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In genetics, chromosome translocation is a phenomenon that results in unusual rearrangement of chromosomes. This includes balanced and unbalanced translocation, with two main types: reciprocal, and Robertsonian translocation. Reciprocal translocation is a chromosome abnormality caused by exchange of parts between non-homologous chromosomes. Two ...
In cancer, c-myc is often constitutively (persistently) expressed. This leads to the increased expression of many genes, some of which are involved in cell proliferation, contributing to the formation of cancer. [1] A common human translocation involving c-myc is critical to the development of most cases of Burkitt lymphoma. [2]
This type involves myc oncogene translocation from chromosome 8 to the Ig lambda locus on chromosome 22. This type of translocation is involved in about 5% of cases of Burkitt lympohoma. The c-myc gene found on chromosome 8 is part of the MYC family of genes that serve as regulators of cellular transcription and is associated with Burkitt lymphoma.
The chromosomal defect in the Philadelphia chromosome is a reciprocal translocation, in which parts of two chromosomes, 9 and 22, swap places. The result is that a fusion gene is created by juxtaposing the ABL1 gene on chromosome 9 (region q34) to a part of the BCR (breakpoint cluster region) gene on chromosome 22 (region q11).
The cancer stem cell hypothesis proposes that the different kinds of cells in a heterogeneous tumor arise from a single cell, termed Cancer Stem Cell. Cancer stem cells may arise from transformation of adult stem cells or differentiated cells within a body. These cells persist as a subcomponent of the tumor and retain key stem cell properties.
There are 2 different types of chromosomal translocations that can occur: translocation events which relocate a proto-oncogene to a new chromosomal site that leads to higher expression; translocation events that lead to a fusion between a proto-oncogene and a 2nd gene (this creates a fusion protein with increased cancerous/oncogenic activity)
The first fusion gene [1] was described in cancer cells in the early 1980s. The finding was based on the discovery in 1960 by Peter Nowell and David Hungerford in Philadelphia of a small abnormal marker chromosome in patients with chronic myeloid leukemia—the first consistent chromosome abnormality detected in a human malignancy, later designated the Philadelphia chromosome. [3]
This results in the two daughter cells receiving an uneven chromatid. [4] Since the two resulting chromatids lack telomeres, when they replicate the BFB cycle will repeat, and will continue every subsequent cell division until those chromatids receive a telomere, usually from a different chromatid through the process of translocation. [4]