J.-E. Sarry

Ferritinophagy is a Druggable Vulnerability of Quiescent Leukemic Stem Cells

The paper identifies ferritinophagy as a therapeutic target in quiescent leukemic stem cells, showing that inhibiting NCOA4 reduces leukemia.

SCD inhibition eradicates AML displaying high de novo fatty acid desaturation and synergizes with chemotherapy

SCD inhibition induces AML cell death and synergizes with chemotherapy to prolong survival in murine AML models.

FAO-supported OxPhos leukemic stem cells are sensitive to cold.

The paper identifies cold sensitivity as a vulnerability in FAO-supported OxPhos leukemic stem cells, which can be exploited for therapeutic targeting.

Adaptation of redox metabolism in drug-tolerant persister cells is a vulnerability to prevent relapse in pancreatic cancer

This study identifies mitochondrial and redox metabolic reprogramming in drug-tolerant persister cells of pancreatic cancer and shows that targeting redox metabolism can prevent relapse.

Cytidine deaminase regulates mitochondrial biogenesis in pancreatic cancer cells

This study shows that Cytidine deaminase (CDA) promotes mitochondrial biogenesis and oxidative phosphorylation in pancreatic cancer cells, independent of its deaminase activity, revealing new therapeutic targets.

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress in FLT3-mutant leukemia

This study identifies C/EBPα's role in promoting lipid anabolism and vulnerability to lipid oxidative stress in FLT3-mutant AML through regulation of the FASN-SCD axis.

SHED-dependent oncogenic signalling of the PEAK3 pseudo-kinase

This study identifies PEAK3 as an oncogenic pseudo-kinase that uses the SHED module to activate AKT signaling and promote cancer growth.

The NADPH oxidase NOX2 is a marker of adverse prognosis involved in chemoresistance of Acute Myeloid Leukemias

This study identifies NOX2 as a marker of poor prognosis and a contributor to chemoresistance in AML, showing its upregulation in drug-resistant cells and association with adverse outcomes.

Mitochondrial determinants of response and resistance to venetoclax plus cytarabine duplet therapy in acute myeloid leukemia

This study identifies mitochondrial determinants of response and resistance to venetoclax plus cytarabine therapy in AML, showing that OxPHOS is a predictive marker and that targeting ETCI improves outcomes.

Adrenomedullin-CALCRL Axis Controls Relapse-Initiating Drug Tolerant Acute Myeloid Leukemia Cells

The paper identifies the ADM-CALCRL axis as a driver of drug-tolerant AML cells that persist after chemotherapy and proposes it as a therapeutic target to prevent relapse.

Extracellular ATP and CD39 activate cAMP-mediated mitochondrial stress response to promote cytarabine resistance in acute myeloid leukemia

This study shows CD39 and extracellular ATP promote cytarabine resistance in AML by enhancing mitochondrial activity via cAMP signaling, suggesting CD39 as a therapeutic target.

Combinatory therapy targeting mitochondrial oxidative phosphorylation improves efficacy of IDH mutant inhibitors in acute myeloid leukemia

This study shows that combining mitochondrial oxidative phosphorylation inhibitors with IDH mutant inhibitors improves anti-AML efficacy in IDH-mutant AML patients, especially those who relapse or are unresponsive.

Targeting the SUMO pathway primes all-trans-retinoic acid-induced differentiation of non promyelocytic Acute Myeloid Leukemias

This study shows that inhibiting the SUMO pathway enhances the effectiveness of all-trans-retinoic acid in treating non-APL AMLs by promoting differentiation and reducing proliferation.