tbuckley/cabot-search huggingface dataset:
Abstract 3269: Impact of gender on survival of the patients with esophageal squamous cell carcinoma at a single institute in China
Authors: Jian Liang Lu, Jian Liang Lu, Rui Ping Xu, Bei Li, Li Xin Wan, Ming Yao Chen, Chun Jiang Liu, Zhan Qiang Han, Fang Fang Shen, Jian Bo Zhao, Hai Zhou Guo, Wei Cao, Bing Yu Fan, Li Dong Wang
Journal: Cancer Research (2017)

Abstract Esophageal cancer (EC) has been well documented with predominant occurrence in male and with major histopathological type of esophageal squamous cell carcinoma (ESCC) in China. However, the influence by gender on ESCC survival is largely unknown in China. The present study was thus undertaken to elucidate the impact by gender on survival of Chinese patients with ESCC. A total of 17,969 ESCC patients was enrolled in this study, including 11,127 males with a mean age of 60.2±8.6 and 6842 females with a mean age of 61.0±8.4.All the patients were from ESCC database in Henan Key Laboratory for Esophageal Cancer Research of the First Affiliated Hospital, Zhengzhou University (1975 to 2015). Only the patients with T2–4N0–1M0–1 were enrolled in this study. Based on the diagnosed time, the patients were classified into two groups, group I (1996–2005, 6885/38.3%) and group II (2006–2015, 11084/61.7%). The followed–up was undertaken until October, 2016. Kaplan–Meier models were for describing the survival curves and Cox proportional hazards models were undertaken to observe the risk of death of male and female. The results demonstrated that the male patients had a poor survival than female (X2=58.17, P&amp;lt;0.001). Furthermore, similar results were observed for the two different periods of 1996–2005 (X2=21.08, P&amp;lt;0.001) and 2006–2015 (X2=34.67, P&amp;lt;0.001). The present results indicate that gender is an independent survival factor for ESCC and the female patients with ESCC have a dramatic prolonged survival than male patients in China. [Supported by Doctoral Team Foundation of the First Affiliated Hospital of Zhengzhou University (2016-BSTDJJ-03), Natural Science Foundation of Henan Province (20161110) and Correspondening author: Li Dong Wang, email:ldwang2007@126.com] Note: This abstract was not presented at the meeting. Citation Format: Jian Liang Lu, Jian Liang Lu, Rui Ping Xu, Bei Li, Li Xin Wan, Ming Yao Chen, Chun Jiang Liu, Zhan Qiang Han, Fang Fang Shen, Jian Bo Zhao, Hai Zhou Guo, Wei Cao, Bing Yu Fan, Li Dong Wang. Impact of gender on survival of the patients with esophageal squamous cell carcinoma at a single institute in China [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3269. doi:10.1158/1538-7445.AM2017-3269
Abstract LB-153: Lotus leaf and Cassia seed extracts, through activating Nrf2 pathway, suppress TPA-induced mouse skin cell transformation
Authors: Yen-Fan Chan, Zi-Han Lin, Pei-Chun Chen, Ping-Hua Sung, Zheng-Yuan Su
Journal: Cancer Research (2017)

Abstract In traditional Chinese medicine, some Chinese herbs to be used as foods can protect and promote human health. Lotus (Nelumbo nucifera) leaves (LL) and Cassia (Cassia tora) seeds (CS) are often used as a food or an ingredient when cooking in Chinese region. LL and CS have been studied to exhibit some biological effects but there is no investigation to study their cancer chemopreventive potential. In this study, the extracts, including water extract (WE), water extraction residue ethanol extract (WREE) and ethanol extract (EE), of LL and CS were prepared. HepG2-C8 cell line, HepG2 cells stably transfected with Nrf2-ARE-luciferase plasmid, were used to screen out the extracts with cancer chemoprevetive potential. Our results showed that CS-WE, LL-WREE and LL-EE has better Nrf2-ARE-luciferase induction activity. Furthermore, we also found that these three extracts can inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced anchorage-independent cell growth of JB6 P+ cells while up-regulating Nrf2 and Nrf2 downstream antioxidant/detoxification enzymes. These results suggested that Chinese herbal Lotus leaves and Cassia seeds to be used as foods might inhibit carcinogenesis through the regulation of Nrf2 pathway. Citation Format: Yen-Fan Chan, Zi-Han Lin, Pei-Chun Chen, Ping-Hua Sung, Zheng-Yuan Su. Lotus leaf and Cassia seed extracts, through activating Nrf2 pathway, suppress TPA-induced mouse skin cell transformation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr LB-153. doi:10.1158/1538-7445.AM2017-LB-153
Abstract 1712: Detection of circulating tumor cells in stage IV non-small cell lung cancer
Authors: Stephanie N. Shishido, Lyudmila Bazhenova, Anders Carlsson, James Hicks, Peter Kuhn
Journal: Cancer Research (2017)

Abstract Non-Small Cell Lung Cancer (NSCLC) is the most common cause of cancer related deaths in both men and women. Some lung cancer patients have a unique challenge of a tissue access due to tumor location or baseline lung disorders such as emphysema and chronic obstructive pulmonary disease (COPD). Liquid biopsy technologies can overcome tissue assess difficulties. However, as of today there are no commercially approved assays for CTC enumeration in lung cancer. Multiple non-commercial assays exist and some show correlation of CTC enumeration and changes in CTC counts on therapy with prognosis and response to therapy. Outside of absolute number of CTC there is little published data regarding prognostic significance of CTC morphologic heterogeneity in late stage NSCLC and its ability to predict treatment outcomes. Here we investigate CTC counts in 81 patients with stage IV NSCLC using a fluid phase biopsy and high definition (HD) diagnostic pathology imaging of all nucleated cells. HD-CTCs were detected in 51 (63%) patients at initiation of therapy with a median of 2.20 (range 0-509.20) and a mean of 26.21 HD-CTCs/mL (±15.64). There was no correlation between the absolute number of HD-CTCs at the time of initiation of new therapy and patient outcomes. A subset of 25 patients was further analyzed to determine the significance of HD-CTC kinetics, which may follow three distinct patterns: an increase in HD-CTCs with therapy, unchanged HD-CTCs numbers (stable), and a decline in HD-CTCs numbers. Patients that experienced an increasing, stable, or decreasing HD-CTC profile had an overall change of 118.40, 0.54, and 81.40 HD-CTCs/mL respectively during the first 3 months. The overall survival (OS) for increasing profiles was 31.08 months (±13.08, median 32.46, range 15.11-43.50), for stable profiles OS was 8.82 months (±3.57, median 7.23, range 3.91-19.75), and for decreasing profiles it was 15.30 months (±6.39, median 14.06, range 3.81-28.06) months. CTCs are identifiable in patients with stage IV NSCLC, but correlation of absolute HD-CTC counts with disease progression was not statistically significant. However, change in CTC counts were predictive of OS in patients with metastatic lung cancer receiving chemotherapy. Citation Format: Stephanie N. Shishido, Lyudmila Bazhenova, Anders Carlsson, James Hicks, Peter Kuhn. Detection of circulating tumor cells in stage IV non-small cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1712. doi:10.1158/1538-7445.AM2017-1712
Infants, animals, and the origins of number
Authors: Eric Margolis
Journal: Behavioral and Brain Sciences (2017)

Where do human numerical abilities come from? Leibovich et al. argue against nativist views of numerical development noting limitations in newborns' vision and limitations regarding newborns' ability to individuate objects. I argue that these considerations do not undermine competing nativist views and that Leibovich et al.'s model itself presupposes that infant learners have numerical representations.
Abstract 837: PSMB8 as a candidate marker of responsiveness to preoperative radiotherapy in rectal cancer patients
Authors: Yejin Ha, Ka hee Tak, Chan wook Kim, Seon Ae Roh, Eun Kyung Choi, Dong Hyung Cho, Jeong-Hwan Kim, Seon-Kyu Kim, Seon-Young Kim, Yong Sung Kim, Jin-Cheon Kim
Journal: Cancer Research (2017)

Abstract Prediction of individual responsiveness is urgently needed, specifically in locally advanced rectal cancer (LARC) patients who underwent preoperative chemoradiotherapy (CRT). The present study, RNA-Seq was used to compare the basal expression profile between responders and non-responders to preoperative CRT, in correlation with the tumor regression grade (TRG) among 22 LARC patients. Eight differentially expressed genes (B3GALT4, HSPA1B, KRBOX1, PPBP, PPP1R18, PSMB8, SLC39A7, and TAP2) associated with preoperative CRT responses were primarily identified among the 22 LARC patients by RNA-Seq (p&amp;lt;0.0005 and &amp;gt;16-fold difference). Among these genes, PSMB8 and SLC39A7 were upregulated in the responsive group in the other 40 LARC patients (p&amp;lt;0.05). PSMB8 overexpression significantly reduced colony formation and increased apoptosis-inducing molecules like cleaved caspase-3 and cleaved PARP in irradiated CRC cells after 6 Gy irradiation. PSMB8 knockdown increased colony formation and decreased caspase-3 activation and cleaved PARP levels after irradiation. In mice treated with ionizing radiation, tumor growth suppression was significantly greater in HCT116/PSMB8-xenografts (81%) than in HCT116/vector-xenografts (53%) (p=0.001). However, SLC39A7 overexpression had no significant effect on irradiated CRC cells. These results suggest that PSMB8 appears to predict radiosensitivity in LARC patients with preoperative CRT, although further clinical validation is needed in a larger cohort. Citation Format: Yejin Ha, Ka hee Tak, Chan wook Kim, Seon Ae Roh, Eun Kyung Choi, Dong Hyung Cho, Jeong-Hwan Kim, Seon-Kyu Kim, Seon-Young Kim, Yong Sung Kim, Jin-Cheon Kim. PSMB8 as a candidate marker of responsiveness to preoperative radiotherapy in rectal cancer patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 837. doi:10.1158/1538-7445.AM2017-837
Abstract 1967: A novel 40kDa CPE-ΔN isoform promotes proliferation and invasion in pancreatic cancer cells
Authors: XuYu Yang, Cong Ling, Hong Lou, Loh Yoke Peng
Journal: Cancer Research (2017)

Abstract Carboxypeptidase E (CPE) is a prohormone processing exopeptidase that cleaves C-terminal basic residues from peptide hormones liberated endoproteolytically from prohormones. It is a 476- amino acid protein with a signal peptide in its N-terminus and is mainly expressed in neuropeptide-rich areas of brain and endocrine tissues. As a multifunctional protein, CPE plays many non-enzymatic roles such as prohormone sorting, vesicle transport, and secretion in addition to its carboxypeptidase activity. Moreover, high expression of CPE is found in metastatic tumor tissues, including liver cancer, renal clear cell carcinoma, colorectal cancer, cervical cancer and melanoma, suggesting CPE may be involved in tumor metastasis and progression. In this study, a novel CPE splice isoform mRNA was identified by Northern blotting, which is ~1.83kb in size. RACE assay and sequence analysis confirmed existence of this CPE isoform mRNA, which partially lacks a N-terminus region, and has a shorter 3’-UTR compared to WT-CPE mRNA, by removal of 188 nucleotides within the first exon and 589 nucleotides out of the 3’-UTR, respectively. Bioinformatics analysis revealed that this CPE isoform mRNA has a shortened ORF, which starts coding from the 3rd ATG relative to wild-type (WT) CPE mRNA and encodes a 40kDa CPE-αN protein with the N-terminus truncated. Western blot analysis showed that 40kD CPE-αN is expressed in multiple cancer cell lines and tumor tissues. In Panc-1pancreatic cancer cells, knockdown of endogenous CPE(s) inhibited cell growth and invasion; in contrast, ectopic expression of 40kD CPE isoform significantly promoted proliferation, colony formation, invasion and migration, whereas overexpression of WT-CPE had only a small effect. These results suggest that the 40kD CPE-αN isoform plays a role in cell growth and metastasis. Note: This abstract was not presented at the meeting. Citation Format: XuYu Yang, Cong Ling, Hong Lou, Loh Yoke Peng. A novel 40kDa CPE-ΔN isoform promotes proliferation and invasion in pancreatic cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1967. doi:10.1158/1538-7445.AM2017-1967
Abstract 1956: ABCE1 regulates the translational profile of neuroblastoma to drive tumor progression
Authors: Jixuan Gao, Klaartje Somers, Katherine M. Hannan, Jamie I. Fletcher, Bing Liu, Ross D. Hannan, Richard B. Pearson, Michelle Haber, Murray D. Norris, Michelle J. Henderson
Journal: Cancer Research (2017)

Abstract Neuroblastoma is the most common extracranial solid tumor in children. A key driver of high-risk neuroblastoma is the MYCN transcription factor which fuels neuroblastoma progression by enhancing metabolic processes including protein translation (1). ABCE1, a member of the ATP-binding cassette (ABC) superfamily of transporters, is a translation factor directly up-regulated by MYCN (2). It is thought to dissociate the 80S ribosome into free 40S and 60S subunits so they can re-initiate translation and provide the protein building blocks required for rapid cell growth and migration (3). High ABCE1 expression is associated with poor clinical outcome in neuroblastoma patients (2). Therefore, we hypothesized that ABCE1 suppression may inhibit the aggressiveness of neuroblastoma by disabling protein synthesis. To test this, we suppressed ABCE1 using siRNAs in MYCN-amplified neuroblastoma cell lines, SK-N-BE(2) and CHP-134, which resulted in severely impaired cell migration (P&amp;lt;0.001) and proliferation (P&amp;lt;0.005). In mice xenografted with SK-N-BE(2) cells, ABCE1 suppression delayed tumor growth (P=0.001) and metastasis (P&amp;lt;0.001). Mechanistically, when polyribosome analysis was used to monitor the impact of ABCE1 expression on protein translation in SK-N-BE(2) cells, loss of ABCE1 reduced the proportion of actively translating ribosomes (P&amp;lt;0.001), leading to lower global protein synthesis (P=0.018). This is the first report of ABCE1 acting as pro-tumorigenic factor in neuroblastoma. Our data imply that targeting the translational machinery through ABCE1 may be an effective therapeutic approach for the treatment of MYC-driven cancers. 1. Boon, K., Caron, H. N., van Asperen, R., Valentijn, L., Hermus, M. C., van Sluis, P., Roobeek, I., Weis, I., Voûte, P.A., Schwab, M. &amp; Versteeg, R. (2001) EMBO J. 20, 1383-1393. 2. Porro, A., Haber, M., Diolaiti, D., Iraci, N., Henderson, M., Gherardi, S., Valli, E., Munoz, M.A., Xue, C., Flemming, C., Schwab, M., Wong, J.H., Marshall, G.M., Della Valle, G., Norris, M.D. &amp; Perini, G. (2010) J. Biol. Chem. 285, 19532-19543. 3. Pisarev, A.V., Skabkin, M.A., Pisareva, V.P., Skabkina, O.V., Rakotondrafara, A.M., Hentze, M.W., Hellen C.U. &amp; Pestova, T.V. (2010). Mol. Cell, 37, 196-210. Citation Format: Jixuan Gao, Klaartje Somers, Katherine M. Hannan, Jamie I. Fletcher, Bing Liu, Ross D. Hannan, Richard B. Pearson, Michelle Haber, Murray D. Norris, Michelle J. Henderson. ABCE1 regulates the translational profile of neuroblastoma to drive tumor progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1956. doi:10.1158/1538-7445.AM2017-1956
Abstract 2020: Synergistic induction of apoptosis of combined mesupron and auranofin treatment in human breast cancer cells
Authors: Joo-Eun Lee, Yeo-Jung Kwon, Kyung-Soo Oh, Young-Jin Chun
Journal: Cancer Research (2017)

Abstract Urokinase-type plasminogen activator (uPA) system may play a crucial role in cancer cell invasion and metastasis. uPA has been validated as a predictive or prognostic biomarker protein and considered as a therapeutic target in human breast cancer. Mesupron is a uPA inhibitor blocking uPA enzymatic activity to reduce tumor cell invasion, migration and cell growth. Auranofin has been known as an antirheumatic drug and a thioredoxin reductase inhibitor and recently its anticancer activity in ovarian and breast cancers has also been identified. To study whether cotreatment with mesupron and auranofin shows a significant anticancer activity, the synergistic induction of apoptosis of mesupron with auranofin was determined. Auranofin or mesupron alone inhibited cancer cell growth in MCF-7 cells with IC50 of 0.25 μM or 25 μM, respectively. Flow cytometric analysis also showed an increased apoptosis. When cells were treated with mesupron (0.125 μM) in combination with auranofin (10 μM), we found a significant induction of apoptosis although the cytotoxic effects of mesupron or auranofin alone at those concentrations were not quite strong. Interestingly, combined mesupron and auranofin treatment significantly suppressed mitochondrial antiapoptotic proteins including Bcl-2 and Bcl-xL. We also found the increase of caspase-3 and PARP cleavages. The combination index (CI) also indicated the synergistic induction of apoptosis by auranofin and mesupron. Taken together, these data suggest that the use of mesupron and auranofin in combination can be valuable to achieve higher anticancer activity. Note: This abstract was not presented at the meeting. Citation Format: Joo-Eun Lee, Yeo-Jung Kwon, Kyung-Soo Oh, Young-Jin Chun. Synergistic induction of apoptosis of combined mesupron and auranofin treatment in human breast cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2020. doi:10.1158/1538-7445.AM2017-2020
Genetic Variability of Methyl-Tetrahydrofolate-Reductase Modifies eNOS Coupling in Human Arteries and Veins: Effects on Vascular Superoxide Generation and Nitric Oxide Bioavailabllity
Authors: C Antoniades, C Shrirodaria, P Leeson, T Van-Assche, C Ratnatunga, R Pillai, D Tousoulis, C Stefanadis, H Refsum, K M Channon
Journal: Circulation (2008)
Abstract 331: Cardiac Stem Cell Therapy in Conjugation with Anti-inflammatory Small molecule enhances function of infarcted rat hearts.
Authors: Sudhish Sharma, David Simpson, Rachana Mishra, savitha Deshmukh, Sunjay Kaushal
Journal: Circulation Research (2013)

The transplantation of human cardiospheres derived cells (hCDCs) in clinical Phase I trials involving adult ischemic patients, results in reduction in scar formation. But this therapy faces three major issues: low survival rate (1-5%) of the transplanted cells and limited ventricular ejection fraction improvement. One of the major causes of decreased hCDCs engraftment is the prolonged and sustained pro-inflammatory response after acute myocardial infarct (MI). Pro-survival cocktail has been used to overcome this problem but it has major disadvantages for human use as a multi-component mixture, it may change the function of the stem cells and this method depends on anti-apoptotic molecules which may have side effects on the overall cellular turnover. A drug screen in our laboratory has discovered potent anti-inflammatory small molecules, Celastrol (CEL), a quinone triterpene. Oral administration of CEL significantly reduced the MI induced inflammatory cytokines release IL-1β by 2.6±0.4 fold (p&lt;0.05, n=5), IL-6 by 2.1±0.2 fold, (p&lt;0.01, n=5), TNF-α by 3.2±1.1 fold, (p&lt;0.001, n=5) and MMP2 1.5±0.2, (p&lt;0.05, n=5:) as analyzed in rat tissue by RT-PCR. This correlates with improved ventricular ejection fraction at day 7 and day 28 post MI (CEL 45.8 ± 2.4% vs. CNT, 34.8±3.3%, p=0.005 (7d), and 44.3 ± 2.8% vs 34.4 ± 4.1%, p=0.01 (28d). After 28 days post MI, MI+CEL group had a higher percentage of viable myocardial tissue as compared to MI group (MI+CEL, n=4: 70.2 ± 0.5%, vs MI, n=5: 56.38 ± 3.8%, n=4 p&lt;0.05) as analyzed Masson’s Trichrome staining. We next combined Celastrol therapy with cardiac stem cell therapy (pretreatment of CDCs for 24 hours with Celastrol prior to their injection in infarcted myocardium) and evaluate the potential of CEL treated hCDCs to repair/preserve infarcted myocardium by ventricular ejection fraction. Echos performed after LAD ligation revealed a preserved ventricular ejection fraction in rats treated with CEL+hCDCs compared to controls (IMDM media) or CDCs by itself. (hCDCs+CEL, n=4: 62.9±1.0% vs IMDM, n=4: 32.95±2.7%, P&lt;0.05; hCDCs, n=4: 53.28±4.0%, P&lt;0.05 at 28 days). These initial studies suggests the effectiveness of combinatorial therapy of CEL and hCDCs. Oral delivery makes CEL a potentially clinically useful adjunct after MI.
Abstract 1938: Exportin-1 (XPO1) is a novel therapeutic biomarker for patients with neuroblastoma
Authors: Basia Galinski, Marcus Luxemburg, Michelle Ewart, Yosef Landesman, Daniel Weiser
Journal: Cancer Research (2017)

Abstract Background: Half of patients with high-risk neuroblastoma succumb to disease, yet these patients with inferior outcome cannot be identified at diagnosis despite contemporary risk stratification that integrates MYCN copy number status, tumor histology, and patient age. We have shown that overexpression of Exportin-1 (XPO1) is associated with poor survival in neuroblastoma, affirming what has been identified across a range of malignancies. Selinexor (KPT-330, Karyopharm Therapeutics), an XPO1 inhibitor in early phase clinical trials, inhibits the nuclear to cytoplasmic translocation of tumor suppressor and growth regulatory proteins implicated in oncogenesis. We hypothesized that protein expression level of XPO1 in neuroblastoma cell lines predict the effective response of treatment with selinexor. Methods: We used a panel of early passage patient derived neuroblastoma cell lines including IMR5, NLF, KELLY, NB-EBC1, and SKNSH that are representative of the spectrum and genetic diversity of human disease. Cell lines were treated with varying concentrations of selinexor. RNA and whole cell protein extract as well as nuclear and cytoplasmic fractionated protein was obtained from untreated and treated conditions. Treated and untreated cells were also pelleted, and, along with patient tumor samples, formalin-fixed and paraffin-embedded for microscopic and immunohistochemical (IHC) evaluation. Results: Compared to noncancerous cell lines, neuroblastoma cell lines have high protein and mRNA expression of XPO1; higher expression correlates with greater sensitivity to selinexor. Selinexor treatment reduced XPO1 protein and increased XPO1 mRNA expression, and it lead to nuclear retention of XPO1 cargo such as p53 and survivin. Comparison of microscopic features and protein staining intensity of patient samples with known XPO1 expression is ongoing. Conclusions: This study provides rationale for XPO1 protein abundance as a potential biomarker of therapeutic response to the drug selinexor. By using patient derived neuroblastoma cell lines, we are able to evaluate the response of selinexor and XPO1 expression in the context of this enigmatic disease. These data suggest that initial drug response to selinexor can be predicted early in the course of disease and more investigation of the high expression of XPO1 seen in patients with poor outcome will provide strategies for combinatorial treatment approaches. Citation Format: Basia Galinski, Marcus Luxemburg, Michelle Ewart, Yosef Landesman, Daniel Weiser. Exportin-1 (XPO1) is a novel therapeutic biomarker for patients with neuroblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1938. doi:10.1158/1538-7445.AM2017-1938