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Article: Targeting the Proline-Glutamine-Asparagine-Arginine Metabolic Axis in Amino Acid Starvation Cancer Therapy.

Kuo, Macus Tien / Chen, Helen H W / Feun, Lynn G / Savaraj, Niramol

2021 Volume 14, Issue 1

Abstract: Proline, glutamine, asparagine, and arginine are conditionally non-essential amino acids that can be produced in our body. However, they are essential for the growth of highly proliferative cells such as cancers. Many cancers express reduced levels of ... ...

Abstract	Proline, glutamine, asparagine, and arginine are conditionally non-essential amino acids that can be produced in our body. However, they are essential for the growth of highly proliferative cells such as cancers. Many cancers express reduced levels of these amino acids and thus require import from the environment. Meanwhile, the biosynthesis of these amino acids is inter-connected but can be intervened individually through the inhibition of key enzymes of the biosynthesis of these amino acids, resulting in amino acid starvation and cell death. Amino acid starvation strategies have been in various stages of clinical applications. Targeting asparagine using asparaginase has been approved for treating acute lymphoblastic leukemia. Targeting glutamine and arginine starvations are in various stages of clinical trials, and targeting proline starvation is in preclinical development. The most important obstacle of these therapies is drug resistance, which is mostly due to reactivation of the key enzymes involved in biosynthesis of the targeted amino acids and reprogramming of compensatory survival pathways via transcriptional, epigenetic, and post-translational mechanisms. Here, we review the interactive regulatory mechanisms that control cellular levels of these amino acids for amino acid starvation therapy and how drug resistance is evolved underlying treatment failure.
Language	English
Publishing date	2021-01-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph14010072
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Article ; Online: Exploiting the Innate Plasticity of the Programmed Cell Death-1 (PD1) Receptor to Design Pembrolizumab H3 Loop Mimics.

Richaud, Alexis D / Zaghouani, Mehdi / Zhao, Guangkuan / Wangpaichitr, Medhi / Savaraj, Niramol / Roche, Stéphane P

Chembiochem : a European journal of chemical biology

2022 Volume 23, Issue 21, Page(s) e202200449

Abstract: Checkpoint blockade of the immunoreceptor programmed cell death-1 (PD1) with its ligand-1 (PDL1) by monoclonal antibodies such as pembrolizumab provided compelling clinical results in various cancer types, yet the molecular mechanism by which this drug ... ...

Abstract	Checkpoint blockade of the immunoreceptor programmed cell death-1 (PD1) with its ligand-1 (PDL1) by monoclonal antibodies such as pembrolizumab provided compelling clinical results in various cancer types, yet the molecular mechanism by which this drug blocks the PD1/PDL1 interface remains unclear. To address this question, we examined the conformational motion of PD1 associated with the binding of pembrolizumab. Our results revealed that the innate plasticity of both C'D and FG loops is crucial to form a deep binding groove (371 Å
MeSH term(s)	Programmed Cell Death 1 Receptor/chemistry ; Programmed Cell Death 1 Receptor/metabolism ; B7-H1 Antigen/chemistry ; B7-H1 Antigen/metabolism ; Antibodies, Monoclonal, Humanized/pharmacology ; Apoptosis
Chemical Substances	Programmed Cell Death 1 Receptor ; pembrolizumab (DPT0O3T46P) ; B7-H1 Antigen ; Antibodies, Monoclonal, Humanized
Language	English
Publishing date	2022-09-27
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2020469-3
ISSN	1439-7633 ; 1439-4227
ISSN (online)	1439-7633
ISSN	1439-4227
DOI	10.1002/cbic.202200449
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Article: Dual inhibition of IDO1/TDO2 enhances anti-tumor immunity in platinum-resistant non-small cell lung cancer.

Wu, Chunjing / Spector, Sydney A / Theodoropoulos, George / Nguyen, Dan J M / Kim, Emily Y / Garcia, Ashley / Savaraj, Niramol / Lim, Diane C / Paul, Ankita / Feun, Lynn G / Bickerdike, Michael / Wangpaichitr, Medhi

Cancer & metabolism

2023 Volume 11, Issue 1, Page(s) 7

Abstract: Background: The impact of non-small cell lung cancer (NSCLC) metabolism on the immune microenvironment is not well understood within platinum resistance. We have identified crucial metabolic differences between cisplatin-resistant (CR) and cisplatin- ... ...

Abstract	Background: The impact of non-small cell lung cancer (NSCLC) metabolism on the immune microenvironment is not well understood within platinum resistance. We have identified crucial metabolic differences between cisplatin-resistant (CR) and cisplatin-sensitive (CS) NSCLC cells with elevated indoleamine 2,3-dioxygenase-1 (IDO1) activity in CR, recognized by increased kynurenine (KYN) production. Methods: Co-culture, syngeneic, and humanize mice models were utilized. C57BL/6 mice were inoculated with either Lewis lung carcinoma mouse cells (LLC) or their platinum-resistant counterpart (LLC-CR) cells. Humanized mice were inoculated with either A (human CS cells) or ALC (human CR cells). Mice were treated with either IDO1 inhibitor or TDO2 (tryptophan 2,3-dioxygenase-2) inhibitor at 200 mg/kg P.O. once a day for 15 days; or with a new-in-class, IDO1/TDO2 dual inhibitor AT-0174 at 170 mg/kg P.O. once a day for 15 days with and without anti-PD1 antibody (10 mg/kg, every 3 days). Immune profiles and KYN and tryptophan (TRP) production were evaluated. Results: CR tumors exhibited a more highly immunosuppressive environment that debilitated robust anti-tumor immune responses. IDO1-mediated KYN production from CR cells suppressed NKG2D on immune effector natural killer (NK) and CD8 Conclusion: Our study reports the presence of platinum-resistant lung tumors that utilize both IDO1/TDO2 enzymes for survival, and to escape immune surveillance as a consequence of KYN metabolites. We also report early in vivo data in support of the potential therapeutic efficacy of the dual IDO1/TDO2 inhibitor AT-0174 as a part of immuno-therapeutic treatment that disrupts tumor metabolism and enhances anti-tumor immunity.
Language	English
Publishing date	2023-05-24
Publishing country	England
Document type	Journal Article
ZDB-ID	2700141-6
ISSN	2049-3002
ISSN	2049-3002
DOI	10.1186/s40170-023-00307-1
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Article ; Online: Cisplatin Resistance and Redox-Metabolic Vulnerability: A Second Alteration.

Wangpaichitr, Medhi / Theodoropoulos, George / Nguyen, Dan J M / Wu, Chunjing / Spector, Sydney A / Feun, Lynn G / Savaraj, Niramol

International journal of molecular sciences

2021 Volume 22, Issue 14

Abstract: The development of drug resistance in tumors is a major obstacle to effective cancer chemotherapy and represents one of the most significant complications to improving long-term patient outcomes. Despite early positive responsiveness to platinum-based ... ...

Abstract	The development of drug resistance in tumors is a major obstacle to effective cancer chemotherapy and represents one of the most significant complications to improving long-term patient outcomes. Despite early positive responsiveness to platinum-based chemotherapy, the majority of lung cancer patients develop resistance. The development of a new combination therapy targeting cisplatin-resistant (CR) tumors may mark a major improvement as salvage therapy in these patients. The recent resurgence in research into cellular metabolism has again confirmed that cancer cells utilize aerobic glycolysis ("the Warburg effect") to produce energy. Hence, this observation still remains a characteristic hallmark of altered metabolism in certain cancer cells. However, recent evidence promotes another concept wherein some tumors that acquire resistance to cisplatin undergo further metabolic alterations that increase tumor reliance on oxidative metabolism (OXMET) instead of glycolysis. Our review focuses on molecular changes that occur in tumors due to the relationship between metabolic demands and the importance of NAD
MeSH term(s)	Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Drug Resistance, Neoplasm ; Energy Metabolism/drug effects ; Glycolysis/drug effects ; Humans ; Kynurenine/metabolism ; Mitochondria/metabolism ; NAD/metabolism ; Neoplasms/metabolism ; Oxidation-Reduction ; Poly (ADP-Ribose) Polymerase-1/metabolism ; Reactive Oxygen Species/metabolism ; Sirtuins/metabolism ; Tumor Microenvironment/drug effects
Chemical Substances	Reactive Oxygen Species ; NAD (0U46U6E8UK) ; Kynurenine (343-65-7) ; PARP1 protein, human (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; Sirtuins (EC 3.5.1.-) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2021-07-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22147379
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Article ; Online: Enhancing the Effect of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Signaling and Arginine Deprivation in Melanoma.

Wu, Chunjing / You, Min / Nguyen, Dao / Wangpaichitr, Medhi / Li, Ying-Ying / Feun, Lynn G / Kuo, Macus T / Savaraj, Niramol

International journal of molecular sciences

2021 Volume 22, Issue 14

Abstract: Melanoma as a very aggressive type of cancer is still in urgent need of improved treatment. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and arginine deiminase (ADI-PEG20) are two of many suggested drugs for treating melanoma. Both ... ...

Abstract	Melanoma as a very aggressive type of cancer is still in urgent need of improved treatment. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and arginine deiminase (ADI-PEG20) are two of many suggested drugs for treating melanoma. Both have shown anti-tumor activities without harming normal cells. However, resistance to both drugs has also been noted. Studies on the mechanism of action of and resistance to these drugs provide multiple targets that can be utilized to increase the efficacy and overcome the resistance. As a result, combination strategies have been proposed for these drug candidates with various other agents, and achieved enhanced or synergistic anti-tumor effect. The combination of TRAIL and ADI-PEG20 as one example can greatly enhance the cytotoxicity to melanoma cells including those resistant to the single component of this combination. It is found that combination treatment generally can alter the expression of the components of cell signaling in melanoma cells to favor cell death. In this paper, the signaling of TRAIL and ADI-PEG20-induced arginine deprivation including the main mechanism of resistance to these drugs and exemplary combination strategies is discussed. Finally, factors hampering the clinical application of both drugs, current and future development to overcome these hurdles are briefly discussed.
MeSH term(s)	Apoptosis/drug effects ; Arginine/deficiency ; Arginine/metabolism ; Autophagy/drug effects ; Cell Line, Tumor ; Drug Resistance, Neoplasm/drug effects ; Humans ; Hydrolases/metabolism ; Hydrolases/pharmacology ; Melanoma/metabolism ; Polyethylene Glycols/metabolism ; Polyethylene Glycols/pharmacology ; Signal Transduction/drug effects ; TNF-Related Apoptosis-Inducing Ligand/genetics ; TNF-Related Apoptosis-Inducing Ligand/metabolism ; TNF-Related Apoptosis-Inducing Ligand/pharmacology
Chemical Substances	TNF-Related Apoptosis-Inducing Ligand ; TNFSF10 protein, human ; Polyethylene Glycols (3WJQ0SDW1A) ; Arginine (94ZLA3W45F) ; Hydrolases (EC 3.-) ; ADI PEG20 (EC 3.5.3.6) ; arginine deiminase (EC 3.5.3.6)
Language	English
Publishing date	2021-07-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22147628
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Article ; Online: Arginine deprivation in cancer therapy.

Feun, Lynn G / Kuo, Macus Tien / Savaraj, Niramol

Current opinion in clinical nutrition and metabolic care

2015 Volume 18, Issue 1, Page(s) 78–82

Abstract: Purpose of review: There has been an increased and renewed interest in metabolic therapy for cancer, particularly Arg deprivation. The purpose of this review is to highlight recent studies that focus on Arg-dependent malignancies with Arginine (Arg)- ... ...

Abstract	Purpose of review: There has been an increased and renewed interest in metabolic therapy for cancer, particularly Arg deprivation. The purpose of this review is to highlight recent studies that focus on Arg-dependent malignancies with Arginine (Arg)-degrading enzymes, including arginase and Arg deiminase. Recent findings: New developments in this area include understanding of the role of most significantly downregulated gene regulating amino acid metabolism, argininosuccinate synthetase and its expression and therapeutic relevance in different tumors. Recent studies have also shed light on the mechanism of tumor cell death with Arg deprivation, with arginase and pegylated Arg deiminase. Particularly important is understanding the mechanism of resistance that cancers develop after such drug exposure. Finally, recent clinical trials have been performed or are ongoing to use Arg deprivation as treatment for advanced malignancies. Summary: Arg deprivation is a promising approach for the treatment of various malignancies.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Arginase/metabolism ; Arginase/pharmacology ; Arginase/therapeutic use ; Arginine/metabolism ; Argininosuccinate Synthase/metabolism ; Humans ; Hydrolases/metabolism ; Hydrolases/pharmacology ; Hydrolases/therapeutic use ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Polyethylene Glycols/metabolism ; Polyethylene Glycols/pharmacology ; Polyethylene Glycols/therapeutic use
Chemical Substances	Antineoplastic Agents ; Polyethylene Glycols (30IQX730WE) ; Arginine (94ZLA3W45F) ; Hydrolases (EC 3.-) ; Arginase (EC 3.5.3.1) ; ADI PEG20 (EC 3.5.3.6) ; arginine deiminase (EC 3.5.3.6) ; Argininosuccinate Synthase (EC 6.3.4.5)
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1460178-3
ISSN	1473-6519 ; 1363-1950
ISSN (online)	1473-6519
ISSN	1363-1950
DOI	10.1097/MCO.0000000000000122
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Zs.A 5586: Show issues

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Article ; Online: A Kinetic Dearomatization Strategy for an Expedient Biomimetic Route to the Bielschowskysin Skeleton.

Scesa, Paul / Wangpaichitr, Medhi / Savaraj, Niramol / West, Lyndon / Roche, Stéphane P

Angewandte Chemie (International ed. in English)

2018 Volume 57, Issue 5, Page(s) 1316–1321

Abstract: Bielschowskysin (1), the flagship of the furanocembranoid diterpene family, has attracted attention from chemists owing to its intriguing and daunting polycyclic architecture and medicinal potential against lung cancer. The high level of ... ...

Abstract	Bielschowskysin (1), the flagship of the furanocembranoid diterpene family, has attracted attention from chemists owing to its intriguing and daunting polycyclic architecture and medicinal potential against lung cancer. The high level of functionalization of 1 poses a considerable challenge to synthesis. Herein, a stereoselective furan dearomatization strategy of furanocembranoids was achieved via the intermediacy of chlorohydrins. The stereochemical course of the kinetic dearomatization was established, and the C3 configuration of the resulting exo-enol ether intermediates proved to be essential to complete the late-stage transannular [2+2] photocycloaddition. Overall, this biomimetic strategy starting from the natural product acerosolide (9) featured an unprecedented regio- and highly stereoselective furan dearomatization, which provided rapid access to the pivotal exo-enol ethers en route to the intricate bielschowskyane skeleton.
Language	English
Publishing date	2018-01-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2011836-3
ISSN	1521-3773 ; 1433-7851
ISSN (online)	1521-3773
ISSN	1433-7851
DOI	10.1002/anie.201711780
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Article: Collaboration Between RSK-EphA2 and Gas6-Axl RTK Signaling in Arginine Starvation Response That Confers Resistance to EGFR Inhibitors.

Kuo, Macus Tien / Long, Yan / Tsai, Wen-Bin / Li, Ying-Ying / Chen, Helen H W / Feun, Lynn G / Savaraj, Niramol

Translational oncology

2019 Volume 13, Issue 2, Page(s) 355–364

Abstract: Many human malignancies require extracellular arginine (Arg) for survival because the key enzyme for de novo Arg biosynthesis, argininosuccinate synthetase 1 (ASS1), is silenced. Recombinant arginine deiminase (ADI-PEG20), which digests extracellular Arg, ...

Abstract	Many human malignancies require extracellular arginine (Arg) for survival because the key enzyme for de novo Arg biosynthesis, argininosuccinate synthetase 1 (ASS1), is silenced. Recombinant arginine deiminase (ADI-PEG20), which digests extracellular Arg, has been in clinical trials for treating ASS1-negative tumors. Reactivation of ASS1 is responsible for the treatment failure. We previously demonstrated that ASS1 reactivation is transcriptionally regulated by c-Myc via the upstream Gas6-Axl tyrosine kinase (RTK) signal. Here, we report that another RTK EphA2 is coactivated via PI3K-ERK/RSK1 pathway in a ligand-independent mechanism. EphA2 is also regulated by c-Myc. Moreover, we found that knockdown Axl upregulates EphA2 expression, demonstrating cross-talk between these RTKs. ADI
Language	English
Publishing date	2019-12-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233 ; 1936-5233 ; 1944-7124
ISSN (online)	1936-5233
ISSN	1936-5233 ; 1944-7124
DOI	10.1016/j.tranon.2019.12.003
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Article ; Online: Topoisomerase I inhibitors for the treatment of brain tumors.

Feun, Lynn / Savaraj, Niramol

Expert review of anticancer therapy

2008 Volume 8, Issue 5, Page(s) 707–716

Abstract: Patients with primary malignant brain tumors have a poor prognosis. Standard treatment includes surgical resection, radiation therapy and chemotherapy. Topoisomerase I inhibitors such as topotecan and irinotecan (CPT-11) represent one class of ... ...

Abstract	Patients with primary malignant brain tumors have a poor prognosis. Standard treatment includes surgical resection, radiation therapy and chemotherapy. Topoisomerase I inhibitors such as topotecan and irinotecan (CPT-11) represent one class of chemotherapy drugs that have been used in this disease. Recent clinical trials have shown major antitumor activity in recurrent glioblastoma when adding the antiangiogenesis drug bevacizumab with CPT-11. The combination of targeted agents to topoisomerase I inhibitors represent a novel and promising approach. This review will summarize clinical trials with topoisomerase I inhibitors and discuss new treatment strategies for primary malignant brain tumors.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Animals ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Bevacizumab ; Brain Neoplasms/drug therapy ; Camptothecin/analogs & derivatives ; Camptothecin/therapeutic use ; Glioblastoma/drug therapy ; Humans ; Neoplasm Recurrence, Local ; Survival Analysis ; Topoisomerase I Inhibitors ; Topotecan/therapeutic use
Chemical Substances	Angiogenesis Inhibitors ; Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antineoplastic Agents ; Topoisomerase I Inhibitors ; Bevacizumab (2S9ZZM9Q9V) ; irinotecan (7673326042) ; Topotecan (7M7YKX2N15) ; Camptothecin (XT3Z54Z28A)
Language	English
Publishing date	2008-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2112544-2
ISSN	1744-8328 ; 1473-7140
ISSN (online)	1744-8328
ISSN	1473-7140
DOI	10.1586/14737140.8.5.707
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Zs.A 5907: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: Phase II trial of SOM230 (pasireotide LAR) in patients with unresectable hepatocellular carcinoma.

Feun, Lynn G / Wangpaichitr, Medhi / Li, Ying-Ying / Kwon, Deukwoo / Richman, Stephen P / Hosein, Peter J / Savaraj, Niramol

Journal of hepatocellular carcinoma

2018 Volume 5, Page(s) 9–15

Abstract: Background: A phase II trial of pasireotide was performed to assess its efficacy and safety in advanced or metastatic hepatocellular carcinoma (HCC).: Patients and methods: Patients with advanced HCC and Child-Pugh score ≤7 received pasireotide LAR ... ...

Abstract	Background: A phase II trial of pasireotide was performed to assess its efficacy and safety in advanced or metastatic hepatocellular carcinoma (HCC). Patients and methods: Patients with advanced HCC and Child-Pugh score ≤7 received pasireotide LAR 60 mg intramuscularly every 28 days. Primary endpoint was disease control rate. Secondary endpoints were time to tumor progression, response rate, treatment-related adverse events, and overall survival. Serum insulin growth factor-1 was measured before and after pasireotide. Results: Twenty patients were treated and evaluable. Eighteen patients (90%) had prior therapy; 16 patients (80%) had multiple therapies. Median age was 65, 75% had Barcelona Clinic Liver Cancer stage C, and 55% had metastatic disease. The main toxicity was hyperglycemia. Rare adverse effects included reversible grade 4 elevation in alanina transaminase/aspartate transaminase in one patient. The best response was stable disease in 9 patients (45%). Median time to tumor progression for the 20 patients was 3 months, and median survival was 9 months. Conclusion: Pasireotide had limited clinical benefit as second-line or third-line treatment in patients with advanced or metastatic HCC. Low baseline insulin growth factor-1 level may be indicative when SOM230 treatment may be ineffective, and decreasing levels after treatment may be indicative of disease control.
Language	English
Publishing date	2018-01-12
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2780784-8
ISSN	2253-5969
ISSN	2253-5969
DOI	10.2147/JHC.S153672
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