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Article ; Online: moDCs, Less Problems.

Gardner, Alycia / Ruffell, Brian

2018 Volume 48, Issue 1, Page(s) 6–8

Abstract: Type 1 conventional dendritic cells are necessary for the development of anti-tumor immunity. In this issue of Immunity, Sharma et al. (2018) identify a phenotypically similar monocyte-derived population within inflamed tumors that promotes T cell ... ...

Abstract	Type 1 conventional dendritic cells are necessary for the development of anti-tumor immunity. In this issue of Immunity, Sharma et al. (2018) identify a phenotypically similar monocyte-derived population within inflamed tumors that promotes T cell responses during therapy.
MeSH term(s)	Cell Differentiation ; Cells, Cultured ; Dendritic Cells ; Monocytes ; T-Lymphocytes
Language	English
Publishing date	2018-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2017.12.017
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Zs.A 4227: 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 ; Online: Dendritic Cells and Their Role in Immunotherapy.

Gardner, Alycia / de Mingo Pulido, Álvaro / Ruffell, Brian

Frontiers in immunology

2020 Volume 11, Page(s) 924

Abstract: Despite significant advances in the field of cancer immunotherapy, the majority of patients still do not benefit from treatment and must rely on traditional therapies. Dendritic cells have long been a focus of cancer immunotherapy due to their role in ... ...

Abstract	Despite significant advances in the field of cancer immunotherapy, the majority of patients still do not benefit from treatment and must rely on traditional therapies. Dendritic cells have long been a focus of cancer immunotherapy due to their role in inducing protective adaptive immunity, but cancer vaccines have shown limited efficacy in the past. With the advent of immune checkpoint blockade and the ability to identify patient-specific neoantigens, new vaccines, and combinatorial therapies are being evaluated in the clinic. Dendritic cells are also emerging as critical regulators of the immune response within tumors. Understanding how to augment the function of these intratumoral dendritic cells could offer new approaches to enhance immunotherapy, in addition to improving the cytotoxic and targeted therapies that are partially dependent upon a robust immune response for their efficacy. Here we will discuss the role of specific dendritic cell subsets in regulating the anti-tumor immune response, as well as the current status of dendritic cell-based immunotherapies, in order to provide an overview for future lines of research and clinical trials.
MeSH term(s)	Animals ; Antineoplastic Agents, Immunological/adverse effects ; Antineoplastic Agents, Immunological/therapeutic use ; Cancer Vaccines/adverse effects ; Cancer Vaccines/therapeutic use ; Dendritic Cells/drug effects ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Dendritic Cells/transplantation ; Humans ; Immune Checkpoint Inhibitors/adverse effects ; Immune Checkpoint Inhibitors/therapeutic use ; Immunotherapy, Adoptive/adverse effects ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/therapy ; Phenotype ; Signal Transduction ; Treatment Outcome
Chemical Substances	Antineoplastic Agents, Immunological ; Cancer Vaccines ; Immune Checkpoint Inhibitors
Language	English
Publishing date	2020-05-21
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.00924
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Article ; Online: Reducing interferon'ce in stem cells.

Gardner, Alycia / Ruffell, Brian

Nature cell biology

2017 Volume 19, Issue 6, Page(s) 597–599

Abstract: Little is known regarding how the interactions of stem cells with the immune system regulate their plasticity. A study now describes a mechanism by which normal breast and cancer stem cells utilize miR-199a to downregulate the corepressor LCOR and ... ...

Abstract	Little is known regarding how the interactions of stem cells with the immune system regulate their plasticity. A study now describes a mechanism by which normal breast and cancer stem cells utilize miR-199a to downregulate the corepressor LCOR and minimize responses to type I interferon.
MeSH term(s)	Animals ; Cell Proliferation ; Humans ; Immune System/metabolism ; Interferons/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Models, Biological ; Neoplastic Stem Cells/pathology ; Stem Cells/metabolism
Chemical Substances	MicroRNAs ; Interferons (9008-11-1)
Language	English
Publishing date	2017-05-31
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/ncb3544
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Zs.A 5169: 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 ; Online: Combating castration-resistant prostate cancer by co-targeting the epigenetic regulators EZH2 and HDAC.

Schade, Amy E / Kuzmickas, Ryan / Rodriguez, Carrie L / Mattioli, Kaia / Enos, Miriam / Gardner, Alycia / Cichowski, Karen

PLoS biology

2023 Volume 21, Issue 4, Page(s) e3002038

Abstract: While screening and early detection have reduced mortality from prostate cancer, castration-resistant disease (CRPC) is still incurable. Here, we report that combined EZH2/HDAC inhibitors potently kill CRPCs and cause dramatic tumor regression in ... ...

Abstract	While screening and early detection have reduced mortality from prostate cancer, castration-resistant disease (CRPC) is still incurable. Here, we report that combined EZH2/HDAC inhibitors potently kill CRPCs and cause dramatic tumor regression in aggressive human and mouse CRPC models. Notably, EZH2 and HDAC both transmit transcriptional repressive signals: regulating histone H3 methylation and histone deacetylation, respectively. Accordingly, we show that suppression of both EZH2 and HDAC are required to derepress/induce a subset of EZH2 targets, by promoting the sequential demethylation and acetylation of histone H3. Moreover, we find that the induction of one of these targets, ATF3, which is a broad stress response gene, is critical for the therapeutic response. Importantly, in human tumors, low ATF3 levels are associated with decreased survival. Moreover, EZH2- and ATF3-mediated transcriptional programs inversely correlate and are most highly/lowly expressed in advanced disease. Together, these studies identify a promising therapeutic strategy for CRPC and suggest that these two major epigenetic regulators buffer prostate cancers from a lethal response to cellular stresses, thereby conferring a tractable therapeutic vulnerability.
MeSH term(s)	Animals ; Humans ; Male ; Mice ; Cell Line, Tumor ; Enhancer of Zeste Homolog 2 Protein/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Histones/metabolism ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Histone Deacetylases
Chemical Substances	Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; EZH2 protein, human (EC 2.1.1.43) ; Histones ; Ezh2 protein, mouse (EC 2.1.1.43) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2023-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2126776-5
ISSN	1545-7885 ; 1544-9173
ISSN (online)	1545-7885
ISSN	1544-9173
DOI	10.1371/journal.pbio.3002038
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Article ; Online: DAB2IP Is a Bifunctional Tumor Suppressor That Regulates Wild-Type RAS and Inflammatory Cascades in KRAS Mutant Colon Cancer.

Miller, Abigail L / Perurena, Naiara / Gardner, Alycia / Hinoue, Toshinori / Loi, Patrick / Laird, Peter W / Cichowski, Karen

Cancer research

2023 Volume 83, Issue 11, Page(s) 1800–1814

Abstract: The DAB2IP tumor suppressor encodes a RAS GTPase-activating protein. Accordingly, DAB2IP has been shown to be mutated or suppressed in tumor types that typically lack RAS mutations. However, here we report that DAB2IP is mutated or selectively silenced ... ...

Abstract	The DAB2IP tumor suppressor encodes a RAS GTPase-activating protein. Accordingly, DAB2IP has been shown to be mutated or suppressed in tumor types that typically lack RAS mutations. However, here we report that DAB2IP is mutated or selectively silenced in the vast majority of KRAS and BRAF mutant colorectal cancers. In this setting, DAB2IP loss promoted tumor development by activating wild-type H- and N-RAS proteins, which was surprisingly required to achieve robust activation of RAS effector pathways in KRAS-mutant tumors. DAB2IP loss also triggered production of inflammatory mediators and the recruitment of protumorigenic macrophages in vivo. Importantly, tumor growth was suppressed by depleting macrophages or inhibiting cytokine/inflammatory mediator expression with a JAK/TBK1 inhibitor. In human tumors, DAB2IP was lost at early stages of tumor development, and its depletion was associated with an enrichment of macrophage and inflammatory signatures. Together, these findings demonstrate that DAB2IP restrains the activation of the RAS pathway and inflammatory cascades in the colon and that its loss represents a common and unappreciated mechanism for amplifying these two critical oncogenic signals in colorectal cancer. Significance: DAB2IP is lost in early-stage tumors, which amplifies RAS signaling, triggers inflammatory mediators, and recruits macrophages in KRAS-mutant colon cancers.
MeSH term(s)	Humans ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Genes, Tumor Suppressor ; Colonic Neoplasms/genetics ; Signal Transduction ; ras GTPase-Activating Proteins/genetics ; ras GTPase-Activating Proteins/metabolism ; Cell Line, Tumor
Chemical Substances	Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras GTPase-Activating Proteins ; KRAS protein, human ; DAB2IP protein, human
Language	English
Publishing date	2023-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-0370
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Article ; Online: Dendritic Cells and Cancer Immunity.

Gardner, Alycia / Ruffell, Brian

Trends in immunology

2016 Volume 37, Issue 12, Page(s) 855–865

Abstract: Dendritic cells (DCs) are central regulators of the adaptive immune response, and as such are necessary for T-cell-mediated cancer immunity. In particular, antitumoral responses depend on a specialized subset of conventional DCs that transport tumor ... ...

Abstract	Dendritic cells (DCs) are central regulators of the adaptive immune response, and as such are necessary for T-cell-mediated cancer immunity. In particular, antitumoral responses depend on a specialized subset of conventional DCs that transport tumor antigens to draining lymph nodes and cross-present antigen to activate cytotoxic T lymphocytes. DC maturation is necessary to provide costimulatory signals to T cells, but while DC maturation occurs within tumors, it is often insufficient to induce potent immunity, particularly in light of suppressive mechanisms within tumors. Bypassing suppressive pathways or directly activating DCs can unleash a T-cell response, and although clinical efficacy has proven elusive, therapeutic targeting of DCs continues to hold translational potential in combinatorial approaches.
MeSH term(s)	Animals ; Antigen Presentation ; Antigens, Neoplasm/immunology ; Cancer Vaccines/immunology ; Cell Differentiation ; Cross-Priming ; Dendritic Cells/immunology ; Dendritic Cells/transplantation ; Humans ; Immunotherapy/methods ; Neoplasms/immunology ; Neoplasms/therapy ; T-Lymphocytes, Cytotoxic/immunology ; Tumor Microenvironment
Chemical Substances	Antigens, Neoplasm ; Cancer Vaccines
Language	English
Publishing date	2016-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2016.09.006
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: TIM-3 blockade enhances IL-12-dependent antitumor immunity by promoting CD8

Gardner, Alycia / de Mingo Pulido, Álvaro / Hänggi, Kay / Bazargan, Sarah / Onimus, Alexis / Kasprzak, Agnieszka / Conejo-Garcia, Jose R / Rejniak, Katarzyna A / Ruffell, Brian

Journal for immunotherapy of cancer

2022 Volume 10, Issue 1

Abstract: Background: T cell immunoglobulin and mucin domain containing-3 (TIM-3) blocking antibodies are currently being evaluated in clinical trials for solid and hematological malignancies. Despite its identification on T cells, TIM-3 is predominantly ... ...

Abstract	Background: T cell immunoglobulin and mucin domain containing-3 (TIM-3) blocking antibodies are currently being evaluated in clinical trials for solid and hematological malignancies. Despite its identification on T cells, TIM-3 is predominantly expressed by myeloid cells, including XCR1 Methods: T cell infiltration, effector function, and spatial localization in relation to XCR1 Results: TIM-3 blockade increased interferon-γ expression by CD8 Conclusions: TIM-3 blockade increases exposure of intratumoral CD8
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/immunology ; Dendritic Cells/immunology ; Hepatitis A Virus Cellular Receptor 2/antagonists & inhibitors ; Humans ; Immunotherapy/methods ; Interleukin-12/metabolism ; Mice ; Receptors, Chemokine/metabolism ; Signal Transduction
Chemical Substances	Havcr2 protein, mouse ; Hepatitis A Virus Cellular Receptor 2 ; Receptors, Chemokine ; XC chemokine receptor 1, mouse ; Interleukin-12 (187348-17-0)
Language	English
Publishing date	2022-01-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2719863-7
ISSN	2051-1426 ; 2051-1426
ISSN (online)	2051-1426
ISSN	2051-1426
DOI	10.1136/jitc-2021-003571
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Article ; Online: A novel role for transcription-coupled nucleotide excision repair for the in vivo repair of 3,N4-ethenocytosine.

Chaim, Isaac A / Gardner, Alycia / Wu, Jie / Iyama, Teruaki / Wilson, David M / Samson, Leona D

Nucleic acids research

2017 Volume 45, Issue 6, Page(s) 3242–3252

Abstract: Etheno (ε) DNA base adducts are highly mutagenic lesions produced endogenously via reactions with lipid peroxidation (LPO) products. Cancer-promoting conditions, such as inflammation, can induce persistent oxidative stress and increased LPO, resulting in ...

Abstract	Etheno (ε) DNA base adducts are highly mutagenic lesions produced endogenously via reactions with lipid peroxidation (LPO) products. Cancer-promoting conditions, such as inflammation, can induce persistent oxidative stress and increased LPO, resulting in the accumulation of ε-adducts in different tissues. Using a recently described fluorescence multiplexed host cell reactivation assay, we show that a plasmid reporter bearing a site-specific 3,N4-ethenocytosine (εC) causes transcriptional blockage. Notably, this blockage is exacerbated in Cockayne Syndrome and xeroderma pigmentosum patient-derived lymphoblastoid and fibroblast cells. Parallel RNA-Seq expression analysis of the plasmid reporter identifies novel transcriptional mutagenesis properties of εC. Our studies reveal that beyond the known pathways, such as base excision repair, the process of transcription-coupled nucleotide excision repair plays a role in the removal of εC from the genome, and thus in the protection of cells and tissues from collateral damage induced by inflammatory responses.
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/metabolism ; Animals ; Cell Line ; Cells, Cultured ; Cockayne Syndrome/genetics ; Cytosine/analogs & derivatives ; Cytosine/metabolism ; DNA Adducts/metabolism ; DNA Repair ; DNA Repair Enzymes/genetics ; Humans ; Mice ; Mice, Knockout ; Mutagenesis ; RNA Polymerase II/metabolism ; Transcription, Genetic ; Xeroderma Pigmentosum/genetics
Chemical Substances	3,N(4)-ethenocytosine ; DNA Adducts ; 1,N(6)-ethenoadenine (13875-63-3) ; Cytosine (8J337D1HZY) ; RNA Polymerase II (EC 2.7.7.-) ; DNA Repair Enzymes (EC 6.5.1.-) ; Adenine (JAC85A2161)
Language	English
Publishing date	2017-01-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkx015
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Zs.A 1067: Show issues

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Article ; Online: TIM-3 Regulates CD103

de Mingo Pulido, Álvaro / Gardner, Alycia / Hiebler, Shandi / Soliman, Hatem / Rugo, Hope S / Krummel, Matthew F / Coussens, Lisa M / Ruffell, Brian

Cancer cell

2018 Volume 33, Issue 1, Page(s) 60–74.e6

Abstract: Intratumoral ... ...

Abstract	Intratumoral CD103
MeSH term(s)	Animals ; Antigens, CD/immunology ; Basic-Leucine Zipper Transcription Factors/deficiency ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Dendritic Cells/immunology ; Female ; Hepatitis A Virus Cellular Receptor 2/genetics ; Humans ; Integrin alpha Chains/immunology ; Interferon Regulatory Factors/immunology ; Mice, Transgenic
Chemical Substances	Antigens, CD ; Basic-Leucine Zipper Transcription Factors ; HAVCR2 protein, human ; Havcr2 protein, mouse ; Hepatitis A Virus Cellular Receptor 2 ; Integrin alpha Chains ; Interferon Regulatory Factors ; alpha E integrins ; interferon regulatory factor-8
Language	English
Publishing date	2018-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2017.11.019
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Zs.A 5650: 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 ; Online: The inhibitory receptor TIM-3 limits activation of the cGAS-STING pathway in intra-tumoral dendritic cells by suppressing extracellular DNA uptake.

de Mingo Pulido, Álvaro / Hänggi, Kay / Celias, Daiana P / Gardner, Alycia / Li, Jie / Batista-Bittencourt, Bruna / Mohamed, Eslam / Trillo-Tinoco, Jimena / Osunmakinde, Olabisi / Peña, Reymi / Onimus, Alexis / Kaisho, Tsuneyasu / Kaufmann, Johanna / McEachern, Kristen / Soliman, Hatem / Luca, Vincent C / Rodriguez, Paulo C / Yu, Xiaoqing / Ruffell, Brian

Immunity

2021 Volume 54, Issue 6, Page(s) 1154–1167.e7

Abstract: Blockade of the inhibitory receptor TIM-3 shows efficacy in cancer immunotherapy clinical trials. TIM-3 inhibits production of the chemokine CXCL9 by ... ...

Abstract	Blockade of the inhibitory receptor TIM-3 shows efficacy in cancer immunotherapy clinical trials. TIM-3 inhibits production of the chemokine CXCL9 by XCR1
MeSH term(s)	Animals ; Biological Transport/physiology ; Cell Line ; Cell Line, Tumor ; Chemokines/metabolism ; Cytoplasm/metabolism ; DNA/metabolism ; Dendritic Cells/metabolism ; Endocytosis/physiology ; Female ; HEK293 Cells ; Hepatitis A Virus Cellular Receptor 2/metabolism ; Humans ; Immunotherapy/methods ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Nucleotidyltransferases/metabolism ; Signal Transduction/physiology
Chemical Substances	Chemokines ; Havcr2 protein, mouse ; Hepatitis A Virus Cellular Receptor 2 ; Membrane Proteins ; Sting1 protein, mouse ; DNA (9007-49-2) ; Nucleotidyltransferases (EC 2.7.7.-) ; cGAS protein, mouse (EC 2.7.7.-)
Language	English
Publishing date	2021-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2021.04.019
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