- Acute Lymphoblastic Leukemia research
- Childhood Cancer Survivors' Quality of Life
- Carcinogens and Genotoxicity Assessment
- Epigenetics and DNA Methylation
- Diabetes and associated disorders
- T-cell and B-cell Immunology
- DNA Repair Mechanisms
- Immune Cell Function and Interaction
- Immunodeficiency and Autoimmune Disorders
- Gene expression and cancer classification
- Cancer-related molecular mechanisms research
- Family Support in Illness
- Gene Regulatory Network Analysis
University of Southern California
2024
Karolinska Institutet
2002
National Institute on Drug Abuse
2000
Johns Hopkins University
2000
<p>Supplementary Figure S3 shows bulk tissue expression for MLH3. This gene is expressed highly in pre-B lymphoblasts which the target transformation childhood ALL.</p>
<p>Supplementary Figure S2 shows bulk tissue expression for TDG. This gene is expressed highly in pre-B lymphoblasts (more than any other tissue) which the target transformation childhood ALL.</p>
<p>Supplementary Figure 1 shows bulk tissue expression for RECQL. This gene is expressed highly in pre-B lymphoblasts which the target transformation childhood ALL.</p>
<p>Supplementary Figure S4 shows bulk tissue expression for SETMAR. This gene is expressed substantially in pre-B lymphoblasts which the target transformation childhood ALL.</p>
<div>AbstractBackground:<p>Acute lymphoblastic leukemia (ALL) is the most common type of cancer among children. Tobacco exposure during gestation has been investigated as a potential risk factor, but its role remains undefined. Given tobacco’s toxicologic profile DNA-damaging agent, we examined impact DNA repair gene variability source vulnerability to tobacco for ALL.</p>Methods:<p>Leveraging demographic and genotype data from two large California-based ALL...
<p>Supplementary Figure S6 shows bulk tissue expression for BARD1. This gene is expressed highly in pre-B lymphoblasts (more than any other tissue) which the target transformation childhood ALL.</p>
<p>Supplementary Figure S7 shows a "interaction effect size of G x E" comparison between Non-Latino white and Latino children with ALL compared to controls. The sizes generally are not associated as group.</p>
<p>Supplementary Figure S5 shows bulk tissue expression for PDS5B. This gene is expressed highly in pre-B lymphoblasts which the target transformation childhood ALL.</p>
<p>Supplementary Figure S8 shows a "coefficient effect size" comparison between Non-Latino white and Latino children with ALL compared to controls. The sizes generally are not associated as group.</p>
Abstract Background: Acute lymphoblastic leukemia (ALL) is the most common type of cancer among children. Tobacco exposure during gestation has been investigated as a potential risk factor, but its role remains undefined. Given tobacco’s toxicologic profile DNA-damaging agent, we examined impact DNA repair gene variability source vulnerability to tobacco for ALL. Methods: Leveraging demographic and genotype data from two large California-based ALL epidemiology studies, used logistic...