Y. M. Shah

Fmo5 plays a sex-specific role in goblet cell maturation and mucus barrier formation

This study identifies Fmo5's sex-specific role in goblet cell maturation and mucus barrier formation in the intestine, with severe effects in female mice.

Recharacterization of RSL3 reveals that the selenoproteome is a druggable target in colorectal cancer

This study recharacterizes RSL3 as a broad selenoprotein inhibitor, showing its potential as a therapeutic target for colorectal cancer by inducing ferroptosis.

Sulfide oxidation promotes hypoxic angiogenesis and neovascularization

This study shows that sulfide oxidation via SQOR promotes hypoxic angiogenesis and neovascularization by reprogramming metabolic pathways in endothelial cells.

Targeting PIKfyve-driven lipid homeostasis as a metabolic vulnerability in pancreatic cancer

This study identifies PIKfyve as a targetable vulnerability in pancreatic cancer by showing its role in lipid metabolism and synthetic lethality with KRAS-MAPK inhibitors.

BRD4-mediated epigenetic regulation of endoplasmic reticulum-mitochondria contact sites is governed by the mitochondrial complex III

The paper identifies fedratinib as a drug that increases endoplasmic reticulum-mitochondria contact sites by inhibiting BRD4, revealing a novel epigenetic pathway linking ERMCS to cellular metabolism.

Glucose-6-phosphate dehydrogenase deficiency accelerates pancreatic acinar-to-ductal metaplasia

This study shows that G6PD deficiency accelerates pancreatic acinar-to-ductal metaplasia by enhancing NADPH production for ROS management, highlighting a metabolic role in early tumorigenesis.

GTP signaling links metabolism, DNA repair, and responses to genotoxic stress

This study identifies a GTP-mediated signaling pathway linking metabolism to DNA repair and resistance to genotoxic stress in glioblastoma and non-malignant cells.

Ras-dependent activation of BMAL2 regulates hypoxic metabolism in pancreatic cancer

This study identifies BMAL2 as a KRAS-dependent regulator of hypoxic metabolism in pancreatic cancer, showing it stabilizes HIF1A and destabilizes HIF2A under hypoxia.

PINK1 supports colorectal cancer growth by regulating the labile iron pool.

This study shows PINK1 supports colorectal cancer growth by regulating the labile iron pool through mitophagy and ferritinophagy.

Microenvironmental Ammonia Enhances T cell Exhaustion in Colorectal Cancer

This study shows that ammonia accumulation in the colorectal cancer microenvironment promotes T cell exhaustion and treatment resistance, and that reducing ammonia improves immunotherapy efficacy.

Microbiota metabolic exchange is critical for colorectal cancer redox homeostasis and growth

This study identifies reuterin as a microbial metabolite that suppresses colorectal cancer growth by altering redox balance and inducing cell death.

Intestinal ferritinophagy is regulated by HIF-2 and is essential for systemic iron homeostasis

This study shows HIF-2 regulates intestinal ferritinophagy via NCOA4, which is essential for systemic iron homeostasis.

The Pancreatic Tumor Microenvironment Compensates for Loss of GOT2

This study shows that the pancreatic tumor microenvironment compensates for loss of GOT2 by providing pyruvate, maintaining redox homeostasis and tumor growth in vivo.

GOT1 Inhibition Primes Pancreatic Cancer for Ferroptosis through the Autophagic Release of Labile Iron

This study shows that inhibiting GOT1 in pancreatic cancer primes cells for ferroptosis by promoting autophagy-mediated release of labile iron.

Hypoxia inducible factor-2α increases sensitivity of colon cancer cells towards oxidative cell death

This study shows that HIF-2α overexpression makes colon cancer cells more sensitive to oxidative cell death, suggesting a potential therapeutic strategy.

Identification, Isolation, and Characterization of Human LGR5-positive Colon Adenoma Cells

The paper isolates and characterizes LGR5-positive cells from human colon adenomas using organoids and RNA-sequencing, identifying correlations with CRC-specific genes.

Cadmium exposure inhibits branching morphogenesis and causes alterations consistent with HIF-1α inhibition in human primary breast organoids

This study shows cadmium exposure inhibits branching morphogenesis and HIF-1α activity in human breast organoids, suggesting it disrupts mammary gland development rather than promoting cancer.