R. J. Shaw

EGFR+ lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth

This study shows EGFR-mutant lung adenocarcinomas exploit alveolar macrophage metabolism via GM-CSF--PPARγ signaling to support tumor growth and EGFR signaling, suggesting new therapeutic strategies combining statins and PPARγ inhibition.

Inter-organelle crosstalk supports acetyl-coenzyme A homeostasis and lipogenesis under metabolic stress

The paper investigates how acetyl-CoA homeostasis and lipogenesis are maintained under metabolic stress through inter-organelle crosstalk using isotope tracing in knockout cell lines.

Circadian disruption enhances HSF1 signaling and tumorigenesis in Kras-driven lung cancer

This study shows that chronic circadian disruption increases tumor burden in KRAS-driven lung cancer by enhancing HSF1 signaling and tumorigenesis.

Non-conserved metabolic regulation by LKB1 distinguishes human and mouse lung adenocarcinoma

This study identifies a metabolic divergence between human and mouse lung adenocarcinomas due to LKB1-dependent regulation of TPI1 phosphorylation, highlighting limitations of mouse models for studying human cancer.

The autophagy initiating kinase ULK1 is required for pancreatic cancer cell growth and survival

This study shows ULK1 is essential for pancreatic cancer cell growth and survival, and ULK1 inhibitors can enhance immunotherapy by increasing MHC Class I expression.

Metabolic adaptation to progressive mitochondrial dysfunction in aging POLGD257A mice

This study examines metabolic changes in aging PolgD257A mice, revealing altered glycolysis, urea cycle dysfunction, and lipidome shifts linked to neuropathy.

HDAC3 regulates senescence and lineage-specific transcriptional programs in non-small cell lung cancer

This study identifies HDAC3's role in regulating senescence and lineage-specific transcription in NSCLC, revealing therapeutic implications for HDAC3 inhibitors.

Inhibition of CAMKK2 impairs autophagy and castration-resistant prostate cancer via suppression of AMPK-ULK1 signaling

This study shows that inhibiting CAMKK2 blocks autophagy and slows castration-resistant prostate cancer by disrupting AMPK-ULK1 signaling.

PHD3 controls energy homeostasis and exercise capacity.

The paper was submitted in error and the authors do not wish it to be cited.