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Article ; Online: Rapamycin enhances adenovirus-mediated cancer imaging and therapy in pre-immunized murine hosts.

Jiang, Ziyue Karen / Johnson, Mai / Moughon, Diana L / Kuo, Jennifer / Sato, Makoto / Wu, Lily

PloS one

2013 Volume 8, Issue 9, Page(s) e73650

Abstract: Tumor-specific adenoviral vectors comprise a fruitful gene-based diagnostic imaging and therapy research area for advanced stage of cancer, including metastatic disease. However, clinical translation of viral vectors has encountered considerable ... ...

Abstract	Tumor-specific adenoviral vectors comprise a fruitful gene-based diagnostic imaging and therapy research area for advanced stage of cancer, including metastatic disease. However, clinical translation of viral vectors has encountered considerable obstacles, largely due to host immune responses against the virus. Here, we explored the utilization of an immunosuppressant, rapamycin, to circumvent the anti-adenovirus immunity in immunocompetent murine prostate cancer models. Rapamycin diminished adenoviral-induced acute immune response by inhibiting NF-κB activation; it also reduced the scale and delayed the onset of inflammatory cytokine secretion. Further, we found that rapamycin abrogated anti-adenovirus antibody production and retarded the function of myeloid cells and lymphocytes that were activated upon viral administration in pre-immunized hosts. Thus, the co-administration of rapamycin prolonged and enhanced adenovirus-delivered transgene expression in vivo, and thereby augmented the imaging capability of adenoviral vectors in both bioluminescent and positron emission tomography modalities. Furthermore, we showed that despite an excellent response of cancer cells to a cytotoxic gene therapeutic vector in vitro, only minimal therapeutic effects were observed in vivo in pre-immunized mice. However, when we combined gene therapy with transient immunosuppression, complete tumor growth arrest was achieved. Overall, transient immunosuppression by rapamycin was able to boost the diagnostic utility and therapeutic potentials of adenoviral vectors.
MeSH term(s)	Adaptive Immunity/drug effects ; Adenoviridae/genetics ; Animals ; Cell Line, Tumor ; Ganciclovir/pharmacology ; Genetic Therapy/adverse effects ; Genetic Vectors/genetics ; Immunity, Innate/drug effects ; Immunization ; Immunosuppression/methods ; Immunosuppressive Agents/pharmacology ; Male ; Mice ; Molecular Imaging/adverse effects ; Prostatic Neoplasms/diagnosis ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/immunology ; Prostatic Neoplasms/therapy ; Safety ; Sirolimus/pharmacology ; Thymidine Kinase/genetics ; Transgenes/genetics
Chemical Substances	Immunosuppressive Agents ; Thymidine Kinase (EC 2.7.1.21) ; Ganciclovir (P9G3CKZ4P5) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2013-09-02
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.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0073650
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: CRISPR-Mediated VHL Knockout Generates an Improved Model for Metastatic Renal Cell Carcinoma.

Schokrpur, Shiruyeh / Hu, Junhui / Moughon, Diana L / Liu, Peijun / Lin, Lucia C / Hermann, Kip / Mangul, Serghei / Guan, Wei / Pellegrini, Matteo / Xu, Hua / Wu, Lily

Scientific reports

2016 Volume 6, Page(s) 29032

Abstract: Metastatic renal cell carcinoma (mRCC) is nearly incurable and accounts for most of the mortality associated with RCC. Von Hippel Lindau (VHL) is a tumour suppressor that is lost in the majority of clear cell RCC (ccRCC) cases. Its role in regulating ... ...

Abstract	Metastatic renal cell carcinoma (mRCC) is nearly incurable and accounts for most of the mortality associated with RCC. Von Hippel Lindau (VHL) is a tumour suppressor that is lost in the majority of clear cell RCC (ccRCC) cases. Its role in regulating hypoxia-inducible factors-1α (HIF-1α) and -2α (HIF-2α) is well-studied. Recent work has demonstrated that VHL knock down induces an epithelial-mesenchymal transition (EMT) phenotype. In this study we showed that a CRISPR/Cas9-mediated knock out of VHL in the RENCA model leads to morphologic and molecular changes indicative of EMT, which in turn drives increased metastasis to the lungs. RENCA cells deficient in HIF-1α failed to undergo EMT changes upon VHL knockout. RNA-seq revealed several HIF-1α-regulated genes that are upregulated in our VHL knockout cells and whose overexpression signifies an aggressive form of ccRCC in the cancer genome atlas (TCGA) database. Independent validation in a new clinical dataset confirms the upregulation of these genes in ccRCC samples compared to adjacent normal tissue. Our findings indicate that loss of VHL could be driving tumour cell dissemination through stabilization of HIF-1α in RCC. A better understanding of the mechanisms involved in this phenomenon can guide the search for more effective treatments to combat mRCC.
MeSH term(s)	Animals ; Bacterial Proteins ; CRISPR-Associated Protein 9 ; CRISPR-Cas Systems ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/secondary ; Cell Line, Tumor ; Cell Movement ; Datasets as Topic ; Disease Models, Animal ; Endonucleases ; Epithelial-Mesenchymal Transition ; Female ; Gene Editing ; Gene Expression Regulation, Neoplastic ; Heterografts ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/physiology ; Kidney Neoplasms/pathology ; Lung Neoplasms/secondary ; Mice ; Mice, Knockout ; Mice, Nude ; Neoplasm Proteins/genetics ; Neoplasm Proteins/physiology ; RNA, Guide, CRISPR-Cas Systems ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Von Hippel-Lindau Tumor Suppressor Protein/physiology
Chemical Substances	Bacterial Proteins ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Neoplasm Proteins ; RNA, Guide, CRISPR-Cas Systems ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; CRISPR-Associated Protein 9 (EC 3.1.-) ; Cas9 endonuclease Streptococcus pyogenes (EC 3.1.-) ; Endonucleases (EC 3.1.-) ; VHL protein, human (EC 6.3.2.-) ; VHL protein, mouse (EC 6.3.2.-)
Language	English
Publishing date	2016-06-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep29032
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Detection of immune responses after immunotherapy in glioblastoma using PET and MRI.

Antonios, Joseph P / Soto, Horacio / Everson, Richard G / Moughon, Diana L / Wang, Anthony C / Orpilla, Joey / Radu, Caius / Ellingson, Benjamin M / Lee, Jason T / Cloughesy, Timothy / Phelps, Michael E / Czernin, Johannes / Liau, Linda M / Prins, Robert M

Proceedings of the National Academy of Sciences of the United States of America

2017 Volume 114, Issue 38, Page(s) 10220–10225

Abstract: Contrast-enhanced MRI is typically used to follow treatment response and progression in patients with glioblastoma (GBM). However, differentiating tumor progression from pseudoprogression remains a clinical dilemma largely unmitigated by current advances ...

Abstract	Contrast-enhanced MRI is typically used to follow treatment response and progression in patients with glioblastoma (GBM). However, differentiating tumor progression from pseudoprogression remains a clinical dilemma largely unmitigated by current advances in imaging techniques. Noninvasive imaging techniques capable of distinguishing these two conditions could play an important role in the clinical management of patients with GBM and other brain malignancies. We hypothesized that PET probes for deoxycytidine kinase (dCK) could be used to differentiate immune inflammatory responses from other sources of contrast-enhancement on MRI. Orthotopic malignant gliomas were established in syngeneic immunocompetent mice and then treated with dendritic cell (DC) vaccination and/or PD-1 mAb blockade. Mice were then imaged with [
MeSH term(s)	Animals ; Cell Line ; Female ; Glioblastoma/diagnostic imaging ; Glioblastoma/therapy ; Humans ; Immunotherapy ; Magnetic Resonance Imaging ; Mice ; Mice, Inbred C57BL ; Positron-Emission Tomography
Language	English
Publishing date	2017-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1706689114
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Rapamycin enhances adenovirus-mediated cancer imaging and therapy in pre-immunized murine hosts.

Ziyue Karen Jiang / Mai Johnson / Diana L Moughon / Jennifer Kuo / Makoto Sato / Lily Wu

PLoS ONE, Vol 8, Iss 9, p e

2013 Volume 73650

Abstract	Tumor-specific adenoviral vectors comprise a fruitful gene-based diagnostic imaging and therapy research area for advanced stage of cancer, including metastatic disease. However, clinical translation of viral vectors has encountered considerable obstacles, largely due to host immune responses against the virus. Here, we explored the utilization of an immunosuppressant, rapamycin, to circumvent the anti-adenovirus immunity in immunocompetent murine prostate cancer models. Rapamycin diminished adenoviral-induced acute immune response by inhibiting NF-κB activation; it also reduced the scale and delayed the onset of inflammatory cytokine secretion. Further, we found that rapamycin abrogated anti-adenovirus antibody production and retarded the function of myeloid cells and lymphocytes that were activated upon viral administration in pre-immunized hosts. Thus, the co-administration of rapamycin prolonged and enhanced adenovirus-delivered transgene expression in vivo, and thereby augmented the imaging capability of adenoviral vectors in both bioluminescent and positron emission tomography modalities. Furthermore, we showed that despite an excellent response of cancer cells to a cytotoxic gene therapeutic vector in vitro, only minimal therapeutic effects were observed in vivo in pre-immunized mice. However, when we combined gene therapy with transient immunosuppression, complete tumor growth arrest was achieved. Overall, transient immunosuppression by rapamycin was able to boost the diagnostic utility and therapeutic potentials of adenoviral vectors.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Macrophage Blockade Using CSF1R Inhibitors Reverses the Vascular Leakage Underlying Malignant Ascites in Late-Stage Epithelial Ovarian Cancer.

Moughon, Diana L / He, Huanhuan / Schokrpur, Shiruyeh / Jiang, Ziyue Karen / Yaqoob, Madeeha / David, John / Lin, Crystal / Iruela-Arispe, M Luisa / Dorigo, Oliver / Wu, Lily

Cancer research

2015 Volume 75, Issue 22, Page(s) 4742–4752

Abstract: Malignant ascites is a common complication in the late stages of epithelial ovarian cancer (EOC) that greatly diminishes the quality of life of patients. Malignant ascites is a known consequence of vascular dysfunction, but current approved treatments ... ...

Abstract	Malignant ascites is a common complication in the late stages of epithelial ovarian cancer (EOC) that greatly diminishes the quality of life of patients. Malignant ascites is a known consequence of vascular dysfunction, but current approved treatments are not effective in preventing fluid accumulation. In this study, we investigated an alternative strategy of targeting macrophage functions to reverse the vascular pathology of malignant ascites using fluid from human patients and an immunocompetent murine model (ID8) of EOC that mirrors human disease by developing progressive vascular disorganization and leakiness culminating in massive ascites. We demonstrate that the macrophage content in ascites fluid from human patients and the ID8 model directly correlates with vascular permeability. To further substantiate macrophages' role in the pathogenesis of malignant ascites, we blocked macrophage function in ID8 mice using a colony-stimulating factor 1 receptor kinase inhibitor (GW2580). Administration of GW2580 in the late stages of disease resulted in reduced infiltration of protumorigenic (M2) macrophages and dramatically decreased ascites volume. Moreover, the disorganized peritoneal vasculature became normalized and sera from GW2580-treated ascites protected against endothelial permeability. Therefore, our findings suggest that macrophage-targeted treatment may be a promising strategy toward a safe and effective means to control malignant ascites of EOC.
MeSH term(s)	Animals ; Anisoles/pharmacology ; Ascites/etiology ; Ascites/prevention & control ; Capillary Permeability/drug effects ; Carcinoma, Ovarian Epithelial ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Flow Cytometry ; Humans ; Immunohistochemistry ; Macrophages/drug effects ; Mice ; Neoplasms, Glandular and Epithelial/complications ; Ovarian Neoplasms/complications ; Pyrimidines/pharmacology ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/antagonists & inhibitors
Chemical Substances	5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine ; Anisoles ; Csf1r protein, mouse ; Pyrimidines ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
Language	English
Publishing date	2015-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-14-3373
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Article ; Online: CSF1 receptor targeting in prostate cancer reverses macrophage-mediated resistance to androgen blockade therapy.

Escamilla, Jemima / Schokrpur, Shiruyeh / Liu, Connie / Priceman, Saul J / Moughon, Diana / Jiang, Ziyue / Pouliot, Frederic / Magyar, Clara / Sung, James L / Xu, Jingying / Deng, Gang / West, Brian L / Bollag, Gideon / Fradet, Yves / Lacombe, Louis / Jung, Michael E / Huang, Jiaoti / Wu, Lily

Cancer research

2015 Volume 75, Issue 6, Page(s) 950–962

Abstract: Growing evidence suggests that tumor-associated macrophages (TAM) promote cancer progression and therapeutic resistance by enhancing angiogenesis, matrix-remodeling, and immunosuppression. In this study, prostate cancer under androgen blockade therapy ( ... ...

Abstract	Growing evidence suggests that tumor-associated macrophages (TAM) promote cancer progression and therapeutic resistance by enhancing angiogenesis, matrix-remodeling, and immunosuppression. In this study, prostate cancer under androgen blockade therapy (ABT) was investigated, demonstrating that TAMs contribute to prostate cancer disease recurrence through paracrine signaling processes. ABT induced the tumor cells to express macrophage colony-stimulating factor 1 (M-CSF1 or CSF1) and other cytokines that recruit and modulate macrophages, causing a significant increase in TAM infiltration. Inhibitors of CSF1 signaling through its receptor, CSF1R, were tested in combination with ABT, demonstrating that blockade of TAM influx in this setting disrupts tumor promotion and sustains a more durable therapeutic response compared with ABT alone.
MeSH term(s)	Androgen Antagonists/therapeutic use ; Animals ; Carcinogenesis ; Cells, Cultured ; Drug Resistance, Neoplasm ; Humans ; Macrophages/physiology ; Male ; Mice ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Receptor, Macrophage Colony-Stimulating Factor/antagonists & inhibitors
Chemical Substances	Androgen Antagonists ; Receptor, Macrophage Colony-Stimulating Factor (EC 2.7.10.1)
Language	English
Publishing date	2015-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-14-0992
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Targeting distinct tumor-infiltrating myeloid cells by inhibiting CSF-1 receptor: combating tumor evasion of antiangiogenic therapy.

Priceman, Saul J / Sung, James L / Shaposhnik, Zory / Burton, Jeremy B / Torres-Collado, Antoni X / Moughon, Diana L / Johnson, Mai / Lusis, Aldons J / Cohen, Donald A / Iruela-Arispe, M Luisa / Wu, Lily

Blood

2009 Volume 115, Issue 7, Page(s) 1461–1471

Abstract: Tumor-infiltrating myeloid cells (TIMs) support tumor growth by promoting angiogenesis and suppressing antitumor immune responses. CSF-1 receptor (CSF1R) signaling is important for the recruitment of CD11b(+)F4/80(+) tumor-associated macrophages (TAMs) ... ...

Abstract	Tumor-infiltrating myeloid cells (TIMs) support tumor growth by promoting angiogenesis and suppressing antitumor immune responses. CSF-1 receptor (CSF1R) signaling is important for the recruitment of CD11b(+)F4/80(+) tumor-associated macrophages (TAMs) and contributes to myeloid cell-mediated angiogenesis. However, the impact of the CSF1R signaling pathway on other TIM subsets, including CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSCs), is unknown. Tumor-infiltrating MDSCs have also been shown to contribute to tumor angiogenesis and have recently been implicated in tumor resistance to antiangiogenic therapy, yet their precise involvement in these processes is not well understood. Here, we use the selective pharmacologic inhibitor of CSF1R signaling, GW2580, to demonstrate that CSF-1 regulates the tumor recruitment of CD11b(+)Gr-1(lo)Ly6C(hi) mononuclear MDSCs. Targeting these TIM subsets inhibits tumor angiogenesis associated with reduced expression of proangiogenic and immunosuppressive genes. Combination therapy using GW2580 with an anti-VEGFR-2 antibody synergistically suppresses tumor growth and severely impairs tumor angiogenesis along with reverting at least one TIM-mediated antiangiogenic compensatory mechanism involving MMP-9. These data highlight the importance of CSF1R signaling in the recruitment and function of distinct TIM subsets, including MDSCs, and validate the benefits of targeting CSF1R signaling in combination with antiangiogenic drugs for the treatment of solid cancers.
MeSH term(s)	Animals ; Anisoles/pharmacology ; Carcinoma, Lewis Lung/drug therapy ; Carcinoma, Lewis Lung/pathology ; Cell Line, Tumor ; Cell Movement/drug effects ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Macrophages/cytology ; Male ; Matrix Metalloproteinase 9/metabolism ; Melanoma/drug therapy ; Melanoma/pathology ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/drug effects ; Myeloid Cells/pathology ; Neoplasm Transplantation ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Pyrimidines/pharmacology ; Rats ; Receptor, Macrophage Colony-Stimulating Factor/antagonists & inhibitors ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction/drug effects ; Skin Neoplasms/drug therapy ; Skin Neoplasms/pathology ; Vascular Endothelial Growth Factor Receptor-2/metabolism
Chemical Substances	5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine ; Anisoles ; Pyrimidines ; Receptor, Macrophage Colony-Stimulating Factor (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2009-12-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2009-08-237412
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Rapamycin enhances adenovirus-mediated cancer imaging and therapy in pre-immunized murine hosts.

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Article ; Online: CRISPR-Mediated VHL Knockout Generates an Improved Model for Metastatic Renal Cell Carcinoma.

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Article ; Online: Detection of immune responses after immunotherapy in glioblastoma using PET and MRI.

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Article ; Online: Rapamycin enhances adenovirus-mediated cancer imaging and therapy in pre-immunized murine hosts.

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Article ; Online: Macrophage Blockade Using CSF1R Inhibitors Reverses the Vascular Leakage Underlying Malignant Ascites in Late-Stage Epithelial Ovarian Cancer.

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Article ; Online: CSF1 receptor targeting in prostate cancer reverses macrophage-mediated resistance to androgen blockade therapy.

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Article ; Online: Targeting distinct tumor-infiltrating myeloid cells by inhibiting CSF-1 receptor: combating tumor evasion of antiangiogenic therapy.

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