Katelyn Becker

The paper analyzes bone marrow microenvironment changes in HMA-resistant MDS patients treated with guadecitabine and atezolizumab, finding that long-term survivors show reduced immunosuppressive monocytes and expanded effector lymphocytes.

This paper shows that a high-fat diet increases endometrial hyperplasia risk by reprogramming stromal fibroblasts to a pro-fibrotic state driven by estrogen.

This study identifies YAP signaling as a driver of resistance to MEK and AKT inhibitors in NF1-related MPNSTs using preclinical models and spatial transcriptomics.

The paper identifies group II p21-activated kinases as regulators of α-synucleinopathy by linking network vulnerability analysis to gene expression and pharmacological interventions.

This study shows that developmental exposure to dieldrin causes sex-specific DNA modifications in neurodevelopmental pathways, potentially increasing Parkinson's disease risk later in life.

The paper uses spatial transcriptomics to identify specific cortical neurons vulnerable to Lewy pathology in PD and discovers a conserved molecular dysfunction signature in both mice and humans.

This study shows that α-synuclein fibrils injected into mouse forebrain cause regional pathology, early neuronal degeneration, and cognitive deficits resembling Lewy body diseases.

This study shows that T cells reduce phosphorylated α-synuclein pathology in a mouse model of α-synucleinopathy.

The paper tests if inhibiting the mitochondrial pyruvate carrier reduces synucleinopathy in PD models but finds no effect on Syn aggregation or neurodegeneration.

This study shows that loss of one Engrailed1 allele in mice increases α-synuclein aggregation after PFF injection, suggesting a role for En1 in PD pathology.