bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 2639: Prognostic significance of non-small cell lung cancer and response to EGFR-TKI of EGFR mutated lung cancer besed on PD-L1 expression
Authors: Kobayashi Kenichi , Seike Masahiro , Noro Rintaro , Hemmi Shinobu , Gemma Akihiko 
Published: August 2018

Abstract
Background: Recent clinical trials have shown that immune checkpoint blockades that target either PD-1 or PD-L1 yield remarkable responses in a subgroup of non-small cell lung cancer (NSCLC) patients.
Materials and Methods: We retrospectively examined, by immunohistochemical analysis, 211 NSCLC patients who had undergone complete surgical resection. Using 32 independent samples, we also evaluated PD-L1 expression in 32 NSCLC patients with epidermal growth factor receptor (EGFR) mutations treated by EGFR-tyrosine kinase inhibitors (EGFR-TKIs).
Results: Overall survival of PD-L1 positive surgical NSCLC patients with stages I-III and stage I disease were significantly shorter than those of PD-L1 negative NSCLC patients (P &lt;0.01 and P = 0.02, respectively). In 86 squamous cell carcinoma (SQ) cases, PD-L1 positive patients showed significantly poorer survival than PD-L1 negative patients (P = 0.01). In stage I NSCLC patients, gender and PD-L1 expression were found to be independent predictors of death after multivariate analysis (Hazard ratio [HR] 3.57, P &lt;0.01 and HR 2.05, P = 0.04, respectively). In SQ patients, p-stage and PD-L1 expression were independent predictors of death (HR 2.53, P &lt;0.01 and HR 2.26, P = 0.02, respectively). Response to EGFR-TKIs, progression-free survival and overall survival were not significantly different between PD-L1 positive and negative NSCLC patients with EGFR mutations.
Conclusion: PD-L1 positive expression in a tumor was a significant independent predictor of poor outcome in patients with lung SQ and in stage I NSCLC patients. Based on PD-L1 expression, the clinical response to EGFR-TKIs and prognosis did not differ in EGFR-mutated NSCLC patients.
Citation Format: Kenichi Kobayashi, Masahiro Seike, Rintaro Noro, Shinobu Hemmi, Akihiko Gemma. Prognostic significance of non-small cell lung cancer and response to EGFR-TKI of EGFR mutated lung cancer besed on PD-L1 expression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2639.
Abstract 2642: CBLC is a potential biomarker for the susceptibility to paclitaxel in lung adenocarcinoma
Authors: Lin Yi-Ping , Hong Shiao-Ya , Kao Yu-Rung , Wu Cheng-Wen 
Published: August 2018

Abstract
CBL family proteins have been reported as E3 ubiquitin ligases of receptor tyrosine kinases. CBLC is the most divergent member of CBL family in human due to lack of the distal part of C terminus found in other two proteins, CBL and CBLB. By data mining from TCGA database, CBLC expression was frequently upregulated in lung adenocarcinoma. However, very little is known about the tumorigenic functions of CBLC compared to other CBL family proteins. Although patients with lung adenocarcinoma harboring EGFR mutations can be treated with tyrosine kinase inhibitors (TKIs), there is no good target therapy for treating lung adenocarcinoma patients with EGFR wild-type or TKIs resistance. Here, this study is to investigate if CBLC can be a good target for treatment to benefit these patients. In lung adenocarcinoma cells, CBLC knockdown significantly decreased cell viability, while CBLC overexpression increased the ability to form colonies in soft agar. Flow cytometry analyses revealed that CBLC depletion decreased the cell population of G2/M phase and increased cell apoptosis. Our study also showed that CBLC knockdown in EGFR wild-type cells increased the drug resistance to paclitaxel, which is widely used as a first-line chemotherapy drug in lung adenocarcinoma patients with EGFR wild-type or TKI resistance. Taken together, these findings indicate that CBLC might play a role in promoting cell mitosis and could be a potential biomarker of paclitaxel susceptibility for patients with EGFR wild-type lung adenocarcinoma.
Citation Format: Yi-Ping Lin, Shiao-Ya Hong, Yu-Rung Kao, Cheng-Wen Wu. CBLC is a potential biomarker for the susceptibility to paclitaxel in lung adenocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2642.
Abstract 266: Disulfiram overcomes docetaxel resistance in prostate cancer by targeting the neddylation pathway and down-regulation of Skp2 expression
Authors: Song Liankun , Yu Bin , Liu Hong-Min , Zi Xiaolin 
Published: August 2018

Abstract
Disulfiram (DSF), an inhibitor of aldehyde dehydrogenase and a dithiocarbamate chelator of copper, has been clinically used for treatment of alcohol dependence for decades. A population-based case control study has suggested that the use of DSF is associated with reduced risk of prostate cancer. In addition, copper is accumulated in prostate cancer and can act synergistically with DSF to inhibit the growth of prostate cancer cells. These accumulating data suggested that DSF is a very promising agent to be repurposed for prostate cancer treatment and prevention. However, the anti-cancer mechanisms of DSF currently remain largely unknown. Here we have shown that DSF treatment decreases the neddylation levels of NEDD8-conjugating enzyme UBE2M and Cullin-1 leading to down-regulation of Skp2 expression in prostate cancer DU145 cells. Further co-immunoprecipitation experiment revealed that DSF disrupted the formation of the defective in Cul neddylation 1 protein (DCN1) and UBE2M complex. DSF synergistically enhanced the growth inhibitory effect of docetaxel on prostate cancer cell lines and overcame the drug resistance. Taken together, these data may provide proof of concept for rationally designed repurpose of DSF to treat docetaxel-resistant prostate cancer by involvement of the neddylation pathway.
Citation Format: Liankun Song, Bin Yu, Hong-Min Liu, Xiaolin Zi. Disulfiram overcomes docetaxel resistance in prostate cancer by targeting the neddylation pathway and down-regulation of Skp2 expression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 266.
Abstract 2716: Development of 4-1BB agonists: Ligand fusion shows greater anti-tumor activity than antibodies in vivo
Authors: Tam Eric , Craig Galina , Ghassemifar Sara , Koshkaryev Alexander , Movassaghian Sara , Cosgrove Cormac , Sampson James , Drummond Daryl , Raue Andreas 
Published: August 2018

Abstract
Members of the tumor necrosis factor (TNF) superfamily of costimulatory receptors have emerged as promising targets for modulation of tumor infiltrating lymphocytes. Among these, 4-1BB (CD137) has a prominent role in promoting survival and expansion of cytotoxic CD8 T cells as well as activation of CD4 T cells, NK cells, and antigen presenting cells. The clinical relevance of 4-1BB agonism is currently being evaluated for two antibodies: urelumab (IgG4) and utomilumab (IgG2). However, it has been established that for the trimeric TNF receptor family, the homotrimeric ligands are superior activators compared to bivalent agonistic antibodies. Here we describe a prototype 4-1BB agonist consisting of three human 4-1BB ligands linked together as a single polypeptide chain and fused to the C-terminus of human IgG1 Fc (STIM-41BBL). Compared to a clinically relevant human 4-1BB antibody, STIM-41BBL shows increased activation of 4-1BB in a NF-kappa B reporter cell line. STIM-4-1BBL also shows augmented cytokine release compared to the antibody in CD8 T cells. Furthermore, we have developed a mouse STIM-41BBL and like the human counterpart, the ligand fusion induced greater cytokine release than an agonistic mouse 4-1BB antibody (IgG2a) in CD8 T cells. We have also introduced mutations (D265A/N297A) to the mouse 4-1BB antibody to make it effectorless in order to better approximate the clinical 4-1BB antibodies. Subsequently, we demonstrate that the murine STIM-41BBL had greater anti-tumor activity than the 4-1BB antibody in a MC38 tumor model. These results support the continued development of a 4-1BB ligand based therapeutic and suggests the greater potential of a STIM-41BBL fusion to a targeting antibody for more precise activation of immune system.
Citation Format: Eric Tam, Galina Craig, Sara Ghassemifar, Alexander Koshkaryev, Sara Movassaghian, Cormac Cosgrove, James Sampson, Daryl Drummond, Andreas Raue. Development of 4-1BB agonists: Ligand fusion shows greater anti-tumor activity than antibodies in vivo [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2716.
Abstract 2751: Regorafenib attenuates IFN-γ-induced PD-L1 expression and enhances antitumor immunity
Authors: Zhu Xiao-Feng 
Published: August 2018

Abstract
Immune checkpoint blocked therapy (ICB) targeting the PD-1/PD-L1 axis induce durable tumor regressions in a sizeable minority of cancer patients. To enhance the efficacy of existing immunotherapies, we implemented a screen of kinase inhibitors capable of increasing the activity of T cells suppressed by PD-L1. Here, we identified regorafenib, which was approved to treat patients with advanced gastrointestinal stromal tumors and metastatic colorectal cancer, as a potent agent significantly attenuating IFN-γ-induced PD-L1 expression without affecting MHC-I expression, contributing to enhanced anti-tumor effects with ICB in vitro and in vivo, due in part to inhibit JAK1/2-STAT1 signaling and the activation of ERK by suppressing the tyrosine kinase receptor RET-Src axis. Additionally, our analysis of GEO database and TCGA database revealed that RET and Src co-high expression was an independent unfavorable prognosis factor in both melanoma patients with or without ICB via inhibiting anti-tumor immune response. Further, gene set enrichment analysis (GSEA) demonstrated, compared to RET and Src co-high expression group, anti-tumor immune response related gene signatures as prominent modules in other group. Collectively, our data unveiled a new mechanism of reducing IFN-γ-induced PD-L1 expression and provided a rationale to explore a new combination of immunotherapies and regorafenib in melanoma treatment.
Citation Format: Xiao-Feng Zhu. Regorafenib attenuates IFN-γ-induced PD-L1 expression and enhances antitumor immunity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2751.
Abstract 2783: Empowering therapeutic monoclonal antibodies with IFN-alpha for cancer immunotherapy
Authors: Guo Jun , Xiao Yu , Lyer Ramesh B. , Lake Marc R. , Ladror Uri S. , Lu Xin , Pappano Bill , Harlan John E. , Tomlinson Medha J. , Bukofzer Gail T. , Donawho Cherrie K. , Shoemaker Alexander R. , Huang Tzu-Hsuan 
Published: August 2018

Abstract
Type 1 IFNs stimulates secretion of IP-10 (CXCL10) which is a critical chemokine to recruit effector T cells to the tumor microenvironment and IP-10 knockout mice exhibit a phenotype with compromised effector T cell generation and trafficking. Type 1 IFNs also induces MHC class 1 upregulation on tumor cells which can enhance anti-tumor CD8 T cell effector response in the tumor microenvironment. Although type 1 IFNs show great promise in potentiating anti-tumor immune response, systemic delivery of type 1 IFNs is associated with toxicity thereby limiting clinical application. In this study, we fused tumor targeting antibodies with IFN-alpha and showed that the fusion proteins can be produced with high yields and purity. IFN fusions selectively induced IP-10 secretion from antigen positive tumor cells, which was critical in recruiting the effector T cells to the tumor microenvironment. Further, we establish a real time in vitro antigen specific CTL killing assay using IncuCyte Zoom and tested the anti-tumor efficacy of anti-PDL1-IFN-alpha fusion using this system. We found anti-PDL1-IFN-alpha as low as 10 pM exhibits potent activity in potentiating OT1 CD8 T cells killing against OVA expressing tumor cells, while control IFN fusion did not exhibit any activity in the same experiment. Furthermore, IFN-alpha fusion antibody was well tolerated in vivo and demonstrated anti-tumor efficacy in an anti-PD-L1 resistant syngeneic mouse tumor model. Our data supports the hypothesis of targeting type 1 IFN to the tumor microenvironment may enhance effector T cell responses in non-inflamed tumors.
Citation Format: Jun Guo, Yu Xiao, Ramesh B. Lyer, Marc R. Lake, Uri S. Ladror, Xin Lu, Bill Pappano, John E. Harlan, Medha J. Tomlinson, Gail T. Bukofzer, Cherrie K. Donawho, Alexander R. Shoemaker, Tzu-Hsuan Huang. Empowering therapeutic monoclonal antibodies with IFN-alpha for cancer immunotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2783.
Abstract 2829: Targeting the DNA damage response and DNA-PK signaling via small molecule Ku inhibitors
Authors: Turchi John J. , Gavande Navnath S. , VanderVere-Carozza Pamela S. , Vernon Tyler , Pawelczak Katherine S. 
Published: August 2018

Abstract
Normal 0 false false false EN-US X-NONE X-NONE /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-parent:""; mso-padding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin-top:0in; mso-para-margin-right:0in; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0in; line-height:115%; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin;} The DNA dependent protein kinase (DNA-PK) is a validated target for cancer therapeutics that drives the DNA damage response (DDR) and plays a critical role as a primary sensor in the non-homologous end joining (NHEJ) DNA double strand break (DSB) repair pathway. Various anti-cancer therapeutic strategies mediate their cytotoxic effects by inducing DSBs, including ionizing radiation (IR), and clinical outcomes are directly related to the repair of DNA damage. Modulating the pathway responsible for repairing DSBs will have a profound impact on the efficacy of DNA damaging agents in the clinic. To date, development of inhibitors for DNA-PK has focused on targeting the active site with ATP mimetics. We have taken the novel and innovative approach to inhibiting DNA-PK via blocking the Ku 70/80 heterodimer interaction with DNA, a necessary step in DNA-PK activation. Exploiting this unique mechanism of kinase activation, we have identified a series of highly potent and specific DNA-PK inhibitors that impart their inhibitory activity via disruption of the binding of Ku protein to DNA ends. This novel approach affords significant advantages to current approaches in kinase inhibition. Novel derivatives of our initial hit inhibit DNA-PK catalytic activity at nanomolar concentrations and potentiate cellular sensitivity to DSB-inducing agents like etoposide and bleomycin. Data demonstrate that the cellular effects observed are a function of Ku inhibition and that this novel class of DNA-PK inhibitors can be further developed as anti-cancer therapeutics that can be used as an adjuvant to, or concomitant with radiotherapy and other cancer therapies that induce DNA damage.
Citation Format: John J. Turchi, Navnath S. Gavande, Pamela S. VanderVere-Carozza, Tyler Vernon, Katherine S. Pawelczak. Targeting the DNA damage response and DNA-PK signaling via small molecule Ku inhibitors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2829.
Abstract 2832: Novel therapy for oral squamous cell carcinoma using non-thermal atmospheric pressure biocompatible plasma activated water
Authors: Han Ihn , Song In Seok , Li Ying , Kang Min Ho , Ryu Jae Jun , Choi Eun Ha 
Published: August 2018

Abstract
Non-thermal atmospheric pressure biocompatible plasma (NBP) has been reported that was possible to induce apoptosis on various cancer cells including lung, ovary, brain, liver, breast, and pancreas cancer. We developed NBP device, which has been reported to have cytotoxicity on cancer cells induce DNA damage and apoptosis. In particular,reactive oxygen and/or nitrogen species (RONS) were generated by plasma device to give oxidative stress and depolarization of mitochondria membrane in cancer cells. Now we developed a microwave plasma jet system, which could generate nitric oxide (NO) and NO-plasma activated water (NO-PAW). Previously, we found that NO-PAW could induce apoptosis and accumulate ROS in human cervical cancer cells (1). In this study we investigated the efficacy of NO-PAW on oral squamous cancer cells (OSCC), a common malignant tumor of the head and neck (2, 3). We observed that cytotoxicity and apoptotic stimulation by NO-PAW were significantly increased. Also, expression level of caspase and PARP in OSCC was increased after treatment by NO-PAW. However, the apoptosis effect was not observed in human gingival fibroblasts (as normal human cells). Additionally, we found that NO-PAW inhibited cancer progression in vivo. In conclusion, NO-PAW could suppress the progress of OSCC by inducing cell apoptosis. This indicated NO-PAW as a novel tool for OSCC therapy, and probably will be also effective for other oral cancer.
Acknowledgments: This work was supported by the Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea (NRF- 2016K1A4A3914113) funded by the Ministry of Science, ICT, and Future Planning (MSIP) of the Korean Government for EH. Choi, I. Han. The Korea government, and the Basic Science Research Program through the NRF of Korea, funded by the Ministry of Education (NRF-2015R1C1A2A01054137) for I. Han.
References:
1. Y. Li, M.H. Kang, H.S. Uhm, G.J. Lee, E.H. Choi, I. Han. Sci Rep 2017;7:1.
2. E. Majchrzak, B. Szybiak, A. Wegner, P. Pienkowski, J. Pazdrowski, L. Luczewski, M. Sowka, P. Golusinski, J. Malicki, W. Golusinski. Radiol Oncol 2014;48:1.
3. B. Wang, S. Zhang, K. Yue, X.D. Wang. Chin J Cancer 2013;32:614.
Citation Format: Ihn Han, In Seok Song, Ying Li, Min Ho Kang, Jae Jun Ryu, Eun Ha Choi. Novel therapy for oral squamous cell carcinoma using non-thermal atmospheric pressure biocompatible plasma activated water [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2832.
Abstract 3158: DLL3 regulates migration and invasion of small cell lung cancer
Authors: Furuta Megumi , Sakakibara Jun Konishi , Shoji Tetsuaki , Takashima Yuta , Kikuchi Hajime , Kikuchi Eiki , Kikuchi Junko , Kinoshita Ichiro , Akita Hirotoshi Dosaka , Nishimura Masaharu 
Published: August 2018

Abstract
Background: Delta-like protein 3 (DLL3) is a ligand of Notch signaling, which is reported to be a tumor suppressor in small cell lung cancer (SCLC). Previous studies suggest that DLL3 might be associated with neuroendocrine tumorigenesis through inhibition of Notch signaling unlike other activating ligands. Moreover, DLL3 was highly expressed in SCLC, but not in normal lung tissue. However, little is known about function of DLL3 in SCLC. In this study, we examine the effect of DLL3 in tumorigenesis of SCLC.
Methods: The mRNA expression levels and proteins of DLL3, Notch receptors (Notch1, Notch2, Notch3 and Notch4), Hes1 and EMT markers (E-cadherin, Snail and Vimentin) were examined using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot in 9 SCLC cell lines (SBC-3, SBC-5, MS-1, RERF-LC-MA, H69, H82, H209, H529 and H1688). We used small interfering RNA (siRNA) to down-regulate the expression of DLL3 in SCLC cell lines. Anchorage-dependent and anchorage-independent cell growth was measured by MTT assay and migration and invasion were assessed by transwell assay.
Results: The mRNA of DLL3 was expressed in all of 9 SCLC cell lines. The expression of DLL3 was especially higher in H82, H69, H209, H529 and H1688 cells. Notch1 protein was expressed in SBC-3, SBC-5, MS-1 and H82. Based on DLL3 expression analysis data, we used H82 and H69 in the following experiments. The suppression of DLL3 by siRNA resulted in the moderate inhibition of cell growth of H82 cells in both anchorage-dependent and anchorage-independent cell proliferation. The depletion of DLL3 prevented migration and invasion in the two cell lines. The expressions of Notch1 and Notch target gene, Hes1 were downregulated by DLL3 knockdown in both SCLC cells. Because Notch pathway was reported to regulate EMT, we evaluated the EMT markers when DLL3 was inhibited in SCLC cells. Snail was downregulated in DLL3 knockdown SCLC cells, while protein expression levels of E-cadherin and Vimentin were not changed in these DLL3 knockdown cells compared to control cells.
Conclusions: DLL3 promotes the migration and invasion in SCLC cells by modulating Notch1 and Snail.
Citation Format: Megumi Furuta, Jun Konishi Sakakibara, Tetsuaki Shoji, Yuta Takashima, Hajime Kikuchi, Eiki Kikuchi, Junko Kikuchi, Ichiro Kinoshita, Hirotoshi Dosaka Akita, Masaharu Nishimura. DLL3 regulates migration and invasion of small cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3158.
Abstract 3159: Rac1 and Cdc42 as drivers in ovarian cancer metastasis
Authors: Rivera Melanie , Dominguez Dayna , Pauken Christine , Romero Elsa , Kenney S. Ray , Shi Yang , Lee Ji-Hyun , Gillette Jennifer , Hudson Laurie G. , Wandinger-Ness Angela 
Published: August 2018

Abstract
Five-year ovarian cancer patient survival has not improved for decades, largely due to disease recurrence. Therefore, drivers of relapse need to be identified. We first reported that Rac1 and Cdc42 GTPases are highly overexpressed in serous ovarian cancer using immunohistochemistry. To correlate GTPase expression with survival outcomes, we analyzed gene expression data in The Cancer Genome Atlas, revealing that ovarian cancer patients with the highest RAC1 RNA levels had significantly worse age-adjusted survival than those with low RAC1. Quantitative analyses of Rac1b, a constitutively active Rac1 splice variant, show dramatic overexpression in tumor epithelia relative to stroma and normal epithelia. Since high Rac1 and Cdc42 levels drive cancer cell adhesion, invasion and metastasis, we used multiple assays to assess the dependence of ovarian cancer cell behaviors on Rac1 and Cdc42. Using Matrigel invasion chambers, treatment of multiple ovarian cancer cell lines with specific Rac1 and Cdc42 inhibitors resulted in significantly decreased cellular invasion. Conversely, with overexpression of Rac1, ovarian cancer cells demonstrated increased invasion. Furthermore, IP injection of ovarian cancer cells overexpressing Rac1 resulted in increased adhesion, invasion and metastasis in the omentum and peritoneum in vivo. These data support Rac1 and Cdc42 as important drivers of invasive and metastatic ovarian cancer and as novel high-value therapeutic targets with potential impact in reducing disease metastasis.
Citation Format: Melanie Rivera, Dayna Dominguez, Christine Pauken, Elsa Romero, S. Ray Kenney, Yang Shi, Ji-Hyun Lee, Jennifer Gillette, Laurie G. Hudson, Angela Wandinger-Ness. Rac1 and Cdc42 as drivers in ovarian cancer metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3159.