Chronic Leukemia

Chronic Myelogenous Leukemia
Overview
Every gene information of an individuals, were passed down to them by their ancestors. The deoxyribonucleic acid (DNA) information is the genetic code double helix that determine our traits, malfunctioning, diseases, and so on. There are numerous deadly diseases and one of them is called Chronic Myelogenous Leukemia. Chronic Myelogenous leukemia is a type of many cancer that exists. As is said by many cancer is when the cells in the body begin to grow out of control. Any cells in the body can produce cancer, and diffuse throughout the other parts of the body. Chronic Myelogenous Leukemia also known as chronic myeloid leukemia (CML), occurs in the blood forming cells of the bone marrow. Bone marrow function
Weeks later, Rudolf Virchow in berlin reported an identical case. They were probably the first two patients that represent the description of the disease that is later on known as chronic myeloid leukemia. Even though their cases had some similarities, Bennett though that the patient had an infection and Virchow believe that it was a neoplastic disorder he called blood disease or leukemia. In 1872, Ernst Neumann observed that leukemia cells originated in the bone marrow. Decades later, they saw the differentiation into myeloid versus lymphoid and acute versus chronic leukemia. An important step was found by Philadelphia cytogeneticists Peter Nowel and David Hungerford of an abnormally small G-group chromosome (PH). This discover was the biggest step yet because it reveal that cancer was a problem of DNA. Few years later, Janet Rowley discover that Philadelphia chromosome was the product of a reciprocal translocation between chromosome 9 and 22. In 1980s, the translocation partners were identified as BCR and ABL. In 1990 a model of the disease was
Transcription factors deregulation in the differentiation of chronic myeloid leukemia stem cells was demonstrated in a transgenic model with deficiency of a transcription factor Jun B. Jun B deficiency, led to the development of a chronic myeloid leukemia like disease with a propensity for myeloid differentiation in which several transcription potential exist only at the level of HSC, according to NCBI. GM-CSF is a mediate and proliferation of Jun B deficient which will associate with anti-apoptotic proteins Bcl-2 and Bcl-x and also cell cycle regulators. Transcription factor GA binding protein (GABP) is a complex transcription factors that contains GABPα, and GABPβ proteins. If we were to delete GABP, it will result in cell cycle arrest and deep loss of hematopoietic progenitor in bone marrow. Another important myeloid transcription factor is GATA2, it upregulated CML CD34 plus cells. Also for the self-renewal and abnormal myelopaiesis, HoxA9 and HoxB4 are well known for that. Hyper methylation mediated inactivation of HoxA4 and HoxA4 found in 30 percent of CD34 plus cell from patients with chronic myeloid leukemia, and more than 90 percent was observed from patients with critical phase of their chronic myeloid