My research centers on the molecular mechanisms of estrogen action and on endocrine therapy resistance in breast cancer and liver responses to environmental pollutants and diet that promote metabolic dysfunction-associated steatotic liver disease (MASLD).  I work with breast cancer cell line models and mice to study tissue-specific estrogen, diet, and polychlorinated biphenyls (PCB)-exposure-regulated transcriptome and epitranscriptomic signaling.  I have expertise in cell-based studies on estrogen receptor-DNA interaction, transcriptional regulation of mRNA and non-coding RNAs, e.g., miRNA and lncRNAs and their gene targets, protein expression, lipidomics, nongenomic signaling by estrogens, mechanisms of endocrine disrupting and metabolism disrupting chemicals, Oxford nanopore long read direct RNA- seq – including identification of site-specific m6A in mRNA transcripts, Illumina short read RNA- and miRNA-seq, m6A-RNA-immunoprecipitation (RIP)- RT-qPCR, mass-spectrometry-based detection of RNA modifications, and quantitative bioinformatic data analyses.  In collaboration with Dr. Brian Clem, my lab recently performed single nuclear RNA seq (snRNA-seq, Parse Biosciences) to define the transcriptome changes in human breast cancer patient derived xenograft (PDX) grown in the milk duct of the mammary gland of female mice following the mouse intra-ductal (MIND) model.  In collaboration with Drs. Matthew Cave and Belinda Petri, we are examining how epitranscriptomic changes in mouse liver following exposure to high fat or low fat diet in combination with PCB exposures regulate m6A epitranscriptome changes, splicing, transcript and protein abundance, and pathways, especially lipid metabolism, in a mouse model of MASLD and its progression to metabolic-dysfunction associated steatohepatitis (MASH).