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Article ; Online: Pseudoprogression in a patient with metastatic melanoma treated with PD-1 and LAG-3 inhibition.

Wu, Lawrence W / Tao, Jacqueline J / McDonnell, Diana / Izar, Benjamin

2024

Abstract: Pseudoprogression encapsulates a process of temporary radiographic growth followed by subsequent regression of metastatic melanoma lesions in response to immune checkpoint blockade (ICB), such as the combination of anti-programmed cell death protein 1 ( ... ...

Abstract	Pseudoprogression encapsulates a process of temporary radiographic growth followed by subsequent regression of metastatic melanoma lesions in response to immune checkpoint blockade (ICB), such as the combination of anti-programmed cell death protein 1 (PD-1) and anticytotoxic T-lymphocyte-associated antigen 4 therapy. This occurs in approximately 5-10% of ICB-treated patients, but has not yet been described in the context of novel combination therapies. Here, we report a case of an 89-year-old patient with metastatic melanoma to the liver, lung and lymph nodes, who underwent treatment with Opdualag (combining anti-PD-1 nivolumab and anti-lymphocyte-activation gene 3 relatlimab ICBs), and developed pseudoprogression after two cycles of therapy. The patient experienced a radiographic increase in liver metastatic lesion size, but was found to have a subsequent reduction in these lesions. The patient has been on therapy for 18 months without evidence of disease progression and continues to be clinically well-appearing.
Language	English
Publishing date	2024-04-18
Publishing country	England
Document type	Journal Article
ZDB-ID	1095779-0
ISSN	1473-5636 ; 0960-8931
ISSN (online)	1473-5636
ISSN	0960-8931
DOI	10.1097/CMR.0000000000000974
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Article ; Online: From patient tissue correlates to molecular mechanisms of cancer immune evasion: the emerging role of CD58 and PD-L1 co-regulation via CMTM6.

Melms, Johannes C / Ho, Patricia / Rogava, Meri / Izar, Benjamin

Genes and immunity

2023 Volume 25, Issue 1, Page(s) 82–84

Abstract: Immune evasion is a hallmark of cancer, yet the underlying mechanisms are often unknown in many patients. Using single-cell transcriptomics analysis, we previously identified the co-stimulator CD58 as part of a cancer cell-intrinsic immune checkpoint ... ...

Abstract	Immune evasion is a hallmark of cancer, yet the underlying mechanisms are often unknown in many patients. Using single-cell transcriptomics analysis, we previously identified the co-stimulator CD58 as part of a cancer cell-intrinsic immune checkpoint resistance signature in patient melanoma tissue. We subsequently validated CD58 loss as a driver of immune evasion using a patient-derived co-culture model of cancer and cytotoxic tumor-infiltrating lymphocytes in a pooled single-cell perturbation experiment, where we additionally observed concurrent upregulation of PD-L1 protein expression in melanoma cells with CD58 loss. In our most recent study, we uncovered the mechanisms of immune evasion mediated by CD58 loss, including impaired T cell activation and infiltration within tumors, as well as inhibitory signaling by PD-L1 via a shared regulator, CMTM6. Thus, cancer cell-intrinsic reduction of CD58 represents a multi-faceted determinant of immune evasion. Furthermore, its reciprocal interaction with PD-L1 via CMTM6 provides critical insights into how co-inhibitory and co-stimulatory immune cues are regulated.
MeSH term(s)	Humans ; B7-H1 Antigen/genetics ; Melanoma/genetics ; Immune Evasion ; Cell Line, Tumor ; Signal Transduction
Chemical Substances	B7-H1 Antigen
Language	English
Publishing date	2023-12-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2060566-3
ISSN	1476-5470 ; 1466-4879
ISSN (online)	1476-5470
ISSN	1466-4879
DOI	10.1038/s41435-023-00224-9
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Article ; Online: CXCR3: Here to stay to enhance cancer immunotherapy?

Rogava, Meri / Izar, Benjamin

EBioMedicine

2019 Volume 49, Page(s) 11–12

MeSH term(s)	Biomarkers ; Humans ; Immunomodulation ; Immunotherapy ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/therapy ; Receptors, CXCR3/metabolism ; Treatment Outcome
Chemical Substances	Biomarkers ; CXCR3 protein, human ; Receptors, CXCR3
Language	English
Publishing date	2019-11-02
Publishing country	Netherlands
Document type	Letter
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2019.09.044
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Article ; Online: Predictable Clinical Benefits without Evidence of Synergy in Trials of Combination Therapies with Immune-Checkpoint Inhibitors.

Palmer, Adam C / Izar, Benjamin / Hwangbo, Haeun / Sorger, Peter K

Clinical cancer research : an official journal of the American Association for Cancer Research

2022 Volume 28, Issue 2, Page(s) 368–377

Abstract: Purpose: Combinations of immune-checkpoint inhibitors (ICI) with other cancer therapies have been approved for advanced cancers in multiple indications, and numerous trials are under way to test new combinations. However, the mechanisms that account for ...

Abstract	Purpose: Combinations of immune-checkpoint inhibitors (ICI) with other cancer therapies have been approved for advanced cancers in multiple indications, and numerous trials are under way to test new combinations. However, the mechanisms that account for the superiority of approved ICI combinations relative to their constituent monotherapies remain unknown. Experimental design: We analyzed 13 phase III clinical trials testing combinations of ICIs with each other or other drugs in patients with advanced melanoma and lung, breast, gastric, kidney, and head and neck cancers. The clinical activity of the individual constituent therapies, measured in the same or a closely matched trial cohort, was used to compute progression-free survival (PFS) curves expected under a model of independent drug action. To identify additive or synergistic efficacy, PFS expected under this null model was compared with observed PFS by Cox regression. Results: PFS elicited by approved combination therapies with ICIs could be accurately predicted from monotherapy data using the independent drug action model (Pearson Conclusions: Combining ICIs with other cancer therapies affords predictable and clinically meaningful benefit by providing patients with multiple chances of response to a single agent. Conversely, there exists no evidence in phase III trials that other therapies interact with and enhance the activity of ICIs. These findings can inform the design and testing of new ICI combination therapies while emphasizing the importance of developing better predictors (biomarkers) of ICI response.
MeSH term(s)	Clinical Trials, Phase III as Topic ; Cohort Studies ; Combined Modality Therapy ; Humans ; Immune Checkpoint Inhibitors/therapeutic use ; Melanoma/drug therapy ; Progression-Free Survival
Chemical Substances	Immune Checkpoint Inhibitors
Language	English
Publishing date	2022-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-2275
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Zs.A 4223: Show issues

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Article ; Online: Filippo Giancotti (1958-2023).

DePinho, Ronald / Massagué, Joan / Manji, Gulam / Rustgi, Anil K / Izar, Benjamin

Nature cancer

2023 Volume 4, Issue 10, Page(s) 1401–1402

Language	English
Publishing date	2023-09-28
Publishing country	England
Document type	Editorial
ISSN	2662-1347
ISSN (online)	2662-1347
DOI	10.1038/s43018-023-00639-3
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Article ; Online: Beyond Tumor PD-L1: Emerging Genomic Biomarkers for Checkpoint Inhibitor Immunotherapy.

Lagos, Galina G / Izar, Benjamin / Rizvi, Naiyer A

American Society of Clinical Oncology educational book. American Society of Clinical Oncology. Annual Meeting

2020 Volume 40, Page(s) 1–11

Abstract: Despite the success of immune checkpoint blockade as a strategy for activating an antitumor immune response and promoting cancer regression, only a subset of patients have durable clinical benefit. Efforts are ongoing to identify robust biomarkers that ... ...

Abstract	Despite the success of immune checkpoint blockade as a strategy for activating an antitumor immune response and promoting cancer regression, only a subset of patients have durable clinical benefit. Efforts are ongoing to identify robust biomarkers that can effectively predict treatment response to immune checkpoint inhibitors (ICIs). Although PD-L1 expression is useful for stratifying patients, it is an imperfect tool. Comprehensive next-generation sequencing platforms that are readily used in clinical practice to identify a tumor's potentially actionable genetic alterations also reveal tumor genomic features, including tumor mutation burden (TMB), that may impact the response to ICIs. High TMB enhances tumor immunogenicity through increased numbers of tumor neoantigens that may promote an immune response. Defective DNA repair, leading to microsatellite instability, is an endogenous mechanism for increased tumor TMB that augments response to anti-PD-1 blockade. Alternatively, DNA damage from exogenous factors is responsible for high TMB seen in melanoma, lung cancer, and urothelial carcinoma, among tumor subtypes with higher response rates to ICIs. In this review, we summarize data supporting the use of TMB as a biomarker as well as its known limitations. We also highlight specific tumor suppressor genes and oncogenes that are under investigation as biomarkers for ICI response and resistance. Efforts are ongoing to delineate which genomic tumor characteristics can eventually be utilized in clinical practice to ascertain the benefit of ICIs for an individual patient.
MeSH term(s)	B7-H1 Antigen/pharmacology ; B7-H1 Antigen/therapeutic use ; Biomarkers, Tumor/genetics ; Genomics/methods ; Humans ; Immunotherapy/methods
Chemical Substances	B7-H1 Antigen ; Biomarkers, Tumor
Language	English
Publishing date	2020-04-21
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2431126-1
ISSN	1548-8756 ; 1548-8748
ISSN (online)	1548-8756
ISSN	1548-8748
DOI	10.1200/EDBK_289967
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Book ; Online ; Thesis: The hepatic response following infection with Listeria monocytogenes

Izar, Benjamin

2013

Title variant	Die hepatische Reaktion auf eine Infektion mit Listeria monocytogenes
Author's details	Benjamin Izar
Language	English
Size	Online-Ressource
Publisher	Universitätsbibliothek
Publishing place	Gießen
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Gießen, Justus-Liebig-Universität, Diss., 2013
Note	In: Giessen : VVB Laufersweiler
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: Rapid evolution of acute kidney injury after initial infusion of pembrolizumab in a melanoma patient concurrently treated with RAF/MEK inhibitors.

Thummalapalli, Rohit / Melms, Johannes C / Mier, James / Izar, Benjamin

Melanoma research

2020 Volume 30, Issue 2, Page(s) 219–222

Abstract: The use of either immune checkpoint blockade or RAF/MEK inhibitors represents standard of care treatment options for metastatic melanoma. Each class of these drugs has distinct response kinetics, adverse effects, and unique clinical challenges. ... ...

Abstract	The use of either immune checkpoint blockade or RAF/MEK inhibitors represents standard of care treatment options for metastatic melanoma. Each class of these drugs has distinct response kinetics, adverse effects, and unique clinical challenges. Combination of immune checkpoint blockade and RAF/MEK inhibitors may result in rapid and durable responses, however, the potential adverse effects of such combinations are poorly characterized. Here, we describe the case of a patient with BRAF-mutant melanoma who received an initial infusion of anti-PD-1 therapy while taking RAF/MEK inhibitors and experienced severe acute kidney injury, an otherwise infrequent side effect of any of these drugs alone. Treatment with corticosteroids rapidly reversed this process, indicating an underlying immune-mediated complication. A deeper understanding of potential adverse effects of combination therapies and their potential mechanisms should be carefully considered in the treatment landscape for melanoma and other cancers.
MeSH term(s)	Acute Kidney Injury/chemically induced ; Aged ; Antibodies, Monoclonal, Humanized/adverse effects ; Antineoplastic Combined Chemotherapy Protocols/adverse effects ; Female ; Humans ; Melanoma/complications ; Melanoma/drug therapy ; Melanoma/pathology ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Skin Neoplasms/complications ; Skin Neoplasms/drug therapy ; Skin Neoplasms/pathology
Chemical Substances	Antibodies, Monoclonal, Humanized ; pembrolizumab (DPT0O3T46P) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2020-02-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1095779-0
ISSN	1473-5636 ; 0960-8931
ISSN (online)	1473-5636
ISSN	0960-8931
DOI	10.1097/CMR.0000000000000646
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Article ; Online: GILA, a Replacement for the Soft-Agar Assay that Permits High-Throughput Drug and Genetic Screens for Cellular Transformation.

Izar, Benjamin / Rotem, Asaf

Current protocols in molecular biology

2016 Volume 116, Page(s) 28.8.1–28.8.12

Abstract: For the last five decades, measuring the ability of cells to grow in soft agar has served as the gold standard assay for in vitro cellular transformation. Nevertheless, the soft agar colony formation assay is time consuming and ill-suited for high- ... ...

Abstract	For the last five decades, measuring the ability of cells to grow in soft agar has served as the gold standard assay for in vitro cellular transformation. Nevertheless, the soft agar colony formation assay is time consuming and ill-suited for high-throughput screens. This unit describes an equally qualitative and quantitative assay known as growth in low attachment or GILA. The GILA assay is suitable for high-throughput pharmacological or genetic screens and allows the simultaneous examination of multiple cell lines and experimental perturbations. GILA conditions are specific and relevant to the transformed state because they depend on a property of cancer cells that is not shared by non-transformed cells. The GILA assay enables ex vivo drug sensitivity testing of patient-derived tumor cells to define precise treatments for individual patients. © 2016 by John Wiley & Sons, Inc.
MeSH term(s)	Agar/chemistry ; Cell Adhesion ; Cell Culture Techniques/methods ; Cell Separation/methods ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/genetics ; Drug Screening Assays, Antitumor/methods ; Genetic Testing/methods ; High-Throughput Screening Assays/methods ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Tumor Cells, Cultured
Chemical Substances	Agar (9002-18-0)
Language	English
Publishing date	2016-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1934-3647
ISSN (online)	1934-3647
DOI	10.1002/cpmb.26
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Article ; Online: LncRNA Malat1 suppresses pyroptosis and T cell-mediated killing of incipient metastatic cells.

Kumar, Dhiraj / Gurrapu, Sreeharsha / Wang, Yan / Bae, Seong-Yeon / Pandey, Poonam R / Chen, Hong / Mondal, Jayanta / Han, Hyunho / Wu, Chang-Jiun / Karaiskos, Spyros / Yang, Fei / Sahin, Aysegul / Wistuba, Ignacio I / Gao, Jianjun / Tripathy, Debasish / Gao, Hua / Izar, Benjamin / Giancotti, Filippo G

Nature cancer

2024 Volume 5, Issue 2, Page(s) 262–282

Abstract: The contribution of antitumor immunity to metastatic dormancy is poorly understood. Here we show that the long noncoding RNA Malat1 is required for tumor initiation and metastatic reactivation in mouse models of breast cancer and other tumor types. ... ...

Abstract	The contribution of antitumor immunity to metastatic dormancy is poorly understood. Here we show that the long noncoding RNA Malat1 is required for tumor initiation and metastatic reactivation in mouse models of breast cancer and other tumor types. Malat1 localizes to nuclear speckles to couple transcription, splicing and mRNA maturation. In metastatic cells, Malat1 induces WNT ligands, autocrine loops to promote self-renewal and the expression of Serpin protease inhibitors. Through inhibition of caspase-1 and cathepsin G, SERPINB6B prevents gasdermin D-mediated induction of pyroptosis. In this way, SERPINB6B suppresses immunogenic cell death and confers evasion of T cell-mediated tumor lysis of incipient metastatic cells. On-target inhibition of Malat1 using therapeutic antisense nucleotides suppresses metastasis in a SERPINB6B-dependent manner. These results suggest that Malat1-induced expression of SERPINB6B can titrate pyroptosis and immune recognition at metastatic sites. Thus, Malat1 is at the nexus of tumor initiation, reactivation and immune evasion and represents a tractable and clinically relevant drug target.
MeSH term(s)	Animals ; Mice ; Cell Line, Tumor ; Pyroptosis ; RNA Splicing ; RNA, Long Noncoding/genetics ; T-Lymphocytes/metabolism
Chemical Substances	RNA, Long Noncoding ; Malat1 long non-coding RNA, mouse
Language	English
Publishing date	2024-01-09
Publishing country	England
Document type	Journal Article
ISSN	2662-1347
ISSN (online)	2662-1347
DOI	10.1038/s43018-023-00695-9
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