Pharmacodynamic characterization of eryaspase (L-asparaginase encapsulated in red blood cells) in combination with chemotherapy in a phase 2/3 trial in patients with relapsed acute lymphoblastic leukemia (NCT01518517).

El‐Hariry, Iman; Aguéra, Karine; Hoke, Frank; Swart, K.J; Hamm, Adam; Kay, Richard; Lorenzi, Philip L.

doi:10.1200/jco.2018.36.15_suppl.7049

Cited by 1 publication

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“…Pegylated enzymes that are covalently linked to polyethylene glycol (PEG), including PEGasparaginase, PEG-arginase, PEG-arginine deiminase and PEGmethioninase, have been developed to decrease the immunogenicity and prolong the half-life (19,23,163,164). Erythrocyte-encapsulated asparaginase (eryaspase) has less toxicity and improves patient survival in clinical trials for the treatment of patients with pancreatic cancer or acute lymphocytic leukemia when combined with chemotherapy (165,166). These findings shed light on the translation of amino acids-depletion enzymes into clinical application in cancer treatment.…”

Section: Enzymatic Degradation-or Dietary Restriction-mediated Nutrient Depletionmentioning

confidence: 99%

Targeting Nutrient Dependency in Cancer Treatment

Fan

Li²,

Gao

et al. 2022

Front. Oncol.

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Metabolic reprogramming is one of the hallmarks of tumor. Growing evidence suggests metabolic changes that support oncogenic progression may cause selective vulnerabilities that can be exploited for cancer treatment. Increasing demands for certain nutrients under genetic determination or environmental challenge enhance dependency of tumor cells on specific nutrient, which could be therapeutically developed through targeting such nutrient dependency. Various nutrients including several amino acids and glucose have been found to induce dependency in genetic alteration- or context-dependent manners. In this review, we discuss the extensively studied nutrient dependency and the biological mechanisms behind such vulnerabilities. Besides, existing applications and strategies to target nutrient dependency in different cancer types, accompanied with remaining challenges to further exploit these metabolic vulnerabilities to improve cancer therapies, are reviewed.

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