to oncogenes are usually acquired and not inherited. These tumor-causing mutations often actuate oncogenes via chromosomal rearrangement or changes in the chromosome, which sequestrates one gene after another, thereby permitting the first gene to prompt the alternative. Search which genes are involved in different cancer types would help scientists proceed with new methods for finding a cure for this disease. This article will depict which genes and their location on which chromosomes, specifically on chromosome 11, are related to different types of cancer.
Publisher
BENTHAM SCIENCE PUBLISHERS
Reference107 articles.
1. Nebral K.; König M.; Schmidt H.H.; Lutz D.; Sperr W.R.; Kalwak K.; Brugger S.; Dworzak M.N.; Haas O.A.; Strehl S.; Screening for NUP98 rearrangements in hematopoietic malignancies by fluorescence in situ hybridization. Haematologica 2005,90(6),746-752
2. Kwong Y.L.; Pang A.; Low frequency of rearrangements of the homeobox geneHOXA9/t(7;11) in adult acute myeloid leukemia. Genes Chromosomes Cancer 1999,25(1),70-74
3. Ahuja H.G.; Popplewell L.; Tcheurekdjian L.; Slovak M.L.; NUP98 gene rearrangements and the clonal evolution of chronic myelogenous leukemia. Genes Chromosomes Cancer 2001,30(4),410-415
4. Dash A.B.; Williams I.R.; Kutok J.L.; Tomasson M.H.; Anastasiadou E.; Lindahl K.; Li S.; Van Etten R.A.; Borrow J.; Housman D.; Druker B.; Gilliland D.G.; A murine model of CML blast crisis induced by cooperation between BCR/ABL and NUP98/HOXA9. Proc Natl Acad Sci USA 2002,99(11),7622-7627
5. Diehl J.A.; Cycling to cancer with cyclin D1. Cancer Biol Ther 2002,1(3),226-231