Issam Ben‐Sahra

This study identifies arginine synthesis pathway and ASS1 as key factors in mRNA translation reprogramming and ICI resistance in cutaneous melanoma, showing that targeting ASS1 can restore sensitivity to anti-PD-1.

This study identifies MELK as a key driver of metabolic adaptation and therapy resistance in melanoma, showing that inhibiting MELK can sensitize resistant cells to immunotherapy.

This study shows that the extracellular matrix promotes guanylate production in pancreatic cancer cells, reducing oxaliplatin-induced DNA damage and enhancing proliferation.

This study identifies PRPS-PRPSAP complexes as regulators of histone chaperone interactions, linking nucleotide biosynthesis to chromatin assembly.

This study shows that succinate dehydrogenase supports de novo purine synthesis in cancer cells, and its inhibition reduces proliferation by impairing purine biosynthesis and inducing a compensatory salvage pathway.

This study identifies serine synthesis as a metabolic vulnerability in sunitinib-resistant renal cell carcinoma, showing that inhibiting key enzymes enhances drug sensitivity.

This study shows that glutamine deprivation promotes podocyte maturation in renal organoids through metabolic and transcriptomic changes during differentiation.

The paper constructs a coessential genetic network to map the dynamic cellular stress response across 625 cancer cell lines, identifying key regulators and modules involved in stress resilience.

The paper identifies a founder variant in SZT2 associated with neurodevelopmental disorder and develops a method to distinguish pathogenic variants from VUSs in SZT2.