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2. 860 Targeting immunosuppressive macrophages overcomes PARP-inhibitor resistance in BRCA1-associated triple-negative breast cancer

Author

Elizabeth Mittendorf, Jennifer Guerriero, Peter Sorger, Nadine Tung, Anita Mehta, Emily Cheney, Christina Hartl, Constantia Pantelidou, Madison Oliwa, Jessica Castrillon, Jia-Ren Lin, Mateus de Oliveira Taveira, Nathan Johnson, William Oldham, Marian Kalocsay, Matthew Berberich, Sarah Boswell, Aditi Kothari, Shawn Johnson, Deborah Dillon, Mikel Lipschitz, Scott Rodig, Sandro Santagata, Judy Garber, José Yélamos, and Geoffrey Shapiro

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Published
2020
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3. Abstract P1-04-05: Independent validation of the HER2DX genomic test in HER2-positive breast cancer treated with neoadjuvant paclitaxel, trastuzumab and pertuzumab (THP): a correlative analysis from the DAPHNe phase II clinical trial

Author

Adrienne Waks, Esther R. Ogayo, Laia Paré, Mercedes Marín-Aguilera, Fara Brasó-Maristany, Patricia Galván, Oleguer Castillo, Olga Martínez-Sáez, Ana Vivancos, Patricia Villagrasa, Paolo Tarantino, Neelam Desai, Jennifer Guerriero, Otto Metzger, Nadine Tung, Ian Krop, Joel S Parker, Charles M. Perou, Aleix Prat, Eric Winer, Sara Tolaney, and Elizabeth A. Mittendorf

Subjects
Cancer Research, Oncology
Abstract

Background: HER2DX is a 27-gene prognostic (risk-score) and predictive (pathological complete response [pCR]-score) assay in early-stage HER2+ breast cancer (BC) based on clinical data and the expression of 4 gene signatures (immune, proliferation, luminal differentiation, and HER2 amplicon). Here we aim to evaluate, for the first time, the ability of HER2DX to predict pCR following neoadjuvant THP in HER2+ BC. Methods: Standardized HER2DX was evaluated centrally on baseline pre-treatment FFPE tumor biopsies from the DAPHNe phase II trial (Waks et al. NPJ Breast 2022; NCT03716180), in which patients (pts) with newly diagnosed stage II-III HER2+ BC were treated with neoadjuvant weekly paclitaxel × 12 and HP every 3 weeks × 4. Primary aim was to test the ability of HER2DX pCR-score to predict pCR (ypT0/isN0). Secondary objectives were to test the ability of HER2DX pCR-score to predict pCR independent of clinical-pathological variables and PAM50 subtype (HER2-enriched vs not) and to evaluate the association of HER2DX pCR-score with HER2DX risk-score. Five patients who received additional neoadjuvant chemotherapy after THP were excluded from this analysis. Logistic regression and receiver-operator curve (ROC) analysis were assessed. Statistical analyses were performed in R code 4.0.5. Results: HER2DX was evaluated in 80 of 97 pts (82.5%) enrolled in the DAPHNe trial who received study treatment. Clinical T2-4 disease represented 81.3% of cases (n=65), clinical node-negative disease (cN0) represented 65.0% of cases (n=52), and 70.0% of tumors (n=56) were hormone receptor-positive. The overall pCR rate was 60.0% (95% confidence interval [CI] 49.3-70.7): 87.0% (95% CI 79.6-94.4) in hormone receptor-negative disease and 48.2% (95% CI 37.2-59.1) in hormone receptor-positive disease. The proportion of HER2DX low-, medium- and high-pCR groups was 38.8%, 27.5% and 33.7%, respectively. HER2DX pCR-score (as a continuous variable from 0 to 100) was significantly associated with pCR (odds ratio [OR]=1.05, p< 0.0001). In the overall population, the pCR rates in HER2DX pCR-high, pCR-med and pCR-low groups were 92.6%, 63.6% and 29.0% (pCR-high vs pCR-low OR=30.6, p< 0.0001), respectively. The AUC ROC of HER2DX pCR score (as a continuous variable) and pCR status was 0.835. In the ER-negative population, the pCR rates in HER2DX pCR-high, pCR-med and pCR-low groups were 94.7%, 66.7%, and 0%, respectively (Table 1). HER2DX pCR-score was significantly associated with pCR independent of hormone receptor status, HER2 immunohistochemistry (IHC) score, clinical stage, and PAM50 HER2-enriched subtype. The correlation between HER2DX pCR-score and HER2DX risk-score was weak (Pearson coefficient=-0.12), as previously described (Prat et al. EBiomedicine 2022). 51.3% of patients were categorized as HER2DX low-risk. Conclusion: The 27-gene HER2DX genomic test predicts pCR following neoadjuvant THP in newly diagnosed stage II-III HER2+ BC. Patients with HER2DX pCR-low score and HER2DX high-risk score, representing 22.5% of pts, warrant further attention in order to optimize therapeutic strategies in this subset. The combination of HER2DX pCR-score and risk-score might guide therapeutic decisions by identifying patients who are ideal candidates for de-escalated or escalated systemic and locoregional treatments. Table 1 Citation Format: Adrienne Waks, Esther R. Ogayo, Laia Paré, Mercedes Marín-Aguilera, Fara Brasó-Maristany, Patricia Galván, Oleguer Castillo, Olga Martínez-Sáez, Ana Vivancos, Patricia Villagrasa, Paolo Tarantino, Neelam Desai, Jennifer Guerriero, Otto Metzger, Nadine Tung, Ian Krop, Joel S Parker, Charles M. Perou, Aleix Prat, Eric Winer, Sara Tolaney, Elizabeth A. Mittendorf. Independent validation of the HER2DX genomic test in HER2-positive breast cancer treated with neoadjuvant paclitaxel, trastuzumab and pertuzumab (THP): a correlative analysis from the DAPHNe phase II clinical trial [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P1-04-05.

Published
2023

4. Abstract P1-04-13: Generation and validation of an estrogen receptor signaling (ERS) gene panel that inversely correlates with antigen presentation and T cell infiltration and activity in hormone receptor positive (HR+) breast cancer

Author

Jonathan S Goldberg, Xiaoyong Cui, Kenichi Shimada, Sandra McAllister, Sara Tolaney, Adrienne Waks, Rinath Jeselsohn, Jennifer Guerriero, Judith Agudo, and Elizabeth Mittendorf

Subjects
Cancer Research, Oncology
Abstract

Background: Tumor infiltrating lymphocytes (TILs) are observed in low numbers in HR+ breast cancer relative to other subtypes. For T cells (TC) to recognize and respond to a tumor, antigens must be presented on the tumor cell surface via human leukocyte antigen class one (HLA-I) molecules. Hence, the lack of immune infiltration into HR+ tumors could be explained by limited antigen or impaired antigen presentation. We hypothesized that ERS inversely correlates with antigen presentation and T cell infiltration in HR+ tumors. The objective of this study was to comprehensively examine the relationship between ERS, antigen presentation machinery (APM) and TC gene expression in HR+ breast cancer.Methods: Comprehensive gene panels for ERS, APM and TC expression were generated from literature review, GO terms, KEGG pathways, REACTOME, and computationally and manually curated gene lists. Genes expressed in both The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) were used for subsequent analyses. Tumors were classified into 4 major subtypes (HR+/HER2-, HR+/HER2+, HR-/HER2+, HR-/HER2-) based on estrogen receptor (ER), progesterone receptor and HER2 expression as defined by immunohistochemistry. To statistically refine each gene panel, the genes were hierarchically clustered based on their pairwise Spearman correlation coefficients among HR+/HER2- samples in TCGA (n = 441) and METABRIC (n = 1028). Specifically, clusters were identified by linkage with 2 hallmark genes for each panel: ESR1 and FOXA1 for the ERS panel, HLA-A and NLRC5 for the APM panel, and CD8A and CD8B for the TC panel. Due to overlapping genes in the APM and TC panels, these two panels were combined for subsequent analyses. Final gene panels for ERS and APM/TC were generated from overlapping genes identified in corresponding TCGA and METABRIC clusters. Internal validity of the final gene panels was assessed through pathway enrichment analysis. The panels were then validated through correlation analysis in an independent single institution cohort (HR+ = 25, HER2+ [regardless of HR] = 25, TNBC = 23). Finally, intra and inter-panel correlation analysis results were compared between breast cancer subtypes in both TCGA and METABRIC datasets. Results: Among the 988 genes identified in our manually curated panels, 788 genes were recognized in both TCGA and METABRIC datasets. Statistical refinement resulted in a final 28-gene ERS panel and a final 135-gene combined APM/TC panel. Early and late-estrogen response pathways were enriched in the ERS panel, whereas interferon-gamma response and other innate and acquired immune-related pathways were enriched in the APM/TC panel. Strong inverse correlations between ERS and APM/TC panels were identified in both TCGA and METABRIC datasets. These findings were validated in the single institution cohort where we noted the strength of the correlations varied with the subtype of disease and extent of HR expression. Further analyses in all 4 breast cancer subtypes, in both TCGA and METABRIC datasets, revealed consistent positive correlations within the APM/TC panel across all subtypes. However, positive correlations within the ERS panel corresponded to the subtypes’ dependency on ER pathway, with a strong correlation in HR+ breast cancer and limited correlation in HR- tumors. Conclusions: Using an unbiased data-driven approach, ERS and APM/TC gene panels were generated. Among HR+ tumors, high levels of ERS gene expression significantly correlated with lower levels of APM/TC gene expression providing one potential mechanism for low TC infiltration in HR+ breast cancer. The prognostic and predictive values of these panels are currently being investigated. Citation Format: Jonathan S Goldberg, Xiaoyong Cui, Kenichi Shimada, Sandra McAllister, Sara Tolaney, Adrienne Waks, Rinath Jeselsohn, Jennifer Guerriero, Judith Agudo, Elizabeth Mittendorf. Generation and validation of an estrogen receptor signaling (ERS) gene panel that inversely correlates with antigen presentation and T cell infiltration and activity in hormone receptor positive (HR+) breast cancer [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P1-04-13.

Published
2022

5. Abstract P5-13-15: High dimensional flow cytometric analysis or the peripheral immune profile and response to HER2-targeted antibody therapy

Author

Esther R Ogayo, Adrienne Waks, Wade Rogers, Matei Ionita, Kenechukwu Adigwe, Jillian Alberti, Sapana Kadel, Jonni Moore, Tari King, Ian Krop, Sara Tolaney, Eric Winer, Jennifer Guerriero, and Elizabeth Mittendorf

Subjects
Cancer Research, Oncology
Abstract

Background: DAPHNe was a prospective trial designed to assess adherence to de-escalated antibody doublet therapy in the adjuvant setting among HER2+ breast cancer patients experiencing a pathologic complete response (pCR) following neoadjuvant taxol (T), trastuzumab (H) and pertuzumab (P). Peripheral blood mononuclear cells (PBMC), were collected from all patients at baseline and after THP completion. The goal of this study was to determine if a patient’s peripheral blood immune profile at baseline, or the longitudinal change with treatment, could predict response to THP. Methods: Blood samples were subjected to high dimensional (28-30 parameter) flow cytometry with comprehensive T- and NK-cell panels. A fully automated computational analysis strategy was undertaken consisting of unsupervised clustering of the high dimensional data into groups of cells with similar immunophenotypic signatures. Clustering was performed using 2 algorithms: Fingerprint-based clustering (Fluster) and High Throughput Mapper (HiTMapper). Clusters were tested using the Wilcoxon rank-sum test for correlation with the clinical response. Responders were those with pCR (=residual cancer burden [RCB] 0) or RCB 1; non-responders were those with RCB 2/3 disease. P values were adjusted with the Benjamini-Hochberg method to control for FDR. In addition to P values, effect size was evaluated using the nonparametric Cliff’s Delta measure. An effect was determined to be large if the magnitude of Delta was >0.4 which corresponded to one cohort coming ahead 70% of the time. In addition, groups of clusters were evaluated using multivariate statistical modeling or dimensionality reduction to determine if there was an association with pCR. Results: Matched baseline and pre-op PBMC were available to perform the NK panel in 66 patients and the T cell panel in 40. In both groups 70% were responders and 30% were non-responders. No cluster produced by Fluster or HiTMapper differed significantly between responders and non-responders however, in the T cell panel, several clusters had a large effect size (table) suggesting the clusters are good at differentiating some, responders from non-responders. Both algorithms agreed that the median responder has more CD4 naïve and CD8 naïve cells than the median non-responder. While no individual cluster differed significantly between responders and non-responders, cross-validated logistic regression analyses showed that 2 clusters, activated CD4 central memory clusters, and activated CD4 naïve clusters, predicted responder status with AUC of 0.70 and 0.68 respectively. Numerous clusters showed robust and significant longitudinal changes between baseline and pre-op samples. Stratifying longitudinal changes by response status revealed no significant differences between responders and non-responders, however evaluation of effect size suggested a naïve CD4 cluster that increased in non-responders and decreased in responders. The latter could be explained as naïve T cells acquiring a memory phenotype in response to treatment in responders. Conclusion: High dimensional flow cytometry suggested a potential role for monitoring several T cell subsets to predict response in HER2+ patients receiving THP. Additional analyses to include cyTOF evaluation of PBMCs are ongoing to further characterize the peripheral immune profile of these HER2+ patients. T cell clusters with high effect sizeMajor PhenotypeOther markersMethodp-valueeffect sizeCD4 CM.actCD38, CD226HiTMapper0.351-0.469CD4 Naive.act.2CD38, CD226HiTMAPPER0.4-0.413CD4 Naive.act.4CD226HiTMapper0.351-0.490CD4 Naive.act.5CD38HiTMapper0.351-0.524CD8 Naive 1CD226HiTMapper0.396-0.427CD3 Neg-Fluster0.3190.476CD3 Neg3CD45RA, CD185, CD197Fluster0.3190.476CD3 Neg4CD45RA, Eomes,tBETFluster0.4240.413CD4 Naive-Fluster0.319-0.517CD8 Naive1-Fluster0.319-0.469Unassigned 20 (CD4)CD45RA, CD27-, CD28-Fluster0.364-0.441 Citation Format: Esther R Ogayo, Adrienne Waks, Wade Rogers, Matei Ionita, Kenechukwu Adigwe, Jillian Alberti, Sapana Kadel, Jonni Moore, Tari King, Ian Krop, Sara Tolaney, Eric Winer, Jennifer Guerriero, Elizabeth Mittendorf. High dimensional flow cytometric analysis or the peripheral immune profile and response to HER2-targeted antibody therapy [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P5-13-15.

Published
2022

6. Abstract F2-3: Immunosuppressive macrophages and PARP inhibitor resistance

Author

Jennifer Guerriero

Subjects
Cancer Research, Oncology
Abstract

Despite objective responses to poly(ADP-ribose) polymerase (PARP) inhibition and improvements in progression-free survival (PFS) compared to standard chemotherapy in patients with BRCA-associated triple-negative breast cancer (TNBC), benefits are transitory. Using high-dimensional single-cell profiling of human TNBC, here we demonstrate that macrophages are the predominant infiltrating immune cell type in breast cancer susceptibility (BRCA)-associated TNBC. Macrophages are an innate immune cell that play a critical role in host defense and maintaining tissue homeostasis, however their infiltration into tumors has been associated with disease progression and resistance to therapy. Tumor associated macrophages (TAMs) represent a significant proportion of solid tumors, including breast cancer. TAMs play a major role in tumorigenesis as they can enhance tumor cell growth, angiogenesis and metastasis. In addition, TAMs can inhibit anti-tumor responses of T cells. Our recent work has shown that removal or conversion of TAMs to an anti-tumor phenotype enhances chemo- and immuno-therapy establishing TAMs as targets for anti-cancer therapy. Through multi-omics profiling, we show that PARP inhibitors enhance both anti- and pro-tumor features of macrophages through glucose and lipid metabolic reprogramming, driven by the sterol regulatory element-binding protein 1 (SREBF1, SREBP1) pathway. Combining PARP inhibitor therapy with colony-stimulating factor 1 receptor (CSF1R)-blocking antibodies significantly enhanced innate and adaptive antitumor immunity and extended survival in mice with BRCA-deficient tumors in vivo, and this was mediated by CD8+ T cells. Collectively, our results uncover macrophage-mediated immune suppression as a liability of PARP inhibitor treatment and demonstrate that combined PARP inhibition and macrophage-targeting therapy induces a durable reprogramming of the tumor microenvironment (TME), thus constituting a promising therapeutic strategy for TNBC. Therefore, targeting TAMs offers great potential to enhance both chemo- and immuno-therapy. Deep analysis of TAMs in solid tumors has revealed the complexity of TAMs and revealed major gaps in our knowledge of the functional and phenotypic characterization of TAM subsets associated with cancer, before and after treatment. Here we will discuss the complexity of TAMs in solid tumors including characterizing TAM subsets, location, and crosstalk with neighboring cells, as well as novel TAM-modulating strategies and combinations that are likely to enhance current therapies and overcome chemo- and immuno-therapy resistance. Citation Format: Jennifer Guerriero. Immunosuppressive macrophages and PARP inhibitor resistance [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr F2-3.

Published
2023

7. A phase II study of biomarker-driven early discontinuation of anti–PD-1 therapy in patients with advanced melanoma (PET-Stop): ECOG-ACRIN EA6192

Author

Geoffrey Thomas Gibney, Sandra J. Lee, Michael B. Atkins, Terence Z. Wong, Jennifer Guerriero, Thomas Urban Marron, Gary Irvin Cohen, Thach-Giao Truong, Richard D. Carvajal, Bradley Snyder, Michael Farwell, John M. Kirkwood, and Jedd D. Wolchok

Subjects
Cancer Research, Oncology
Abstract

TPS9591 Background: In patients (pts) with advanced, metastatic melanoma (aMM) anti-PD-1 monotherapy and anti-PD-1/anti-CTLA-4 combination regimens yield durable responses, yet the optimal therapy duration remains unclear. Most prospective studies have treated responding pts for at least 2 years unless there has been a prohibitive treatment related adverse event (TRAE). Durable treatment-free survival has been observed in pts where anti-PD-1 therapy is discontinued after short courses due to TRAEs. Biomarkers are needed to define which pts may safely discontinue anti-PD-1 therapy in order to reduce financial toxicity and risk of late TRAEs, and to improve quality of life. 18FDG-PET/CT scan and tumor biopsy may better assess for active residual disease and identify pts who can safely discontinue treatment. A retrospective study at G-LCCC demonstrated responding pts with aMM who elected to discontinue their anti-PD-1 therapy (median treatment duration 12 months) after a negative PET/CT scan and/or tumor biopsy had event free survival (EFS) of 95% at 3 years (Gibney et al JITC 2021). We hypothesize that pts with disease control by CT scan after 12 months on anti-PD-1 therapy can be safely discontinued from treatment if no hypermetabolic activity on PET/CT scan or negative biopsy for active disease. Methods: EA6192 is a multicenter phase II study to evaluate the EFS after discontinuation of anti-PD-1-based therapy in aMM pts with PET/CT scan and/or biopsy that is negative for active disease. Pts with unresectable stage IIIB-IV aMM treated with nivolumab/ipilimumab (nivo/ipi), nivo, pembrolizumab (pembro), or pembro/ipi are eligible. Pts with uveal melanoma are excluded. Pts must receive 52 weeks of therapy, have disease control (CR, PR or SD by imRECIST) and no prohibitive TRAEs. Eligible pts undergo screening including 18FDG-PET/CT scan at 52 weeks (+/- 2 weeks) from start of anti-PD-1 therapy. Pts with hypermetabolic tumor site(s) undergo biopsy. Pts with non-hypermetabolic PET/CT scan or negative biopsy are assigned to Arm A and are monitored off active treatment. Pts with hypermetabolic PET/CT scan and positive or non-feasible biopsy are assigned to Arm B and remain on active treatment for another 48 weeks. Restaging scans are performed every 12 weeks. Arm B pts with disease control undergo a second PET/CT scan and biopsy, and then are monitored off active treatment. 150 patients are planned for accrual. The primary objective is to accurately define the 12-month EFS rate of Arm A, distinguishing between the null and alternative hypotheses of 12-month EFS rate of 88% and 95% with 92% power and one-sided type 1 error rate of 0.072. Secondary and exploratory objectives include assessment of pathologic response, EFS for Arm B, overall survival, incidence of late TRAEs, and correlative biomarker studies. This study is actively enrolling pts. Clinical trial information: NCT04462406.

Published
2022

8. 31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016): part two

Author

Casey Ager, Matthew Reilley, Courtney Nicholas, Todd Bartkowiak, Ashvin Jaiswal, Michael Curran, Tina C. Albershardt, Anshika Bajaj, Jacob F. Archer, Rebecca S. Reeves, Lisa Y. Ngo, Peter Berglund, Jan ter Meulen, Caroline Denis, Hormas Ghadially, Thomas Arnoux, Fabien Chanuc, Nicolas Fuseri, Robert W. Wilkinson, Nicolai Wagtmann, Yannis Morel, Pascale Andre, Michael B. Atkins, Matteo S. Carlino, Antoni Ribas, John A. Thompson, Toni K. Choueiri, F. Stephen Hodi, Wen-Jen Hwu, David F. McDermott, Victoria Atkinson, Jonathan S. Cebon, Bernie Fitzharris, Michael B. Jameson, Catriona McNeil, Andrew G. Hill, Eric Mangin, Malidi Ahamadi, Marianne van Vugt, Mariëlle van Zutphen, Nageatte Ibrahim, Georgina V. Long, Robyn Gartrell, Zoe Blake, Ines Simoes, Yichun Fu, Takuro Saito, Yingzhi Qian, Yan Lu, Yvonne M. Saenger, Sadna Budhu, Olivier De Henau, Roberta Zappasodi, Kyle Schlunegger, Bruce Freimark, Jeff Hutchins, Christopher A. Barker, Jedd D. Wolchok, Taha Merghoub, Elena Burova, Omaira Allbritton, Peter Hong, Jie Dai, Jerry Pei, Matt Liu, Joel Kantrowitz, Venus Lai, William Poueymirou, Douglas MacDonald, Ella Ioffe, Markus Mohrs, William Olson, Gavin Thurston, Cristian Capasso, Federica Frascaro, Sara Carpi, Siri Tähtinen, Sara Feola, Manlio Fusciello, Karita Peltonen, Beatriz Martins, Madeleine Sjöberg, Sari Pesonen, Tuuli Ranki, Lukasz Kyruk, Erkko Ylösmäki, Vincenzo Cerullo, Fabio Cerignoli, Biao Xi, Garret Guenther, Naichen Yu, Lincoln Muir, Leyna Zhao, Yama Abassi, Víctor Cervera-Carrascón, Mikko Siurala, João Santos, Riikka Havunen, Suvi Parviainen, Akseli Hemminki, Angus Dalgleish, Satvinder Mudan, Mark DeBenedette, Ana Plachco, Alicia Gamble, Elizabeth W. Grogan, John Krisko, Irina Tcherepanova, Charles Nicolette, Pooja Dhupkar, Ling Yu, Eugenie S. Kleinerman, Nancy Gordon, Italia Grenga, Lauren Lepone, Sofia Gameiro, Karin M. Knudson, Massimo Fantini, Kwong Tsang, James Hodge, Renee Donahue, Jeffrey Schlom, Elizabeth Evans, Holm Bussler, Crystal Mallow, Christine Reilly, Sebold Torno, Maria Scrivens, Cathie Foster, Alan Howell, Leslie Balch, Alyssa Knapp, John E. Leonard, Mark Paris, Terry Fisher, Siwen Hu-Lieskovan, Ernest Smith, Maurice Zauderer, William Fogler, Marilyn Franklin, Matt Thayer, Dan Saims, John L. Magnani, Jian Gong, Michael Gray, George Fromm, Suresh de Silva, Louise Giffin, Xin Xu, Jason Rose, Taylor H. Schreiber, Sofia R. Gameiro, Paul E. Clavijo, Clint T. Allen, James W. Hodge, Kwong Y. Tsang, Jane Grogan, Nicholas Manieri, Eugene Chiang, Patrick Caplazi, Mahesh Yadav, Patrick Hagner, Hsiling Chiu, Michelle Waldman, Anke Klippel, Anjan Thakurta, Michael Pourdehnad, Anita Gandhi, Ian Henrich, Laura Quick, Rob Young, Margaret Chou, Andrew Hotson, Stephen Willingham, Po Ho, Carmen Choy, Ginna Laport, Ian McCaffery, Richard Miller, Kimberly A. Tipton, Kenneth R. Wong, Victoria Singson, Chihunt Wong, Chanty Chan, Yuanhiu Huang, Shouchun Liu, Jennifer H. Richardson, W. Michael Kavanaugh, James West, Bryan A. Irving, Ritika Jaini, Matthew Loya, Charis Eng, Melissa L. Johnson, Alex A. Adjei, Mateusz Opyrchal, Suresh Ramalingam, Pasi A. Janne, George Dominguez, Dmitry Gabrilovich, Laura de Leon, Jeannette Hasapidis, Scott J. Diede, Peter Ordentlich, Scott Cruickshank, Michael L. Meyers, Matthew D. Hellmann, Pawel Kalinski, Amer Zureikat, Robert Edwards, Ravi Muthuswamy, Nataša Obermajer, Julie Urban, Lisa H. Butterfield, William Gooding, Herbert Zeh, David Bartlett, Olga Zubkova, Larissa Agapova, Marina Kapralova, Liudmila Krasovskaia, Armen Ovsepyan, Maxim Lykov, Artem Eremeev, Vladimir Bokovanov, Olga Grigoryeva, Andrey Karpov, Sergey Ruchko, Alexandr Shuster, Danny N. Khalil, Luis Felipe Campesato, Yanyun Li, Adam S. Lazorchak, Troy D. Patterson, Yueyun Ding, Pottayil Sasikumar, Naremaddepalli Sudarshan, Nagaraj Gowda, Raghuveer Ramachandra, Dodheri Samiulla, Sanjeev Giri, Rajesh Eswarappa, Murali Ramachandra, David Tuck, Timothy Wyant, Jasmin Leshem, Xiu-fen Liu, Tapan Bera, Masaki Terabe, Birgit Bossenmaier, Gerhard Niederfellner, Yoram Reiter, Ira Pastan, Leiming Xia, Yang Xia, Yangyang Hu, Yi Wang, Yangyi Bao, Fu Dai, Shiang Huang, Elaine Hurt, Robert E. Hollingsworth, Lawrence G. Lum, Alfred E. Chang, Max S. Wicha, Qiao Li, Thomas Mace, Neil Makhijani, Erin Talbert, Gregory Young, Denis Guttridge, Darwin Conwell, Gregory B. Lesinski, Rodney JM Macedo Gonzales, Austin P. Huffman, Ximi K. Wang, Ran Reshef, Andy MacKinnon, Jason Chen, Matt Gross, Gisele Marguier, Peter Shwonek, Natalija Sotirovska, Susanne Steggerda, Francesco Parlati, Amani Makkouk, Mark K. Bennett, Ethan Emberley, Tony Huang, Weiqun Li, Silinda Neou, Alison Pan, Jing Zhang, Winter Zhang, Netonia Marshall, Thomas U. Marron, Judith Agudo, Brian Brown, Joshua Brody, Christopher McQuinn, Matthew Farren, Hannah Komar, Reena Shakya, Thomas Ludwug, Y. Maurice Morillon, Scott A. Hammond, John W. Greiner, Pulak R. Nath, Anthony L. Schwartz, Dragan Maric, David D. Roberts, Aung Naing, Kyriakos P. Papadopoulos, Karen A. Autio, Deborah J. Wong, Manish Patel, Gerald Falchook, Shubham Pant, Patrick A. Ott, Melinda Whiteside, Amita Patnaik, John Mumm, Filip Janku, Ivan Chan, Todd Bauer, Rivka Colen, Peter VanVlasselaer, Gail L. Brown, Nizar M. Tannir, Martin Oft, Jeffrey Infante, Evan Lipson, Ajay Gopal, Sattva S. Neelapu, Philippe Armand, Stephen Spurgeon, John P. Leonard, Rachel E. Sanborn, Ignacio Melero, Thomas F. Gajewski, Matthew Maurer, Serena Perna, Andres A. Gutierrez, Raphael Clynes, Priyam Mitra, Satyendra Suryawanshi, Douglas Gladstone, Margaret K. Callahan, James Crooks, Sheila Brown, Audrey Gauthier, Marc Hillairet de Boisferon, Andrew MacDonald, Laura Rosa Brunet, William T. Rothwell, Peter Bell, James M. Wilson, Fumi Sato-Kaneko, Shiyin Yao, Shannon S. Zhang, Dennis A. Carson, Cristina Guiducci, Robert L. Coffman, Kazutaka Kitaura, Takaji Matsutani, Ryuji Suzuki, Tomoko Hayashi, Ezra E. W. Cohen, David Schaer, Yanxia Li, Julie Dobkin, Michael Amatulli, Gerald Hall, Thompson Doman, Jason Manro, Frank Charles Dorsey, Lillian Sams, Rikke Holmgaard, Krishnadatt Persaud, Dale Ludwig, David Surguladze, John S. Kauh, Ruslan Novosiadly, Michael Kalos, Kyla Driscoll, Hardev Pandha, Christy Ralph, Kevin Harrington, Brendan Curti, Wallace Akerley, Sumati Gupta, Alan Melcher, David Mansfield, David R. Kaufman, Emmett Schmidt, Mark Grose, Bronwyn Davies, Roberta Karpathy, Darren Shafren, Katerina Shamalov, Cyrille Cohen, Naveen Sharma, James Allison, Tala Shekarian, Sandrine Valsesia-Wittmann, Christophe Caux, Aurelien Marabelle, Brian M. Slomovitz, Kathleen M. Moore, Hagop Youssoufian, Marshall Posner, Poonam Tewary, Alan D. Brooks, Ya-Ming Xu, Kithsiri Wijeratne, Leslie A. A. Gunatilaka, Thomas J. Sayers, John P. Vasilakos, Tesha Alston, Simon Dovedi, James Elvecrog, Iwen Grigsby, Ronald Herbst, Karen Johnson, Craig Moeckly, Stefanie Mullins, Kristen Siebenaler, Julius SternJohn, Ashenafi Tilahun, Mark A. Tomai, Katharina Vogel, Eveline E. Vietsch, Anton Wellstein, Martin Wythes, Stefano Crosignani, Joseph Tumang, Shilpa Alekar, Patrick Bingham, Sandra Cauwenberghs, Jenny Chaplin, Deepak Dalvie, Sofie Denies, Coraline De Maeseneire, JunLi Feng, Kim Frederix, Samantha Greasley, Jie Guo, James Hardwick, Stephen Kaiser, Katti Jessen, Erick Kindt, Marie-Claire Letellier, Wenlin Li, Karen Maegley, Reece Marillier, Nichol Miller, Brion Murray, Romain Pirson, Julie Preillon, Virginie Rabolli, Chad Ray, Kevin Ryan, Stephanie Scales, Jay Srirangam, Jim Solowiej, Al Stewart, Nicole Streiner, Vince Torti, Konstantinos Tsaparikos, Xianxian Zheng, Gregory Driessens, Bruno Gomes, Manfred Kraus, Chunxiao Xu, Yanping Zhang, Giorgio Kradjian, Guozhong Qin, Jin Qi, Xiaomei Xu, Bo Marelli, Huakui Yu, Wilson Guzman, Rober Tighe, Rachel Salazar, Kin-Ming Lo, Jessie English, Laszlo Radvanyi, Yan Lan, Michael Postow, Yasin Senbabaoglu, Billel Gasmi, Hong Zhong, Cailian Liu, Daniel Hirschhorhn-Cymerman, Yuanyuan Zha, Gregory Malnassy, Noreen Fulton, Jae-Hyun Park, Wendy Stock, Yusuke Nakamura, Hongtao Liu, Xiaoming Ju, Rachelle Kosoff, Kimberly Ramos, Brandon Coder, Robert Petit, Michael Princiotta, Kyle Perry, Jun Zou, Ainhoa Arina, Christian Fernandez, Wenxin Zheng, Michael A. 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Pachynski, Rosa M. Santana Carrero, Sarai Rivas, Figen Beceren-Braun, Scott Anthony, Kimberly S. Schluns, Deepali Sawant, Maria Chikina, Hiroshi Yano, Creg Workman, Elise Salerno, Ileana Mauldin, Donna Deacon, Sofia Shea, Joel Pinczewski, Thomas Gajewski, Stefani Spranger, Brendan Horton, Akiko Suzuki, Pamela Leland, Bharat H. Joshi, Raj K. Puri, Randy F. Sweis, Riyue Bao, Jason Luke, Marie-Nicole Theodoraki, Frances-Mary Mogundo, Haejung Won, Dayson Moreira, Chan Gao, Xingli Zhao, Priyanka Duttagupta, Jeremy Jones, Massimo D’Apuzzo, and Sumanta Pal

Subjects
0301 basic medicine, Pharmacology, Cancer Research, medicine.medical_specialty, business.industry, medicine.medical_treatment, Immunology, Cancer, Immunotherapy, medicine.disease, 3. Good health, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Oncology, 030220 oncology & carcinogenesis, Family medicine, Molecular Medicine, Immunology and Allergy, Medicine, business
Abstract

O1 IL-15 primes an mTOR-regulated gene-expression program to prolong anti-tumor capacity of human natural killer cells #### Andreas Lundqvist1, Vincent van Hoef1, Xiaonan Zhang1, Erik Wennerberg2, Julie Lorent1, Kristina Witt1, Laia Masvidal Sanz1, Shuo Liang1, Shannon Murray3, Ola Larsson1

Published
2016

Catalog

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