Xinran Wang

ORCID: 0009-0000-1805-3280
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About
Contact & Profiles
Research Areas
  • 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>

10.1158/1055-9965.28171663 preprint EN cc-by 2025-01-09

<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>

10.1158/1055-9965.28171666 preprint EN cc-by 2025-01-09

<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>

10.1158/1055-9965.28171669 preprint EN cc-by 2025-01-09

<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>

10.1158/1055-9965.28171660 preprint EN cc-by 2025-01-09

<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...

10.1158/1055-9965.c.7618117 preprint EN 2025-01-09

<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>

10.1158/1055-9965.28171654 preprint EN cc-by 2025-01-09

<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>

10.1158/1055-9965.28171651 preprint EN cc-by 2025-01-09

<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>

10.1158/1055-9965.28171657 preprint EN cc-by 2025-01-09

<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>

10.1158/1055-9965.28171648 preprint EN cc-by 2025-01-09

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...

10.1158/1055-9965.epi-24-1037 article EN Cancer Epidemiology Biomarkers & Prevention 2024-11-04
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