Development Of Leukemia In Children Research Articles

The Effect of Parents’ Education on the Prevalence of Acute Leukemia in Children

Background: Cancer is one of the most common causes of death in children. The aim of this study was to evaluate the effect of parents’ education on the prevention of leukemia in children. Methods: This study was a survey performed in Mahak and Bahrami hospitals in 2019. Checklists were completed in two groups of parents, those who had a child with leukemia and those who had a healthy child. Data were analyzed by SPSS statistical software. Results: In this study, 365 individuals in the healthy group and 81 in the cancer group participated. More than sixty percent (62.3%) were females. The highest frequency of age in both groups was 31 - 40 years. The highest frequency of parents’ education in the healthy group was associate degree and bachelor (about 51%) and in the cancer group, lowers than associate degree (about 73%). There was a significant relationship between parents’ education and the prevalence of leukemia in children (P < 0.05). Conclusions: Based on the study, parents’ higher education can be effective in preventing the development of leukemia in children.

Molecular epidemiology of acute leukemia in children: causal model, interaction of three factors—susceptibility, environmental exposure and vulnerability period

Acute leukemias have a huge morphological, cytogenetic and molecular heterogeneity and genetic polymorphisms associated with susceptibility. Every leukemia presents causal factors associated with the development of the disease. Particularly, when three factors are present, they result in the development of acute leukemia. These phenomena are susceptibility, environmental exposure and a period that, for this model, has been called the period of vulnerability. This framework shows how the concepts of molecular epidemiology have established a reference from which it is more feasible to identify the environmental factors associated with the development of leukemia in children. Subsequently, the arguments show that only susceptible children are likely to develop leukemia once exposed to an environmental factor. For additional exposure, if the child is not susceptible to leukemia, the disease does not develop. In addition, this exposure should occur during a time window when hematopoietic cells and their environment are more vulnerable to such interaction, causing the development of leukemia. This model seeks to predict the time when the leukemia develops and attempts to give a context in which the causality of childhood leukemia should be studied. This information can influence and reduce the risk of a child developing leukemia.

Familial history of cancer and leukemia in children younger than 2 years of age in Brazil

The objective of this study was to determine the contribution of a familial history of cancer (FHC) to the development of leukemia in children below 2 years of age. This is a national hospital-based case-control study of children 0-24 months of age recruited from 15 Brazilian hospitals from several regions providing oncological care and local general hospitals. Participants' FHC antecedents were obtained through face-to-face interviews with the mothers of cases and controls using a standardized questionnaire. Unconditional logistic regression was used to determine crude and adjusted (adj.) odds ratios (OR), and the respective 95% confidence intervals (CI), of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) after adjustment for selected variables. FHC antecedents were obtained from 178 ALL, 51 AML, and 428 controls. FHC in second-degree relatives (grandparents, uncles, cousins) showed an adj. OR=1.66 (95% CI 1.12-2.45) for ALL. Antecedents of two or more relatives with cancer showed a statistically significant two-fold higher risk of either ALL or AML. Paternal, and joint paternal and maternal antecedents of cancer also showed statistically significant higher adj. OR, respectively: 1.80 and 1.89 for ALL, and 2.34 and 3.23 for AML. Hematological malignancies among second-degree relatives showed an adj. OR=3.48 (95% CI 1.72-7.09) for ALL. According to the anatomic site, antecedents of leukemia/lymphoma among case relatives, compared with the control ones, showed an OR=2.98 (95% CI 1.52-5.82) for ALL, whereas stomach cancer antecedents showed an OR=3.55 (95% CI 1.02-12.39) for AML. The observed results support the hypothesis that FHC antecedents are associated with leukemogenesis in children below 2 years of age.

Manipulating piggyBac Transposon Chromosomal Integration Site Selection in Human Cells

The ability to direct gene delivery to a user-defined chromosomal location would greatly improve gene transfer applications. The piggyBac transposon system is a nonviral gene transfer system proven effective in a variety of cells and tissues, including human cells. We fused a highly site-specific synthetic zinc-finger DNA-binding domain (ZFP) to the N-terminus of the piggyBac transposase and evaluated site-directed genomic integration in human cells. Chimeric ZFP-piggyBac transposase exhibited robust gene transfer activity, targeted binding to a cognate endogenous chromosomal ZFP site in the human genome, and site-directed transposon integration into an episomal plasmid target containing a single ZFP site in human cells. We evaluated the ability of ZFP-piggyBac to direct gene integration into an engineered chromosomal ZFP target site in the human genome and consistently observed a higher degree of ZFP-piggyBac site-directed genomic integration when compared to native piggyBac. Chromatin immunoprecipitation (ChIP) experiments revealed binding of native piggyBac to our engineered TTAA-containing chromosomal target which supported integration, but not a TTAA-deficient chromosomal target which lacked integration. Our results offer insight into the requirements for using a chimeric zinc finger-piggyBac transposase to direct integration into a user-defined chromosomal location.

Childhood leukemia in the vicinity of nuclear power plants in Germany.

The causes of leukemia are largely unclear. The question whether leukemia rates are increased near nuclear power plants is controversial. The German Childhood Cancer Registry has published an epidemiological case-control study on childhood cancer and nuclear power plants. The study was based on the distance of children's residences from nuclear power plants and addressed the question whether children under age 5 with cancer live closer, on average, to nuclear power plants than randomly selected controls. Odds Ratios (OR) for distance categories and standardized incidence ratios (SIR) were calculated. An association was found between the nearness of residence to nuclear power plants and the risk of leukemia (593 cases, 1766 controls). Within the 5-km zone, the OR for the development of leukemia in children under 5 years of age was 2.19 compared to the rest of the region, and this elevation of the OR was statistically significant. The incidence of leukemia in the overall study region was the same as that in Germany as a whole (SIR=0.99; 95% confidence interval 0.92-1.07). Based on the available information about radiation emissions from German nuclear power plants, a direct relation to radiation seems implausible. Many factors may conceivably cause leukemia, possibly operating in combination, and these factors may be present to a greater extent in the vicinity of German nuclear power plants.

Patterns of Hematopoietic Lineage Involvement in Children With Neurofibromatosis Type 1 and Malignant Myeloid Disorders

AbstractChildren with neurofibromatosis type 1 (NF1) are at increased risk of developing malignant myeloid disorders, particularly juvenile chronic myelogenous leukemia/juvenile myelomonocytic leukemia (JCML/JMML). We investigated bone marrows from 11 such patients (8 boys and 3 girls) and detected allelic losses at the NF1 locus in 4 of them and probable losses in 2 others. To determine which hematopoietic cell lineages were derived from the abnormal clones, Epstein-Barr virus (EBV)-transformed cell lines and CD34+ cells were analyzed from 3 children with JCML with allelic losses in unfractionated marrow. CD34 cells from these 3 patients lacked the normal NF1 allele, whereas EBV cell lines retained it. Erythroblasts plucked from the burst-forming unit-erythroid colonies of one of these children lacked the normal NF1 allele. We also studied a 10-month-old boy with NF1 who developed an unusual myeloproliferative syndrome. His bone marrow and EBV cell line both showed loss of the normal NF1 allele. In our series and in the literature, male sex and maternal transmission of NF1 were associated with the highest risk of myeloid leukemia. These data (1) provide strong genetic evidence that NF1 functions as a tumor-suppressor in early myelopoiesis, (2) confirm the clonal nature of JCML/JMML, (3) suggest that the elevation in fetal hemoglobin seen in JCML/JMML is a result of primary involvement of erythroid progenitors in the malignant clone, (4) show consistent loss of NF1 in the CD34 cells of affected children and show that the malignant clone may also give rise to pre-B cells in some cases, and (5) implicate epigenetic factors in the development of leukemia in children with NF1.

Patterns of hematopoietic lineage involvement in children with neurofibromatosis type 1 and malignant myeloid disorders

Children with neurofibromatosis type 1 (NF1) are at increased risk of developing malignant myeloid disorders, particularly juvenile chronic myelogenous leukemia/juvenile myelomonocytic leukemia (JCML/JMML). We investigated bone marrows from 11 such patients (8 boys and 3 girls) and detected allelic losses at the NF1 locus in 4 of them and probable losses in 2 others. To determine which hematopoietic cell lineages were derived from the abnormal clones, Epstein-Barr virus (EBV)-transformed cell lines and CD34+ cells were analyzed from 3 children with JCML with allelic losses in unfractionated marrow. CD34 cells from these 3 patients lacked the normal NF1 allele, whereas EBV cell lines retained it. Erythroblasts plucked from the burst-forming unit-erythroid colonies of one of these children lacked the normal NF1 allele. We also studied a 10-month-old boy with NF1 who developed an unusual myeloproliferative syndrome. His bone marrow and EBV cell line both showed loss of the normal NF1 allele. In our series and in the literature, male sex and maternal transmission of NF1 were associated with the highest risk of myeloid leukemia. These data (1) provide strong genetic evidence that NF1 functions as a tumor-suppressor in early myelopoiesis, (2) confirm the clonal nature of JCML/JMML, (3) suggest that the elevation in fetal hemoglobin seen in JCML/JMML is a result of primary involvement of erythroid progenitors in the malignant clone, (4) show consistent loss of NF1 in the CD34 cells of affected children and show that the malignant clone may also give rise to pre-B cells in some cases, and (5) implicate epigenetic factors in the development of leukemia in children with NF1.

The Epidemiology Of Leukemia

Publisher Summary This chapter reviews the etiology of leukemia and discusses the contributions made by a wide range of epidemiological studies. It focuses on the exploring aspects of etiology that are potentially suitable for primary prevention. Epidemiology can contribute to the aspects of the identification of high risk groups suitable for screening, to the reduction of delay in diagnosis, to the organization and deployment of treatment facilities, and to the support of the patient and family during treatment. The chapter reviews what is known about leukemia from published national mortality statistics; some data are available also from national publications on incidence, discussing leukemia mortality by age and sex and leukemia incidence by age, sex, color, and trends. It also discusses the factors relevant to the development of leukemia in children and to the development of leukemia in adults. This division is somewhat arbitrary, but it has an advantage because of the much closer time relationship between factors operating on the fetus and childhood leukemia compared with more general environmental agents and adult leukemia such as maternal irradiation, genetic factors, drugs, or irradiation. Immunological deficiencies and a number of other very rare diseases are associated with an increased risk of leukemia.