Publications
258
Citations
6,728
Est. group size
~1
Recurring co-author estimate
Active years
34
Publishing since 1993
Xiaoping Wan's work centers on the molecular biology of endometrial cancer, particularly how a protein called NSD1 chemically modifies (methylates) another protein, PPARγ, to regulate PTEN activity and control tumor cell metabolism (glycolysis) and cancer progression. The recent record consists largely of supplementary materials tied to a single detailed study on this gene-regulation pathway in endometrial cancer. Broader listed interests span epigenetics, cancer metabolism, and cellular signaling, though the available publication data is dominated by one project.
Publication counts have fluctuated over the past decade with a notable spike in 2020 and again in 2026, suggesting bursty rather than steadily increasing output, likely tied to large multi-part publications.
Generated by claude-sonnet-5 from public bibliographic data · Jul 20, 2026
- Supplementary Figure S12 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Table S7 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Table S5 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S4 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S24 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S14 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Table S3 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S2 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S9 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S11 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S20 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S21 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S10 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Table S1 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Supplementary Figure S6 from NSD1-Mediated PPARγ Methylation Enhances PTEN Activity to Suppress Glycolysis and Tumor Progression in Endometrial Cancer
2026
- Figshare×4
- Nature Communications×3
- eLife×3
- Oncogene×3
- Oncotarget×3
- Dmitry Terentyev
Medicine · The Ohio State University
- Angelina Ramirez‐Navarro
Medicine · The Ohio State University
- Brian R. Overholser
Medicine · Purdue University West Lafayette
- Apoorva Purohit
Medicine · The Ohio State University
- Drew Nassal
Medicine · The Ohio State University
This profile was generated automatically from public scholarly data (OpenAlex). Group size and activity levels are estimates derived from co-authorship patterns.
Last updated Jul 19, 2026.
Claim or correct this profile