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Article: Targeting carcinoembryonic antigen-expressing tumors using a novel transcriptional and translational dual-regulated oncolytic herpes simplex virus type 1.

Chouljenko, Dmitry V / Murad, Yanal M / Lee, I-Fang / Delwar, Zahid / Ding, Jun / Liu, Guoyu / Liu, Xiaohu / Bu, Xuexian / Sun, Yi / Samudio, Ismael / Jia, William Wei-Guo

Molecular therapy oncolytics

2023 Volume 28, Page(s) 334–348

Abstract: VG2025 is a recombinant oncolytic herpes simplex virus type 1 (HSV-1) that uses transcriptional and translational dual regulation (TTDR) of critical viral genes to enhance virus safety and promote tumor-specific virus replication without reducing ... ...

Abstract	VG2025 is a recombinant oncolytic herpes simplex virus type 1 (HSV-1) that uses transcriptional and translational dual regulation (TTDR) of critical viral genes to enhance virus safety and promote tumor-specific virus replication without reducing virulence. The TTDR platform is based on transcriptional control of the essential HSV-1 immediate-early protein ICP27 using a tumor-specific carcinoembryonic antigen (CEA) promoter, coupled with translational control of the neurovirulence factor ICP34.5 using multiple microRNA (miR)-binding sites. VG2025 further incorporates IL-12 and the IL-15/IL-15 receptor alpha subunit complex to enhance the antitumor and immune stimulatory properties of oncolytic HSVs. The TTDR strategy was verified
Language	English
Publishing date	2023-02-11
Publishing country	United States
Document type	Journal Article
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2023.02.003
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Article ; Online: Pre-Existing HSV-1 Immunity Enhances Anticancer Efficacy of a Novel Immune-Stimulating Oncolytic Virus.

Ding, Jun / Murad, Yanal M / Sun, Yi / Lee, I-Fang / Samudio, Ismael / Liu, Xiaohu / Jia, William Wei-Guo / Zhao, Ronghua

Viruses

2022 Volume 14, Issue 11

Abstract: Oncolytic viruses (OVs) can specifically replicate in the host and cause cancer cell lysis while inducing an antitumor immune response. The aim of this study is to investigate the impact of either pre-existing immunity against herpes simplex virus type-1 ...

Abstract	Oncolytic viruses (OVs) can specifically replicate in the host and cause cancer cell lysis while inducing an antitumor immune response. The aim of this study is to investigate the impact of either pre-existing immunity against herpes simplex virus type-1 (HSV-1) or multicycle treatment with OVs on anticancer efficacy of VG161, an HSV-1 OV in phase 2 clinical trial. VG161 efficacy was tested in CT26 mouse models by comparing the efficacy and immune response in naïve mice or in mice that were immunized with VG161. Moreover, VG161 efficacy in HLA-matched CD34+ humanized intrahepatic cholangiocarcinoma (ICC) patient-derived xenograft (PDX) models was also tested in multicycle treatment and was compared to standard chemotherapy for this type of cancer (gemcitabine). The HSV-1-immunized mice significantly inhibited tumor growth in VG161-treated mice compared to control naïve treated mice. RNA expression profiling and ELISPOT analyses indicated changes in the tumor's immune profile in the immunized and treated group compared to naïve and treated mice, as well as enhanced T cell function depicted by higher numbers of tumor specific lymphocytes, which was enhanced by immunization. In the ICC PDX model, repeated treatment of VG161 with 2 or 3 cycles seemed to increase the anticancer efficacy of VG161. In conclusion, the anticancer efficacy of VG161 can be enhanced by pre-immunization with HSV-1 and multicycle administration when the virus is given intratumorally, indicating that pre-existing antiviral immunity might enhance OV-induced antitumor immunity. Our results suggest potential clinical benefits of HSV-1-based OV therapy in HSV-1-seropositive patients and multicycle administration of VG161 for long-term maintenance treatment.
MeSH term(s)	Humans ; Mice ; Animals ; Oncolytic Viruses/physiology ; Herpesvirus 1, Human/genetics ; Neoplasms/therapy ; Immunity ; Disease Models, Animal ; Oncolytic Virotherapy/methods
Language	English
Publishing date	2022-10-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14112327
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Article ; Online: Targeting leukemia's "fatty tooth".

Samudio, Ismael / Konopleva, Marina

Blood

2015 Volume 126, Issue 16, Page(s) 1874–1875

Abstract: In this issue of Blood, Ricciardi et al report a novel fatty acid oxidation (FAO) inhibitor, ST1326, that effectively inhibits proliferation, survival, and chemoresistance in leukemia cell lines and primary samples. ...

Abstract	In this issue of Blood, Ricciardi et al report a novel fatty acid oxidation (FAO) inhibitor, ST1326, that effectively inhibits proliferation, survival, and chemoresistance in leukemia cell lines and primary samples.
MeSH term(s)	Carnitine/analogs & derivatives ; Carnitine O-Palmitoyltransferase/antagonists & inhibitors ; Drug Delivery Systems ; Fatty Acids/metabolism ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Neoplasm Proteins/antagonists & inhibitors
Chemical Substances	Fatty Acids ; Neoplasm Proteins ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21) ; Carnitine (S7UI8SM58A)
Language	English
Publishing date	2015-10-14
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2015-08-665125
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Article ; Online: Cell-surface proteomics for the identification of novel therapeutic targets in cancer.

Kuhlmann, Laura / Cummins, Emma / Samudio, Ismael / Kislinger, Thomas

Expert review of proteomics

2018 Volume 15, Issue 3, Page(s) 259–275

Abstract: Introduction: Cancer is the second most common cause of death worldwide and its heterogeneity complicates therapy. Standard cytotoxic regiments disrupt rapidly dividing cells, regardless of their neoplastic status. The introduction of less toxic ... ...

Abstract	Introduction: Cancer is the second most common cause of death worldwide and its heterogeneity complicates therapy. Standard cytotoxic regiments disrupt rapidly dividing cells, regardless of their neoplastic status. The introduction of less toxic targeted therapies has partially contributed to the observed decrease in cancer-related mortality. Cell-surface proteins represent attractive targets for therapy, due to their easily-accessible localization and their involvement in essential signaling pathways, often dysregulated in cancer. Despite their clinical appeal, cell-surface proteins are often underrepresented in standard proteomic data sets, due to their poor solubility and lower expression levels compared to intracellular proteins. Areas covered: This review will summarize some of the available techniques for enriching the cell-surface proteome, and discuss their advantages, limitations and applicability to clinical sample-testing. Moreover, we discuss currently available strategies for the development of novel targeted therapies in cancer. Expert commentary: The interest in elucidating the cancer-associated surfaceome is growing and will likely benefit from recent advancements in instrument sensitivity, method development, and a growing body of high-quality proteomics databases. Multiomics studies, in combination with functional validations (e.g. dropout screens), and evaluation of the healthy surfaceome, will likely aid in the selection of relevant targets for future therapy development.
MeSH term(s)	Animals ; Antigens, Neoplasm/chemistry ; Antigens, Neoplasm/metabolism ; Biomarkers, Tumor/chemistry ; Biomarkers, Tumor/metabolism ; Humans ; Mass Spectrometry/methods ; Molecular Targeted Therapy/methods ; Proteomics/methods
Chemical Substances	Antigens, Neoplasm ; Biomarkers, Tumor
Language	English
Publishing date	2018-01-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2299100-1
ISSN	1744-8387 ; 1478-9450
ISSN (online)	1744-8387
ISSN	1478-9450
DOI	10.1080/14789450.2018.1429924
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Article ; Online: Oncolytic virotherapy in hepato-bilio-pancreatic cancer: The key to breaking the log jam?

Li, Yuwei / Shen, Yinan / Zhao, Ronghua / Samudio, Ismael / Jia, William / Bai, Xueli / Liang, Tingbo

Cancer medicine

2020 Volume 9, Issue 9, Page(s) 2943–2959

Abstract: Traditional therapies have limited efficacy in hepatocellular carcinoma, pancreatic cancer, and biliary tract cancer, especially for advanced and refractory cancers. Through a deeper understanding of antitumor immunity and the tumor microenvironment, ... ...

Abstract	Traditional therapies have limited efficacy in hepatocellular carcinoma, pancreatic cancer, and biliary tract cancer, especially for advanced and refractory cancers. Through a deeper understanding of antitumor immunity and the tumor microenvironment, novel immunotherapies are becoming available for cancer treatment. Oncolytic virus (OV) therapy is an emerging type of immunotherapy that has demonstrated effective antitumor efficacy in many preclinical studies and clinical studies. Thus, it may represent a potential feasible treatment for hard to treat gastrointestinal (GI) tumors. Here, we summarize the research progress of OV therapy for the treatment of hepato-bilio-pancreatic cancers. In general, most OV therapies exhibits potent, specific oncolysis both in cell lines in vitro and the animal models in vivo. Currently, several clinical trials have suggested that OV therapy may also be effective in patients with refractory hepato-bilio-pancreatic cancer. Multiple strategies such as introducing immunostimulatory genes, modifying virus capsid and combining various other therapeutic modalities have been shown enhanced specific oncolysis and synergistic anti-cancer immune stimulation. Combining OV with other antitumor therapies may become a more effective strategy than using virus alone. Nevertheless, more studies are needed to better understand the mechanisms underlying the therapeutic effects of OV, and to design appropriate dosing and combination strategies.
MeSH term(s)	Animals ; Biliary Tract Neoplasms/pathology ; Biliary Tract Neoplasms/therapy ; Humans ; Liver Neoplasms/pathology ; Liver Neoplasms/therapy ; Oncolytic Virotherapy/methods ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/therapy
Language	English
Publishing date	2020-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2045-7634
ISSN (online)	2045-7634
DOI	10.1002/cam4.2949
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Article ; Online: Human Fc gamma receptor IIIA blockade inhibits platelet destruction in a humanized murine model of ITP.

Blood advances

2024 Volume 8, Issue 8, Page(s) 1869–1879

Abstract: Abstract: Fc gamma receptor (FcγR) IIIA is an important receptor for immunoglobulin G (IgG) and is involved in immune defense mechanisms as well as tissue destruction in some autoimmune diseases including immune thrombocytopenia (ITP). FcγRIIIA on ... ...

Abstract	Abstract: Fc gamma receptor (FcγR) IIIA is an important receptor for immunoglobulin G (IgG) and is involved in immune defense mechanisms as well as tissue destruction in some autoimmune diseases including immune thrombocytopenia (ITP). FcγRIIIA on macrophages can trigger phagocytosis of IgG-sensitized platelets, and prior pilot studies observed blockade of FcγRIIIA increased platelet counts in patients with ITP. Unfortunately, although blockade of FcγRIIIA in patients with ITP increased platelet counts, its engagement by the blocking antibody drove serious adverse inflammatory reactions. These adverse events were postulated to originate from the antibody's Fc and/or bivalent nature. The blockade of human FcγRIIIA in vivo with a monovalent construct lacking an active Fc region has not yet been achieved. To effectively block FcγRIIIA in vivo, we developed a high affinity monovalent single-chain variable fragment (scFv) that can bind and block human FcγRIIIA. This scFv (17C02) was expressed in 3 formats: a monovalent fusion protein with albumin, a 1-armed human IgG1 antibody, and a standard bivalent mouse (IgG2a) antibody. Both monovalent formats were effective in preventing phagocytosis of ITP serum-sensitized human platelets. In vivo studies using FcγR-humanized mice demonstrated that both monovalent therapeutics were also able to increase platelet counts. The monovalent albumin fusion protein did not have adverse event activity as assessed by changes in body temperature, whereas the 1-armed antibody induced some changes in body temperature even though the Fc region function was impaired by the Leu234Ala and Leu235Ala mutations. These data demonstrate that monovalent blockade of human FcγRIIIA in vivo can potentially be a therapeutic strategy for patients with ITP.
MeSH term(s)	Humans ; Mice ; Animals ; Purpura, Thrombocytopenic, Idiopathic/drug therapy ; Receptors, IgG/metabolism ; Disease Models, Animal ; Thrombocytopenia ; Immunoglobulin G/therapeutic use ; Albumins/therapeutic use
Chemical Substances	Receptors, IgG ; Immunoglobulin G ; Albumins
Language	English
Publishing date	2024-02-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023012155
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Article ; Online: Asparaginase unveils glutamine-addicted AML.

Samudio, Ismael / Konopleva, Marina

Blood

2013 Volume 122, Issue 20, Page(s) 3398–3400

Abstract: In this issue of Blood, Willems et al describe the dependence of acute myeloid leukemia (AML) cells on glutamine for maintaining protein synthesis downstream of mammalian target of rapamycin (mTOR) and show that the enzyme asparaginase can be used to ... ...

Abstract	In this issue of Blood, Willems et al describe the dependence of acute myeloid leukemia (AML) cells on glutamine for maintaining protein synthesis downstream of mammalian target of rapamycin (mTOR) and show that the enzyme asparaginase can be used to target this dependence. Using various AML cell lines, primary samples, and CD341 stem cells from healthy donors, the authors support the notion that asparaginase may offer a therapeutic benefit in AML—not from its well-known enzymatic activity, but from its “off-target” effects on glutamine levels that result in inhibition of downstream mTOR signaling, inhibition of protein synthesis, and ultimately loss of viability.
MeSH term(s)	Animals ; Female ; Glutamine/antagonists & inhibitors ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Male
Chemical Substances	Glutamine (0RH81L854J)
Language	English
Publishing date	2013-11-13
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2013-09-526392
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Article: Targeting a Tumor-Specific Epitope on Podocalyxin Increases Survival in Human Tumor Preclinical Models.

Canals Hernaez, Diana / Hughes, Michael R / Li, Yicong / Mainero Rocca, Ilaria / Dean, Pamela / Brassard, Julyanne / Bell, Erin M / Samudio, Ismael / Mes-Masson, Anne-Marie / Narimatsu, Yoshiki / Clausen, Henrik / Blixt, Ola / Roskelley, Calvin D / McNagny, Kelly M

Frontiers in oncology

2022 Volume 12, Page(s) 856424

Abstract: Podocalyxin (Podxl) is a CD34-related cell surface sialomucin that is normally highly expressed by adult vascular endothelia and kidney podocytes where it plays a key role in blocking adhesion. Importantly, it is also frequently upregulated on a wide ... ...

Abstract	Podocalyxin (Podxl) is a CD34-related cell surface sialomucin that is normally highly expressed by adult vascular endothelia and kidney podocytes where it plays a key role in blocking adhesion. Importantly, it is also frequently upregulated on a wide array of human tumors and its expression often correlates with poor prognosis. We previously showed that, in xenograft studies, Podxl plays a key role in metastatic disease by making tumor initiating cells more mobile and invasive. Recently, we developed a novel antibody, PODO447, which shows exquisite specificity for a tumor-restricted glycoform of Podxl but does not react with Podxl expressed by normal adult tissue. Here we utilized an array of glycosylation defective cell lines to further define the PODO447 reactive epitope and reveal it as an O-linked core 1 glycan presented in the context of the Podxl peptide backbone. Further, we show that when coupled to monomethyl auristatin E (MMAE) toxic payload, PODO447 functions as a highly specific and effective antibody drug conjugate (ADC) in killing ovarian, pancreatic, glioblastoma and leukemia cell lines
Language	English
Publishing date	2022-05-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.856424
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Article ; Online: The mitochondria target drug avocatin B synergizes with induction chemotherapeutics to induce leukemia cell death.

Tcheng, Matthew / Samudio, Ismael / Lee, Eric A / Minden, Mark D / Spagnuolo, Paul A

Leukemia & lymphoma

2016 Volume 58, Issue 4, Page(s) 986–988

MeSH term(s)	Antineoplastic Agents/pharmacology ; Cell Death/drug effects ; Cell Line, Tumor ; Drug Synergism ; Fatty Acids/metabolism ; Humans ; Leukemia/drug therapy ; Leukemia/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Oxidation-Reduction/drug effects
Chemical Substances	Antineoplastic Agents ; Fatty Acids
Language	English
Publishing date	2016-08-25
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2016.1218005
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Article: Induction of Durable Antitumor Response by a Novel Oncolytic Herpesvirus Expressing Multiple Immunomodulatory Transgenes.

Chouljenko, Dmitry V / Ding, Jun / Lee, I-Fang / Murad, Yanal M / Bu, Xuexian / Liu, Guoyu / Delwar, Zahid / Sun, Yi / Yu, Sheng / Samudio, Ismael / Zhao, Ronghua / Jia, William Wei-Guo

Biomedicines

2020 Volume 8, Issue 11

Abstract: Oncolytic virotherapy is a promising new tool for cancer treatment, but direct lytic destruction of tumor cells is not sufficient and must be accompanied by strong immune activation to elicit anti-tumor immunity. We report here the creation of a novel ... ...

Abstract	Oncolytic virotherapy is a promising new tool for cancer treatment, but direct lytic destruction of tumor cells is not sufficient and must be accompanied by strong immune activation to elicit anti-tumor immunity. We report here the creation of a novel replication-competent recombinant oncolytic herpes simplex virus type 1 (VG161) that carries genes coding for IL-12, IL-15, and IL-15 receptor alpha subunit, along with a peptide fusion protein capable of disrupting PD-1/PD-L1 interactions. The VG161 virus replicates efficiently and exhibits robust cytotoxicity in multiple tumor cell lines. Moreover, the encoded cytokines and the PD-L1 blocking peptide work cooperatively to boost immune cell function. In vivo testing in syngeneic CT26 and A20 tumor models reveals superior efficacy when compared to a backbone virus that does not express exogenous genes. Intratumoral injection of VG161 induces abscopal responses in non-injected distal tumors and grants resistance to tumor re-challenge. The robust anti-tumor effect of VG161 is associated with T cell and NK cell tumor infiltration, expression of Th1 associated genes in the injection site, and increased frequency of splenic tumor-specific T cells. VG161 also displayed a superb safety profile in GLP acute and repeated injection toxicity studies performed using cynomolgus monkeys. Overall, we demonstrate that VG161 can induce robust oncolysis and stimulate a robust anti-tumor immune response without sacrificing safety.
Language	English
Publishing date	2020-11-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines8110484
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