Xiao, W. (Weihua)

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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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    Overexpression of adrenomedullin gene markedly inhibits proliferation of PC3 prostate cancer cells in vitro and in vivo
    (Elsevier, 2003) Pio, R. (Rubén); Yang, L. (Luping); Wang, Z. (Zhou); Abasolo, I. (Ibane); Xiao, W. (Weihua); Montuenga-Badia, L.M. (Luis M.); Kozlowski, J.M. (James M.); Cuttitta, F. (Frank); Calvo-González, A. (Alfonso); Haleem, R. (R.)
    The expression of the gene encoding adrenomedullin (AM), a multifunctional peptide hormone, in the prostate is localized to the epithelial cells. Prostate cancer cells are derived from prostatic epithelial cells. To elucidate the potential role of the AM gene in prostate cancer progression, we have stably-transfected the PC3 human prostate cancer cell line with an AM gene expression vector. The AM-transfected PC3 sublines were studied along with parental and empty vector transfected PC3 cells as controls. The average level of AM in the conditioned media of AM-transfected cells was 0.959+/-0.113 nM, a physiologically relevant concentration. The ectopic expression of AM gene inhibited the proliferation of PC3 cells in culture dishes. In addition, anchorage-independent growth of the transfected sublines was virtually abolished in soft agar assays. Flow cytometry studies showed that overexpression of AM gene caused a very significant G(1)/G(0) cell cycle arrest. In vivo experiments demonstrated that AM gene expression markedly inhibited the growth of xenograft tumors in nude mice. Our in vivo and in vitro studies suggest that AM could strongly suppress the malignancy of prostate cancer cells, via autocrine and/or paracrine mechanisms.