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  1. AU="Manrique, Soraya Zorro"
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  1. Article ; Online: Influence of injection technique, drug formulation and tumor microenvironment on intratumoral immunotherapy delivery and efficacy.

    Muñoz, Nina M / Williams, Malea / Dixon, Katherine / Dupuis, Crystal / McWatters, Amanda / Avritscher, Rony / Manrique, Soraya Zorro / McHugh, Kevin / Murthy, Ravi / Tam, Alda / Naing, Aung / Patel, Sapna P / Leach, David / Hartgerink, Jeffrey D / Young, Simon / Prakash, Punit / Hwu, Patrick / Sheth, Rahul A

    Journal for immunotherapy of cancer

    2021  Volume 9, Issue 2

    Abstract: Background: Intratumoral delivery of immunotherapeutics represents a compelling solution to directly address local barriers to tumor immunity. However, we have previously shown that off-target delivery is a substantial problem during intratumoral ... ...

    Abstract Background: Intratumoral delivery of immunotherapeutics represents a compelling solution to directly address local barriers to tumor immunity. However, we have previously shown that off-target delivery is a substantial problem during intratumoral injections; this can lead to diminished drug efficacy and systemic toxicities. We have identified three variables that influence intratumoral drug delivery: injection technique, drug formulation and tumor microenvironment. The purpose of this study was to characterize the impact of modifications in each variable on intratumoral drug delivery and immunotherapy efficacy.
    Methods: Intratumoral injections were performed in a hybrid image-guided intervention suite with ultrasound, fluoroscopy and CT scanning capabilities in both rat and mouse syngeneic tumor models. Intratumoral drug distribution was quantified by CT volumetric imaging. The influence of varying needle design and hydrogel-based drug delivery on the immune response to a stimulator of interferon genes (STING) agonist was evaluated using flow cytometry and single cell RNA sequencing. We also evaluated the influence of tumor stiffness on drug injection distribution.
    Results: Variations in needle design, specifically with the use of a multiside hole needle, led to approximately threefold improvements in intratumoral drug deposition relative to conventional end-hole needles. Likewise, delivery of a STING agonist through a multiside hole needle led to significantly increased expression of type I interferon-associated genes and 'inflammatory' dendritic cell gene signatures relative to end-hole STING agonist delivery. A multidomain peptide-based hydrogel embedded with a STING agonist led to substantial improvements in intratumoral deposition; however, the hydrogel was noted to generate a strong immune response against itself within the target tumor. Evaluation of tumor stroma on intratumoral drug delivery revealed that there was a greater than twofold improvement in intratumoral distribution in soft tumors (B16 melanoma) compared with firm tumors (MC38 colorectal).
    Conclusions: Injection technique, drug formulation and tumor stiffness play key roles in the accurate delivery of intratumoral immunotherapeutics.
    MeSH term(s) Adaptor Proteins, Signal Transducing/agonists ; Adaptor Proteins, Signal Transducing/immunology ; Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/chemistry ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/immunology ; Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/pathology ; Drug Carriers ; Drug Compounding ; Female ; Hydrogels ; Immunotherapy ; Injections, Intralesional ; Liver Neoplasms/drug therapy ; Liver Neoplasms/immunology ; Liver Neoplasms/pathology ; Melanoma, Experimental/drug therapy ; Melanoma, Experimental/immunology ; Melanoma, Experimental/pathology ; Membrane Proteins/agonists ; Membrane Proteins/immunology ; Mice, Inbred C57BL ; Peptides/administration & dosage ; Peptides/chemistry ; Rats, Inbred BUF ; Skin Neoplasms/drug therapy ; Skin Neoplasms/immunology ; Skin Neoplasms/pathology ; Tumor Microenvironment ; Mice ; Rats
    Chemical Substances Adaptor Proteins, Signal Transducing ; Antineoplastic Agents ; Drug Carriers ; Hydrogels ; Membrane Proteins ; Peptides ; Sting1 protein, rat
    Language English
    Publishing date 2021-02-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2719863-7
    ISSN 2051-1426 ; 2051-1426
    ISSN (online) 2051-1426
    ISSN 2051-1426
    DOI 10.1136/jitc-2020-001800
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Blockade of CCL1 inhibits T regulatory cell suppressive function enhancing tumor immunity without affecting T effector responses.

    Hoelzinger, Dominique B / Smith, Shannon E / Mirza, Noweeda / Dominguez, Ana Lucia / Manrique, Soraya Zorro / Lustgarten, Joseph

    Journal of immunology (Baltimore, Md. : 1950)

    2010  Volume 184, Issue 12, Page(s) 6833–6842

    Abstract: Intratumoral accumulation of T regulatory cells (Tregs) creates an immunosuppressive environment that reduces the efficacy of antitumor immunotherapy. The immunosuppressive milieu within tumors is largely brought about by the presence of Tregs, which ... ...

    Abstract Intratumoral accumulation of T regulatory cells (Tregs) creates an immunosuppressive environment that reduces the efficacy of antitumor immunotherapy. The immunosuppressive milieu within tumors is largely brought about by the presence of Tregs, which maintain self-tolerance by directly inhibiting T cells, NK cells, and dendritic cells. Depletion of Tregs enhances antitumor immune responses; however, current depletion therapies also affect the function of CD4 and CD8 T effector cells. Previous studies from our laboratory indicate that intratumoral delivery of CpG-ODN strongly reduces the levels of Tregs within the tumor, which is mainly mediated by IL-6. Because IL-6 promotes growth of some human cancers, alternate pathways to inactivate Tregs were sought through microarray analysis, resulting in gene candidates that can be exploited to modulate the function of Tregs. Analysis of these candidates indicates that neutralization of chemokine (C-C motif) ligand 1 (CCL1) prevented de novo conversion and suppressive function of Tregs without affecting the function of T effector cells. The combination of CpG-ODN and anti-CCL1 treatments induced complete rejection of tumors in BALB-neuT tolerant mice, and result in the generation of long-term protective memory responses. Tumor rejection correlated with changes in the lymphocyte composition within the tumor; we observed decreased Treg numbers and a concomitant accumulation of tumoricidal cells such as CD8+NKG2D+ and NK cells. These studies demonstrate that neutralization of CCL1 can be used as an adjuvant to antitumor immunotherapy, as a means of reversing the immunosuppressive function of Tregs without compromising T cell effector function.
    MeSH term(s) Animals ; Blotting, Western ; Cell Separation ; Chemokine CCL1/antagonists & inhibitors ; Chemokine CCL1/immunology ; Flow Cytometry ; Gene Expression ; Gene Expression Regulation/immunology ; Immune Tolerance/immunology ; Immunotherapy/methods ; Interleukin-6/immunology ; Interleukin-6/metabolism ; Mice ; Mice, Inbred BALB C ; Oligodeoxyribonucleotides/immunology ; Oligonucleotide Array Sequence Analysis ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/immunology ; Tumor Escape/immunology
    Chemical Substances CPG-oligonucleotide ; Chemokine CCL1 ; Interleukin-6 ; Oligodeoxyribonucleotides
    Language English
    Publishing date 2010-05-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.0904084
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Definitive activation of endogenous antitumor immunity by repetitive cycles of cyclophosphamide with interspersed Toll-like receptor agonists.

    Manrique, Soraya Zorro / Dominguez, Ana L / Mirza, Noweeda / Spencer, Christopher D / Bradley, Judy M / Finke, James H / Lee, James J / Pease, Larry R / Gendler, Sandra J / Cohen, Peter A

    Oncotarget

    2016  Volume 7, Issue 28, Page(s) 42919–42942

    Abstract: Many cancers both evoke and subvert endogenous anti-tumor immunity. However, immunosuppression can be therapeutically reversed in subsets of cancer patients by treatments such as checkpoint inhibitors or Toll-like receptor agonists (TLRa). Moreover, ... ...

    Abstract Many cancers both evoke and subvert endogenous anti-tumor immunity. However, immunosuppression can be therapeutically reversed in subsets of cancer patients by treatments such as checkpoint inhibitors or Toll-like receptor agonists (TLRa). Moreover, chemotherapy can leukodeplete immunosuppressive host elements, including myeloid-derived suppressor cells (MDSCs) and regulatory T-cells (Tregs). We hypothesized that chemotherapy-induced leukodepletion could be immunopotentiated by co-administering TLRa to emulate a life-threatening infection. Combining CpG (ODN 1826) or CpG+poly(I:C) with cyclophosphamide (CY) resulted in uniquely well-tolerated therapeutic synergy, permanently eradicating advanced mouse tumors including 4T1 (breast), Panc02 (pancreas) and CT26 (colorectal). Definitive treatment required endogenous CD8+ and CD4+ IFNγ-producing T-cells. Tumor-specific IFNγ-producing T-cells persisted during CY-induced leukopenia, whereas Tregs were progressively eliminated, especially intratumorally. Spleen-associated MDSCs were cyclically depleted by CY+TLRa treatment, with residual monocytic MDSCs requiring only continued exposure to CpG or CpG+IFNγ to effectively attack malignant cells while sparing non-transformed cells. Such tumor destruction occurred despite upregulated tumor expression of Programmed Death Ligand-1, but could be blocked by clodronate-loaded liposomes to deplete phagocytic cells or by nitric oxide synthase inhibitors. CY+TLRa also induced tumoricidal myeloid cells in naive mice, indicating that CY+TLRa's immunomodulatory impacts occurred in the complete absence of tumor-bearing, and that tumor-induced MDSCs were not an essential source of tumoricidal myeloid precursors. Repetitive CY+TLRa can therefore modulate endogenous immunity to eradicate advanced tumors without vaccinations or adoptive T-cell therapy. Human blood monocytes could be rendered similarly tumoricidal during in vitro activation with TLRa+IFNγ, underscoring the potential therapeutic relevance of these mouse tumor studies to cancer patients.
    Language English
    Publishing date 2016-07-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.10190
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Systemic targeting of CpG-ODN to the tumor microenvironment with anti-neu-CpG hybrid molecule and T regulatory cell depletion induces memory responses in BALB-neuT tolerant mice.

    Sharma, Sanjay / Dominguez, Ana Lucia / Manrique, Soraya Zorro / Cavallo, Federica / Sakaguchi, Shimon / Lustgarten, Joseph

    Cancer research

    2008  Volume 68, Issue 18, Page(s) 7530–7540

    Abstract: We have shown that neu transgenic mice are immunotolerant and that immunizations with dendritic cells (DC) pulsed with neu-derived antigens were not able to control tumor growth in these animals. We tested whether, by modulating the tumor ... ...

    Abstract We have shown that neu transgenic mice are immunotolerant and that immunizations with dendritic cells (DC) pulsed with neu-derived antigens were not able to control tumor growth in these animals. We tested whether, by modulating the tumor microenvironment with Toll-like receptor ligands, it could be possible to induce the activation of antitumor responses in neu mice. Our results indicate that only intratumoral (i.t.) injections of CpG-ODN induce an antitumor response in neu mice. To target the CpG-ODN to the tumor site anywhere within the body, we chemically conjugated an anti-Her-2/neu monoclonal antibody (mAb) with CpG-ODN. The anti-neu-CpG hybrid molecule retained its ability to bind to Her-2/neu(+) tumors, activate DCs, and induce antitumor responses. Our results indicated that injections of anti-neu-CpG induced the rejection of primary tumors in 100% of BALB/c mice and only in approximately 30% of BALB-neuT mice. After challenging the BALB/c and BALB-neuT mice, we observed that BALB/c mice developed a protective memory response; in contrast, BALB-neuT mice succumbed to the challenge. After injections of anti-neu-CpG, T regulatory cells (T-reg) were drastically reduced at the tumor site, but a large number were still present in the lymphoid organs. When BALB-neuT mice were treated with anti-neu-CpG plus anti-GITR mAb, but not with anti-CD25 mAb, 100% of the BALB-neuT mice rejected the primary tumor and developed a protective memory response indicating the critical role of T-regs in regulating the repertoire against self antigens. Taken together, these results indicate that CpG-ODN-targeted therapy and depletion of T-regs optimally activate a primary response and generate a protective memory response against self-tumor antigens.
    MeSH term(s) Adjuvants, Immunologic/administration & dosage ; Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/immunology ; Drug Delivery Systems ; Female ; Immunoconjugates/administration & dosage ; Immunoconjugates/genetics ; Immunoconjugates/immunology ; Immunologic Memory ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/immunology ; Mammary Neoplasms, Experimental/therapy ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Oligodeoxyribonucleotides/administration & dosage ; Oligodeoxyribonucleotides/genetics ; Oligodeoxyribonucleotides/immunology ; Receptor, ErbB-2/biosynthesis ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/immunology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Adjuvants, Immunologic ; Antibodies, Monoclonal ; CPG-oligonucleotide ; Immunoconjugates ; Oligodeoxyribonucleotides ; Erbb2 protein, mouse (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2008-09-15
    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-08-1635
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Aurora kinase inhibition sensitizes melanoma cells to T-cell-mediated cytotoxicity.

    Punt, Simone / Malu, Shruti / McKenzie, Jodi A / Manrique, Soraya Zorro / Doorduijn, Elien M / Mbofung, Rina M / Williams, Leila / Silverman, Deborah A / Ashkin, Emily L / Dominguez, Ana Lucía / Wang, Zhe / Chen, Jie Qing / Maiti, Sourindra N / Tieu, Trang N / Liu, Chengwen / Xu, Chunyu / Forget, Marie-Andrée / Haymaker, Cara / Khalili, Jahan S /
    Satani, Nikunj / Muller, Florian / Cooper, Laurence J N / Overwijk, Willem W / Amaria, Rodabe N / Bernatchez, Chantale / Heffernan, Timothy P / Peng, Weiyi / Roszik, Jason / Hwu, Patrick

    Cancer immunology, immunotherapy : CII

    2020  Volume 70, Issue 4, Page(s) 1101–1113

    Abstract: Although immunotherapy has achieved impressive durable clinical responses, many cancers respond only temporarily or not at all to immunotherapy. To find novel, targetable mechanisms of resistance to immunotherapy, patient-derived melanoma cell lines were ...

    Abstract Although immunotherapy has achieved impressive durable clinical responses, many cancers respond only temporarily or not at all to immunotherapy. To find novel, targetable mechanisms of resistance to immunotherapy, patient-derived melanoma cell lines were transduced with 576 open reading frames, or exposed to arrayed libraries of 850 bioactive compounds, prior to co-culture with autologous tumor-infiltrating lymphocytes (TILs). The synergy between the targets and TILs to induce apoptosis, and the mechanisms of inhibiting resistance to TILs were interrogated. Gene expression analyses were performed on tumor samples from patients undergoing immunotherapy for metastatic melanoma. Finally, the effect of inhibiting the top targets on the efficacy of immunotherapy was investigated in multiple preclinical models. Aurora kinase was identified as a mediator of melanoma cell resistance to T-cell-mediated cytotoxicity in both complementary screens. Aurora kinase inhibitors were validated to synergize with T-cell-mediated cytotoxicity in vitro. The Aurora kinase inhibition-mediated sensitivity to T-cell cytotoxicity was shown to be partially driven by p21-mediated induction of cellular senescence. The expression levels of Aurora kinase and related proteins were inversely correlated with immune infiltration, response to immunotherapy and survival in melanoma patients. Aurora kinase inhibition showed variable responses in combination with immunotherapy in vivo, suggesting its activity is modified by other factors in the tumor microenvironment. These data suggest that Aurora kinase inhibition enhances T-cell cytotoxicity in vitro and can potentiate antitumor immunity in vivo in some but not all settings. Further studies are required to determine the mechanism of primary resistance to this therapeutic intervention.
    MeSH term(s) Animals ; Apoptosis ; Aurora Kinase A/antagonists & inhibitors ; Aurora Kinase A/genetics ; Aurora Kinase A/metabolism ; Aurora Kinase B/antagonists & inhibitors ; Aurora Kinase B/genetics ; Aurora Kinase B/metabolism ; Cell Proliferation ; Drug Resistance, Neoplasm/immunology ; Female ; Humans ; Immunotherapy/methods ; Lymphocytes, Tumor-Infiltrating/immunology ; Melanoma/genetics ; Melanoma/immunology ; Melanoma/metabolism ; Melanoma/therapy ; Mice ; Prognosis ; Survival Rate ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/transplantation ; Tumor Cells, Cultured ; Tumor Microenvironment/immunology ; Xenograft Model Antitumor Assays
    Chemical Substances AURKA protein, human (EC 2.7.11.1) ; AURKB protein, human (EC 2.7.11.1) ; Aurora Kinase A (EC 2.7.11.1) ; Aurora Kinase B (EC 2.7.11.1)
    Language English
    Publishing date 2020-10-29
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 195342-4
    ISSN 1432-0851 ; 0340-7004
    ISSN (online) 1432-0851
    ISSN 0340-7004
    DOI 10.1007/s00262-020-02748-9
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  6. Article ; Online: Foxp3-positive macrophages display immunosuppressive properties and promote tumor growth.

    Manrique, Soraya Zorro / Correa, Maria Adelaida Duque / Hoelzinger, Dominique B / Dominguez, Ana Lucia / Mirza, Noweeda / Lin, Hsi-Hsien / Stein-Streilein, Joan / Gordon, Siamon / Lustgarten, Joseph

    publication RETRACTED

    The Journal of experimental medicine

    2011  Volume 208, Issue 7, Page(s) 1485–1499

    Abstract: Regulatory T cells (T reg cells) are characterized by the expression of the forkhead lineage-specific transcription factor Foxp3, and their main function is to suppress T cells. While evaluating T reg cells, we identified a population of Foxp3-positive ... ...

    Abstract Regulatory T cells (T reg cells) are characterized by the expression of the forkhead lineage-specific transcription factor Foxp3, and their main function is to suppress T cells. While evaluating T reg cells, we identified a population of Foxp3-positive cells that were CD11b(+)F4/80(+)CD68(+), indicating macrophage origin. These cells were observed in spleen, lymph nodes, bone marrow, thymus, liver, and other tissues of naive animals. To characterize this subpopulation of macrophages, we devised a strategy to purify CD11b(+)F4/80(+)Foxp3(+) macrophages using Foxp3-GFP mice. Analysis of CD11b(+)F4/80(+)Foxp3(+) macrophage function indicated that these cells inhibited the proliferation of T cells, whereas Foxp3(-) macrophages did not. Suppression of T cell proliferation was mediated through soluble factors. Foxp3(-) macrophages acquired Foxp3 expression after activation, which conferred inhibitory properties that were indistinguishable from natural Foxp3(+) macrophages. The cytokine and transcriptional profiles of Foxp3(+) macrophages were distinct from those of Foxp3(-) macrophages, indicating that these cells have different biological functions. Functional in vivo analyses indicated that CD11b(+)F4/80(+)Foxp3(+) macrophages are important in tumor promotion and the induction of T reg cell conversion. For the first time, these studies demonstrate the existence of a distinct subpopulation of naturally occurring macrophage regulatory cells in which expression of Foxp3 correlates with suppressive function.
    MeSH term(s) Animals ; Antigens, Differentiation/metabolism ; Base Sequence ; CD11b Antigen/metabolism ; Cell Proliferation ; Chemokines/metabolism ; Cytokines/metabolism ; Forkhead Transcription Factors/antagonists & inhibitors ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/immunology ; Forkhead Transcription Factors/metabolism ; Gene Expression Profiling ; Immune Tolerance/physiology ; Macrophage Activation ; Macrophages/classification ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Melanoma, Experimental/immunology ; Melanoma, Experimental/metabolism ; Melanoma, Experimental/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; RNA, Small Interfering/genetics ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
    Chemical Substances Antigens, Differentiation ; CD11b Antigen ; Chemokines ; Cytokines ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; RNA, Small Interfering ; monocyte-macrophage differentiation antigen
    Language English
    Publishing date 2011-06-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Retracted Publication
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20100730
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