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Article ; Online: Natural killer cell therapies.

Vivier, Eric / Rebuffet, Lucas / Narni-Mancinelli, Emilie / Cornen, Stéphanie / Igarashi, Rob Y / Fantin, Valeria R

2024 Volume 626, Issue 8000, Page(s) 727–736

Abstract: Natural killer (NK) cells are lymphocytes of the innate immune system. A key feature of NK cells is their ability to recognize a wide range of cells in distress, particularly tumour cells and cells infected with viruses. They combine both direct effector ...

Abstract	Natural killer (NK) cells are lymphocytes of the innate immune system. A key feature of NK cells is their ability to recognize a wide range of cells in distress, particularly tumour cells and cells infected with viruses. They combine both direct effector functions against their cellular targets and participate in the generation, shaping and maintenance of a multicellular immune response. As our understanding has deepened, several therapeutic strategies focused on NK cells have been conceived and are currently in various stages of development, from preclinical investigations to clinical trials. Here we explore in detail the complexity of NK cell biology in humans and highlight the role of these cells in cancer immunity. We also analyse the harnessing of NK cell immunity through immune checkpoint inhibitors, NK cell engagers, and infusions of preactivated or genetically modified, autologous or allogeneic NK cell products.
MeSH term(s)	Humans ; Immunotherapy, Adoptive/methods ; Killer Cells, Natural/immunology ; Killer Cells, Natural/transplantation ; Neoplasms/immunology ; Neoplasms/therapy ; Immunity, Innate
Language	English
Publishing date	2024-02-21
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06945-1
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Article ; Online: Self-eating limits EGFR-dependent tumor growth.

Fantin, Valeria R / Abraham, Robert T

Cell

2013 Volume 154, Issue 6, Page(s) 1184–1186

Abstract: Autophagy is a cell-autonomous, catabolic process that plays context-dependent roles in tumor growth and progression. Wei et al. report that EGFR signaling promotes tumor growth through phosphorylation and functional inactivation of Beclin 1 and the ... ...

Abstract	Autophagy is a cell-autonomous, catabolic process that plays context-dependent roles in tumor growth and progression. Wei et al. report that EGFR signaling promotes tumor growth through phosphorylation and functional inactivation of Beclin 1 and the consequent suppression of autophagy.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/metabolism ; Autophagy ; Beclin-1 ; Drug Resistance, Neoplasm ; Humans ; Membrane Proteins/metabolism ; Receptor, Epidermal Growth Factor/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; BECN1 protein, human ; Beclin-1 ; Membrane Proteins ; EGFR protein, human (EC 2.7.10.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2013-09-12
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2013.08.040
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Article ; Online: Survival of the fittest: metabolic adaptations in cancer.

Berardi, Marcelo J / Fantin, Valeria R

Current opinion in genetics & development

2011 Volume 21, Issue 1, Page(s) 59–66

Abstract: Malignant transformation is often a multistep process characterized by an initial period of avascular growth. Rapid cell proliferation creates areas within the emerging preneoplastic lesion with limited diffusion of oxygen and nutrients. In this context, ...

Abstract	Malignant transformation is often a multistep process characterized by an initial period of avascular growth. Rapid cell proliferation creates areas within the emerging preneoplastic lesion with limited diffusion of oxygen and nutrients. In this context, activation of oncogenes, loss of tumor suppressors as well as additional adaptive mechanisms drive a profound metabolic rewiring to overcome the environmental constraints. The emerging cells are in principle better suited to proliferate and survive in the hostile tumor microenvironment. Furthermore, some of the acquired metabolic traits impact their metastatic behavior and response to therapy. It is becoming increasingly clear that malignant cells are highly dependent on certain nutrients, an Achilles' heel of cancer and an opportunity for therapeutic intervention.
MeSH term(s)	Adaptation, Biological ; Animals ; Cell Proliferation ; Glucose/metabolism ; Glutamine/metabolism ; Humans ; Mitochondria/metabolism ; Neoplasms/metabolism ; Neoplasms/pathology
Chemical Substances	Glutamine (0RH81L854J) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2011-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1077312-5
ISSN	1879-0380 ; 0959-437X
ISSN (online)	1879-0380
ISSN	0959-437X
DOI	10.1016/j.gde.2010.10.001
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Article: Palbociclib and Fulvestrant Act in Synergy to Modulate Central Carbon Metabolism in Breast Cancer Cells.

Warth, Benedikt / Palermo, Amelia / Rattray, Nicholas J W / Lee, Nathan V / Zhu, Zhou / Hoang, Linh T / Cai, Yuping / Mazurek, Anthony / Dann, Stephen / VanArsdale, Todd / Fantin, Valeria R / Shields, David / Siuzdak, Gary / Johnson, Caroline H

Metabolites

2019 Volume 9, Issue 1

Abstract: The aims of this study were to determine whether combination chemotherapeutics exhibit a synergistic effect on breast cancer cell metabolism. Palbociclib, is a selective inhibitor of cyclin-dependent kinases 4 and 6, and when patients are treated in ... ...

Abstract	The aims of this study were to determine whether combination chemotherapeutics exhibit a synergistic effect on breast cancer cell metabolism. Palbociclib, is a selective inhibitor of cyclin-dependent kinases 4 and 6, and when patients are treated in combination with fulvestrant, an estrogen receptor antagonist, they have improved progression-free survival. The mechanisms for this survival advantage are not known. Therefore, we analyzed metabolic and transcriptomic changes in MCF-7 cells following single and combination chemotherapy to determine whether selective metabolic pathways are targeted during these different modes of treatment. Individually, the drugs caused metabolic disruption to the same metabolic pathways, however fulvestrant additionally attenuated the pentose phosphate pathway and the production of important coenzymes. A comprehensive effect was observed when the drugs were applied together, confirming the combinatory therapy's synergism in the cell model. This study also highlights the power of merging high-dimensional datasets to unravel mechanisms involved in cancer metabolism and therapy.
Language	English
Publishing date	2019-01-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo9010007
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Article ; Online: Leveraging model-based study designs and serial micro-sampling techniques to understand the oral pharmacokinetics of the potent LTB4 inhibitor, CP-105696, for mouse pharmacology studies.

Spilker, Mary E / Chung, Heekyung / Visswanathan, Ravi / Bagrodia, Shubha / Gernhardt, Steven / Fantin, Valeria R / Ellies, Lesley G

Xenobiotica; the fate of foreign compounds in biological systems

2017 Volume 47, Issue 7, Page(s) 600–606

Abstract: 1. Leukotriene B4 (LTB4) is a proinflammatory mediator important in the progression of a number of inflammatory diseases. Preclinical models can explore the role of LTB4 in pathophysiology using tool compounds, such as CP-105696, that modulate its ... ...

Abstract	1. Leukotriene B4 (LTB4) is a proinflammatory mediator important in the progression of a number of inflammatory diseases. Preclinical models can explore the role of LTB4 in pathophysiology using tool compounds, such as CP-105696, that modulate its activity. To support preclinical pharmacology studies, micro-sampling techniques and mathematical modeling were used to determine the pharmacokinetics of CP-105696 in mice within the context of systemic inflammation induced by a high-fat diet (HFD). 2. Following oral administration of doses > 35 mg/kg, CP-105696 kinetics can be described by a one-compartment model with first order absorption. The compound's half-life is 44-62 h with an apparent volume of distribution of 0.51-0.72 L/kg. Exposures in animals fed an HFD are within 2-fold of those fed a normal chow diet. Daily dosing at 100 mg/kg was not tolerated and resulted in a >20% weight loss in the mice. 3. CP-105696's long half-life has the potential to support a twice weekly dosing schedule. Given that most chronic inflammatory diseases will require long-term therapies, these results are useful in determining the optimal dosing schedules for preclinical studies using CP-105696.
MeSH term(s)	Administration, Oral ; Animals ; Benzopyrans/pharmacokinetics ; Carboxylic Acids/pharmacokinetics ; Diet, High-Fat ; Half-Life ; Inflammation ; Leukotriene B4/antagonists & inhibitors ; Mice ; Models, Biological ; Neutrophils
Chemical Substances	Benzopyrans ; Carboxylic Acids ; Leukotriene B4 (1HGW4DR56D) ; CP 105696 (Z7354TW4BM)
Language	English
Publishing date	2017-07
Publishing country	England
Document type	Journal Article
ZDB-ID	120287-x
ISSN	1366-5928 ; 0049-8254
ISSN (online)	1366-5928
ISSN	0049-8254
DOI	10.1080/00498254.2016.1207112
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Article: Mechanisms of resistance to histone deacetylase inhibitors and their therapeutic implications.

Fantin, Valeria R / Richon, Victoria M

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

2007 Volume 13, Issue 24, Page(s) 7237–7242

Abstract: Histone deacetylase inhibitors (HDI) are a promising new approach to the treatment of cancer. HDIs have been shown to induce differentiation, cell cycle arrest, and apoptosis in a variety of transformed cell lines; inhibit tumor growth in animal models; ... ...

Abstract	Histone deacetylase inhibitors (HDI) are a promising new approach to the treatment of cancer. HDIs have been shown to induce differentiation, cell cycle arrest, and apoptosis in a variety of transformed cell lines; inhibit tumor growth in animal models; and show antitumor activity in clinical trials. Vorinostat, which has shown clinical responses in approximately 30% of patients with advanced cutaneous T-cell lymphoma, is the first HDI approved for the treatment of cancer, and it is currently being evaluated in other indications. A better understanding of the molecular determinants of resistance to HDIs may provide the basis for therapeutic combinations with improved clinical efficacy. Poor response to treatment could be linked to systemic factors like pharmacokinetics or to tumor-specific factors both at the level of the malignant cells (tumor intrinsic) or the tumor microenvironment. This review focuses on the tumor intrinsic mechanisms of drug resistance (excluding mechanism of acquired resistance due to chronic exposure). In particular, attention is given to selected mechanisms that are relevant across chemical classes of HDIs and that can aid in the design of rational combination strategies.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis/physiology ; Drug Resistance, Neoplasm/physiology ; Enzyme Inhibitors/pharmacology ; Histone Deacetylase Inhibitors ; Humans ; Neoplasms/drug therapy ; Neoplasms/enzymology
Chemical Substances	Enzyme Inhibitors ; Histone Deacetylase Inhibitors
Language	English
Publishing date	2007-12-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-07-2114
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Article ; Online: Discovery of a Potent Steroidal Glucocorticoid Receptor Antagonist with Enhanced Selectivity against the Progesterone and Androgen Receptors (OP-3633).

Du, Xiaohui / Eksterowicz, John / Zhou, Haiying / Rew, Yosup / Zhu, Liusheng / Yan, Xuelei / Medina, Julio C / Huang, Tom / Chen, Xi / Sutimantanapi, Dena / Jahchan, Nadine / Kong, Wayne / Sun, Jessica / Zavorotinskaya, Tatiana / Ye, Qiuping / Fantin, Valeria R / Sun, Daqing

Journal of medicinal chemistry

2019 Volume 62, Issue 14, Page(s) 6751–6764

Abstract: Structure-based modification of mifepristone ( ...

Abstract	Structure-based modification of mifepristone (
MeSH term(s)	Androgen Receptor Antagonists/chemistry ; Androgen Receptor Antagonists/pharmacology ; Drug Discovery ; Humans ; Mifepristone/analogs & derivatives ; Mifepristone/pharmacology ; Models, Molecular ; Receptors, Androgen/metabolism ; Receptors, Glucocorticoid/antagonists & inhibitors ; Receptors, Glucocorticoid/metabolism ; Receptors, Progesterone/antagonists & inhibitors ; Receptors, Progesterone/metabolism
Chemical Substances	Androgen Receptor Antagonists ; Receptors, Androgen ; Receptors, Glucocorticoid ; Receptors, Progesterone ; Mifepristone (320T6RNW1F)
Language	English
Publishing date	2019-07-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.9b00711
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Article ; Online: Orally Bioavailable Small-Molecule CD73 Inhibitor (OP-5244) Reverses Immunosuppression through Blockade of Adenosine Production.

Journal of medicinal chemistry

2020 Volume 63, Issue 18, Page(s) 10433–10459

Abstract: The adenosinergic pathway represents an attractive new therapeutic approach in cancer immunotherapy. In this pathway, ecto-5-nucleotidase CD73 has the unique function of regulating production of immunosuppressive adenosine (ADO) through the hydrolysis of ...

Abstract	The adenosinergic pathway represents an attractive new therapeutic approach in cancer immunotherapy. In this pathway, ecto-5-nucleotidase CD73 has the unique function of regulating production of immunosuppressive adenosine (ADO) through the hydrolysis of AMP. CD73 is overexpressed in many cancers, resulting in elevated levels of ADO that correspond to poor patient prognosis. Therefore, reducing the level of ADO via inhibition of CD73 is a potential strategy for treating cancers. Based on the binding mode of adenosine 5'-(α,β-methylene)diphosphate (AOPCP) with human CD73, we designed a series of novel monophosphonate small-molecule CD73 inhibitors. Among them, OP-5244 (
MeSH term(s)	5'-Nucleotidase/antagonists & inhibitors ; Adenosine/antagonists & inhibitors ; Administration, Oral ; Animals ; CD8-Positive T-Lymphocytes/drug effects ; Cell Line, Tumor ; Dogs ; Enzyme Inhibitors/administration & dosage ; Enzyme Inhibitors/chemical synthesis ; Enzyme Inhibitors/pharmacokinetics ; Enzyme Inhibitors/pharmacology ; GPI-Linked Proteins/antagonists & inhibitors ; Humans ; Immunologic Factors/administration & dosage ; Immunologic Factors/chemical synthesis ; Immunologic Factors/pharmacokinetics ; Immunologic Factors/pharmacology ; Macaca fascicularis ; Mice, Inbred BALB C ; Molecular Structure ; Nucleosides/administration & dosage ; Nucleosides/chemical synthesis ; Nucleosides/pharmacokinetics ; Nucleosides/pharmacology ; Organophosphonates/administration & dosage ; Organophosphonates/chemical synthesis ; Organophosphonates/pharmacokinetics ; Organophosphonates/pharmacology ; Rats ; Stereoisomerism ; Structure-Activity Relationship
Chemical Substances	Enzyme Inhibitors ; GPI-Linked Proteins ; Immunologic Factors ; Nucleosides ; Organophosphonates ; 5'-Nucleotidase (EC 3.1.3.5) ; NT5E protein, human (EC 3.1.3.5) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2020-09-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.0c01086
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Article: Survival of the fittest: metabolic adaptations in cancer

Berardi, Marcelo J / Fantin, Valeria R

Current Opinion in Genetics & Development. 2011 Feb., v. 21, no. 1

2011

Abstract	Malignant transformation is often a multistep process characterized by an initial period of avascular growth. Rapid cell proliferation creates areas within the emerging preneoplastic lesion with limited diffusion of oxygen and nutrients. In this context, activation of oncogenes, loss of tumor suppressors as well as additional adaptive mechanisms drive a profound metabolic rewiring to overcome the environmental constraints. The emerging cells are in principle better suited to proliferate and survive in the hostile tumor microenvironment. Furthermore, some of the acquired metabolic traits impact their metastatic behavior and response to therapy. It is becoming increasingly clear that malignant cells are highly dependent on certain nutrients, an Achilles’ heel of cancer and an opportunity for therapeutic intervention.
Keywords	cell proliferation ; metastasis ; nutrients ; oncogenes ; oxygen ; therapeutics
Language	English
Dates of publication	2011-02
Size	p. 59-66.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1077312-5
ISSN	1879-0380 ; 0959-437X
ISSN (online)	1879-0380
ISSN	0959-437X
DOI	10.1016/j.gde.2010.10.001
Database	NAL-Catalogue (AGRICOLA)

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Article: F16, a mitochondriotoxic compound, triggers apoptosis or necrosis depending on the genetic background of the target carcinoma cell.

Fantin, Valeria R / Leder, Philip

Cancer research

2003 Volume 64, Issue 1, Page(s) 329–336

Abstract: Mutations that lead to the emergence of resistance to apoptosis are commonly observed among tumor cells. Some of the proteins affected are integral parts of the apoptotic cascade such as pro- and antiapoptotic members of the Bcl-2 family. F16 is a small ... ...

Abstract	Mutations that lead to the emergence of resistance to apoptosis are commonly observed among tumor cells. Some of the proteins affected are integral parts of the apoptotic cascade such as pro- and antiapoptotic members of the Bcl-2 family. F16 is a small molecule that accumulates in mitochondria of a variety of tumor cells and interferes with their physiological function. Because this interference ultimately triggers apoptosis in many affected cell lines, we examined the effect of antiapoptotic Bcl-2 overexpression on the response of cells to F16. Our results showed that high levels of Bcl-2 did not block the ability of F16 to induce cell death. However, unlike the apoptotic response that followed F16 treatment of cells with moderate Bcl-2 levels, cells resistant to a variety of apoptotic stimuli by virtue of Bcl-2 overexpression succumbed to F16 by necrosis. Thus, this dual ability of the mitochondriotoxic compound F16 to induce apoptosis and necrosis may represent an added advantage by expanding its spectrum of action toward genetically altered tumor cells incapable of apoptosis.
MeSH term(s)	Apoptosis/drug effects ; Carcinoma/genetics ; Carcinoma/pathology ; Caspase Inhibitors ; Cell Death/drug effects ; Cell Division/drug effects ; Cell Line, Tumor ; Cysteine Proteinase Inhibitors/pharmacology ; Flow Cytometry ; Homeostasis ; Humans ; Indoles/toxicity ; Mitochondria/drug effects ; Mitochondria/pathology ; Necrosis ; Oxidation-Reduction ; Proto-Oncogene Proteins c-bcl-2/genetics ; Pyridinium Compounds/toxicity
Chemical Substances	Caspase Inhibitors ; Cysteine Proteinase Inhibitors ; Indoles ; Proto-Oncogene Proteins c-bcl-2 ; Pyridinium Compounds ; 4-(2-(indol-3-yl)vinyl)-1-methylpyridinium (64651-39-4)
Language	English
Publishing date	2003-12-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.can-03-0899
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