Christopher J. Clarke

Neutral Sphingomyelinase-2 Restrains TAZ to Suppress Breast Tumor Growth

This study identifies nSMase2 as a metabolic tumor suppressor in breast cancer by restraining TAZ and inhibiting tumorigenesis.

Oncogene-driven metabolic regulation of Dihydroceramide Desaturase 1 (DES1) converges on GAPDH in matrix-detached conditions

This study identifies a novel pathway where oncogenic PI3K pathway drives DES1 activity through GAPDH in matrix-detached conditions, linking glucose and sphingolipid metabolism.

Metabolic plasticity enables cancer adaptation to acidic tumor ecosystems

This study shows cancer cells adapt to acidic tumor environments through sphingolipid metabolic plasticity, revealing that targeting metabolic flexibility, not individual pathways, may be more effective.

SERUM AND PLASMA SPHINGOLIPIDS AS BIOMARKERS OFANTHRACYCLINE-INDUCED CARDIOTOXICITY

This study identifies serum and plasma sphingolipids as potential biomarkers for anthracycline-induced cardiotoxicity, showing correlations with cardiac outcomes during and after therapy.

A Critical Role for Neutral Sphingomyelinase-2 in Doxorubicin-induced Cardiotoxicity

This study identifies nSMase2 as a critical mediator of Doxorubicin-induced cardiotoxicity and shows its loss protects against cardiac damage.

Remote organ cancer adversely alters renal function and induces kidney injury, inflammation, and fibrosis.

This study shows that certain cancers alter kidney function and cause injury, inflammation, and fibrosis, independent of chemotherapy or metastasis.