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Article ; Online: A BAFFling

Eldering, Eric

2022 Volume 107, Issue 12, Page(s) 2774–2775

MeSH term(s)	Adult ; Humans ; Lymphoma, Mantle-Cell/diagnosis ; Cell Cycle Proteins
Chemical Substances	Cell Cycle Proteins
Language	English
Publishing date	2022-12-01
Publishing country	Italy
Document type	Editorial ; Comment
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2022.280721
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Article ; Online: The Therapeutic Potential of Targeting NIK in B Cell Malignancies.

Haselager, Marco V / Eldering, Eric

Frontiers in immunology

2022 Volume 13, Page(s) 930986

Abstract: NF-κB-inducing kinase (NIK) is a key player in non-canonical NF-κB signaling, involved in several fundamental cellular processes, and is crucial for B cell function and development. In response to certain signals and ligands, such as CD40, BAFF and ... ...

Abstract	NF-κB-inducing kinase (NIK) is a key player in non-canonical NF-κB signaling, involved in several fundamental cellular processes, and is crucial for B cell function and development. In response to certain signals and ligands, such as CD40, BAFF and lymphotoxin-β activation, NIK protein stabilization and subsequent NF-κB activation is achieved. Overexpression or overactivation of NIK is associated with several malignancies, including activating mutations in multiple myeloma (MM) and gain-of-function in MALT lymphoma as a result of post-translational modifications. Consequently, drug discovery studies are devoted to pharmacologic modulation of NIK and development of specific novel small molecule inhibitors. However, disease-specific
MeSH term(s)	Humans ; NF-kappa B/metabolism ; Neoplasms ; Protein Serine-Threonine Kinases ; Signal Transduction/genetics ; NF-kappaB-Inducing Kinase
Chemical Substances	NF-kappa B ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-07-12
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.930986
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Article ; Online: Metabolic reprogramming in the CLL TME; potential for new therapeutic targets.

Simon-Molas, Helga / Montironi, Chiara / Kabanova, Anna / Eldering, Eric

Seminars in hematology

2024

Abstract: Chronic lymphocytic leukemia (CLL) cells circulate between peripheral (PB) blood and lymph node (LN) compartments, and strictly depend on microenvironmental factors for proliferation, survival and drug resistance. All cancer cells display metabolic ... ...

Abstract	Chronic lymphocytic leukemia (CLL) cells circulate between peripheral (PB) blood and lymph node (LN) compartments, and strictly depend on microenvironmental factors for proliferation, survival and drug resistance. All cancer cells display metabolic reprogramming and CLL is no exception - though the inert status of the PB CLL cells has hampered detailed insight into these processes. We summarize previous work on reactive oxygen species (ROS), oxidative stress, and hypoxia, as well as the important roles of Myc, and PI3K/Akt/mTor pathways. In vitro co-culture systems and gene expression analyses have provided a partial picture of CLL LN metabolism. New broad omics techniques allow to obtain molecular and also single-cell level understanding of CLL plasticity and metabolic reprogramming. We summarize recent developments and describe the new concept of glutamine addiction for CLL, which may hold therapeutic promise.
Language	English
Publishing date	2024-02-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	206923-4
ISSN	1532-8686 ; 0037-1963
ISSN (online)	1532-8686
ISSN	0037-1963
DOI	10.1053/j.seminhematol.2024.02.001
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Article: Negligible role of TRAIL death receptors in cell death upon endoplasmic reticulum stress in B-cell malignancies.

Favaro, Francesca / Both, Demi / Derks, Ingrid A M / Spaargaren, Marcel / Muñoz-Pinedo, Cristina / Eldering, Eric

Oncogenesis

2023 Volume 12, Issue 1, Page(s) 6

Abstract: Impairments in protein folding in the endoplasmic reticulum (ER) lead to a condition called ER stress, which can trigger apoptosis via the mitochondrial or the death receptor (extrinsic) pathway. There is controversy concerning involvement of the death ... ...

Abstract	Impairments in protein folding in the endoplasmic reticulum (ER) lead to a condition called ER stress, which can trigger apoptosis via the mitochondrial or the death receptor (extrinsic) pathway. There is controversy concerning involvement of the death receptor (DR)4 and DR5-Caspase-8 -Bid pathway in ER stress-mediated cell death, and this axis has not been fully studied in B-cell malignancies. Using three B-cell lines from Mantle Cell Lymphoma, Waldenström's macroglobulinemia and Multiple Myeloma origins, we engineered a set of CRISPR KOs of key components of these cell death pathways to address this controversy. We demonstrate that DR4 and/or DR5 are essential for killing via TRAIL, however, they were dispensable for ER-stress induced-cell death, by Thapsigargin, Brefeldin A or Bortezomib, as were Caspase-8 and Bid. In contrast, the deficiency of Bax and Bak fully protected from ER stressors. Caspase-8 and Bid were cleaved upon ER-stress stimulation, but this was DR4/5 independent and rather a result of mitochondrial-induced feedback loop subsequent to Bax/Bak activation. Finally, combined activation of the ER-stress and TRAIL cell-death pathways was synergistic with putative clinical relevance for B-cell malignancies.
Language	English
Publishing date	2023-02-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2674437-5
ISSN	2157-9024
ISSN	2157-9024
DOI	10.1038/s41389-023-00450-w
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Article ; Online: Tipping the balance: toward rational combination therapies to overcome venetoclax resistance in mantle cell lymphoma.

Thus, Yvonne J / Eldering, Eric / Kater, Arnon P / Spaargaren, Marcel

Leukemia

2022 Volume 36, Issue 9, Page(s) 2165–2176

Abstract: Mantle cell lymphoma (MCL), an aggressive, but incurable B-cell lymphoma, is genetically characterized by the t(11;14) translocation, resulting in the overexpression of Cyclin D1. In addition, deregulation of the B-cell lymphoma-2 (BCL-2) family proteins ...

Abstract	Mantle cell lymphoma (MCL), an aggressive, but incurable B-cell lymphoma, is genetically characterized by the t(11;14) translocation, resulting in the overexpression of Cyclin D1. In addition, deregulation of the B-cell lymphoma-2 (BCL-2) family proteins BCL-2, B-cell lymphoma-extra large (BCL-X
MeSH term(s)	Adult ; Antineoplastic Agents ; Bridged Bicyclo Compounds, Heterocyclic ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Humans ; Lymphoma, B-Cell ; Lymphoma, Mantle-Cell ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2 ; Sulfonamides ; Tumor Microenvironment ; bcl-X Protein
Chemical Substances	Antineoplastic Agents ; Bridged Bicyclo Compounds, Heterocyclic ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2 ; Sulfonamides ; bcl-X Protein ; venetoclax (N54AIC43PW)
Language	English
Publishing date	2022-06-20
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-022-01627-9
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Zs.A 2295: Show issues

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Article: Hematopoietic versus Solid Cancers and T Cell Dysfunction: Looking for Similarities and Distinctions.

Montironi, Chiara / Muñoz-Pinedo, Cristina / Eldering, Eric

Cancers

2021 Volume 13, Issue 2

Abstract: Cancer cells escape, suppress and exploit the host immune system to sustain themselves, and the tumor microenvironment (TME) actively dampens T cell function by various mechanisms. Over the last years, new immunotherapeutic approaches, such as adoptive ... ...

Abstract	Cancer cells escape, suppress and exploit the host immune system to sustain themselves, and the tumor microenvironment (TME) actively dampens T cell function by various mechanisms. Over the last years, new immunotherapeutic approaches, such as adoptive chimeric antigen receptor (CAR) T cell therapy and immune checkpoint inhibitors, have been successfully applied for refractory malignancies that could only be treated in a palliative manner previously. Engaging the anti-tumor activity of the immune system, including CAR T cell therapy to target the CD19 B cell antigen, proved to be effective in acute lymphocytic leukemia. In low-grade hematopoietic B cell malignancies, such as chronic lymphocytic leukemia, clinical outcomes have been tempered by cancer-induced T cell dysfunction characterized in part by a state of metabolic lethargy. In multiple myeloma, novel antigens such as BCMA and CD38 are being explored for CAR T cells. In solid cancers, T cell-based immunotherapies have been applied successfully to melanoma and lung cancers, whereas application in e.g., breast cancer lags behind and is modestly effective as yet. The main hurdles for CAR T cell immunotherapy in solid tumors are the lack of suitable antigens, anatomical inaccessibility, and T cell anergy due to immunosuppressive TME. Given the wide range of success and failure of immunotherapies in various cancer types, it is crucial to comprehend the underlying similarities and distinctions in T cell dysfunction. Hence, this review aims at comparing selected, distinct B cell-derived versus solid cancer types and at describing means by which malignant cells and TME might dampen T cell anti-tumor activity, with special focus on immunometabolism. Drawing a meaningful parallel between the efficacy of immunotherapy and the extent of T cell dysfunction will shed light on areas where we can improve immune function to battle cancer.
Language	English
Publishing date	2021-01-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13020284
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Article ; Online: Kinase inhibitors developed for treatment of hematologic malignancies: implications for immune modulation in COVID-19.

Jacobs, Chaja F / Eldering, Eric / Kater, Arnon P

Blood advances

2021 Volume 5, Issue 3, Page(s) 913–925

Abstract: Tyrosine kinase inhibitors (TKIs) are used to target dysregulated signaling pathways in virtually all hematologic malignancies. Many of the targeted signaling pathways are also essential in nonmalignant immune cells. The current coronavirus severe acute ... ...

Abstract	Tyrosine kinase inhibitors (TKIs) are used to target dysregulated signaling pathways in virtually all hematologic malignancies. Many of the targeted signaling pathways are also essential in nonmalignant immune cells. The current coronavirus severe acute respiratory syndrome coronavirus 2 pandemic catalyzed clinical exploration of TKIs in the treatment of the various stages of COVID-19, which are characterized by distinct immune-related complications. Most of the reported effects of TKIs on immune regulation have been explored in vitro, with different class-specific drugs having nonoverlapping target affinities. Moreover, many of the reported in vivo effects are based on artificial animal models or on observations made in symptomatic patients with a hematologic malignancy who often already suffer from disturbed immune regulation. Based on in vitro and clinical observations, we attempt to decipher the impact of the main TKIs approved or in late-stage development for the treatment of hematological malignancies, including inhibitors of Bruton's tyrosine kinase, spleen tyrosine kinase, BCR-Abl, phosphatidylinositol 3-kinase/ mammalian target of rapamycin, JAK/STAT, and FMS-like tyrosine kinase 3, to provide a rationale for how such inhibitors could modify clinical courses of diseases, such as COVID-19.
MeSH term(s)	Adaptive Immunity ; Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors ; Agammaglobulinaemia Tyrosine Kinase/metabolism ; COVID-19/complications ; COVID-19/immunology ; COVID-19/pathology ; COVID-19/virology ; Cytokines/metabolism ; Fusion Proteins, bcr-abl/antagonists & inhibitors ; Fusion Proteins, bcr-abl/metabolism ; Hematologic Neoplasms/complications ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/pathology ; Humans ; Immunity, Innate ; Protein Kinase Inhibitors/therapeutic use ; SARS-CoV-2/isolation & purification
Chemical Substances	Cytokines ; Protein Kinase Inhibitors ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2) ; Fusion Proteins, bcr-abl (EC 2.7.10.2)
Language	English
Publishing date	2021-02-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2020003768
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Zs.A 7153: Show issues

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Article ; Online: Electron transport chain and mTOR inhibition synergistically decrease CD40 signaling and counteract venetoclax resistance in chronic lymphocytic leukemia.

Chen, Zhenghao / Cretenet, Gaspard / Carnazzo, Valeria / Simon-Molas, Helga / Kater, Arnon P / Windt, Gerritje J W van der / Eldering, Eric

Haematologica

2024 Volume 109, Issue 1, Page(s) 151–162

Abstract: CD40 signaling upregulates BCL-XL and MCL-1 expression in the chronic lymphocytic leukemia (CLL) lymph node microenvironment, affording resistance to the BCL-2 inhibitor, venetoclax. Venetoclax resistance in the therapeutic setting and after long-term ... ...

Abstract	CD40 signaling upregulates BCL-XL and MCL-1 expression in the chronic lymphocytic leukemia (CLL) lymph node microenvironment, affording resistance to the BCL-2 inhibitor, venetoclax. Venetoclax resistance in the therapeutic setting and after long-term laboratory selection has been linked to metabolic alterations, but the underlying mechanism(s) are unknown. We aimed here to discover how CD40 stimulation as a model for tumor microenvironment-mediated metabolic changes, affects venetoclax sensitivity/resistance. CD40 stimulation increased oxidative phosphorylation and glycolysis, but only inhibition of oxidative phosphorylation countered venetoclax resistance. Furthermore, blocking mitochondrial import of pyruvate, glutamine or fatty acids affected CLL metabolism, but did not prevent CD40-mediated resistance to venetoclax. In contrast, inhibition of the electron transport chain (ETC) at complex I, III or V attenuated CLL activation and ATP production, and downregulated MCL-1 and BCL-XL, correlating with reduced CD40 surface expression. Moreover, ETC inhibition equaled mTOR1/2 but not mTOR1 inhibition alone for venetoclax resistance, and all three pathways were linked to control of general protein translation. In line with this, ETC plus mTOR inhibition synergistically counteracted venetoclax resistance. These findings link oxidative CLL metabolism to CD40 expression and cellular signaling, and may hold clinical potential.
MeSH term(s)	Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Electron Transport ; Drug Resistance, Neoplasm ; TOR Serine-Threonine Kinases/metabolism ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Bridged Bicyclo Compounds, Heterocyclic/therapeutic use ; CD40 Antigens/metabolism ; Apoptosis ; Tumor Microenvironment
Chemical Substances	venetoclax (N54AIC43PW) ; Myeloid Cell Leukemia Sequence 1 Protein ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Bridged Bicyclo Compounds, Heterocyclic ; CD40 Antigens
Language	English
Publishing date	2024-01-01
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.282760
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Article ; Online: Metabolic signature and response to glutamine deprivation are independent of p53 status in B cell malignancies.

Montironi, Chiara / Chen, Zhenghao / Derks, Ingrid A M / Cretenet, Gaspard / Krap, Esmée A / Eldering, Eric / Simon-Molas, Helga

iScience

2024 Volume 27, Issue 5, Page(s) 109640

Abstract: The tumor suppressor p53 has been described to control various aspects of metabolic reprogramming in solid tumors, but in B cell malignancies that role is as yet unknown. We generated pairs of p53 functional and knockout (KO) clones from distinct B cell ... ...

Abstract	The tumor suppressor p53 has been described to control various aspects of metabolic reprogramming in solid tumors, but in B cell malignancies that role is as yet unknown. We generated pairs of p53 functional and knockout (KO) clones from distinct B cell malignancies (acute lymphoblastic leukemia, chronic lymphocytic leukemia, diffuse large B cell lymphoma, and multiple myeloma). Metabolomics and isotope tracing showed that p53 loss did not drive a common metabolic signature. Instead, cell lines segregated according to cell of origin. Next, we focused on glutamine as a crucial energy source in the B cell tumor microenvironment. In both
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.109640
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Book ; Thesis: Structure function studies on the serpin C1 inhibitor

Eldering, Eric F.

1992

Author's details	door Eric Frederik Eldering
Size	106 S. : Ill., graph. Darst.
Publishing country	Netherlands
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Amsterdam, Univ., Diss., 1992
HBZ-ID	HT004304489
ISBN	90-900-4974-6 ; 978-90-900-4974-8
Database	Catalogue ZB MED Medicine, Health

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92 E 2860	order for loan	Magazin

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