Asparaginase Erwinia chrysanthemi for acute lymphoblastic leukemia and
                        lymphoblastic lymphoma

Gao, Congying; Ma, Xiangyu; Zhang, Zifan; Lu, Qisi; Ashby, Charles R.; Wei, Liuya; Chen, Zhe‐Sheng

doi:10.1358/dot.2022.58.6.3413459

Cited by 5 publications

(6 citation statements)

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“…Asparaginase converts asparagine and glutamine to aspartate and glutamate, respectively, thereby decreasing plasma concentrations of asparagine and glutamine which ultimately reduces glutamine availability to the cancer cells 56 . Recent studies support the use of asparaginase and asparaginase derivatives as cancer therapeutics 9,10,52,57,58 . Mesothelioma is a highly aggressive and treatment‐resistant cancer, and our findings suggest that asparaginase‐dependent glutamine depletion may be a useful mesothelioma treatment strategy.…”

Section: Discussionmentioning

confidence: 69%

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Mesothelioma cancer cells are glutamine addicted and glutamine restriction reduces YAP1 signaling to attenuate tumor formation

Adhikary

Shrestha

Naselsky

et al. 2022

Molecular Carcinogenesis

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Glutamine addiction is an important phenotype displayed in some types of cancer. In these cells, glutamine depletion results in a marked reduction in the aggressive cancer phenotype. Mesothelioma is an extremely aggressive disease that lacks effective therapy. In this study, we show that mesothelioma tumors are glutamine addicted suggesting that glutamine depletion may be a potential therapeutic strategy. We show that glutamine restriction, by removing glutamine from the medium or treatment with inhibitors that attenuate glutamine uptake (V-9302) or conversion to glutamate (CB-839), markedly reduces mesothelioma cell proliferation, spheroid formation, invasion, and migration. Inhibition of the SLC1A5 glutamine importer, by knockout or treatment with V-9302, an SLC1A5 inhibitor, also markedly reduces mesothelioma cell tumor growth. A relationship between glutamine utilization and YAP1/TEAD signaling has been demonstrated in other tumor types, and the YAP1/TEAD signaling cascade is active in mesothelioma cells and drives cell survival and proliferation. We therefore assessed the impact of glutamine depletion on YAP1/TEAD signaling. We show that glutamine restriction, SLC1A5 knockdown/ knockout, or treatment with V-9302 or CB-839, reduces YAP1 level, YAP1/TEADdependent transcription, and YAP1/TEAD target protein (e.g., CTGF, cyclin D1, COL1A2, COL3A1, etc.) levels. These changes are observed in both cells and tumors. These findings indicate that mesothelioma is a glutamine addicted cancer, show that glutamine depletion attenuates YAP1/TEAD signaling and tumor growth, and suggest that glutamine restriction may be useful as a mesothelioma treatment strategy.

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Section: Discussionmentioning

confidence: 69%

“…56 Recent studies support the use of asparaginase and asparaginase derivatives as cancer therapeutics. 9,10,52,57,58 Mesothelioma is a highly aggressive and treatment-resistant cancer, and our findings suggest that asparaginase-dependent glutamine depletion may be a useful mesothelioma treatment strategy.…”

Section: Glutamine Starvation and Tumor Growthmentioning

confidence: 71%

Mesothelioma cancer cells are glutamine addicted and glutamine restriction reduces YAP1 signaling to attenuate tumor formation

Adhikary

Shrestha

Naselsky

et al. 2022

Molecular Carcinogenesis

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“…It is derived from a novel Pseudomonas fluorescens expression that was created to be genetically similar to Erwina asparaginase and has been shown to have the same effect in treatment. 9 Lastly, the most recently developed formulation is calaspargase, as what was used in our patient. Calaspargase is similar to peg-asparaginase, except it uses a different linker molecule increasing the stability and half-life.…”

Section: F I G U R E 1 Patient Pictures Showing Progression Of Sympto...mentioning

confidence: 99%

Delayed serum sickness reaction after initial hypersensitivity reaction to calaspargase during treatment for B‐cell acute lymphoblastic leukemia

Gay,

Smink,

Mulieri

et al. 2024

Pediatric Blood & Cancer

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“…Previously, it had been demonstrated that this formulation and dosage was similar in achieving sufficient ASNase activity when compared to the non-recombinant Erwinia c. ASNase (based on the dosage of 25,000 IU/m 2 ). 55 Lin et al concluded that a single IM dose of JZP-458 (25 mg/m 2 ) resulted in similar ASNase activity levels com-pared to 25,000 IU/m 2 of the non-recombinant Erwinia c. ASNase. 54 In 2021, based on the clinical and pharmacological data derived from the studies described, the FDA granted the approval of JZP-458.…”

Section: Erwinia C Asparaginase As Second-line Therapy: the Journey C...mentioning

confidence: 99%

Back to the future: the amazing journey of the therapeutic anti-leukemia enzyme asparaginase <i>Erwinia chrysanthemi</i>

Tong

Rizzari

2023

haematol

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For several decades asparaginase has been considered world-wide as an essential component of combination chemotherapy for the treatment of childhood acute lymphoblastic leukemia (ALL). Discovered over 60 years ago, two main unmanipulated asparaginase products originated from primary bacteria sources, namely Escherichia coli and Erwinia chrysanthemi, have been available for clinical use. A pegylated product of the Escherichia coli asparaginase was subsequently developed and is now the main product used by several international cooperative groups. The various asparaginase products all display the same mechanism of action (hydrolysis of circulating asparagine) and are associated with similar efficacy and toxicity patterns. However, their different pharmacokinetics, pharmacodynamics and immunological properties require distinctive modalities of application and monitoring. Erwinia chrysanthemi asparaginase was initially used as a first-line product, but subsequently became a preferred second-line product for children who experienced immunological reactions to the Escherichia coli asparaginase products. An asparaginase product displaying the same characteristics of the Erwinia chrysanthemi asparaginase recently has been produced by use of recombinant technology, thus securing a preparation available for use as an alternative, or as a back-up in case of shortages, for the non-recombinant product. The long journey of the Erwinia chrysanthemi asparaginase product as it has developed throughout the last several decades has made it possible for almost every child and adult with ALL to complete the asparaginase-based protocol treatment when an immunological reaction has occurred to any Escherichia coli asparaginase product.

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Asparaginase Erwinia chrysanthemi for acute lymphoblastic leukemia and lymphoblastic lymphoma

Cited by 5 publications

References 0 publications

Mesothelioma cancer cells are glutamine addicted and glutamine restriction reduces YAP1 signaling to attenuate tumor formation

Mesothelioma cancer cells are glutamine addicted and glutamine restriction reduces YAP1 signaling to attenuate tumor formation

Delayed serum sickness reaction after initial hypersensitivity reaction to calaspargase during treatment for B‐cell acute lymphoblastic leukemia

Back to the future: the amazing journey of the therapeutic anti-leukemia enzyme asparaginase <i>Erwinia chrysanthemi</i>

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