Combining cancer immunotherapy and targeted therapy

被引:57
作者
Ribas, Antoni [1 ,2 ,3 ,4 ]
Wolchok, Jedd D. [5 ,6 ,7 ]
机构
[1] Univ Calif Los Angeles, Dept Med, Div Hematol Oncol, Los Angeles, CA 90024 USA
[2] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA
[3] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA
[4] Univ Calif Los Angeles, Dept Med & Mol Pharmacol, Los Angeles, CA USA
[5] Weill Cornell Med Coll, Dept Med, Mem Sloan Kettering Canc Ctr, New York, NY USA
[6] Weill Cornell Med Coll, Ludwig Ctr Canc Immunotherapy, Mem Sloan Kettering Canc Ctr, Program Immunol, New York, NY USA
[7] Ludwig Inst Canc Res, New York, NY USA
关键词
HISTONE DEACETYLASE INHIBITORS; MHC CLASS-I; T-CELL RESPONSES; SUBERIC BISHYDROXAMATE; ANTITUMOR-ACTIVITY; KINASE INHIBITOR; RAS MUTATIONS; TUMOR; BRAF; MELANOMA;
D O I
10.1016/j.coi.2013.02.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The ability to pharmacologically modulate key signaling pathways that drive tumor growth and progression, but do not negatively impact the function of lymphocytes, provides avenues for rational combinatorial approaches to improve the antitumor activity of tumor immunotherapies. Novel targeted agents can very specifically block oncogenic events in cancer cells, leading to a pro-apoptotic milieu and a potential increase in sensitivity to recognition and attack by cytotoxic T lymphocytes (CTLs). Furthermore, targeted pathway modulation in lymphocytes may change their function and have activating effects in some instances. When tested together with recently developed powerful tumor immunotherapies, such combinations may exploit the highly specific targeting of oncogenes with small molecule inhibitors to lead to high frequency of tumor regressions, and merge this benefit with the durable responses achievable with effective tumor immunotherapies.
引用
收藏
页码:291 / 296
页数:6
相关论文
共 53 条
[1]   mTOR regulates memory CD8 T-cell differentiation [J].
Araki, Koichi ;
Turner, Alexandra P. ;
Shaffer, Virginia Oliva ;
Gangappa, Shivaprakash ;
Keller, Susanne A. ;
Bachmann, Martin F. ;
Larsen, Christian P. ;
Ahmed, Rafi .
NATURE, 2009, 460 (7251) :108-U124
[2]   Natural killer cell-mediated lysis of hepatoma cells via specific induction of NKG2D Ligands by the histone deacetylase inhibitor sodium valproate [J].
Armeanu, S ;
Bitzer, M ;
Lauer, UM ;
Venturelli, S ;
Pathil, A ;
Krusch, M ;
Kaiser, S ;
Jobst, K ;
Smirnow, I ;
Wagner, A ;
Steinle, A ;
Salih, HR .
CANCER RESEARCH, 2005, 65 (14) :6321-6329
[3]   Imatinib potentiates antitumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido [J].
Balachandran, Vinod P. ;
Cavnar, Michael J. ;
Zeng, Shan ;
Bamboat, Zubin M. ;
Ocuin, Lee M. ;
Obaid, Hebroon ;
Sorenson, Eric C. ;
Popow, Rachel ;
Ariyan, Charlotte ;
Rossi, Ferdinand ;
Besmer, Peter ;
Guo, Tianhua ;
Antonescu, Cristina R. ;
Taguchi, Takahiro ;
Yuan, Jianda ;
Wolchok, Jedd D. ;
Allison, James P. ;
DeMatteo, Ronald P. .
NATURE MEDICINE, 2011, 17 (09) :1094-U99
[4]   Targeted therapies to improve tumor immunotherapy [J].
Begley, Jonathan ;
Ribas, Antoni .
CLINICAL CANCER RESEARCH, 2008, 14 (14) :4385-4391
[5]   Selective BRAFV600E Inhibition Enhances T-Cell Recognition of Melanoma without Affecting Lymphocyte Function [J].
Boni, Andrea ;
Cogdill, Alexandria P. ;
Dang, Ping ;
Udayakumar, Durga ;
Njauw, Ching-Ni Jenny ;
Sloss, Callum M. ;
Ferrone, Cristina R. ;
Flaherty, Keith T. ;
Lawrence, Donald P. ;
Fisher, David E. ;
Tsao, Hensin ;
Wargo, Jennifer A. .
CANCER RESEARCH, 2010, 70 (13) :5213-5219
[6]   Novel mode of action of c-kit tyrosine kinase inhibitors leading to NK cell-dependent antitumor effects [J].
Borg, C ;
Terme, M ;
Taïeb, J ;
Ménard, C ;
Flament, C ;
Robert, C ;
Maruyama, K ;
Wakasugi, H ;
Angevin, E ;
Thielemans, K ;
Le Cesne, A ;
Chung-Scott, V ;
Lazar, V ;
Tchou, I ;
Crépineau, F ;
Lemoine, F ;
Bernard, J ;
Fletcher, JA ;
Turhan, A ;
Blay, JY ;
Spatz, A ;
Emile, JF ;
Heinrich, MC ;
Mécheri, S ;
Tursz, T ;
Zitvogel, L .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (03) :379-388
[7]   Histone deacetylase activities are required for innate immune cell control of Th1 but not Th2 effector cell function [J].
Brogdon, Jennifer L. ;
Xu, Yongyao ;
Szabo, Susanne J. ;
An, Shaojian ;
Buxton, Francis ;
Cohen, Dalia ;
Huang, Qian .
BLOOD, 2007, 109 (03) :1123-1130
[8]   Progression of RAS-Mutant Leukemia during RAF Inhibitor Treatment [J].
Callahan, Margaret K. ;
Rampal, Raajit ;
Harding, James J. ;
Klimek, Virginia M. ;
Chung, Young Rock ;
Merghoub, Taha ;
Wolchok, Jedd D. ;
Solit, David B. ;
Rosen, Neal ;
Abdel-Wahab, Omar ;
Levine, Ross L. ;
Chapman, Paul B. .
NEW ENGLAND JOURNAL OF MEDICINE, 2012, 367 (24) :2316-2321
[9]   Eradication of solid tumors using histone deacetylase inhibitors combined with immune-stimulating antibodies [J].
Christiansen, Ailsa J. ;
West, Alison ;
Banks, Kellie-Marie ;
Haynes, Nicole M. ;
Teng, Michele W. ;
Smyth, Mark J. ;
Johnstone, Ricky W. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2011, 108 (10) :4141-4146
[10]   The Oncogenic BRAF Kinase Inhibitor PLX4032/RG7204 Does Not Affect the Viability or Function of Human Lymphocytes across a Wide Range of Concentrations [J].
Comin-Anduix, Begona ;
Chodon, Thinle ;
Sazegar, Hooman ;
Matsunaga, Douglas ;
Mock, Stephen ;
Jalil, Jason ;
Escuin-Ordinas, Helena ;
Chmielowski, Bartosz ;
Koya, Richard C. ;
Ribas, Antoni .
CLINICAL CANCER RESEARCH, 2010, 16 (24) :6040-6048