Acute Lymphoblastic Leukemia - Annotated Bibliography Example

Acute Lymphoblastic Leukemia Haslam, K., Kelly, J., Morris, T., Connaghan, G., Gilligan, O., Browne, P., & Langabeer, S. E. (January 01, 2011). Screening for CRLF2 overexpression in adult acute lymphoblastic leukemia. International Journal of Laboratory Hematology, 33, 6, 17-9. According to Haslam et al. (2011), prognosis of the acute lymphoblastic leukemia is adults are normally poor with a long-term survival rate of less than forty percent within the patients younger than 60 years. Emergence of molecular technologies offers proper means of interrogation of leukemia. Abnormalities that results to overexpression of the cytokine receptor-like factor 2 gene within pediatric B-ALL and adults B-ALL encodes a subunit of the thymic stromal lymphopoietic receptor thus forming a heterodimeric complex having interleukin-7 receptor alpha chain before the TSLP ligand binding. Overexpression of the CRLF2 occurs by the interstitial deletion of the pseudoautosomal region through sex chromosome thus resulting to P2RY8-CRLF2 fusion. Haslam et al. (2011) depict that a high proportion of children with Down syndrome related to B-ALL with concomitant of JAK2 that result in constitutive activation of the JAK –STAT signaling pathway. Moreover, CRLF2 and JAK2 mutations contribute to development factor independence depicting that inhibitors of the CRLF2/JAK2 signaling pathways have therapeutic importance in the process. Moreover, in this article, Haslam et al. highlight the treatment options and the genes therapy used to treat acute lymphoblastic leukemia. According to Haslam et al. (2011), acute lymphoblastic leukemia is treated by subjection to numerous chemotherapy drugs via mouth or via special intravenous line that is normally placed within a vein in the arm or chest and maintain for several months. Radiation treatment I used particularly if there is involvement of the spinal fluid. Blood and marrow transplantation is applied the treatment of the acute lymphoblastic leukemia. BMT entails administration of high dose of chemotherapy to the whole body thus lowering the blood counts. Baraz, R., Cisterne, A., Saunders, P. O., Hewson, J., Thien, M., Weiss, J., Basnett, J., ... Bendall, L. J. (January 01, 2014). mTOR inhibition by everolimus in childhood acute lymphoblastic leukemia induces caspase-independent cell death. Plos One, 9, 7.) The authors acknowledge Acute Lymphoblastic Leukemia as the most common childhood malignancy and designating approximately one-third of the completely pediatric cancers with the most incidences in children between two to five years. Acute lymphoblastic leukemia, also known as acute lymphoid leukemia, is a cancer that mainly attacks the bone marrow and arises from cancerous and immature white blood cells called lymphoblast. The two subtypes of lymphocytes are T and B cells. The authors stipulate that 80% of acute lymphoblastic leukemia arise from immature B-lymphocytes. The disease is most prevalent in children; nevertheless, it has also increased in elderly populace mostly of ages 60 years and over. The authors acknowledge that causes of acute lymphoblastic leukemia are not known, but in children, generic disorders such as Down syndrome can be predisposing to the development of the disease. Massive exposure to radiation and toxic chemical also cause the disease. The main symptoms of acute lymphoblastic leukemia are buildup of the abnormal and immature white blood cells within the bone marrow and blood. Blast cells collect out of the normal cells within the bone marrow thus lowering blood counts. The disease results to decrease in normal white cells making an individual to be susceptible to infection such as sinuses, bronchitis, and pneumonia. The main signs are; enlargement of the lymph nodes within the neck and arms coupled with enlargement of the spleen. This journal also describes the treatment options for acute lymphoblastic leukemia. Acute lymphoblastic leukemia is treated by multiple chemotherapy drugs via mouth or via special intravenous line that is normally placed within a vein in the arm or chest and maintain for several months (Baraz, Cisterne, Saunders, Hewson, Thien, Weiss & Bendall, 2014). Radiation treatment I used particularly if there is involvement of the spinal fluid. Blood and marrow transplantation is also used in the treatment of the acute lymphoblastic leukemia. BMT entails administration of high dose of chemotherapy to the whole body thus lowering the blood counts. Advani, A., & Lazarus, H. M. (2011). Adult acute lymphocytic leukemia: Biology and treatment. Totowa, N.J: Humana. Advani and Lazarus (2011) give credit to the Greeks whom they say to have discovered leukemia between third and fourth century Before Christ (B.C). Consequently, according to the authors, Louis Leakey made a discovery on the Kenyan Homo erectus or Australopithecus in 1932. The authors then contend that George Statholopous, a researcher, believed that the mandible discovered, was a malignant tumor, which according to David Stathopolous may have been a cancer of the jaw common in east Africa. The authors further explain how the bones of dinosaurs believed to be affected by cancer have been discovered from 150 million years ago. It was until 1827 when John Hughes Benett made an official discovery of acute lymphoblastic leukemia in Edinburg (Advani et al., 2011). Additionally, the authors state that in 19th century, most European physicians discovered that some of their patients peculiarly high levels of white blood cells hence calling the disease “weisses blut,” to mean “white blood cells.” The year 1913 saw the classification of leukemia with Acute Lymphocytic being among the four classifications. Bacher, U., Schnittger, S., Haferlach, C., & Haferlach, T. (2009). Molecular diagnostics in acute leukemias. Clinical Chemistry & Laboratory Medicine, 47(11), 1333-1341. doi:10.1515/CCLM.2009.324 Additionally, Bacher et al (2009) point out that Acute Lymphoblastic Leukemia was discovered in 1827 with the aid of emphasis of radiation therapy. Virchow discovered acute Lymphoblastic Leukemia in the year 1857, and its diagnosis was undertaken by microscopy, which was increasingly enabled by the cytogenetic and immunophenotyping of definitive diagnosis of subtypes. The author stipulates that the PT-PRC gene, regulator of B and T-cell receptor signaling, normally encode the protein tyrosine phosphatase CD45. CD45 negatively regulates the JAK family kinases downstream of cytokine receptors. Thus, the presence of CD45 results to inactivating mutations within the T-cell Acute Lymphoblastic Leukemia. Loss of function mutations of the CD45 results to detection of activating mutations within IL-7R, JAK1 or LCK, coupled with down-regulation of the CD45 expression thus causing an increase in signaling downstream of the oncoproteins. Moreover, demonstration of downstream of CD45 sensitizes T cells to cytokine stimulation. Knowles, D. M. (1992). Neoplastic hematopathology. Baltimore: Williams & Wilkins According to Knowles (1992), translocation of chromosomes is the main the cause of acute lymphoblastic leukemia. Knowles describes chromosomes as long molecules of DNA found in every cell. DNA, on the other hand, is the chemical, which creates our genes. Normally when a cell divides into two cells that are new, the outcome in the chromosomes is a new copy of the DNA. Usually, this process is never perfect, and plenty of errors that may affect the DNA occur (Knowles, 1992). As stated earlier, the author contends that a translocation is the most common cause of acute lymphoblastic leukemia as far as the DNA is concerned. According to this book, DNA in human is packaged in 23 pairs of chromosomes. In this book, translocation occurs when a DNA from one chromosome separates and becomes attached to a different chromosome. According to Knowles (1992), the point on the chromosome where the DNA breaks can affect the gene positively or negatively; it is capable of turning on the oncogenes or turning off the gene that assist the cell mature. According to this book, Philadelphia chromosome is the common translocation in Acute Lymphoblastic leukemia in Adults, and it involves a swapping DNA between chromosomes 9 and 22, usually abbreviated as t(9; 22). The condition usually occurs in approximately one out of four adults in cases of acute lymphoblastic leukemia. Knowles comprehensively explains how other translocations such as between 4 and 11, or t(4; 11) and 8 and 14, or t(8;14) can also lead to the development of ALL. Consequently, changes in chromosomes such as deletion, which involves the loss of certain parts of a chromosome and inversion, which is the rearrangement of DNA within a chromosome section can also lead to the development of acute lymphoblastic leukemia. However, Knowles describes the cause of this development as less common. According to Knowles (1992), the chromosomes that lead to the development of Acute Lymphoblastic leukemia is not known. Optimal approach to treatment of patients with Philadelphia chromosome-positive acute lymphoblastic leukemia: how to best use all the available tools. (2013). Leukemia & Lymphoma, 54(1), 21-27. doi:10.3109/10428194.2012.708753 The articles stipulate that Acute lymphoblastic leukemia express the t(9;22) chromosome translation with the BCR-ABL rearrangement. The utilization of the tyrosine kinase inhibitors results higher rate of completion of the remission and numerous patients are normally capable of receiving allogeneic hematopoietic stem cell transplant. TKI containing induction is followed by the myeloablative allogeneic HSCT resulting to long-term survival amidst 50 to 60% within the young adults. The prognosis of the adults Philadelphia chromosome-positive (Ph+) ALL is poor despite a lofty complete remission rate with the TKts coupled with the minimal chemotherapy challenges regarding the treatment of patients with PH+ALL. According to the article, initial treatment of the adult patients regarding the treatment of the ALL was carried out using the TKIs in the treatment of the Ph+ALL. Nevertheless, combination of the imatinib with the chemotherapy has demonstrated an improved complete hematological response rate and an increased applicability within the allogeneic stem cells transplantation, thus allowing a better short-term result within adults Ph+ALL. DeVries, M. L. (2009). Impact of Childhood Acute Lymphoblastic Leukemia and its Treatment on Social-Emotional, Intellectual, and Academic Abilities. The University of Arizona. According to Devries (2009), adolescents and children, suffering from Acute Lymphoblastic leukemia and treated using chemotherapy, are likely to develop treatment-related cognitive and inadequate academic. Leukemia wastes the resources of red blood cells thus leading to a reduction in production of the effective blood cells. The symptoms for ALL include fever and high risk of infection such as bacterial infection (pneumonia) because of neutropenia. Shortness in breath, vomiting, chest pain, bladder, and bowel changes are the signs of these infections (Devries, 2009). Other symptoms include high bleeding tendency, perhaps due to thrombocytopenia, headache, and fatigue. Grody, W. W. (2010). Molecular diagnostics: Techniques and applications for the clinical laboratory. London: Academic According to Grody, Nakamura, Kiechle and Strom (2009), one of the most essential prognostic factors in acute lymphoblastic leukemia, is the initial response to remission induction therapy. Consequently, Grody et al state that the technique used to detect acute lymphoblastic leukemia during initial stages includes using flow cytometry solely for aberrant immunophenoytypes detection. Additionally, the authors contend that for detection of rearrangement of antigen receptors genes, the analysis of polymerase chain reaction is acquired. These methods make it easy to search for MRD that implies minimal residual disease. On the other hand, the authors state that the current molecular detection used in detecting ALL include fluorescence in situ hybridization, commonly known as FISH, real-time quantitative rtPCR and reverse transcriptase polymerase reaction rtPCR. The authors then explain how these methods are used to the transcripts of BCR-ABL or the genes of BCR-ABL. Basically, the current molecular technique used to detect acute lymphoblastic leukemia enhances our ability of estimating risk relapse and measuring residual diseases. References Advani, A., & Lazarus, H. M. (2011). Adult acute lymphocytic leukemia: Biology and treatment. Totowa, N.J: Humana. Knowles, D. M. (1992). Neoplastic hematopathology. Baltimore: Williams & Wilkins DeVries, M. L. (2009). Impact of Childhood Acute Lymphoblastic Leukemia and its Treatment on Social-Emotional, Intellectual, and Academic Abilities. The University of Arizona. Haslam, K., Kelly, J., Morris, T., Connaghan, G., Gilligan, O., Browne, P., & Langabeer, S. E. (January 01, 2011). Screening for CRLF2 overexpression in adult acute lymphoblastic leukemia. International Journal of Laboratory Hematology, 33, 6, 17-9. Bacher, U., Schnittger, S., Haferlach, C., & Haferlach, T. (2009). Molecular diagnostics in acute leukemias. Clinical Chemistry & Laboratory Medicine, 47(11), 1333-1341. doi:10.1515/CCLM.2009.324 Baraz, R., Cisterne, A., Saunders, P. O., Hewson, J., Thien, M., Weiss, J., Basnett, J., ... Bendall, L. J. (January 01, 2014). mTOR inhibition by everolimus in childhood acute lymphoblastic leukemia induces caspase-independent cell death. Plos One, 9, 7.) Read More