The Genetic Effects on Acute Lymphoblastic Leukemia
Following the American Psychological Association Guidelines
Christina Taylor
Baker University
October 7, 2015 Pathophysiology:
Acute Lymphoblastic Leukemia (ALL) contains malignant cells that are lymphoid precursor cells, also known as lymphoblasts. During the early development of these cells, they experience an interruption of their cell development. This is usually due to an abnormal gene expression, mostly caused by chromosomal translocation. Chromosomal translocation happens because of a chromosome abnormality that occurs in the rearrangement of the nonhomoglous chromosomes. The lymphoblasts then replace the normal elements in the bone marrow causing a decrease in production of …show more content…
They are most common in adults and pediatric patients. The authors of this study found that 70% of near haploid ALL was caused by harboring alterations of targeting tyrosine kinase, IKZF3 (AIOLOS), activating Ras- and RTK signaling in chromosomes 24-31. They also found that 91.2% of adult cases and 90.9% of pediatric cases of low hypodiploid cases were due to harboring of TP53 alterations in chromosomes 32-39. For both forms of ALL, they found that inactivation of HELIOS and AIOLOS increased the drive for cell proliferation, which would explain why the outcomes for ALL are so poor. The research in the article primarily focused on low hypodiploid, as there was more finding for their genetic …show more content…
With this finding it suggests that alterations in the tumor protein 53 is of significant importance. The study found that, in half of the pediatric cases, the TP53 mutation was presented as a mutation in the T-cell population. In those pediatric cases they also found that by studying the non-hematopoietic cells, researchers were able to identify the origin of TP53 inheritance. This has allowed for low hypodiploid to be considered a manifestation of Li- Fraumeni syndrome, which is a cancer pre-disposition hereditary disorder that is characterized as autosomal dominant. Low hypodiploid ALL is seen to arise from earlier disruption of cellular development of the lymphoblasts than near haploid. (Holmfeldt, Wei, Diaz- Flores, Walsh, Zhang, & al, 2013) (Seiter & Besa,
Following the American Psychological Association Guidelines
Christina Taylor
Baker University
October 7, 2015 Pathophysiology:
Acute Lymphoblastic Leukemia (ALL) contains malignant cells that are lymphoid precursor cells, also known as lymphoblasts. During the early development of these cells, they experience an interruption of their cell development. This is usually due to an abnormal gene expression, mostly caused by chromosomal translocation. Chromosomal translocation happens because of a chromosome abnormality that occurs in the rearrangement of the nonhomoglous chromosomes. The lymphoblasts then replace the normal elements in the bone marrow causing a decrease in production of …show more content…
They are most common in adults and pediatric patients. The authors of this study found that 70% of near haploid ALL was caused by harboring alterations of targeting tyrosine kinase, IKZF3 (AIOLOS), activating Ras- and RTK signaling in chromosomes 24-31. They also found that 91.2% of adult cases and 90.9% of pediatric cases of low hypodiploid cases were due to harboring of TP53 alterations in chromosomes 32-39. For both forms of ALL, they found that inactivation of HELIOS and AIOLOS increased the drive for cell proliferation, which would explain why the outcomes for ALL are so poor. The research in the article primarily focused on low hypodiploid, as there was more finding for their genetic …show more content…
With this finding it suggests that alterations in the tumor protein 53 is of significant importance. The study found that, in half of the pediatric cases, the TP53 mutation was presented as a mutation in the T-cell population. In those pediatric cases they also found that by studying the non-hematopoietic cells, researchers were able to identify the origin of TP53 inheritance. This has allowed for low hypodiploid to be considered a manifestation of Li- Fraumeni syndrome, which is a cancer pre-disposition hereditary disorder that is characterized as autosomal dominant. Low hypodiploid ALL is seen to arise from earlier disruption of cellular development of the lymphoblasts than near haploid. (Holmfeldt, Wei, Diaz- Flores, Walsh, Zhang, & al, 2013) (Seiter & Besa,