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  1. Article: Fueling the engine and releasing the break: combinational therapy of cancer vaccines and immune checkpoint inhibitors.

    Kleponis, Jennifer / Skelton, Richard / Zheng, Lei

    Cancer biology & medicine

    2015  Volume 12, Issue 3, Page(s) 201–208

    Abstract: Immune checkpoint inhibitors are increasingly drawing much attention in the therapeutic development for cancer treatment. However, many cancer patients do not respond to treatments with immune checkpoint inhibitors, partly because of the lack of tumor- ... ...

    Abstract Immune checkpoint inhibitors are increasingly drawing much attention in the therapeutic development for cancer treatment. However, many cancer patients do not respond to treatments with immune checkpoint inhibitors, partly because of the lack of tumor-infiltrating effector T cells. Cancer vaccines may prime patients for treatments with immune checkpoint inhibitors by inducing effector T-cell infiltration into the tumors and immune checkpoint signals. The combination of cancer vaccine and an immune checkpoint inhibitor may function synergistically to induce more effective antitumor immune responses, and clinical trials to test the combination are currently ongoing.
    Language English
    Publishing date 2015-09-23
    Publishing country China
    Document type Journal Article ; Review
    ZDB-ID 2676322-9
    ISSN 2095-3941
    ISSN 2095-3941
    DOI 10.7497/j.issn.2095-3941.2015.0046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: IDO1 inhibition potentiates vaccine-induced immunity against pancreatic adenocarcinoma.

    Blair, Alex B / Kleponis, Jennifer / Thomas, Dwayne L / Muth, Stephen T / Murphy, Adrian G / Kim, Victoria / Zheng, Lei

    The Journal of clinical investigation

    2019  Volume 129, Issue 4, Page(s) 1742–1755

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) represents an immune quiescent tumor that is resistant to immune checkpoint inhibitors. Previously, our group has shown that a GM-CSF-secreting allogenic pancreatic tumor cell vaccine (GVAX) may prime the tumor ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) represents an immune quiescent tumor that is resistant to immune checkpoint inhibitors. Previously, our group has shown that a GM-CSF-secreting allogenic pancreatic tumor cell vaccine (GVAX) may prime the tumor microenvironment by inducing intratumoral T cell infiltration. Here, we show that untreated PDACs express minimal indoleamine-2,3-dioxygenase (IDO1); however, GVAX therapy induced IDO1 expression on tumor epithelia as well as vaccine-induced tertiary lymphoid aggregates. IDO1 expression plays a role in regulating the polarization of Th1, Th17, and possibly T regulatory cells in PDAC tumors. IDO1 inhibitor enhanced antitumor efficacy of GVAX in a murine model of PDACs. The combination of vaccine and IDO1 inhibitor enhanced intratumoral T cell infiltration and function, but adding anti-PD-L1 antibody to the combination did not offer further synergy and in fact may have had a negative interaction, decreasing the number of intratumoral effector T cells. Additionally, IDO1 inhibitor in the presence of vaccine therapy did not significantly modulate intratumoral myeloid-derived suppressor cells quantitatively, but diminished their suppressive effect on CD8+ proliferation. Our study supports the combination of IDO1 inhibitor and vaccine therapy; however, it does not support the combination of IDO1 inhibitor and anti-PD-1/PD-L1 antibody for T cell-inflamed tumors such as PDACs treated with vaccine therapy.
    MeSH term(s) Adenocarcinoma/immunology ; Adenocarcinoma/pathology ; Adenocarcinoma/therapy ; Animals ; Cancer Vaccines/immunology ; Cancer Vaccines/pharmacology ; Carcinoma, Pancreatic Ductal/immunology ; Carcinoma, Pancreatic Ductal/pathology ; Carcinoma, Pancreatic Ductal/therapy ; Cell Line, Tumor ; Enzyme Inhibitors/pharmacology ; Humans ; Indoleamine-Pyrrole 2,3,-Dioxygenase/antagonists & inhibitors ; Indoleamine-Pyrrole 2,3,-Dioxygenase/immunology ; Mice ; Neoplasms, Experimental/immunology ; Neoplasms, Experimental/pathology ; Neoplasms, Experimental/therapy ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/therapy ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/pathology
    Chemical Substances Cancer Vaccines ; Enzyme Inhibitors ; GVAX vaccine ; IDO1 protein, human ; IDO1 protein, mouse ; Indoleamine-Pyrrole 2,3,-Dioxygenase
    Language English
    Publishing date 2019-03-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI124077
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Anti-pancreatic tumor efficacy of a Listeria-based, Annexin A2-targeting immunotherapy in combination with anti-PD-1 antibodies.

    Kim, Victoria M / Blair, Alex B / Lauer, Peter / Foley, Kelly / Che, Xu / Soares, Kevin / Xia, Tao / Muth, Stephen T / Kleponis, Jennifer / Armstrong, Todd D / Wolfgang, Christopher L / Jaffee, Elizabeth M / Brockstedt, Dirk / Zheng, Lei

    Journal for immunotherapy of cancer

    2019  Volume 7, Issue 1, Page(s) 132

    Abstract: Background: Immune checkpoint inhibitors are not effective for pancreatic ductal adenocarcinoma (PDAC) as single agents. Vaccine therapy may sensitize PDACs to checkpoint inhibitor treatments. Annexin A2 (ANXA2) is a pro-metastasis protein, previously ... ...

    Abstract Background: Immune checkpoint inhibitors are not effective for pancreatic ductal adenocarcinoma (PDAC) as single agents. Vaccine therapy may sensitize PDACs to checkpoint inhibitor treatments. Annexin A2 (ANXA2) is a pro-metastasis protein, previously identified as a relevant PDAC antigen that is expressed by a GM-CSF-secreting allogenic whole pancreatic tumor cell vaccine (GVAX) to induce an anti-ANXA2 antibody response in patients with PDAC. We hypothesized that an ANXA2-targeting vaccine approach not only provokes an immune response but also mounts anti-tumor effects.
    Methods: We developed a Listeria-based, ANXA2-targeting cancer immunotherapy (Lm-ANXA2) and investigated its effectiveness within two murine models of PDAC.
    Results: We show that Lm-ANXA2 prolonged the survival in a transplant model of mouse PDACs. More importantly, priming with the Lm-ANXA2 treatment prior to administration of anti-PD-1 antibodies increased cure rates in the implanted PDAC model and resulted in objective tumor responses and prolonged survival in the genetically engineered spontaneous PDAC model. In tumors treated with Lm-ANXA2 followed by anti-PD-1 antibody, the T cells specific to ANXA2 had significantly increased INFγ expression.
    Conclusions: For the first time, a listeria vaccine-based immunotherapy was shown to be able to induce a tumor antigen-specific T cell response within the tumor microenvironment of a "cold" tumor such as PDAC and sensitize the tumor to checkpoint inhibitor therapy. Moreover, this combination immunotherapy led to objective tumor responses and survival benefit in the mice with spontaneously developed PDAC tumors. Therefore, our study supports developing Lm-ANXA2 as a therapeutic agent in combination with anti-PD-1 antibody for PDAC treatment.
    MeSH term(s) Animals ; Annexin A2/antagonists & inhibitors ; Annexin A2/genetics ; Annexin A2/immunology ; Antigens, Neoplasm/immunology ; Antineoplastic Agents, Immunological/administration & dosage ; Cancer Vaccines/administration & dosage ; Cancer Vaccines/immunology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/immunology ; Carcinoma, Pancreatic Ductal/pathology ; Carcinoma, Pancreatic Ductal/therapy ; Cell Line, Tumor/transplantation ; Disease Models, Animal ; Female ; Humans ; Listeria/immunology ; Mice ; Mice, Transgenic ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/therapy ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Programmed Cell Death 1 Receptor/immunology ; Proto-Oncogene Proteins p21(ras)/genetics ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/immunology ; Tumor Suppressor Protein p53/genetics ; Vaccines, Synthetic/administration & dosage ; Vaccines, Synthetic/immunology
    Chemical Substances ANXA2 protein, human ; Annexin A2 ; Antigens, Neoplasm ; Antineoplastic Agents, Immunological ; Cancer Vaccines ; PDCD1 protein, human ; Programmed Cell Death 1 Receptor ; Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Vaccines, Synthetic ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2019-05-22
    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 10.1186/s40425-019-0601-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Heterogeneous Stromal Signaling within the Tumor Microenvironment Controls the Metastasis of Pancreatic Cancer.

    Rucki, Agnieszka A / Foley, Kelly / Zhang, Pingbo / Xiao, Qian / Kleponis, Jennifer / Wu, Annie A / Sharma, Rajni / Mo, Guanglan / Liu, Angen / Van Eyk, Jennifer / Jaffee, Elizabeth M / Zheng, Lei

    Cancer research

    2017  Volume 77, Issue 1, Page(s) 41–52

    Abstract: Understanding how stromal signals regulate the development of pancreatic ductal adenocarcinoma (PDAC) may suggest novel therapeutic interventions in this disease. In this study, we assessed the metastatic role of stromal signals suggested to be important ...

    Abstract Understanding how stromal signals regulate the development of pancreatic ductal adenocarcinoma (PDAC) may suggest novel therapeutic interventions in this disease. In this study, we assessed the metastatic role of stromal signals suggested to be important in the PDAC microenvironment. Src and IGF-1R phosphorylated the prometastatic molecule Annexin A2 (AnxA2) at Y23 and Y333 in response to stromal signals HGF and IGF-1, respectively, and IGF-1 expression was regulated by the Sonic Hedgehog (Shh) pathway. Both Shh and HGF were heterogeneously expressed in PDAC stroma, and only dual inhibition of these pathways could significantly suppress AnxA2 phosphorylation, PDAC growth, and metastasis. Taken together, our results illuminate tumor-stromal interactions, which drive metastasis, and provide a mechanism-based rationale for a stroma-directed therapy for PDAC. Cancer Res; 77(1); 41-52. ©2016 AACR.
    MeSH term(s) Animals ; Blotting, Western ; Carcinoma, Pancreatic Ductal/pathology ; Chromatography, Liquid ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation, Neoplastic/physiology ; Heterografts ; Humans ; Immunohistochemistry ; Mice ; Neoplasm Invasiveness/pathology ; Pancreatic Neoplasms/pathology ; Real-Time Polymerase Chain Reaction ; Signal Transduction/physiology ; Stromal Cells/metabolism ; Tandem Mass Spectrometry ; Tumor Microenvironment/physiology
    Language English
    Publishing date 2017-01-01
    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-16-1383
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Dual Inhibition of Hedgehog and c-Met Pathways for Pancreatic Cancer Treatment.

    Rucki, Agnieszka A / Xiao, Qian / Muth, Stephen / Chen, Jianlin / Che, Xu / Kleponis, Jennifer / Sharma, Rajni / Anders, Robert A / Jaffee, Elizabeth M / Zheng, Lei

    Molecular cancer therapeutics

    2017  Volume 16, Issue 11, Page(s) 2399–2409

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) is one of the most chemotherapy- and radiotherapy-resistant tumors. The c-Met and Hedgehog (Hh) pathways have been shown previously by our group to be key regulatory pathways in the primary tumor growth and ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most chemotherapy- and radiotherapy-resistant tumors. The c-Met and Hedgehog (Hh) pathways have been shown previously by our group to be key regulatory pathways in the primary tumor growth and metastases formation. Targeting both the HGF/c-Met and Hh pathways has shown promising results in preclinical studies; however, the benefits were not readily translated into clinical trials with PDAC patients. In this study, utilizing mouse models of PDAC, we showed that inhibition of either HGF/c-Met or Hh pathways sensitize the PDAC tumors to gemcitabine, resulting in decreased primary tumor volume as well as significant reduction of metastatic tumor burden. However, prolonged treatment of single HGF/c-Met or Hh inhibitor leads to resistance to these single inhibitors, likely because the single c-Met treatment leads to enhanced expression of Shh, and vice versa. Targeting both the HGF/c-Met and Hh pathways simultaneously overcame the resistance to the single-inhibitor treatment and led to a more potent antitumor effect in combination with the chemotherapy treatment.
    MeSH term(s) Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Animals ; Benzamides/administration & dosage ; Biphenyl Compounds/administration & dosage ; Bridged Bicyclo Compounds, Heterocyclic/administration & dosage ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Deoxycytidine/administration & dosage ; Deoxycytidine/analogs & derivatives ; Disease Models, Animal ; Drug Resistance, Neoplasm/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Hedgehog Proteins/antagonists & inhibitors ; Hedgehog Proteins/genetics ; Hepatocyte Growth Factor/antagonists & inhibitors ; Hepatocyte Growth Factor/genetics ; Humans ; Mice ; Mice, Transgenic ; Neoplasm Metastasis ; Proto-Oncogene Proteins c-met/antagonists & inhibitors ; Proto-Oncogene Proteins c-met/genetics ; Pyridines/administration & dosage ; Tumor Microenvironment/drug effects
    Chemical Substances Benzamides ; Biphenyl Compounds ; Bridged Bicyclo Compounds, Heterocyclic ; HGF protein, human ; Hedgehog Proteins ; Pyridines ; SHH protein, human ; sonidegib (0RLU3VTK5M) ; Deoxycytidine (0W860991D6) ; Hepatocyte Growth Factor (67256-21-7) ; gemcitabine (B76N6SBZ8R) ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; capmatinib (TY34L4F9OZ)
    Language English
    Publishing date 2017-09-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-16-0452
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    Zs.A 5750: Show issues Location:
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  6. Article ; Online: Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by Tumor-Induced Alterations in Genomic DNA Methylation.

    Xiao, Qian / Zhou, Donger / Rucki, Agnieszka A / Williams, Jamila / Zhou, Jiaojiao / Mo, Guanglan / Murphy, Adrian / Fujiwara, Kenji / Kleponis, Jennifer / Salman, Bulent / Wolfgang, Christopher L / Anders, Robert A / Zheng, Shu / Jaffee, Elizabeth M / Zheng, Lei

    Cancer research

    2016  Volume 76, Issue 18, Page(s) 5395–5404

    Abstract: Stromal fibrosis is a prominent histologic characteristic of pancreatic ductal adenocarcinoma (PDAC), but how stromal fibroblasts are regulated in the tumor microenvironment (TME) to support tumor growth is largely unknown. Here we show that PDAC cells ... ...

    Abstract Stromal fibrosis is a prominent histologic characteristic of pancreatic ductal adenocarcinoma (PDAC), but how stromal fibroblasts are regulated in the tumor microenvironment (TME) to support tumor growth is largely unknown. Here we show that PDAC cells can induce DNA methylation in cancer-associated fibroblasts (CAF). Upon direct contact with PDAC cells, DNA methylation of SOCS1 and other genes is induced in mesenchymal stem cells or in CAF that lack SOCS1 methylation at baseline. Silencing or decitabine treatment to block the DNA methylation enzyme DNMT1 inhibited methylation of SOCS1. In contrast, SOCS1 gene methylation and downregulation in CAF activated STAT3 and induced insulin-like growth factor-1 expression to support PDAC cell growth. Moreover, CAF facilitated methylation-dependent growth of PDAC tumor xenografts in mice. The ability of patient-derived CAF with SOCS1 methylation to promote PDAC growth was more robust than CAF without SOCS1 methylation. Overall, our results reveal how PDAC cells can reprogram CAF to modify tumor-stromal interactions in the TME, which promote malignant growth and progression. Cancer Res; 76(18); 5395-404. ©2016 AACR.
    MeSH term(s) Animals ; Cancer-Associated Fibroblasts/pathology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; DNA Methylation/genetics ; Heterografts ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Oligonucleotide Array Sequence Analysis ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Polymerase Chain Reaction ; Suppressor of Cytokine Signaling 1 Protein/genetics ; Tumor Microenvironment
    Chemical Substances Suppressor of Cytokine Signaling 1 Protein
    Language English
    Publishing date 2016-09-15
    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-15-3264
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Semaphorin 3D autocrine signaling mediates the metastatic role of annexin A2 in pancreatic cancer.

    Foley, Kelly / Rucki, Agnieszka A / Xiao, Qian / Zhou, Donger / Leubner, Ashley / Mo, Guanglan / Kleponis, Jennifer / Wu, Annie A / Sharma, Rajni / Jiang, Qingguang / Anders, Robert A / Iacobuzio-Donahue, Christine A / Hajjar, Katherine A / Maitra, Anirban / Jaffee, Elizabeth M / Zheng, Lei

    Science signaling

    2015  Volume 8, Issue 388, Page(s) ra77

    Abstract: Most patients with pancreatic ductal adenocarcinoma (PDA) present with metastatic disease at the time of diagnosis or will recur with metastases after surgical treatment. Semaphorin-plexin signaling mediates the migration of neuronal axons during ... ...

    Abstract Most patients with pancreatic ductal adenocarcinoma (PDA) present with metastatic disease at the time of diagnosis or will recur with metastases after surgical treatment. Semaphorin-plexin signaling mediates the migration of neuronal axons during development and of blood vessels during angiogenesis. The expression of the gene encoding semaphorin 3D (Sema3D) is increased in PDA tumors, and the presence of antibodies against the pleiotropic protein annexin A2 (AnxA2) in the sera of some patients after surgical resection of PDA is associated with longer recurrence-free survival. By knocking out AnxA2 in a transgenic mouse model of PDA (KPC) that recapitulates the progression of human PDA from premalignancy to metastatic disease, we found that AnxA2 promoted metastases in vivo. The expression of AnxA2 promoted the secretion of Sema3D from PDA cells, which coimmunoprecipitated with the co-receptor plexin D1 (PlxnD1) on PDA cells. Mouse PDA cells in which SEMA3D was knocked down or ANXA2-null PDA cells exhibited decreased invasive and metastatic potential in culture and in mice. However, restoring Sema3D in AnxA2-null cells did not entirely rescue metastatic behavior in culture and in vivo, suggesting that AnxA2 mediates additional prometastatic mechanisms. Patients with primary PDA tumors that have abundant Sema3D have widely metastatic disease and decreased survival compared to patients with tumors that have relatively low Sema3D abundance. Thus, AnxA2 and Sema3D may be new therapeutic targets and prognostic markers of metastatic PDA.
    MeSH term(s) Animals ; Annexin A2/genetics ; Annexin A2/metabolism ; Autocrine Communication/genetics ; Blotting, Western ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Female ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic ; Humans ; Intracellular Signaling Peptides and Proteins ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microscopy, Fluorescence/classification ; Neoplasm Metastasis ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Protein Binding ; RNA Interference ; Reverse Transcriptase Polymerase Chain Reaction ; Semaphorins/genetics ; Semaphorins/metabolism ; Signal Transduction/genetics ; Survival Analysis ; Tumor Cells, Cultured ; Pancreatic Neoplasms
    Chemical Substances Annexin A2 ; Intracellular Signaling Peptides and Proteins ; Membrane Glycoproteins ; Nerve Tissue Proteins ; Plxnd1 protein, mouse ; Sema 3D protein, mouse ; Semaphorins
    Language English
    Publishing date 2015-08-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.aaa5823
    Database MEDical Literature Analysis and Retrieval System OnLINE

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