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Gary R. Hudes, Michael A. Carducci, Toni K. Choueiri, Peg Esper, Eric Jonasch, Rashmi Kumar, Kim A. Margolin, M. Dror Michaelson, Robert J. Motzer, Roberto Pili, Susan Roethke, and Sandy Srinivas

-pathway targeting agents (temsirolimus and everolimus). Immunotherapeutic agents (interleukin-2 and interferon-α) are playing a much smaller role, and cytotoxic agents (e.g., gemcitabine and doxorubicin) are used on rare occasions. VHL mutation, HIF upregulation

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Robert J. Motzer, Neeraj Agarwal, Clair Beard, Sam Bhayani, Graeme B. Bolger, Michael A. Carducci, Sam S. Chang, Toni K. Choueiri, Steven L. Hancock, Gary R. Hudes, Eric Jonasch, David Josephson, Timothy M. Kuzel, Ellis G. Levine, Daniel W. Lin, Kim A. Margolin, M. Dror Michaelson, Thomas Olencki, Roberto Pili, Thomas W. Ratliff, Bruce G. Redman, Cary N. Robertson, Charles J. Ryan, Joel Sheinfeld, Philippe E. Spiess, Jue Wang, and Richard B. Wilder

, temsirolimus, everolimus, and bevacizumab in combination with interferon. Tumor histology and risk stratification of patients is important in targeted therapy selection. The most widely used model for risk stratification is the MSKCC model, 46 which

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Toni K. Choueiri

limits the utility of this combination), and temsirolimus for poor-prognosis patients (category 2B for other risk groups). Sorafenib is acceptable for selected patients but is not a preferred agent. High-dose interleukin-2 is also acceptable in some cases

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Robert J. Motzer, Eric Jonasch, Neeraj Agarwal, Sam Bhayani, William P. Bro, Sam S. Chang, Toni K. Choueiri, Brian A. Costello, Ithaar H. Derweesh, Mayer Fishman, Thomas H. Gallagher, John L. Gore, Steven L. Hancock, Michael R. Harrison, Won Kim, Christos Kyriakopoulos, Chad LaGrange, Elaine T. Lam, Clayton Lau, M. Dror Michaelson, Thomas Olencki, Phillip M. Pierorazio, Elizabeth R. Plimack, Bruce G. Redman, Brian Shuch, Brad Somer, Guru Sonpavde, Jeffrey Sosman, Mary Dwyer, and Rashmi Kumar

-line treatments. To date, 7 such agents have been approved by the FDA for the treatment of advanced RCC: sunitinib, sorafenib, pazopanib, axitinib, temsirolimus, everolimus, and bevacizumab in combination with interferon. Tumor histology and risk stratification

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Robert J. Motzer, Eric Jonasch, Neeraj Agarwal, Ajjai Alva, Michael Baine, Kathryn Beckermann, Maria I. Carlo, Toni K. Choueiri, Brian A. Costello, Ithaar H. Derweesh, Arpita Desai, Yasser Ged, Saby George, John L. Gore, Naomi Haas, Steven L. Hancock, Payal Kapur, Christos Kyriakopoulos, Elaine T. Lam, Primo N. Lara, Clayton Lau, Bryan Lewis, David C. Madoff, Brandon Manley, M. Dror Michaelson, Amir Mortazavi, Lakshminarayanan Nandagopal, Elizabeth R. Plimack, Lee Ponsky, Sundhar Ramalingam, Brian Shuch, Zachary L. Smith, Jeffrey Sosman, Mary A. Dwyer, Lisa A. Gurski, and Angela Motter

for poor-/intermediate-risk patients). Temsirolimus (Poor-/Intermediate-Risk Groups) Temsirolimus is an inhibitor of the mTOR protein. The randomized, open-label phase III ARCC study enrolled previously untreated patients with advanced RCC who

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Eric Jonasch and Robert J. Motzer

-risk features has also advanced in the past 10 years. A randomized phase III study comparing the mTOR inhibitor temsirolimus versus IFN showed a significant prolongation of OS in patients who received upfront temsirolimus. 3 Although this improvement is modest

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Noa Efrat Ben-Baruch, Ron Bose, Shyam M. Kavuri, Cynthia X. Ma, and Matthew J. Ellis

targeted therapy drugs, such as trastuzumab and temsirolimus. 11 , 12 A phase I trial of a 3-drug, neratinib-containing regimen (neratinib, trastuzumab, and paclitaxel) for HER2 -positive breast cancer showed good patient tolerability. 13 The main

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Saurabh Rajguru and Brad S. Kahl

regulated by the mTOR kinase, which is a key component of the PI3K/Akt intracellular pathway. On this basis, the mTOR inhibitor temsirolimus was evaluated in R/R MCL. In a phase III study, 162 heavily pretreated patients underwent a 1:1:1 randomization to

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James Brugarolas

approved drugs, lenvatinib and cabozantinib) and inhibitors of mTOR complex 1 (mTORC1), specifically the sirolimus analogues temsirolimus and everolimus. Response rates (almost always partial) to targeted therapies in the first or second line range between

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Metastatic Breast Cancer, Version 1.2012

Featured Updates to the NCCN Guidelines

Robert W. Carlson, D. Craig Allred, Benjamin O. Anderson, Harold J. Burstein, Stephen B. Edge, William B. Farrar, Andres Forero, Sharon Hermes Giordano, Lori J. Goldstein, William J. Gradishar, Daniel F. Hayes, Clifford A. Hudis, Steven Jay Isakoff, Britt-Marie E. Ljung, David A. Mankoff, P. Kelly Marcom, Ingrid A. Mayer, Beryl McCormick, Lori J. Pierce, Elizabeth C. Reed, Mary Lou Smith, Hatem Soliman, George Somlo, Richard L. Theriault, John H. Ward, Antonio C. Wolff, Richard Zellars, Rashmi Kumar, and Dorothy A. Shead

temsirolimus. 18 In this study, progression-free survival was not different between the treatment arms (hazard rate, 0.89; 95% CI, 0.75–1.05; long-rank P = .18). The reasons for the difference in the outcomes of the 2 endocrine therapy with or without an