Area of research
Genetics · Molecular Biology
Research interest
Research interests include Estrogen and related hormone effects, Endometrial and Cervical Cancer Treatments, Genomics and Chromatin Dynamics, and 14-3-3 protein interactions.
Progesterone receptor-dependent downregulation of MHC class I promotes tumor immune evasion and growth in breast cancer.
Estrogen-induced chromatin looping changes identify a subset of functional regulatory elements.
Supplemental Figure 3 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplementary Materials and Methods from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Data from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplemental Figure 5 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplemental Figure 7 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplementary Tables 1-5 from FOXA1 Reprogramming Dictates Retinoid X Receptor Response in <i>ESR1</i>-Mutant Breast Cancer
Identification of genomic features that uniquely impact estrogen receptor alpha binding and its effects on gene expression in endometrial cancer
Supplemental Table 1 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplemental Table 3 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplemental Table 2 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Characterizing intra- and inter-tumor heterogeneity in Ovarian high-grade serous carcinoma subtypes using single-cell and spatial transcriptomics
Supplemental Table 4 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplementary Figures 1-8 from FOXA1 Reprogramming Dictates Retinoid X Receptor Response in <i>ESR1</i>-Mutant Breast Cancer
Supplemental Figure 2 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplemental Figure 1 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplemental Table 5 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
Supplemental Figure 6 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
ZNF865 (BLST) Regulates Back Pain via Cell Senescence and DNA Damage Mechanisms
Supplemental Figure 4 from Allele-Specific Gene Regulation, Phenotypes, and Therapeutic Vulnerabilities in Estrogen Receptor Alpha–Mutant Endometrial Cancer
3D genomic analysis reveals novel enhancer-hijacking caused by complex structural alterations that drive oncogene overexpression
3D genomic analysis reveals novel enhancer-hijacking caused by complex structural alterations that drive oncogene overexpression.
Estrogen Receptor Alpha Mutations, Truncations, Heterodimers, and Therapies
ASPSCR1-TFE3 reprograms transcription by organizing enhancer loops around hexameric VCP/p97
Estrogen Receptor Alpha Mutations, Truncations, Heterodimers, and Therapies.
ASPSCR1-TFE3 reprograms transcription by organizing enhancer loops around hexameric VCP/p97.
Cis-regulatory control of transcriptional timing and noise in response to estrogen.
The EstroGene2.0 database for endocrine therapy response and resistance in breast cancer.
A Stronger IMPACT on Career Development for Early- and Mid-career Faculty.