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  1. AU="Qiu, Jingya"
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  1. Artikel ; Online: Cancer cells resistant to immune checkpoint blockade acquire interferon-associated epigenetic memory to sustain T cell dysfunction.

    Qiu, Jingya / Xu, Bihui / Ye, Darwin / Ren, Diqiu / Wang, Shangshang / Benci, Joseph L / Xu, Yuanming / Ishwaran, Hemant / Beltra, Jean-Christophe / Wherry, E John / Shi, Junwei / Minn, Andy J

    Nature cancer

    2023  Band 4, Heft 1, Seite(n) 43–61

    Abstract: Prolonged interferon (IFN) signaling in cancer cells can promote resistance to immune checkpoint blockade (ICB). How cancer cells retain effects of prolonged IFN stimulation to coordinate resistance is unclear. We show that, across human and/or mouse ... ...

    Abstract Prolonged interferon (IFN) signaling in cancer cells can promote resistance to immune checkpoint blockade (ICB). How cancer cells retain effects of prolonged IFN stimulation to coordinate resistance is unclear. We show that, across human and/or mouse tumors, immune dysfunction is associated with cancer cells acquiring epigenetic features of inflammatory memory. Here, inflammatory memory domains, many of which are initiated by chronic IFN-γ, are maintained by signal transducer and activator of transcription (STAT)1 and IFN regulatory factor (IRF)3 and link histone 3 lysine 4 monomethylation (H3K4me1)-marked chromatin accessibility to increased expression of a subset of IFN-stimulated genes (ISGs). These ISGs include the RNA sensor OAS1 that amplifies type I IFN (IFN-I) and immune inhibitory genes. Abrogating cancer cell IFN-I signaling restores anti-programmed cell death protein 1 (PD1) response by increasing IFN-γ in immune cells, promoting dendritic cell and CD8
    Mesh-Begriff(e) Animals ; Humans ; Mice ; Epigenetic Memory ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Interferon Type I/metabolism ; Interferon Type I/pharmacology ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Interferon-gamma/pharmacology ; Neoplasms/drug therapy ; Neoplasms/genetics ; Signal Transduction ; T-Lymphocytes/immunology
    Chemische Substanzen Immune Checkpoint Inhibitors ; Interferon Type I ; Interferon-gamma (82115-62-6)
    Sprache Englisch
    Erscheinungsdatum 2023-01-16
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-022-00490-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: AN INTEGRATED NETWORK APPROACH TO IDENTIFYING BIOLOGICAL PATHWAYS AND ENVIRONMENTAL EXPOSURE INTERACTIONS IN COMPLEX DISEASES.

    Darabos, Christian / Qiu, Jingya / Moore, Jason H

    Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing

    2016  Band 21, Seite(n) 9–20

    Abstract: Complex diseases are the result of intricate interactions between genetic, epigenetic and environmental factors. In previous studies, we used epidemiological and genetic data linking environmental exposure or genetic variants to phenotypic disease to ... ...

    Abstract Complex diseases are the result of intricate interactions between genetic, epigenetic and environmental factors. In previous studies, we used epidemiological and genetic data linking environmental exposure or genetic variants to phenotypic disease to construct Human Phenotype Networks and separately analyze the effects of both environment and genetic factors on disease interactions. To better capture the intricacies of the interactions between environmental exposure and the biological pathways in complex disorders, we integrate both aspects into a single "tripartite" network. Despite extensive research, the mechanisms by which chemical agents disrupt biological pathways are still poorly understood. In this study, we use our integrated network model to identify specific biological pathway candidates possibly disrupted by environmental agents. We conjecture that a higher number of co-occurrences between an environmental substance and biological pathway pair can be associated with a higher likelihood that the substance is involved in disrupting that pathway. We validate our model by demonstrating its ability to detect known arsenic and signal transduction pathway interactions and speculate on candidate cell-cell junction organization pathways disrupted by cadmium. The validation was supported by distinct publications of cell biology and genetic studies that associated environmental exposure to pathway disruption. The integrated network approach is a novel method for detecting the biological effects of environmental exposures. A better understanding of the molecular processes associated with specific environmental exposures will help in developing targeted molecular therapies for patients who have been exposed to the toxicity of environmental chemicals.
    Mesh-Begriff(e) Computational Biology/methods ; Computational Biology/statistics & numerical data ; Disease/etiology ; Environmental Exposure ; Epigenesis, Genetic ; Gene-Environment Interaction ; Genome-Wide Association Study ; Humans ; Models, Biological ; Nonlinear Dynamics ; Phenotype ; Polymorphism, Single Nucleotide ; Signal Transduction ; Systems Biology
    Sprache Englisch
    Erscheinungsdatum 2016-01-18
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2335-6936
    ISSN (online) 2335-6936
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Studying the Genetics of Complex Disease With Ancestry-Specific Human Phenotype Networks: The Case of Type 2 Diabetes in East Asian Populations.

    Qiu, Jingya / Moore, Jason H / Darabos, Christian

    Genetic epidemiology

    2016  Band 40, Heft 4, Seite(n) 293–303

    Abstract: Genome-wide association studies (GWAS) have led to the discovery of over 200 single nucleotide polymorphisms (SNPs) associated with type 2 diabetes mellitus (T2DM). Additionally, East Asians develop T2DM at a higher rate, younger age, and lower body mass ...

    Abstract Genome-wide association studies (GWAS) have led to the discovery of over 200 single nucleotide polymorphisms (SNPs) associated with type 2 diabetes mellitus (T2DM). Additionally, East Asians develop T2DM at a higher rate, younger age, and lower body mass index than their European ancestry counterparts. The reason behind this occurrence remains elusive. With comprehensive searches through the National Human Genome Research Institute (NHGRI) GWAS catalog literature, we compiled a database of 2,800 ancestry-specific SNPs associated with T2DM and 70 other related traits. Manual data extraction was necessary because the GWAS catalog reports statistics such as odds ratio and P-value, but does not consistently include ancestry information. Currently, many statistics are derived by combining initial and replication samples from study populations of mixed ancestry. Analysis of all-inclusive data can be misleading, as not all SNPs are transferable across diverse populations. We used ancestry data to construct ancestry-specific human phenotype networks (HPN) centered on T2DM. Quantitative and visual analysis of network models reveal the genetic disparities between ancestry groups. Of the 27 phenotypes in the East Asian HPN, six phenotypes were unique to the network, revealing the underlying ancestry-specific nature of some SNPs associated with T2DM. We studied the relationship between T2DM and five phenotypes unique to the East Asian HPN to generate new interaction hypotheses in a clinical context. The genetic differences found in our ancestry-specific HPNs suggest different pathways are involved in the pathogenesis of T2DM among different populations. Our study underlines the importance of ancestry in the development of T2DM and its implications in pharmocogenetics and personalized medicine.
    Mesh-Begriff(e) Asian Continental Ancestry Group/genetics ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Far East ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Models, Genetic ; Myocardial Infarction/genetics ; Odds Ratio ; Ovarian Neoplasms/genetics ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Schizophrenia/genetics
    Sprache Englisch
    Erscheinungsdatum 2016-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 605785-8
    ISSN 1098-2272 ; 0741-0395
    ISSN (online) 1098-2272
    ISSN 0741-0395
    DOI 10.1002/gepi.21964
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: The interferon-stimulated gene RIPK1 regulates cancer cell intrinsic and extrinsic resistance to immune checkpoint blockade.

    Cucolo, Lisa / Chen, Qingzhou / Qiu, Jingya / Yu, Yongjun / Klapholz, Max / Budinich, Krista A / Zhang, Zhaojun / Shao, Yue / Brodsky, Igor E / Jordan, Martha S / Gilliland, D Gary / Zhang, Nancy R / Shi, Junwei / Minn, Andy J

    Immunity

    2022  Band 55, Heft 4, Seite(n) 671–685.e10

    Abstract: Interferon-gamma (IFN-γ) has pleiotropic effects on cancer immune checkpoint blockade (ICB), including roles in ICB resistance. We analyzed gene expression in ICB-sensitive versus ICB-resistant tumor cells and identified a strong association between ... ...

    Abstract Interferon-gamma (IFN-γ) has pleiotropic effects on cancer immune checkpoint blockade (ICB), including roles in ICB resistance. We analyzed gene expression in ICB-sensitive versus ICB-resistant tumor cells and identified a strong association between interferon-mediated resistance and expression of Ripk1, a regulator of tumor necrosis factor (TNF) superfamily receptors. Genetic interaction screening revealed that in cancer cells, RIPK1 diverted TNF signaling through NF-κB and away from its role in cell death. This promoted an immunosuppressive chemokine program by cancer cells, enhanced cancer cell survival, and decreased infiltration of T and NK cells expressing TNF superfamily ligands. Deletion of RIPK1 in cancer cells compromised chemokine secretion, decreased ARG1
    Mesh-Begriff(e) Animals ; Drug Resistance, Neoplasm ; Immune Checkpoint Inhibitors ; Immunotherapy ; Interferon-gamma/metabolism ; Interferons/metabolism ; Mice ; NF-kappa B/metabolism ; Neoplasms/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
    Chemische Substanzen Immune Checkpoint Inhibitors ; NF-kappa B ; Interferon-gamma (82115-62-6) ; Interferons (9008-11-1) ; RIPK1 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk1 protein, mouse (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2022-04-13
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2022.03.007
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Clinical and molecular features of acquired resistance to immunotherapy in non-small cell lung cancer.

    Memon, Danish / Schoenfeld, Adam J / Ye, Darwin / Fromm, George / Rizvi, Hira / Zhang, Xiang / Keddar, Mohamed Reda / Mathew, Divij / Yoo, Kyung Jin / Qiu, Jingya / Lihm, Jayon / Miriyala, Jayalaksmi / Sauter, Jennifer L / Luo, Jia / Chow, Andrew / Bhanot, Umesh K / McCarthy, Caroline / Vanderbilt, Chad M / Liu, Cailian /
    Abu-Akeel, Mohsen / Plodkowski, Andrew J / McGranahan, Nicholas / Łuksza, Marta / Greenbaum, Benjamin D / Merghoub, Taha / Achour, Ikbel / Barrett, J Carl / Stewart, Ross / Beltrao, Pedro / Schreiber, Taylor H / Minn, Andy J / Miller, Martin L / Hellmann, Matthew D

    Cancer cell

    2024  Band 42, Heft 2, Seite(n) 209–224.e9

    Abstract: Although immunotherapy with PD-(L)1 blockade is routine for lung cancer, little is known about acquired resistance. Among 1,201 patients with non-small cell lung cancer (NSCLC) treated with PD-(L)1 blockade, acquired resistance is common, occurring in > ... ...

    Abstract Although immunotherapy with PD-(L)1 blockade is routine for lung cancer, little is known about acquired resistance. Among 1,201 patients with non-small cell lung cancer (NSCLC) treated with PD-(L)1 blockade, acquired resistance is common, occurring in >60% of initial responders. Acquired resistance shows differential expression of inflammation and interferon (IFN) signaling. Relapsed tumors can be separated by upregulated or stable expression of IFNγ response genes. Upregulation of IFNγ response genes is associated with putative routes of resistance characterized by signatures of persistent IFN signaling, immune dysfunction, and mutations in antigen presentation genes which can be recapitulated in multiple murine models of acquired resistance to PD-(L)1 blockade after in vitro IFNγ treatment. Acquired resistance to PD-(L)1 blockade in NSCLC is associated with an ongoing, but altered IFN response. The persistently inflamed, rather than excluded or deserted, tumor microenvironment of acquired resistance may inform therapeutic strategies to effectively reprogram and reverse acquired resistance.
    Mesh-Begriff(e) Humans ; Animals ; Mice ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Signal Transduction ; Immunotherapy ; Antigen Presentation ; B7-H1 Antigen/metabolism ; Tumor Microenvironment
    Chemische Substanzen B7-H1 Antigen
    Sprache Englisch
    Erscheinungsdatum 2024-01-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2023.12.013
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Opposing Functions of Interferon Coordinate Adaptive and Innate Immune Responses to Cancer Immune Checkpoint Blockade.

    Benci, Joseph L / Johnson, Lexus R / Choa, Ruth / Xu, Yuanming / Qiu, Jingya / Zhou, Zilu / Xu, Bihui / Ye, Darwin / Nathanson, Katherine L / June, Carl H / Wherry, E John / Zhang, Nancy R / Ishwaran, Hemant / Hellmann, Matthew D / Wolchok, Jedd D / Kambayashi, Taku / Minn, Andy J

    Cell

    2019  Band 178, Heft 4, Seite(n) 933–948.e14

    Abstract: Interferon-gamma (IFNG) augments immune function yet promotes T cell exhaustion through PDL1. How these opposing effects are integrated to impact immune checkpoint blockade (ICB) is unclear. We show that while inhibiting tumor IFNG signaling decreases ... ...

    Abstract Interferon-gamma (IFNG) augments immune function yet promotes T cell exhaustion through PDL1. How these opposing effects are integrated to impact immune checkpoint blockade (ICB) is unclear. We show that while inhibiting tumor IFNG signaling decreases interferon-stimulated genes (ISGs) in cancer cells, it increases ISGs in immune cells by enhancing IFNG produced by exhausted T cells (T
    Mesh-Begriff(e) Adaptive Immunity/immunology ; Adoptive Transfer ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; CD8-Positive T-Lymphocytes/immunology ; CTLA-4 Antigen/antagonists & inhibitors ; Cell Line, Tumor ; Cohort Studies ; Female ; Gene Knockout Techniques ; Humans ; Immunity, Innate/immunology ; Interferon-gamma/antagonists & inhibitors ; Interferon-gamma/genetics ; Interferon-gamma/metabolism ; Killer Cells, Natural/immunology ; Lung Neoplasms/drug therapy ; Lung Neoplasms/immunology ; Melanoma/drug therapy ; Melanoma/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Progression-Free Survival ; RNA-Seq ; Transfection
    Chemische Substanzen Antineoplastic Agents ; CTLA-4 Antigen ; CTLA4 protein, human ; Ctla4 protein, mouse ; IFNG protein, human ; IFNG protein, mouse ; PDCD1 protein, human ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Interferon-gamma (82115-62-6)
    Sprache Englisch
    Erscheinungsdatum 2019-08-09
    Erscheinungsland United States
    Dokumenttyp 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 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2019.07.019
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: Opposing Functions of Interferon Coordinate Adaptive and Innate Immune Responses to Cancer Immune Checkpoint Blockade

    Benci, Joseph L / Johnson, Lexus R / Choa, Ruth / Xu, Yuanming / Qiu, Jingya / Zhou, Zilu / Xu, Bihui / Ye, Darwin / Nathanson, Katherine L / June, Carl H / Wherry, E. John / Zhang, Nancy R / Ishwaran, Hemant / Hellmann, Matthew D / Wolchok, Jedd D / Kambayashi, Taku / Minn, Andy J

    Cell. 2019 Aug. 08, v. 178, no. 4

    2019  

    Abstract: Interferon-gamma (IFNG) augments immune function yet promotes T cell exhaustion through PDL1. How these opposing effects are integrated to impact immune checkpoint blockade (ICB) is unclear. We show that while inhibiting tumor IFNG signaling decreases ... ...

    Abstract Interferon-gamma (IFNG) augments immune function yet promotes T cell exhaustion through PDL1. How these opposing effects are integrated to impact immune checkpoint blockade (ICB) is unclear. We show that while inhibiting tumor IFNG signaling decreases interferon-stimulated genes (ISGs) in cancer cells, it increases ISGs in immune cells by enhancing IFNG produced by exhausted T cells (TEX). In tumors with favorable antigenicity, these TEX mediate rejection. In tumors with neoantigen or MHC-I loss, TEX instead utilize IFNG to drive maturation of innate immune cells, including a PD1+TRAIL+ ILC1 population. By disabling an inhibitory circuit impacting PD1 and TRAIL, blocking tumor IFNG signaling promotes innate immune killing. Thus, interferon signaling in cancer cells and immune cells oppose each other to establish a regulatory relationship that limits both adaptive and innate immune killing. In melanoma and lung cancer patients, perturbation of this relationship is associated with ICB response independent of tumor mutational burden.
    Schlagwörter T-lymphocytes ; immune response ; innate immunity ; interferon-gamma ; lung neoplasms ; major histocompatibility complex ; melanoma ; neoplasm cells ; patients
    Sprache Englisch
    Erscheinungsverlauf 2019-0808
    Umfang p. 933-948.e14.
    Erscheinungsort Elsevier Inc.
    Dokumenttyp Artikel
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2019.07.019
    Datenquelle NAL Katalog (AGRICOLA)

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