Current Issue : October - December Volume : 2014 Issue Number : 4 Articles : 5 Articles
Acute lymphoblastic leukemia (ALL) is a malignant disorder that originates from one single hematopoietic precursor committed\nto B- or T-cell lineage. Ordinarily, these cells express CCR5 chemokine receptor, which directs the immune response to a cellular\npattern and is involved in cancer pathobiology. The genetic rs333 polymorphism of CCR5 (?32), results in a diminished receptor\nexpression, thus leading to impaired cell trafficking. The objective of the present study was to investigate the effect of CCR5\nchemokine receptor rs333 polymorphism in the pathogenesis of ALL. The genotype distribution was studied in 79 patients and\ncompared with 80 control subjects, in a childhood population of Southern Brazil. Genotyping was performed using DNA samples\namplified by polymerase chain reaction with sequence-specific primers (PCR-SSP). The homozygous (?32/?32) deletion was not\nobserved in any subject involved in the study. Heterozygous genotype was not associated with ALL risk (OR 0.7%; 95% CI 0.21ââ?¬â??\n2.32; P > 0.05), nor recurrence status of ALL (OR 0.86; 95% CI 0.13ââ?¬â??5.48; P > 0.05). This work demonstrated, for the first time,\nno significant differences in the frequency of the CCR5/?32 genotype between ALL and control groups, indicating no effect of this\ngenetic variant on the ALL susceptibility and recurrence risk....
Introduction. Different ferric and ferrous iron preparations can be used as oral iron supplements. Our aim was to compare the\neffects of oral ferric and ferrous iron therapies in women with iron deficiency anaemia. Methods.The present study included 104\nwomen diagnosed with iron deficiency anaemia after evaluation. In the evaluations performed to detect the aetiology underlying the\niron deficiency anaemia, it was found and treated. After the detection of the iron deficiency anaemia aetiology and treatment of the\nunderlying aetiology, the ferric group consisted of 30 patients treatedwith oral ferric protein succinylate tablets (2 Ã?â?? 40mg elemental\niron/day), and the second group consisted of 34 patients treated with oral ferrous glycine sulphate tablets (2 Ã?â?? 40mg elemental\niron/day) for three months. In all patients, the following laboratory evaluations were performed before beginning treatment and\nafter treatment. Results.Themean haemoglobin and haematocrit increases were 0.95 g/dL and 2.62% in the ferric group, while they\nwere 2.25 g/dL and 5.91% in the ferrous group, respectively. A significant difference was found between the groups regarding the\nincrease in haemoglobin and haematocrit values (P < 0.05). Conclusion.Data are submitted on the good tolerability, higher efficacy,\nand lower cost of the ferrous preparation used in our study....
Thalassemia and hemoglobin E (Hb E) are common in Thailand. Individuals with thalassemia trait usually have a normal\nhemoglobin concentration or mild anemia. Therefore, thalassemic individuals who have minimum acceptable Hb level may be\naccepted as blood donors. This study was aimed at determining the frequency of ?-thalassemia 1 trait, ?-thalassemia trait, and\nHb E-related syndromes in Southern Thai blood donors. One hundred and sixteen voluntary blood donors, Southern Thailand\norigin, were recruited for thalassemia and Hb E screening by red blood cell indices/dichlorophenolindophenol precipitation test.\n?-Thalassemia and Hb E were then identified by high performance liquid chromatography and 4 common ?-thalassemia deletions\nwere characterized by a single tube-multiplex gap-polymerase chain reaction. Overall frequency of hemoglobinopathies was 12.9%,\nclassified as follows: homozygous ?-thalassemia 2 (1.7%), heterozygous ?-thalassemia 1 (1.7%), heterozygous ?-thalassemia without\n?-thalassemia (0.9%), heterozygous Hb E without ?-thalassemia (5.2%), double heterozygotes for Hb E/?-thalassemia 1 (1.7%),\nhomozygous Hb E without ?-thalassemia (0.9%), and homozygousHb E with heterozygous ?-thalassemia 2 (0.9%). The usefulness\nof thalassemia screening is not only for receiving highly effective red blood cells in the recipients but also for encouraging the control\nand prevention program of thalassemia in blood donors....
Acute myeloid leukemia (AML) is a genetically heterogeneous disease. Certain cytogenetic and molecular genetic mutations are\nrecognized to have an impact on prognosis, leading to their inclusion in some prognostic stratification systems. Recently, the advent\nof high-throughput whole genome or exome sequencing has led to the identification of several novel recurrent mutations in AML,\na number of which have been found to involve genes concerned with epigenetic regulation. These genes include in particular\nDNMT3A, TET2, and IDH1/2, involved with regulation of DNA methylation, and EZH2 and ASXL-1, which are implicated in\nregulation of histones. However, the precise mechanisms linking these genes to AML pathogenesis have yet to be fully elucidated\nas has their respective prognostic relevance. As massively parallel DNA sequencing becomes increasingly accessible for patients,\nthere is a need for clarification of the clinical implications of these mutations. This review examines the literature surrounding the\nbiology of these epigenetic modifying genes with regard to leukemogenesis and their clinical and prognostic relevance in AML\nwhen mutated....
Multiple myeloma is a malignant proliferation of monoclonal plasma cells leading to clinical features that include hypercalcaemia,\nrenal dysfunction, anaemia, and bone disease (frequently referred to by the acronym CRAB) which represent evidence of end organ\nfailure. Recent evidence has revealed myeloma to be a highly heterogeneous disease composed of multiple molecularly-defined\nsubtypes each with varying clinicopathological features and disease outcomes. The major division within myeloma is between\nhyperdiploid and nonhyperdiploid subtypes. In this division, hyperdiploid myeloma is characterised by trisomies of certain odd\nnumbered chromosomes, namely, 3, 5, 7, 9, 11, 15, 19, and 21 whereas nonhyperdiploid myeloma is characterised by translocations\nof the immunoglobulin heavy chain alleles at chromosome 14q32 with various partner chromosomes, the most important of\nwhich being 4, 6, 11, 16, and 20. Hyperdiploid and nonhyperdiploid changes appear to represent early or even initiating mutagenic\nevents that are subsequently followed by secondary aberrations including copy number abnormalities, additional translocations,\nmutations, and epigenetic modifications which lead to plasma cell immortalisation and disease progression. The following review\nprovides a comprehensive coverage of the genetic and epigenetic events contributing to the initiation and progression of multiple\nmyeloma and where possible these abnormalities have been linked to disease prognosis....
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