Hodi, F.S. (F. Stephen)

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    Defining the Critical Hurdles in Cancer Immunotherapy
    (Biomed Central, 2011) Kotlan, B. (Beatrix); Ottensmeier, C. (Christian); Zwierzina, H. (Heinz); Butterfield, L.H. (Lisa H.); Nelief, C. (Cornelious); Gajewski, T.F. (Thomas F.); Borden, E. (Ernest); Bonorino, C. C. (Cristina C.); Song, W. (Wenru); Hoos, A. (Axel); Grizzi, F. (Fabio); Characiejus, D. (Dainius); Galon, J. (Jerome); Kaufman, H.L. (Howard L.); Coukos, G. (George); Kawakami, K. (Koji); Dillman, R.O. (Robert O.); Ribas, A. (Antoni); Herberman, R.B. (Ronald B.); Kalinski, P. (Pawel); Durrant, L.G. (Lindy G.); Hwu, P. (Patrick); Aamdal, S. (Steinar); Straten, P.T. (Per Thor); Wang, E. (Ena); Finke, J.H. (James H.); Romero, P.J. (Pedro J.); Withington, T. (Tara); Schendel, D. J. (Dolores J.); Scheper, R.J. (Rik J.); Disis, M.L. (Mary L.); Old, LL.J. (LLoyd J.); Allison, J.P. (James P.); Singh-Jasuja, H. (Harpreet); Kroemer, G. (Guido); Guida, M. (Michele); Dranoff, G. (Glenn); Kawakami, Y. (Yutaka); Hodi, F.S. (F. Stephen); Jaffee, E.M. (Elizabeth M.); Maio, M. (Michele); Maccalli, C. (Cristina); Salem, M.L. (Mohamed L.); Van-Der-Burg, S.H. (Sjoerd H.); Gollob, J.A. (Jared A.); Khleif, S.N. (Samir N.); Bergmann, L. (Lothar); Wigginton, J.M. (Jon M.); Xiao, W. (Weihua); Qin, S. (Shukui); Bartunkova, J. (Jirina); Britten, C.M. (Cedrik M.); Nelson, B. (Brad); Berinstein, N. (Neil); Rivoltini, L. (Licia); Proietti, E. (Enrico); Melero, I. (Ignacio); Mastrangelo, M.J. (Michael J.); Kiessling, R. (Rolf); Chang, A.E. (Alfred E.); Keilholtz, U. (Ulrich); Parmiani, G. (Giorgio); Janetzki, S. (Sylvia); Zitvogel, L. (Laurence); Seliger, B. (Barbara); Rees, R. (Robert); O'Donnell-Tormey, J. (Jill); Levitsky, H.I. (Hyam I.); Hakansson, L. (Leif); Nishimura, M.I. (Michael I.); Marschner, J-P. (Jens-Peter); Wolchok, J.D. (Jedd D.); Ohashi, P.S. (Pamela S.); Sharma, P. (Padmanee); Imai, K. (Kohzoh); Winter, H. (Hauke); Ritter, G. (Gerd); Odunsi, K. (Kunle); Fox, B.A. (Bernard A.); Von Hoegen, P. (Paul); Gruijl, T. (Tanja); Nicolini, A. (Andrea); Welters, M. J. (Maris J.); Hege, K. (Kristen); Lotze, M.T. (Michael T.); Murphy, W.J. (William J.); Atkins, M.B. (Michael B.); Dolstra, H. (Harry); Lapointe, R. (Rejean); Masucci, G. (Giuseppe); Cao, X. (Xuetao); Tian, Z. (Zigang); Ascierto, P.A. (Paolo Antonio); Huber, C. (Christoph); Tahara, H. (Hideaki); Pawelec, G. (Graham); June, C.H. (Carl H.); Carson, W.E. (William E.); Papamichail, M. (Michael); Choudhury, A.R. (A. Raja); Marincola, F.M. (Francesco M.); Shiku, H. (Hiroshi); Bramson, J.L. (Jonathan L.); Ridolfi, R. (Ruggero); Gouttefangeas, C. (Cecile)
    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 be overcome to improve outcomes of patients with cancer.
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    Conserved interferon-g signaling drives clinical response to immune checkpoint blockade therapy in melanoma
    (Elsevier, 2020) Vega-Crespo, A. (Agustin); Kalbasi, A. (Anusha); Onyshchenko, M. (Mykola); Grasso, C.S. (Catherine S.); Speiser, D.E. (Daniel E.); Wind-Rotolo, M. (Megan); Ribas, A. (Antoni); Ross-Macdonald, P. (Petra); Diab, A. (Adi); Martin-Algarra, S. (Salvador); Sanghoon-Shin, D. (Daniel); Urba, W.J. (Walter J.); Campbell, K. (Katie); Champhekar, A. (Ameya); Medina, E. (Egmidio); Hodi, F.S. (F. Stephen); Johnson, D.B. (Douglas B.); Anagnostou, V. (Valsamo); Luke, J.J. (Jason J.); Tsoi, J. (Jennifer); Haanen, J. (J.); Tran, P. (Phuong); Velculescu, V.E. (Victor E.); Bhatia, S. (Shailender); Wolchok, J.D. (Jedd D.); Abril-Rodriguez, G. (Gabriel); Topalian, S.L. (Suzanne L.); Chmielowski, B. (Bartosz); Puig-Saus, C. (Cristina); Torrejon, D.Y. (Davis Y.); Joo-Kim, Y. (Yeon); Quist, M. (Michael); Martignier, C. (Christophe); Sharfman, W. (William); Slingluff, C.L. (Craig L.); Pardoll, D.M. (Drew M.)
    We analyze the transcriptome of baseline and on-therapy tumor biopsies from 101 patients with advanced melanoma treated with nivolumab (anti-PD-1) alone or combined with ipilimumab (anti-CTLA-4). We find that T cell infiltration and interferon-γ (IFN-γ) signaling signatures correspond most highly with clinical response to therapy, with a reciprocal decrease in cell-cycle and WNT signaling pathways in responding biopsies. We model the interaction in 58 human cell lines, where IFN-γ in vitro exposure leads to a conserved transcriptome response unless cells have IFN-γ receptor alterations. This conserved IFN-γ transcriptome response in melanoma cells serves to amplify the antitumor immune response. Therefore, the magnitude of the antitumor T cell response and the corresponding downstream IFN-γ signaling are the main drivers of clinical response or resistance to immune checkpoint blockade therapy.