M. Black

Investigating the mode of action for liver toxicity and wasting-like responses produced by high dose exposures to longer chain perfluoroacid substances (PFAS) using high throughput transcriptomics

This study identifies pathway perturbations in liver caused by PFAS exposure, showing longer-chain PFAS downregulate lipid and steroid metabolism genes, similar to TCDD, suggesting a common MOA involving PPAR inhibition.

Empowering high-throughput high-content analysis of 3D tumor models: Open-source software for automated non-confocal image analysis

This paper develops open-source software for automated analysis of 3D tumor models using non-confocal microscopy, achieving accurate drug sensitivity measurements and significantly reducing processing time.

TRIB1 modulates transcriptional programming in breast cancer cells to regulate cell proliferation

This study shows TRIB1 promotes breast cancer cell proliferation by regulating MYC expression and cell cycle progression through interactions with β-catenin and ER-driven transcription.

The fate of intracoelomic acoustic transmitters in Atlantic Salmon (Salmo salar) post-smolts and wider considerations for casual factors driving tag retention and mortality in fishes

This study assesses tag retention and post-surgical mortality in Atlantic salmon post-smolts and finds high tag expulsion rates and weak negative correlation with tag:body mass ratio.

RBFOX2 deregulation promotes pancreatic cancer metastasis through alternative splicing

This study identifies RBFOX2 deregulation as a driver of pancreatic cancer metastasis through alternative splicing of ABI1, enhancing cancer cell stemness and invasiveness.

Structural and mechanistic basis for protein glutamylation by the kinase fold

This study reveals how the kinase fold of SidJ catalyzes protein glutamylation and identifies SdjA as a glutamylase regulating SidE-ligases during Legionella infection.

Modeling adaptive therapy in non-muscle invasive bladder cancer

This study models adaptive therapy for non-muscle invasive bladder cancer to control tumor size and reduce recurrence by analyzing mutational heterogeneity and cytokine profiles.

Recurrent loss of heterozygosity correlates with clinical outcome in pancreatic neuroendocrine cancer

The paper identifies two distinct aneuploidy patterns in pancreatic neuroendocrine tumors (pNETs) associated with poor and good clinical outcomes, respectively, and highlights MEN1 mutations as a significant driver.