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1. Supplementary Figure S1 from Sunitinib-Induced Myeloid Lineage Redistribution in Renal Cell Cancer Patients: CD1c+ Dendritic Cell Frequency Predicts Progression-Free Survival

Author

van Cruijsen, Hester, primary, van der Veldt, Astrid A.M., primary, Vroling, Laura, primary, Oosterhoff, Dinja, primary, Broxterman, Henk J., primary, Scheper, Rik J., primary, Giaccone, Giuseppe, primary, Haanen, John B.A.G., primary, van den Eertwegh, Alfons J.M., primary, Boven, Epie, primary, Hoekman, Klaas, primary, and de Gruijl, Tanja D., primary

Published
2023
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2. Supplementary Figure Legends 1-3 from Potent Antitumor Immunity Generated by a CD40-Targeted Adenoviral Vaccine

Author

Hangalapura, Basav N., primary, Oosterhoff, Dinja, primary, de Groot, Jan, primary, Boon, Louis, primary, Tüting, Thomas, primary, van den Eertwegh, Alfons J., primary, Gerritsen, Winald R., primary, van Beusechem, Victor W., primary, Pereboev, Alexander, primary, Curiel, David T., primary, Scheper, Rik J., primary, and de Gruijl, Tanja D., primary

Published
2023
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3. Supplementary Figure 1 from Potent Antitumor Immunity Generated by a CD40-Targeted Adenoviral Vaccine

Author

Hangalapura, Basav N., primary, Oosterhoff, Dinja, primary, de Groot, Jan, primary, Boon, Louis, primary, Tüting, Thomas, primary, van den Eertwegh, Alfons J., primary, Gerritsen, Winald R., primary, van Beusechem, Victor W., primary, Pereboev, Alexander, primary, Curiel, David T., primary, Scheper, Rik J., primary, and de Gruijl, Tanja D., primary

Published
2023
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5. Supplementary Figure 3 from Potent Antitumor Immunity Generated by a CD40-Targeted Adenoviral Vaccine

Author

Hangalapura, Basav N., primary, Oosterhoff, Dinja, primary, de Groot, Jan, primary, Boon, Louis, primary, Tüting, Thomas, primary, van den Eertwegh, Alfons J., primary, Gerritsen, Winald R., primary, van Beusechem, Victor W., primary, Pereboev, Alexander, primary, Curiel, David T., primary, Scheper, Rik J., primary, and de Gruijl, Tanja D., primary

Published
2023
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6. Supplementary Figure 2 from Potent Antitumor Immunity Generated by a CD40-Targeted Adenoviral Vaccine

Author

Hangalapura, Basav N., primary, Oosterhoff, Dinja, primary, de Groot, Jan, primary, Boon, Louis, primary, Tüting, Thomas, primary, van den Eertwegh, Alfons J., primary, Gerritsen, Winald R., primary, van Beusechem, Victor W., primary, Pereboev, Alexander, primary, Curiel, David T., primary, Scheper, Rik J., primary, and de Gruijl, Tanja D., primary

Published
2023
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15. Constitutively active GSK3β as a means to bolster dendritic cell functionality in the face of tumour-mediated immune suppression

Author

López González, Marta, primary, Oosterhoff, Dinja, additional, Lindenberg, Jelle J., additional, Milenova, Ioanna, additional, Lougheed, Sinead M., additional, Martiáñez, Tania, additional, Dekker, Henk, additional, Quixabeira, Dafne Carolina Alves, additional, Hangalapura, Basav, additional, Joore, Jos, additional, Piersma, Sander R., additional, Cervera-Carrascon, Victor, additional, Santos, Joao Manuel, additional, Scheper, Rik J., additional, Verheul, Henk M.W., additional, Jiménez, Connie R., additional, Van De Ven, Rieneke, additional, Hemminki, Akseli, additional, Van Beusechem, Victor W., additional, and De Gruijl, Tanja D., additional

Published
2019
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17. Conditionally replicating adenoviruses as anticancer agents and ways to improve their efficacy

Author

Oosterhoff, Dinja and van Beusechem, Victor W

Abstract

Conditionally replicating adenoviruses (CRAds) were developed as new tools for cancer therapy. CRAds specifically replicate in and kill cancer cells. Within a solid tumor mass, release of newly formed infectious particles from infected cancer cells allows additional cell layers to be infected and destroyed. When used as monotherapeutic agents, CRAds showed only limited effects in clinical trials. Combination studies consisting of CRAd virotherapy with chemo-, radio-or enzyme prodrug therapy, however, showed additive or even synergistic effects and encouraging results in clinical studies. Furthermore, increased CRAd efficacy could be achieved in preclinical models by targeting CRAd infection specifically to tumor cells or via insertion of therapeutic genes in the CRAd genome. In this review, different mechanisms to achieve CRAd specificity, the efficacy of CRAds in clinical trials and ways to enhance their oncolytic potency are discussed.

Published
2004

19. Gene-directed enzyme prodrug therapy for osteosarcoma:sensitization to CPT-11 in vitro and in vivo by adenoviral delivery of a gene encoding secreted carboxylesterase-2

Author

Oosterhoff, Dinja, Witlox, M Adhiambo, van Beusechem, Victor W, Haisma, Hidde J, Schaap, Gerard R, Bras, Johannes, Kruyt, Frank A, Molenaar, Bonnie, Boven, Epie, Wuisman, Paul I J M, Pinedo, Herbert M, and Gerritsen, Winald R

Abstract

Despite improvement in the treatment of osteosarcoma (OS), there are still many patients who cannot benefit from current treatment modalities. This warrants exploration of new treatment options. To that end, we investigated gene-directed enzyme prodrug therapy (GDEPT) with the use of human liver carboxylesterase-2 (CE2) and the anticancer agent CPT-11. CPT-11 is a clinically approved prodrug that needs to be metabolized into the active drug SN-38 by CEs, which occurs rather inefficiently in humans. GDEPT aims at high production of CE2 at the tumor site, resulting in efficient local conversion of CPT-11 into SN-38. Here, we show that OS cells transduced with an adenoviral vector containing the cDNA encoding a secreted form of CE2 (Ad-sCE2) expressed and efficiently secreted CE2. In vitro, transduction of a panel of OS cell lines with Ad-sCE2 resulted in sensitization up to 2800-fold to CPT-11 treatment. Primary OS short-term cultures, derived from patients suffering from a classic high-grade OS, demonstrated increased CPT-11 sensitivity up to 70-fold after transduction with Ad-sCE2 in vitro. When mice bearing s.c. MG-63 OS xenografts were intratumorally injected with Ad-sCE2 and CPT-11, this resulted in a significant difference in time to reach 2000 mm(3) in tumor volume as compared with animals receiving Ad-sCE2 or CPT-11 treatment (P < 0.05). Taken together, these data suggest that OS cells are sensitive for the combination of Ad-sCE2 and CPT-11.

Published
2003

20. Gene-directed enzyme prodrug therapy for osteosarcoma: sensitization to CPT-11 in vitro and in vivo by adenoviral delivery of a gene encoding secreted carboxylesterase-2

Author

Oosterhoff, Dinja, Witlox, M Adhiambo, van Beusechem, Victor W, Haisma, Hidde J, Schaap, Gerard R, Bras, Johannes, Kruyt, Frank A, Molenaar, Bonnie, Boven, Epie, Wuisman, Paul I J M, Pinedo, Herbert M, Gerritsen, Winald R, Orthopedic Surgery and Sports Medicine, Pathology, Medical oncology, Medical oncology laboratory, and CCA - Cancer biology and immunology

Abstract

Despite improvement in the treatment of osteosarcoma (OS), there are still many patients who cannot benefit from current treatment modalities. This warrants exploration of new treatment options. To that end, we investigated gene-directed enzyme prodrug therapy (GDEPT) with the use of human liver carboxylesterase-2 (CE2) and the anticancer agent CPT-11. CPT-11 is a clinically approved prodrug that needs to be metabolized into the active drug SN-38 by CEs, which occurs rather inefficiently in humans. GDEPT aims at high production of CE2 at the tumor site, resulting in efficient local conversion of CPT-11 into SN-38. Here, we show that OS cells transduced with an adenoviral vector containing the cDNA encoding a secreted form of CE2 (Ad-sCE2) expressed and efficiently secreted CE2. In vitro, transduction of a panel of OS cell lines with Ad-sCE2 resulted in sensitization up to 2800-fold to CPT-11 treatment. Primary OS short-term cultures, derived from patients suffering from a classic high-grade OS, demonstrated increased CPT-11 sensitivity up to 70-fold after transduction with Ad-sCE2 in vitro. When mice bearing s.c. MG-63 OS xenografts were intratumorally injected with Ad-sCE2 and CPT-11, this resulted in a significant difference in time to reach 2000 mm(3) in tumor volume as compared with animals receiving Ad-sCE2 or CPT-11 treatment (P < 0.05). Taken together, these data suggest that OS cells are sensitive for the combination of Ad-sCE2 and CPT-11.

Published
2003

21. IL-10 Conditioning of Human Skin Affects the Distribution of Migratory Dendritic Cell Subsets and Functional T Cell Differentiation

Author

Lindenberg, Jelle J., primary, Oosterhoff, Dinja, additional, Sombroek, Claudia C., additional, Lougheed, Sinéad M., additional, Hooijberg, Erik, additional, Stam, Anita G. M., additional, Santegoets, Saskia J. A. M., additional, Tijssen, Henk J., additional, Buter, Jan, additional, Pinedo, Herbert M., additional, van den Eertwegh, Alfons J. M., additional, Scheper, Rik J., additional, Koenen, Hans J. P. M., additional, van de Ven, Rieneke, additional, and de Gruijl, Tanja D., additional

Published
2013
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22. Intradermal Delivery of TLR Agonists in a Human Explant Skin Model: Preferential Activation of Migratory Dendritic Cells by Polyribosinic-Polyribocytidylic Acid and Peptidoglycans

Author

Oosterhoff, Dinja, primary, Heusinkveld, Moniek, additional, Lougheed, Sinéad M., additional, Kosten, Ilona, additional, Lindstedt, Malin, additional, Bruijns, Sven C. M., additional, van Es, Thomas, additional, van Kooyk, Yvette, additional, van der Burg, Sjoerd H., additional, and de Gruijl, Tanja D., additional

Published
2013
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23. Functional characterization of a STAT3-dependent dendritic cell-derived CD14+cell population arising upon IL-10-driven maturation

Author

Lindenberg, Jelle J., primary, van de Ven, Rieneke, additional, Lougheed, Sinéad M., additional, Zomer, Anoek, additional, Santegoets, Saskia JAM, additional, Griffioen, Arjan W., additional, Hooijberg, Erik, additional, van den Eertwegh, Alfons J.M., additional, Thijssen, Victor L., additional, Scheper, Rik J., additional, Oosterhoff, Dinja, additional, and de Gruijl, Tanja D., additional

Published
2013
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26. Tumor-mediated inhibition of human dendritic cell differentiation and function is consistently counteracted by combined p38 MAPK and STAT3 inhibition

Author

Oosterhoff, Dinja, primary, Lougheed, Sinéad, additional, van de Ven, Rieneke, additional, Lindenberg, Jelle, additional, van Cruijsen, Hester, additional, Hiddingh, Lotte, additional, Kroon, Jan, additional, van den Eertwegh, Alfons J.M., additional, Hangalapura, Basav, additional, Scheper, Rik J., additional, and de Gruijl, Tanja D., additional

Published
2012
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27. Glioblastoma-induced inhibition of Langerhans cell differentiation from CD34+precursors is mediated by IL-6 but unaffected by JAK2/STAT3 inhibition

Author

van Cruijsen, Hester, primary, Oosterhoff, Dinja, additional, Lindenberg, Jelle J, additional, Lougheed, Sinéad M, additional, Fehres, Cynthia, additional, Weijers, Karin, additional, van Boerdonk, Robert, additional, Giaccone, Giuseppe, additional, Scheper, Rik J, additional, Hoekman, Klaas, additional, and de Gruijl, Tanja D, additional

Published
2011
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28. Potent Antitumor Immunity Generated by a CD40-Targeted Adenoviral Vaccine

Author

Hangalapura, Basav N., primary, Oosterhoff, Dinja, additional, de Groot, Jan, additional, Boon, Louis, additional, Tüting, Thomas, additional, van den Eertwegh, Alfons J., additional, Gerritsen, Winald R., additional, van Beusechem, Victor W., additional, Pereboev, Alexander, additional, Curiel, David T., additional, Scheper, Rik J., additional, and de Gruijl, Tanja D., additional

Published
2011
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29. Delivery route, MyD88 signaling and cross-priming events determine the anti-tumor efficacy of an adenovirus based melanoma vaccine

Author

Hangalapura, Basav N., primary, Oosterhoff, Dinja, additional, Gupta, Tarun, additional, de Groot, Jan, additional, Wijnands, Pepijn G.J.T.B., additional, van Beusechem, Victor W., additional, den Haan, Joke, additional, Tüting, Thomas, additional, van den Eertwegh, Alfons J.M., additional, and Curiel, David T., additional

Published
2011
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31. Selective Transduction of Dendritic Cells in Human Lymph Nodes and Superior Induction of High-avidity Melanoma-reactive Cytotoxic T Cells by a CD40-targeted Adenovirus

Author

Hangalapura, Basav N., primary, Oosterhoff, Dinja, additional, Aggarwal, Shikhar, additional, Wijnands, Pepijn G.J.T.B., additional, van de Ven, Rieneke, additional, Santegoets, Saskia J.A.M., additional, van den Tol, Monique Petrousjka, additional, Hooijberg, Erik, additional, Pereboev, Alexander, additional, van den Eertwegh, Alfons J.M., additional, Curiel, David T., additional, Scheper, Rik J., additional, and de Gruijl, Tanja D., additional

Published
2010
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32. Selective Transduction of Mature DC in Human Skin and Lymph Nodes by CD80/CD86-targeted Fiber-modified Adenovirus-5/3

Author

van de Ven, Rieneke, primary, Lindenberg, Jelle J., additional, Oosterhoff, Dinja, additional, van den Tol, M. Petrousjka, additional, Rosalia, Rodney A., additional, Murakami, Miho, additional, Everts, Maaike, additional, Scheffer, George L., additional, Scheper, Rik J., additional, de Gruijl, Tanja D., additional, and Curiel, David T., additional

Published
2009
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33. Sunitinib-Induced Myeloid Lineage Redistribution in Renal Cell Cancer Patients: CD1c+ Dendritic Cell Frequency Predicts Progression-Free Survival

Author

van Cruijsen, Hester, primary, van der Veldt, Astrid A.M., additional, Vroling, Laura, additional, Oosterhoff, Dinja, additional, Broxterman, Henk J., additional, Scheper, Rik J., additional, Giaccone, Giuseppe, additional, Haanen, John B.A.G., additional, van den Eertwegh, Alfons J.M., additional, Boven, Epie, additional, Hoekman, Klaas, additional, and de Gruijl, Tanja D., additional

Published
2008
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36. Dendritic cell plasticity in tumor-conditioned skin: CD14+ cells at the cross-roads of immune activation and suppression.

Author

van de Ven, Rieneke, Lindenberg, Jelle J., Oosterhoff, Dinja, and de Gruijl, Tanja D.

Subjects
DENDRITIC cells, TUMORS, ONCOLOGY, T cells, CANCER invasiveness, ANTIGEN presenting cells
Abstract

Tumors abuse myeloid plasticity to re-direct dendritic cell (DC) differentiation from T cell stimulatory subsets to immune-suppressive subsets that can interfere with anti-tumor immunity. Lined by a dense network of easily accessible DC the skin is a preferred site for the delivery of DC-targeted vaccines. Various groups have recently been focusing on functional aspects of DC subsets in the skin and how these may be affected by tumor-derived suppressive factors. IL-6, Prostaglandin-E2, and IL-10 were identified as factors in cultures of primary human tumors responsible for the inhibited development and activation of skin DC as well as monocyte-derived DC. IL-10 was found to be uniquely able to convert fully developed DC to immature macrophage-like cells with functional M2 characteristics in a physiologically highly relevant skin explant model in which the phenotypic and functional traits of "crawl-out" DC were studied. Mostly from mouse studies, the JAK2/STAT3 signaling pathway has emerged as a "master switch" of tumor-induced immune suppression. Our lab has additionally identified p38-MAPK as an important signaling element in human DC suppression, and recently validated it as such in ex vivo cultures of single-cell suspensions from melanoma metastases. Through the identification of molecular mechanisms and signaling events that drive myeloid immune suppression in human tumors, more effective DC-targeted cancer vaccines may be designed. [ABSTRACT FROM AUTHOR]

Published
2013
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37. Functional characterization of a STAT3-dependent dendritic cell-derived CD14+ cell population arising upon IL-10-driven maturation.

Author

Lindenberg, Jelle J., van de Ven, Rieneke, Lougheed, Sinéad M., Zomer, Anoek, Santegoets, Saskia J.A.M., Griffioen, Arjan W., Hooijberg, Erik, Van den Eertwegh, Alfons J.M., Thijssen, Victor L., Scheper, Rik J., Oosterhoff, Dinja, and de Gruijl, Tanja D.

Subjects
INTERLEUKIN-10, CELL proliferation, DENDRITIC cells, MACROPHAGE activation, CYTOKINES
Abstract

Interleukin (IL)-10 is a major cancer-related immunosuppressive factor, exhibiting a unique ability to hamper the maturation of dendritic cells (DCs). We have previously reported that IL-10 induces the conversion of activated, migratory CD1a+ DCs found in the human skin to CD14+CD141+ macrophage-like cells. Here, as a model of tumor-conditioned DC maturation, we functionally assessed CD14- and CD14+ DCs that matured in vitro upon exposure to IL-10. IL-10-induced CD14+ DCs were phenotypically characterized by a low maturation state as well as by high levels of BDCA3 and DC-SIGN, and as such they closely resembled CD14+ cells infiltrating melanoma metastases. Compared with DC matured under standard conditions, CD14+ DCs were found to express high levels of B7-H1 on the cell surface, to secrete low levels of IL- 12p70, to preferentially induce TH2 cells, to have a lower allogeneic TH cell and tumor antigen-specific CD8+ T-cell priming capacity and to induce proliferative T-cell anergy. In contrast to their CD14+ counterparts, CD14- monocyte-derived DCs retained allogeneic TH priming capacity but induced a functionally anergic state as they completely abolished the release of effector cytokines. Transcriptional and cytokine release profiling studies indicated a more profound angiogenic and pro-invasive signature of CD14+ DCs as compared with DCs matured in standard conditions or CD14- DCs matured in the presence of IL-10. Importantly, signal transducer and activator of transcription 3 (STAT3) depletion by RNA interference prevented the development of the IL-10-associated CD14+ phenotype, allowing for normal DC maturation and providing a potential means of therapeutic intervention. [ABSTRACT FROM AUTHOR]

Published
2013
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39. Functional characterization of a STAT3-dependent dendritic cell-derived CD14 + cell population arising upon IL-10-driven maturation.

Author

Lindenberg JJ, van de Ven R, Lougheed SM, Zomer A, Santegoets SJ, Griffioen AW, Hooijberg E, van den Eertwegh AJ, Thijssen VL, Scheper RJ, Oosterhoff D, and de Gruijl TD

Abstract

Interleukin (IL)-10 is a major cancer-related immunosuppressive factor, exhibiting a unique ability to hamper the maturation of dendritic cells (DCs). We have previously reported that IL-10 induces the conversion of activated, migratory CD1a + DCs found in the human skin to CD14 + CD141 + macrophage-like cells. Here, as a model of tumor-conditioned DC maturation, we functionally assessed CD14 - and CD14 + DCs that matured in vitro upon exposure to IL-10. IL-10-induced CD14 + DCs were phenotypically characterized by a low maturation state as well as by high levels of BDCA3 and DC-SIGN, and as such they closely resembled CD14 + cells infiltrating melanoma metastases. Compared with DC matured under standard conditions, CD14 + DCs were found to express high levels of B7-H1 on the cell surface, to secrete low levels of IL-12p70, to preferentially induce TH2 cells, to have a lower allogeneic TH cell and tumor antigen-specific CD8 + T-cell priming capacity and to induce proliferative T-cell anergy. In contrast to their CD14 + counterparts, CD14 - monocyte-derived DCs retained allogeneic TH priming capacity but induced a functionally anergic state as they completely abolished the release of effector cytokines. Transcriptional and cytokine release profiling studies indicated a more profound angiogenic and pro-invasive signature of CD14 + DCs as compared with DCs matured in standard conditions or CD14 - DCs matured in the presence of IL-10. Importantly, signal transducer and activator of transcription 3 (STAT3) depletion by RNA interference prevented the development of the IL-10-associated CD14 + phenotype, allowing for normal DC maturation and providing a potential means of therapeutic intervention.

Published
2013
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40. Conditionally replicating adenoviruses as anticancer agents and ways to improve their efficacy.

Author

Oosterhoff D and van Beusechem VW

Subjects
Antineoplastic Agents therapeutic use, Cell Death, Combined Modality Therapy, Genetic Therapy, Humans, Neoplasms genetics, Neoplasms virology, Adenoviruses, Human physiology, Neoplasms therapy, Virus Replication
Abstract

Conditionally replicating adenoviruses (CRAds) were developed as new tools for cancer therapy. CRAds specifically replicate in and kill cancer cells. Within a solid tumor mass, release of newly formed infectious particles from infected cancer cells allows additional cell layers to be infected and destroyed. When used as monotherapeutic agents, CRAds showed only limited effects in clinical trials. Combination studies consisting of CRAd virotherapy with chemo-, radio-or enzyme prodrug therapy, however, showed additive or even synergistic effects and encouraging results in clinical studies. Furthermore, increased CRAd efficacy could be achieved in preclinical models by targeting CRAd infection specifically to tumor cells or via insertion of therapeutic genes in the CRAd genome. In this review, different mechanisms to achieve CRAd specificity, the efficacy of CRAds in clinical trials and ways to enhance their oncolytic potency are discussed.

Published
2004

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