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315 results on '"Dranoff, G."'

2. Induction of myeloproliferative disease in mice by tyrosine kinase fusion oncogenes does not require granulocyte-macrophage colony-stimulating factor or interleukin-3.

Author

Tomasson, M H, Williams, I R, Li, S, Kutok, J, Cain, D, Gillessen, S, Dranoff, G, Van Etten, R A, and Gilliland, D G

Subjects
Animals, Bone Marrow Transplantation, Cell Transformation, Neoplastic: drug effects, genetics, Disease Models, Animal, Granulocyte-Macrophage Colony-Stimulating Factor: genetics, pharmacology, Interleukin-3: genetics, pharmacology, Mice, Mice, Knockout, Myeloproliferative Disorders: etiology, pathology, Neoplasm Proteins: genetics, pharmacology, Oncogene Proteins, Fusion: genetics, pharmacology, Paracrine Communication, Transduction, Genetic, cytokine, granulocyte macrophage colony stimulating factor, hybrid protein, interleukin 3, neurotrophin 3 receptor, platelet derived growth factor beta receptor, protein tyrosine kinase, animal tissue, apoptosis, article, cell proliferation, chromosome translocation, controlled study, leukemia cell, mouse, myelopoiesis, myeloproliferative disorder, nonhuman, oncogene, pathogenesis, priority journal, Animals, Bone Marrow Transplantation, Cell Transformation, Neoplastic, Disease Models, Animal, Granulocyte-Macrophage Colony-Stimulating Factor, Interleukin-3, Mice, Mice, Knockout, Myeloproliferative Disorders, Neoplasm Proteins, Oncogene Proteins, Fusion, Paracrine Communication, Transduction, Genetic
Abstract

Tyrosine kinase fusion oncogenes that occur as a result of chromosomal translocations have been shown to activate proliferative and antiapoptotic pathways in leukemic cells, but the importance of autocrine and paracrine expression of hematopoietic cytokines in leukemia pathogenesis is not understood. Evidence that leukemic transformation may be, at least in part, cytokine dependent includes data from primary human leukemia cells, cell culture experiments, and murine models of leukemia. This report demonstrates that interleukin (IL)-3 plasma levels are elevated in myeloproliferative disease (MPD) caused by the TEL/tyrosine kinase fusions TEL/platelet-derived growth factor beta receptor (PDGFbetaR), TEL/Janus kinase 2 (JAK2), and TEL/neurotrophin-3 receptor (TRKC). Plasma granulocyte-macrophage colony-stimulating factor (GM-CSF) levels were elevated by TEL/PDGFbetaR and TEL/JAK2. However, all of the fusions tested efficiently induced MPD in mice genetically deficient for both GM-CSF and IL-3, demonstrating that these cytokines are not necessary for the development of disease in this model system. Furthermore, in experiments using normal marrow transduced with TEL/PDGFbetaR retrovirus mixed with marrow transduced with an enhanced green fluorescent protein (EGFP) retrovirus, the MPD induced in these mice demonstrated minimal stimulation of normal myelopoiesis by the TEL/PDGFbetaR-expressing cells. In contrast, recipients of mixed GM-CSF-transduced and EGFP-transduced marrow exhibited significant paracrine expansion of EGFP-expressing cells. Collectively, these data demonstrate that, although cytokine levels are elevated in murine bone marrow transplant models of leukemia using tyrosine kinase fusion oncogenes, GM-CSF and IL-3 are not required for myeloproliferation by any of the oncogenes tested.

Published
2001

3. Interleukin 3 and granulocyte-macrophage colony-stimulating factor are not required for induction of chronic myeloid leukemia-like myeloproliferative disease in mice by BCR/ABL.

Author

Li, S, Gillessen, S, Tomasson, M H, Dranoff, G, Gilliland, D G, and Van Etten, R A

Subjects
Animals, Bone Marrow Transplantation, Cell Transformation, Neoplastic: drug effects, Disease Models, Animal, Fusion Proteins, bcr-abl: genetics, pharmacology, Granulocyte-Macrophage Colony-Stimulating Factor: genetics, metabolism, pharmacology, Interleukin-3: genetics, metabolism, pharmacology, Leukemia, Myelogenous, Chronic, BCR-ABL Positive: etiology, metabolism, pathology, Mice, Mice, Inbred C57BL, Mice, Knockout, Myeloproliferative Disorders: etiology, metabolism, pathology, Survival Rate, Tissue Distribution, Transduction, Genetic
Abstract

Primitive hematopoietic progenitors from some patients with Philadelphia chromosome (Ph)-positive chronic myeloid leukemia (CML) express aberrant transcripts for interleukin 3 (IL-3) and granulocyte colony-stimulating factor (G-CSF), and exhibit autonomous proliferation in serum-free cultures that is inhibited by anti-IL-3 and anti-IL-3 receptor antibodies. Expression of the product of the Ph chromosome, the BCR/ABL oncogene, in mice by retroviral bone marrow transduction and transplantation induces CML-like leukemia, and some leukemic mice have increased circulating IL-3, and perhaps granulocyte-macrophage colony-stimulating factor (GM-CSF). These observations raise the possibility of autocrine or paracrine cytokine production in the pathogenesis of human CML. Mice with homozygous inactivation of the Il-3 gene, the Gm-csf gene, or both, were used to test the requirement for these cytokines for induction of CML-like disease by BCR/ABL. Neither IL-3 nor GM-CSF was required in donor, recipient, or both for induction of CML-like leukemia by p210 BCR/ABL. Use of novel mice deficient in both IL-3 and GM-CSF demonstrated that the lack of effect on leukemogenesis was not due to redundancy between these hematopoietic growth factors. Analysis of cytokine levels in leukemic mice where either donor or recipient was Il-3(-/-) indicated that the increased IL-3 originated from the recipient, suggestive of a host reaction to the disease. These results demonstrate that IL-3 and GM-CSF are not required for BCR/ABL-induced CML-like leukemia in mice and suggest that autocrine production of IL-3 does not play a role in established chronic phase CML in humans.

Published
2001

9. Gene therapy in allergic encephalomyelitis using myelin basic protein-specific T cells engineered to express latent transforming growth factor-beta1

Author

Chen, L.Z., Hochwald, G.M., Huang, C., Dakin, G., Tao, H., Cheng, C., Simmons, W.J., Dranoff, G., and Thorbecke, G.J.

Subjects
Gene therapy -- Research, Encephalomyelitis -- Research, T cells -- Research, Gene expression -- Research, Growth factors -- Research, Science and technology
Abstract

A myelin basic protein (MBP)-specific BALB/c T helper 1 (Th1) clone was transduced with cDNA for murine latent transforming growth factor-[Beta]1 (TGF-[Beta]1) by coculture with fibroblasts producing a genetically engineered retrovirus. When SJL x BALB/c F1 mice, immunized 12-15 days earlier with proteolipid protein in complete Freund's adjuvant, were injected with 3 x [10.sup.6] cells from MBP-activated untransduced cloned Th1 cells, the severity of experimental allergic encephaiomyelitis (EAE) was slightly increased. In contrast, MBP-activated (but not resting) latent TGF-[Beta]1-transduced T cells significantly delayed and ameliorated EAE development. This protective effect was negated by simultaneously injected anti.TGF-[Beta]1. The transduced cells secreted 2-4 ng/ml of latent TGF-[Beta]1 into their culture medium, whereas control cells secreted barely detectable amounts. mRNA profiles for tumor necrosis factor, lymphotoxin, and interferon-[Gamma] were similar before and after transduction; interleukin-4 and -10 were absent. TGF-[Beta]1-transduced and antigen-activated BALB/c Th1 clones, specific for hemocyanin or ovalbumin, did not ameliorate EAE. Spinal cords from mice, taken 12 days after receiving TGF-[Beta]1-transduced, antigen-activated cells, contained detectable amounts of TGF-[Beta]1 cDNA. We conclude that latent TGF-[Beta]1-transduced, self-reactive T cell clones may be useful in the therapy of autoimmune diseases.

Published
1998

13. Immunotherapy advances for glioblastoma

Author

Reardon, D. A., primary, Freeman, G., additional, Wu, C., additional, Chiocca, E. A., additional, Wucherpfennig, K. W., additional, Wen, P. Y., additional, Fritsch, E. F., additional, Curry, W. T., additional, Sampson, J. H., additional, and Dranoff, G., additional

Published
2014
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15. Defining the Critical Hurdles in Cancer Immunotherapy

Author

Fox, BA, Schendel, D.J., Butterfield, L.H., Aamdal, S., Allison, J.P., Ascierto, P.A., Atkins, M.B., Bartunkova, J., Bergmann, L., Berinstein, N., Bonorino, C.C., Borden, E., Bramson, J.L., Britten, C.M., Cao, X., Carson, W.E., Chang, A.E., Characiejus, D., Choudhury, A.R., Coukos, G., de Gruijl, T.D., Dillman, R.O., Dolstra, H., Dranoff, G., Durrant, L.G., Finke, J.H., Galon, J., Gollob, J.A., Gouttefangeas, C., Grizzi, F., Guida, M., Hakansson, L., Hege, K., Herberman, R.B., Hodi, F.S., Hoos, A., Huber, C., Hwu, P., Imai, K., Jaffee, E.M., Janetzki, S., June, C.H., Kalinski, P., Kaufmann, H.L., Kawakami, K., Kawakami, Y., Keilholtz, U., Khleif, S.N., Kiessling, R., Kotlan, B., Kroemer, G., Lapointe, R., Levitsky, H.I., Lotze, M.T., Di Maio, M., Marschner, J.P., Mastrangelo, M.J., Masucci, G., Melero, I., Nelief, C., Murphy, W.J., Nelson, B., Nicolini, A., Nishimura, M.I., Odunsi, K., Ohashi, P.S., O'Donnell-Tormey, J., Old, L.J., Ottensmeier, C., Papamichail, M., Parmiani, G., Pawelec, G., Proietti, E., Qin, S., Rees, R., Ribas, A., Ridolfi, R., Ritter, G., Rivoltini, L., Romero, P.J., Salem, M.L., Scheper, R.J., Seliger, B., Sharma, P., Shiku, H., Singh-Jasuja, H., Song, W., Straten, P.T., Tahara, H., Tian, Z., van der Burg, S.H., von Hoegen, P., Wang, E., Welters, M.J., Winter, H., Withington, T., Wolchok, J.D., Xiao, W., Zitvogel, L., Zwierzina, H., Marincola, F.M., Gajewski, T.F., Wigginton, J.M., Disis, M.L.A., Fox, BA, Schendel, D.J., Butterfield, L.H., Aamdal, S., Allison, J.P., Ascierto, P.A., Atkins, M.B., Bartunkova, J., Bergmann, L., Berinstein, N., Bonorino, C.C., Borden, E., Bramson, J.L., Britten, C.M., Cao, X., Carson, W.E., Chang, A.E., Characiejus, D., Choudhury, A.R., Coukos, G., de Gruijl, T.D., Dillman, R.O., Dolstra, H., Dranoff, G., Durrant, L.G., Finke, J.H., Galon, J., Gollob, J.A., Gouttefangeas, C., Grizzi, F., Guida, M., Hakansson, L., Hege, K., Herberman, R.B., Hodi, F.S., Hoos, A., Huber, C., Hwu, P., Imai, K., Jaffee, E.M., Janetzki, S., June, C.H., Kalinski, P., Kaufmann, H.L., Kawakami, K., Kawakami, Y., Keilholtz, U., Khleif, S.N., Kiessling, R., Kotlan, B., Kroemer, G., Lapointe, R., Levitsky, H.I., Lotze, M.T., Di Maio, M., Marschner, J.P., Mastrangelo, M.J., Masucci, G., Melero, I., Nelief, C., Murphy, W.J., Nelson, B., Nicolini, A., Nishimura, M.I., Odunsi, K., Ohashi, P.S., O'Donnell-Tormey, J., Old, L.J., Ottensmeier, C., Papamichail, M., Parmiani, G., Pawelec, G., Proietti, E., Qin, S., Rees, R., Ribas, A., Ridolfi, R., Ritter, G., Rivoltini, L., Romero, P.J., Salem, M.L., Scheper, R.J., Seliger, B., Sharma, P., Shiku, H., Singh-Jasuja, H., Song, W., Straten, P.T., Tahara, H., Tian, Z., van der Burg, S.H., von Hoegen, P., Wang, E., Welters, M.J., Winter, H., Withington, T., Wolchok, J.D., Xiao, W., Zitvogel, L., Zwierzina, H., Marincola, F.M., Gajewski, T.F., Wigginton, J.M., and Disis, M.L.A.

Abstract

Scientific discoveries that provide strong evidence of antitumor effects in preclinical models often encounter significant delays before being tested in patients with cancer. While some of these delays have a scientific basis, others do not. We need to do better. Innovative strategies need to move into early stage clinical trials as quickly as it is safe, and if successful, these therapies should efficiently obtain regulatory approval and widespread clinical application. In late 2009 and 2010 the Society for Immunotherapy of Cancer (SITC), convened an "Immunotherapy Summit" with representatives from immunotherapy organizations representing Europe, Japan, China and North America to discuss collaborations to improve development and delivery of cancer immunotherapy. One of the concepts raised by SITC and defined as critical by all parties was the need to identify hurdles that impede effective translation of cancer immunotherapy. With consensus on these hurdles, international working groups could be developed to make recommendations vetted by the participating organizations. These recommendations could then be considered by regulatory bodies, governmental and private funding agencies, pharmaceutical companies and academic institutions to facilitate changes necessary to accelerate clinical translation of novel immune-based cancer therapies. The critical hurdles identified by representatives of the collaborating organizations, now organized as the World Immunotherapy Council, are presented and discussed in this report. Some of the identified hurdles impede all investigators; others hinder investigators only in certain regions or institutions or are more relevant to specific types of immunotherapy or first-in-humans studies. Each of these hurdles can significantly delay clinical translation of promising advances in immunotherapy yet if overcome, have the potential to improve outcomes of patients with cancer. © 2011 Fox et al; licensee BioMed Central Ltd.

Published
2011
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16. Macrophage growth factors introduced into the kidney initiate renal injury

Author

Naito, T., Yokoyama, H., Moore, K. J., Dranoff, G., Mulligan, R. C., and Kelley, V. R.

Subjects
Mice, Inbred C3H, Cell Transplantation, Macrophage Colony-Stimulating Factor, Macrophages, Recombinant Fusion Proteins, Gene Expression, Granulocyte-Macrophage Colony-Stimulating Factor, urologic and male genital diseases, Kidney, Transfection, beta-Galactosidase, Epithelium, Mice, Mutant Strains, Autoimmune Diseases, Mice, Kidney Tubules, Retroviridae, Animals, Cells, Cultured, Research Article
Abstract

BACKGROUND: CSF-1 expression precedes renal injury in autoimmune MRL-lpr mice and is responsible for macrophage (M phi) proliferation and survival in the kidney. By comparison, C3H-lpr mice do not express CSF-1 in the kidney, and despite the lpr mutation, kidneys remain normal. The purpose of this study was to test the capacity of local and systemic expression of M phi growth factor, CSF-1 to initiate renal injury in normal (C3H-(++), MRL-(++) and autoimmune (C3H-lpr, MRL-lpr) mice. MATERIALS AND METHODS: We designed a gene transfer system to deliver cytokines into the kidney by transducing renal tubular epithelial cells (TEC) using retroviral vectors expressing CSF-1 or another M phi growth factor, GM-CSF. We placed transduced syngeneic cytokine-TEC under the renal capsule of normal and autoimmune prone mice prior to renal injury and evaluated renal pathology at 3, 7, 14, 28, and 90 days postimplant. RESULTS: CSF-1-TEC and GM-CSF-TEC, but not uninfected TEC, caused extensive local renal injury in strains with the lpr mutation. At 3-7 days the infiltrating cells were mainly M phi, and by 28 days they were predominantly lymphocytes. By comparison, the kidneys of MRL-(++) and C3H-(++) mice remained normal. Implanted genetically modified TEC caused a sustained increase of CSF-1 or GM-CSF in the circulation which did not modify the contralateral kidney. CONCLUSIONS: Gene transfer of M phi growth factors into the kidney initiates severe local renal injury in autoimmune prone mice with the lpr mutation, but does not compromise the kidney in nonautoimmune hosts. Of note, introduction of M phi growth factors into the kidney of C3H-lpr mice which do not spontaneously develop renal injury incites renal damage. These studies offer a gene transfer approach to explore the impact of local and systemic cytokine production on renal injury.

Published
1996

17. Early Post-Transplant Whole Tumor Cell Vaccination Elicits Anti-Tumor T Cell Responses in Patients With Advanced Chronic Lymphocytic Leukemia (CLL)

Author

Hainz, U., primary, Stevenson, K., additional, Ho, V.T., additional, Alonso, A., additional, Goldstein, N.R., additional, Lokko, N., additional, Sievers, Q., additional, Brusic, A.M., additional, Zhang, W., additional, Pasek, M., additional, Zeng, W., additional, Choi, J., additional, Brown, J.R., additional, Canning, C.M., additional, Koreth, J., additional, Cutler, C., additional, Armand, P., additional, Antin, J.H., additional, Sasada, T., additional, Ritz, J., additional, Dranoff, G., additional, Soiffer, R.J., additional, Alyea, E.P., additional, and Wu, C.J., additional

Published
2011
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19. Safety And Clinical Efficacy Of Early Vaccination After Nonmyeloablative Transplant For Advanced Chronic Lymphocytic Leukemia

Author

Wu, C.J., primary, Hainz, U., additional, Stevenson, K.E., additional, Goldstein, N.P., additional, Brusic, A.M., additional, Choi, J.J., additional, Pasek, M., additional, Brown, J.R., additional, Canning, C.M., additional, Armand, P.J., additional, Koreth, J., additional, Cutler, C., additional, Soiffer, R.J., additional, Sasada, T., additional, Ritz, J., additional, Dranoff, G., additional, and Alyea, E.P., additional

Published
2010
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20. A phase I study of an autologous GM-CSF-secreting breast cancer vaccine.

Author

Anderson, KS, primary, Hodi, FS, additional, Sasada, T, additional, Canning, C, additional, Hassett, M, additional, Mayer, E, additional, Hannagan, K, additional, Wong, J, additional, Colson, Y, additional, Shoji, B, additional, Najita, J, additional, Sibani, S, additional, LaBaer, J, additional, Winer, EP, additional, and Dranoff, G, additional

Published
2009
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24. Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) antibody blockade in patients previously vaccinated with irradiated, autologous tumor cells engineered to secrete granulocyte-macrophage colony stimulating factor (GM-CSF)

Author

Hodi, F. S., primary, Seiden, M., additional, Butler, M., additional, Haluska, F. G., additional, Lowy, I., additional, Vincent-Brunick, E., additional, Lautz, D., additional, Mihm, M., additional, and Dranoff, G., additional

Published
2004
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25. A phase I study of vaccination with lethally irradiated, autologous nonsmall cell lung carcinoma cells engineered by adenoviral mediated gene transfer to secrete human granulocyte-macrophage colony stimulating factor

Author

Salgia, R, primary, Lynch, T.J, additional, Skarin, A.T, additional, Lynch, C, additional, Lucca, J, additional, Jaklitsch, M, additional, Mentzer, S, additional, Swanson, S, additional, Lukanich, J, additional, Bueno, R, additional, DeCamp, M, additional, Wain, J, additional, Mathiesen, D, additional, Wright, C, additional, Carey, R, additional, Sommer, K, additional, Boral, A, additional, Fidias, P, additional, Donahue, D, additional, Ando, D, additional, Clift, S, additional, Hardy, S, additional, Webb, I.J, additional, Mulligan, R, additional, Sugarbaker, D, additional, Mihm, M, additional, and Dranoff, G, additional

Published
2000
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27. Bioactivity of Autologous Irradiated Renal Cell Carcinoma Vaccines Generated by Ex Vivo Granulocyte-Macrophage Colony-Stimulating Factor Gene Transfer

Author

Simons, J. W., primary, Jaffee, E. M., additional, Weber, C. E., additional, Levitsky, H. J., additional, Nelson, W. G., additional, Carducci, M. A., additional, Lazenby, A. J., additional, Cohen, L. K., additional, Finn, C. C., additional, Clift, S. M., additional, Hauda, K. M., additional, Beck, L. A., additional, Leiferman, K. M., additional, Owens, A. H., additional, Piantadosi, S., additional, Dranoff, G., additional, Mulligan, R. C., additional, Pardoll, D. M., additional, and Marshall, F. F., additional

Published
1998
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30. A Phase I Study of Vaccination with Autologous, Irradiated Melanoma Cells Engineered to Secrete Human Granulocyte-Macrophage Colony Stimulating Factor. Dana-Farber Cancer Institute, Boston, Massachusetts

Author

Dranoff, G., primary, Soiffer, R., additional, Lynch, T., additional, Mihm, M., additional, Jung, K., additional, Kolesar, K., additional, Liebster, L., additional, Lam, P., additional, Duda, R., additional, Mentzer, S., additional, Singer, S., additional, Tanabe, K., additional, Johnson, R., additional, Sober, A., additional, Bhan, A., additional, Clift, S., additional, Cohen, L., additional, Parry, G., additional, Rokovieh, J., additional, Richards, L., additional, Drayer, J., additional, Berns, A., additional, and Mulligan, R. C., additional

Published
1997
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33. A cell surface marker gene transferred with a retroviral vector into CD34+ cord blood cells is expressed by their T-cell progeny in the SCID- hu thymus

Author

Champseix, C, primary, Marechal, V, additional, Khazaal, I, additional, Schwartz, O, additional, Fournier, S, additional, Schlegel, N, additional, Dranoff, G, additional, Danos, O, additional, Blot, P, additional, Vilmer, E, additional, Heard, JM, additional, Peault, B, additional, and Lehn, P, additional

Published
1996
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38. Tumor cell vaccine elicits potent antitumor immunity after allogeneic T-cell-depleted bone marrow transplantation

Author

Teshima T, Mach N, Gr, Hill, Pan L, Silke Gillessen, Dranoff G, and Jl, Ferrara

Subjects
T-Lymphocytes, Graft vs Tumor Effect, Melanoma, Experimental, Graft vs Host Disease, Granulocyte-Macrophage Colony-Stimulating Factor, Lymphocyte Activation, Cancer Vaccines, Mice, Inbred C57BL, Mice, Histocompatibility Antigens, Immune Tolerance, Animals, Female, Bone Marrow Transplantation
Abstract

Allogeneic bone marrow transplantation (BMT) is currently restricted to hematological malignancies because of a lack of antitumor activity against solid cancers. We have tested a novel treatment strategy to stimulate specific antitumor activity against a solid tumor after BMT by vaccination with irradiated tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor (GM-CSF). Using the B16 melanoma model, we found that vaccination elicited potent antitumor activity in recipients of syngeneic BMT in a time-dependent fashion, and that immune reconstitution was critical for the development of antitumor activity. Vaccination did not stimulate antitumor immunity after allogeneic BMT because of the post-BMT immunodeficiency associated with graft-versus-host disease (GVHD). Remarkably, vaccination was effective in stimulating potent and long-lasting antitumor activity in recipients of T-cell-depleted (TCD) allogeneic bone marrow. Recipients of TCD bone marrow who showed significant immune reconstitution by 6 weeks after BMT developed B16-specific T-cell-cytotoxic, proliferative, and cytokine responses as a function of vaccination. T cells derived from donor stem cells were, therefore, able to recognize tumor antigens, although they remained tolerant to host histocompatibility antigens. These results demonstrate that GM-CSF-based tumor cell vaccines after allogeneic TCD BMT can stimulate potent antitumor effects without the induction of GVHD, and this strategy has important implications for the treatment of patients with solid malignancies.

39. Differences in dendritic cells stimulated in vivo by tumors engineered to secrete granulocyte-macrophage colony-stimulating factor or Flt3-ligand

Author

Mach N, Silke Gillessen, Sb, Wilson, Sheehan C, Mihm M, and Dranoff G

Subjects
Time Factors, CD8 Antigens, T-Lymphocytes, Melanoma, Experimental, Integrin alphaXbeta2, Cancer Vaccines, Antigens, CD1, Mice, Adjuvants, Immunologic, Tumor Cells, Cultured, Animals, Humans, Melanoma, Mice, Inbred BALB C, Gene Transfer Techniques, Granulocyte-Macrophage Colony-Stimulating Factor, Membrane Proteins, Dendritic Cells, Th1 Cells, Flow Cytometry, Mice, Inbred C57BL, Retroviridae, Female, Antigens, CD1d, Interleukin-5, Spleen
Abstract

Both granulocyte-macrophage colony-stimulating factor (GM-CSF) and flt3-ligand (FL) induce the development of dendritic cells (DCs). To compare the functional properties of DCs stimulated by these cytokines in vivo, we used retroviral-mediated gene transfer to generate murine tumor cells secreting high levels of each molecule. Injection of tumor cells expressing either GM-CSF or FL resulted in the dramatic increase of CD11c+ cells in the spleen and tumor infiltrate. However, vaccination with irradiated, GM-CSF-secreting tumor cells stimulated more potent antitumor immunity than vaccination with irradiated, FL-secreting tumor cells. The superior antitumor immunity elicited by GM-CSF involved a broad T cell cytokine response, in contrast to the limited Thl response elicited by FL. DCs generated by GM-CSF were CD8alpha- and expressed higher levels of B7-1 and CD1d than DCs cells generated by FL. Injection sites of metastatic melanoma patients vaccinated with irradiated, autologous tumor cells engineered to secrete GM-CSF demonstrated similar, dense infiltrates of DCs expressing high levels of B7-1. These findings reveal critical differences in the abilities of GM-CSF and FL to enhance the function of DCs in vivo and have important implications for the crafting of tumor vaccines.

42. A phase I study of vaccination with autologous, irradiated melanoma cells engineered to secrete human granulocyte-macrophage colony stimulating factor

Author

Dranoff, G., Soiffer, R., Lynch, T., Mihm, M., Jung, K., Kolesar, K., Liebster, L., Lam, P., Duda, R., Mentzer, S., Samuel Singer, Tanabe, K., Johnson, R., Sober, A., Bhan, A., Clift, S., Cohen, L., Parry, G., Rokovich, J., Richards, L., Drayer, J., Berns, A., and Mulligan, R. C.

Subjects
Patient Selection, Statistics as Topic, Vaccination, Tumor Cells, Cultured, Granulocyte-Macrophage Colony-Stimulating Factor, Humans, Immunotherapy, Genetic Engineering, Melanoma

44. Protective immunity induced by tumor vaccines requires interaction between CD40 and its ligand, CD154

Author

Mackey, M.F., Gunn, J.R., Ting, P.P., Kikutani, H., Dranoff, G., Noelle, R.J., and Barth, R.J.

Subjects
Physiological aspects, Cancer vaccines -- Physiological aspects
Abstract

Mackey, M.F.; Gunn, J.R.; Ting, P.P.; Kikutani, H.; Dranoff, G.; Noelle, R.J.; Barth, R.J. 'Protective Immunity Induced by Tumor Vaccines Requires Interac- tion Between CD40 and Its Ligand, CD154.' Cancer [...]

Published
1997

45. Bioactivity of autologous irradiated renal cell carcinoma vaccines generated by ex vivo granulocyte-macrophage colony-stimulating factor gene transfer

Author

Simons, J.W., Jaffe, E.M., Weber, C.E., Levitsky, H.I., Nelson, W.G., Carducci, M.A., Lazenby, A.J., Cohen, L.K., Finn, C.C., Clift, S.M., Hauda, K.M., Beck, L.A., Leiferman, K.M., Owens, A.H., Piantadosi, S., Dranoff, G., and Mulligan, R.C.

Subjects
Care and treatment, Research, Health aspects, Cancer vaccines -- Research -- Health aspects, Granulocyte-macrophage colony stimulating factor -- Health aspects -- Research, Renal cell carcinoma -- Care and treatment -- Research -- Health aspects, Carcinoma, Renal cell -- Care and treatment -- Research -- Health aspects
Abstract

Simons, J.W.; Jaffee, E.M.; Weber, C.E.; Levitsky, H.I.; Nelson, W.G.; Carducci, M.A.; Lazenby, A.J.; Cohen, L.K.; Finn, C.C.; Clift, S.M.; Hauda, K.M.; Beck, L.A.; Leiferman, K.M.; Owens, A.H.; Piantadosi, S.; [...]

Published
1997

46. GM-CSF tumor cell vaccines are more effective than B7-1 vaccines in murine acute myeloid leukemia (AML)

Author

Dunussi-Joannopoulos, K., Dranoff, G., Weinstein, H.J., Burakoff, S.J., Ferrara, J.L.M., Bierer, B., and Croop, J.M.

Subjects
Physiological aspects, Research, Health aspects, Vaccines -- Research -- Health aspects -- Physiological aspects, Granulocyte-macrophage colony stimulating factor -- Health aspects -- Research -- Physiological aspects, Acute myelocytic leukemia -- Physiological aspects -- Research -- Health aspects
Abstract

GM-CSF Tumor Cell Vaccines are More Effective than B7-1 Vaccines in Murine Acute Myeloid Leukemia (AML).' K. Dunussi-Joannopoulos, G. Dranoff, H.J. Weinstein, S.J. Burakoff, J.L.M. Ferrara, B. Bierer and J.M. [...]

Published
1997

47. Subcutaneous vaccination with irradiated, cytokine-producing tumor cells stimulates CD8+ cell-mediated immunity against tumors located in the 'immunologically privileged' central nervous system

Author

Sampson, J.H., Archer, G.E., Ashley, D.M., Fuchs, H.E., Hale, L.P., Dranoff, G., and Bigner, D.D.

Subjects
Care and treatment, Research, Health aspects, Nervous system tumors -- Care and treatment -- Research, Cytokines -- Health aspects -- Research, Vaccination -- Research -- Health aspects
Abstract

Cancer Vaccines Sampson, J.H.; Archer, G.E.; Ashley, D.M.; Fuchs, H.E.; Hale, L.P.; Dranoff, G.; Bigner, D.D. 'Subcutaneous Vaccination with Irradiated, Cytokine-Producing Tumor Cells Stimulates CD8(+) Cell-Mediated Immunity Against Tumors Located [...]

Published
1996

48. Demonstration of a rational strategy for human prostate cancer gene therapy

Author

Sanda, M.G., Ayyagari, S.R., Jaffee, E.M., Epstein, J.I., Clift, S.L., Cohen, L.K., Dranoff, G., Pardoll, D.M., Mulligan, R.C., and Simons, J.W.

Subjects
Testing, Care and treatment, Gene therapy -- Testing, Prostate cancer -- Care and treatment
Abstract

SOURCE: Journal of Urology, March 1994;151(3):622-628. According to the authors' abstract of an article published in the Journal of Urology, 'The potential efficacy and clinical feasibility of gene therapy for [...]

Published
1994

49. Granulocyte-macrophage colony stimulating factor based melanoma vaccines

Author

Soiffer, R., Lynch, T., Mihm, M., Jung, K., Kolesar, K., Liebster, L., Lam, P., Duda, R., Mentzer, S., Singer, S., Tanabe, K., Johnson, R., Sober, A., Bhan, A., Clift, S., Cohen, L., Parry, G., Rokovich, J., Richards, L., Drayer, J., Berns, A., Mulligan, R.C., and Dranoff, G.

Subjects
Physiological aspects, Research, Health aspects, Vaccines -- Research -- Health aspects -- Physiological aspects, Granulocyte-macrophage colony stimulating factor -- Health aspects -- Research -- Physiological aspects, Melanoma -- Physiological aspects -- Research -- Health aspects
Abstract

According to an abstract submitted by the authors at the annual meeting for the Association of American Physicians, American Society for Clinical Investigation, and American Federation for Clinical Research, entitled [...]

Published
1996

50. Gene therapy of metastatic cancer by in vivo retroviral gene targeting

Author

Hurford, R.K., Dranoff, G., Mulligan, R.C., and Tepper, R.I.

Subjects
Care and treatment, Methods, Gene therapy -- Methods, Cancer metastasis -- Care and treatment, Metastasis -- Care and treatment
Abstract

According to the authors' abstract of an article published in Nature Genetics, 'We have achieved efficient transduction of tumour metastases in vivo by the vascular delivery of retroviral producer cells. [...]

Published
1995

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