tbuckley/cabot-search huggingface dataset:
Abstract 341: Investigating a novel GPCR ITIM motif in regulating Shp2 binding, signaling, and migration
Authors: Ryan D. Paulukinas, Lili T. Belcastro, Catherine C. Moore
Journal: Cancer Research (2017)

Abstract Aberrant expression of CXCR4, a chemokine G protein-coupled receptor (GPCR), promotes a migratory and invasive phenotype during breast cancer metastasis, however the mechanism is unknown. Here we investigate the role of CXCR4 tyrosine phosphorylation within a novel ITIM motif. Following activation, CXCR4 is normally phosphorylated on Ser/Thr residues, which promotes receptor desensitization and internalization. We found previously that Ser/Thr phosphorylation of CXCR4 is delayed upon SDF gradient sensing, and correlates with sustained signaling to SHP2, a protein that drives hyperproliferation and invasion of breast cancer. Since SHP2 is known to be recruited to tyrosine phosphorylated ITIM motifs (immmunoreceptor tyrosine-based inhibitory consensus motifs), we investigated if CXCR4 contains an ITIM motif, and if tyrosine phosphorylation within this motif regulates SHP2 binding, signaling, and migration. Specifically, we assessed 1) if CXCR4 is tyrosine phosphorylated as measured by recombinant phosphatase assay, phospho-Ab development, and tyrosine mutagenesis (YF); 2) if tyrosine mutagenesis alters CXCR4 membrane localization, internalization, and SDF gradient sensing, by ELISA; 3) if tyrosine mutagenesis disrupts CXCR4 interaction with SHP2, by co-IP; 4) if tyrosine mutagenesis alters CXCR4 sustained signaling to SHP2, by Western; and 5) if tyrosine mutation (YF) within the novel ITIM motif in CXCR4 alters migration of metastatic breast cancer cells, by transwell motility assays. Our results demonstrate that CXCR4 phosphorylation is sensitive to recombinant tyrosine phosphatase treatment and tyrosine mutagenesis, suggesting that CXCR4 is indeed tyrosine phosphorylated within the ITIM motif. We determined that while tyrosine phosphorylation within the ITIM motif is not required for CXCR4 membrane localization, internalization, or SDF gradient sensing, it does regulate CXCR4 binding and signaling to SHP2. Investigating the role in CXCR4 mediated migration is on going. To date, our data support a working model that tyrosine phosphorylation of CXCR4 within an ITIM motif is critical for binding to SHP2 and transducing sustained signaling to SHP2. These data have implications on aggressive breast cancers with dysregulated CXCR4 and SHP2. These studies were supported by NIH grant GM-097718, PA Department of Health grant SAP4100057688, and the Milton Lev Memorial Faculty Research Fund. Citation Format: Ryan D. Paulukinas, Lili T. Belcastro, Catherine C. Moore. Investigating a novel GPCR ITIM motif in regulating Shp2 binding, signaling, and migration [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 341. doi:10.1158/1538-7445.AM2017-341
Abstract 666: CD37 tetraspanin as a novel biomarker for PD-1 blockade in diffuse large B-cell lymphoma
Authors: Zijun Y. Xu-Monette, Ken H. Young
Journal: Cancer Research (2017)

Abstract PD-1 immune checkpoint blockade reconstituting antitumor immunity has changed the cancer treatment paradigm. PD-1 blockade has been successful in many types of solid tumors and Hodgkin lymphoma, but not yet for diffuse large B cell lymphoma (DLBCL), the most common aggressive B-cell lymphoma. We found several biomarkers including loss of CD37 tetraspanin expression in DLBCL correlated with increased PD-1 expression suggesting potential sensitivity of these DLBCL subsets to PD-1 blockade. CD37 (TSPAN26) is a member of the tetraspanin superfamily, widely expressed on normal and malignant mature B-cells and downregulated in plasma cells. It has been documented that CD37 plays important roles in T-cell-B-cell interactions, B-cell humoral response triggered by B-cell receptor cross-linking, and a balance between immune responses and tolerance. Interestingly, in a large cohort of DLBCL patients, we found that loss of CD37 expression in DLBCL predicts strikingly decreased overall and progression-free survival rates, and that PDCD1 gene expression was upregulated in CD37-negative activated B-cell-like (ABC) DLBCL by gene expression profiling, whereas the costimulatory molecule ICOSLG was upregulated in CD37+ germinal center B-cell-like (GCB) DLBCL. Using the new fluorescent multiplex technology, we further measured PD-1 and PD-L1 expression at the protein level on lymphoma cells and immune cells in the tumor microenvironment, and found that PD-1 protein levels were increased on both cytotoxic and helper T-cells infiltrating in CD37-negative DLBCL either of GCB or ABC subtype. These novel discoveries suggest that CD37 is important for sustained antitumor adaptive immunity, that immune dysregulation plays an important role for poor clinical outcomes in DLBCL, and that CD37-negative DLBCL may be sensitive to PD-1 blockade. In summary, loss of a CD37 tetraspanin was found to correlate with PD-1 overexpression in DLBCL clinical samples, and CD37 may serve as a novel biomarker for anti-PD-1 immunotherapy clinical trials in DLBCL. Note: This abstract was not presented at the meeting. Citation Format: Zijun Y. Xu-Monette, Ken H. Young. CD37 tetraspanin as a novel biomarker for PD-1 blockade in diffuse large B-cell lymphoma [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 666. doi:10.1158/1538-7445.AM2017-666
Abstract 418: Adaptive resistance to chemotherapy in triple-negative breast cancer revealed by single cell DNA and RNA sequencing
Authors: Charissa Kim, Ruli Gao, Emi Sei, Rachel Brandt, Nicola Crosetto, Theodoros Foukakis, Nicholas Navin
Journal: Cancer Research (2017)

Abstract Triple-negative breast cancer (TNBC) is an aggressive subtype that displays extensive intratumor heterogeneity and frequently (46%) develops resistance to neoadjuvant chemotherapy (NAC). Currently, the genomic basis of chemoresistance remains poorly understood. An important question is whether resistance to chemotherapy is driven by the selection of rare pre-existing subclones with genomic mutations and transcriptional programs that confer resistance to chemotherapy (adaptive resistance) or by the spontaneous induction of new mutations and expression changes that confer a resistant phenotype (acquired resistance). To investigate this question we applied single cell DNA and RNA sequencing methods and deep-exome sequencing to longitudinal time-point samples collected from a cohort of 20 TNBC patients. Deep-exome sequencing of the cohort at three time points revealed a random death model, wherein multiple clones were targeted, as opposed to the selection of specific somatic mutations. In contrast, single cell copy number profiling of ~800 cells from 8 patients identified an adaptive resistance model, wherein minor subclones from the pre-treatment tumors were selected and expanded in response to NAC. Similarly, single cell RNA sequencing of ~8000 cells from 8 patients identified subclones with chemoresistant phenotypes that were selected in response to NAC, resulting in the expansion of the resistant tumor mass. These data suggest that chemoresistance evolves through the selection of copy number changes and expression changes in signaling pathways associated with chemoresistance, rather than point mutations. This adaptive resistance model has important translational implications in clinical diagnostics, by suggesting that resistant clones can be detected in TNBC patients prior to the administration of chemotherapy. Citation Format: Charissa Kim, Ruli Gao, Emi Sei, Rachel Brandt, Nicola Crosetto, Theodoros Foukakis, Nicholas Navin. Adaptive resistance to chemotherapy in triple-negative breast cancer revealed by single cell DNA and RNA sequencing [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 418. doi:10.1158/1538-7445.AM2017-418
Errata: “Temporal Variability of Tungsten and Cobalt in Fallon, Nevada” & “A Retrospective Assessment of Occupational Exposure to Elemental Carbon in the U.S. Trucking Industry”
Authors: Paul R. Sheppard, Robert J. Speakman, Gary Ridenour, Mark L. Witten, Mary E. Davis, Jaime E. Hart, Francine Laden, Eric Garshick, Thomas J. Smith
Journal: Environmental Health Perspectives (2012)
Abstract LB-288: An allosteric PRC2 inhibitor targeting the H3K27me3 binding pocket of EED
Authors: Wei Qi, Kehao Zhao, Justin Gu, Ying Huang, Youzhen Wang, Hailong Zhang, Man Zhang, Jeff Zhang, Zhengtian Yu, Ling Li, Lin Teng, Shannon Chuai, Chao Zhang, Mengxi Zhao, HoMan Chan, Zijun Chen, Douglas Fang, Fei Qi, Leying Feng, Lijian Feng, Yuan Gao, Hui Ge, Xinjian Ge, Andreas Lingel, Guobin Li, Ying Lin, Yueqin Liu, Fangjun Luo, Minlong Shi, Long Wang, Zhaofu Wang, Yanyan Yu, Jue Zeng, Chenhui Zeng, Lijun Zhang, Qiong Zhang, Shaolian Zhou, Counde Oyang, Peter Atadja, En Li
Journal: Cancer Research (2017)

Abstract Polycomb repressive complex 2 (PRC2) consists of three core subunits, EZH2, EED and SUZ12 and plays pivotal roles in transcriptional regulation through its histone H3K27 methyltransferase activity. Dysregulation of PRC2 is observed in multiple human cancers, for example, the catalytic subunit EZH2 is overexpressed in a wide range of human cancers and gain-of-function mutations of EZH2 within its catalytic site have been reported in human B-cell lymphoma, parathyroid carcinoma and melanoma. Small molecule inhibitors that compete with the cofactor S-adenosylmethionine (SAM) have been reported and showed anti-lymphoma efficacy in pre-clinical studies. EED within the PRC2 complex allosterically activate the enzymatic activity by binding to tri-methylated H3K27 (H3K27me3). Here we report the discovery of EED226, a potent and selective PRC2 inhibitor directly binding to the H3K27me3 binding pocket of EED. EED226 induces conformational change upon binding EED leading to loss of PRC2 activity. EED226 shows similar activity as SAM-competitive inhibitors in blocking H3K27 methylation of PRC2 target genes and inducing regression of human lymphoma xenograft tumors. Interestingly, EED226 also effectively inhibits PRC2 containing mutant EZH2 protein resistant to SAM-competitive inhibitors. Together, we show EED226 inhibits PRC2 activity via an allosteric mechanism and offers opportunity for treatment of PRC2-dependent cancers. Citation Format: Wei Qi, Kehao Zhao, Justin Gu, Ying Huang, Youzhen Wang, Hailong Zhang, Man Zhang, Jeff Zhang, Zhengtian Yu, Ling Li, Lin Teng, Shannon Chuai, Chao Zhang, Mengxi Zhao, HoMan Chan, Zijun Chen, Douglas Fang, Fei Qi, Leying Feng, Lijian Feng, Yuan Gao, Hui Ge, Xinjian Ge, Andreas Lingel, Guobin Li, Ying Lin, Yueqin Liu, Fangjun Luo, Minlong Shi, Long Wang, Zhaofu Wang, Yanyan Yu, Jue Zeng, Chenhui Zeng, Lijun Zhang, Qiong Zhang, Shaolian Zhou, Counde Oyang, Peter Atadja, En Li. An allosteric PRC2 inhibitor targeting the H3K27me3 binding pocket of EED [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-288. doi:10.1158/1538-7445.AM2017-LB-288
Reproducibility and sensitivity to change of various methods of joint space width (JSW) measurements in osteoarthritis of the hip (OAH). A double reading of three different radiographic views taken within a 3-year time-interval.
Authors: E Maheu, C Cadet, M Marty, S Ghabri, I Kerloch, B Mazieres, Tim Spector, E Vignon, M Dougados, M Lequesne
Journal: Annals of the Rheumatic Diseases (2005)
Abstract 2095: E7090, a novel and selective FGFR inhibitor, for the treatment of cholangiocarcinoma cells harboring FGFR2-fusion genes
Authors: Saori W. Miyano, Yasuhito Arai, Junji Matsui, Tatsuhiro Shibata
Journal: Cancer Research (2017)

Abstract Genetic abnormalities (gene fusion, mutation and amplification) of fibroblast growth factor receptor (FGFR) family members are known to cause constitutive activation of their signaling pathways, which play an important role in proliferation, survival and migration of cancer cells, as well as tumor angiogenesis. Several recent studies have identified that FGFR2 gene fusions were found in about 10% of intrahepatic cholangiocarcinoma and acted as oncogenes. E7090, an orally available FGFR1, 2 and 3 inhibitor, whose chemical-structure and basic kinase inhibitory profile have been disclosed at AACR2015, is currently under a first-in-human study (NCT02275910). The antitumor activity of E7090 against NIH3T3 and human cholangiocarcinoma cells harboring FGFR2-fusion genes was investigated. NIH3T3 cells stably infected of five FGFR2-fusion genes (FGFR2-AHCYL1, FGFR2-BICC1 type1, FGFR2-BICC1 type2, FGFR2-TXLNA, or FGFR2-KCTD1), all of which were discovered in human intrahepatic cholangiocarcinoma patients, were successfully established and exhibited anchorage-independent cell growth in soft agar assay. E7090 revealed an inhibitory activity on soft agar colony formation of these cells with IC50 values of 0.9 to 17.3 nmol/L in a dose dependent manner. E7090 also reduced activation of downstream pathways of FGFR signaling (MAPK and STAT3) in these cells. Subcutaneous transplantation of FGFR2-BICC1 type2, FGFR2-TXLNA, or FGFR2-KCTD1 expressing cells into immune-deficient mice produced tumor growth, and then oral administration of E7090 at 12.5, 25 and 50 mg/kg showed significant tumor growth inhibition. Finally, antitumor activity of E7090 was examined in a patient derived xenograft (PDX) model of human cholangiocarcinoma harboring FGFR2-BICC1 fusion gene. E7090 also showed dose-dependent antitumor activity and more than 50% of tumor regression was achieved at a dose of 50 mg/kg. In conclusion, E7090 showed potent antitumor activity against FGFR2-fusion genes found in intrahepatic cholangiocarcinoma both in vitro and in vivo models, suggesting that E7090 may provide therapeutic opportunities for cholangiocarcinoma harboring FGFR2-fusion genes. Citation Format: Saori W. Miyano, Yasuhito Arai, Junji Matsui, Tatsuhiro Shibata. E7090, a novel and selective FGFR inhibitor, for the treatment of cholangiocarcinoma cells harboring FGFR2-fusion genes [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 2095. doi:10.1158/1538-7445.AM2017-2095
The Importance of Independent Evaluation
Authors: Kelly A. Johnson, Joseph S. Ross
Journal: JAMA Internal Medicine (2017)

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Abstract 3748: Development of anti-human mesothelin chimeric antigen receptor (CAR) messenger RNA (mRNA) transfected peripheral blood mononuclear cells (CARMA) for the treatment of mesothelin-expressing cancers
Authors: Chien-Fu Hung, Xuequn Xu, Linhong Li, Ying Ma, Qiu Jin, Angelia Viley, Cornell Allen, Pachai Natarajan, Rama Shivakumar, Madhusudan V. Peshwa, Leisha A. Emens
Journal: Cancer Research (2017)

Abstract CD19-targeted chimeric antigen receptor (CAR)-engineered T/NK-cell therapies can result in durable clinical responses in B-cell malignancies. However, CAR-based immunotherapies have been less successful in solid cancers. This is partly due to specificity for shared tumor antigens also present on normal host tissues that leads to ‘on-target/off-tumor’ toxicity. We therefore developed a non-viral approach using repeated infusions of mesothelin-specific messenger RNA (mRNA) CAR-transfected T cells to permit prospective control of ‘on-target/off-tumor’ toxicity. Early trials provided preliminary evidence of the safety and anti-tumor activity of this strategy, but the ex vivo selection, activation and expansion of lymphocytes is laborious and expensive. We therefore explored the feasibility of using a rapid, automated, closed system for cGMP-compliant mRNA CAR transfection into freshly isolated peripheral blood mononuclear cells for clinical scale manufacture (CARMA). The resulting cryopreserved cellular product expressed CAR in &amp;gt;95% of cells, and recognized and lysed tumor cells in an antigen-specific manner. Expression of CAR was detectable for 5-7 days in vitro, with a progressive decline of CAR expression related to in vitro cell expansion. In a murine ovarian cancer model, a single intra-peritoneal (IP) injection of CARMA resulted in the dose-dependent inhibition of tumor growth and prolonged the overall survival (OS) of mice. Multiple weekly IP injections of the optimal CARMA dose enhanced disease control and further prolonged OS, both of which improved with an increasing number of injections. No significant off-tumor toxicities were observed. These data support further investigation of serial IP CARMA administration as a potential treatment for ovarian cancer and other mesothelin-expressing tumors involving the peritoneum, and provide preclinical proof of principle of CARMA for solid tumors. Citation Format: Chien-Fu Hung, Xuequn Xu, Linhong Li, Ying Ma, Qiu Jin, Angelia Viley, Cornell Allen, Pachai Natarajan, Rama Shivakumar, Madhusudan V. Peshwa, Leisha A. Emens. Development of anti-human mesothelin chimeric antigen receptor (CAR) messenger RNA (mRNA) transfected peripheral blood mononuclear cells (CARMA) for the treatment of mesothelin-expressing cancers [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 3748. doi:10.1158/1538-7445.AM2017-3748
Abstract 1241: A preclinical study of the combined treatment of arginase and canavanine in pancreatic cancer
Authors: Tsz Tung Kwong, Chi Hang Wong, Herbert Ho Fung Loong, Stephen Lam Chan
Journal: Cancer Research (2017)

Abstract Background: Arginine deprivation is a novel approach for cancer treatment as some cancers were found to be arginine auxotrophic. PEG-BCT-100, a pegylated form of recombinant human arginase, was used to investigate the effect of arginine deprivation on pancreatic cell lines. On the other hand, Canavanine (CAV), a natural toxic analog of arginine isolated from leguminous plant, has also demonstrated its ability in inhibiting cancer cell proliferation. It alters the protein structure and causes critical metabolic defects in the cells by replacing arginine into newly synthesized proteins during translation. In this study, we have also tested the efficacy of combined arginase and CAV treatment on pancreatic cell lines. Methods: Pancreatic cell lines (MIA PaCa-2, CFPAC-1) and normal fibroblast cell line (WI-38), were either incubated in normal or arginine free condition. The corresponding IC50 of CAV was determined by cell viability assay. To evaluate the responsiveness to the combined treatment, cells were monitored by live cell imaging under the conditions of PEG-BCT-100 treatment alone (0.3IU/ml) or in combination with CAV (10μM or 50μM). The apoptotic effect of the combined treatment was examined by Western blotting and Annexin V assay. Results: Either arginase or CAV treatment could inhibit pancreatic cancer cell growth. The cells treated with CAV in arginine free condition demonstrated an inhibition of cell proliferation and its corresponding IC50 was significantly lowered from millimolar to micromolar concentration when arginine was withdrawn. Strong synergism of CAV and PEG-BCT-100 was observed after 48-hour treatment with enhanced apoptosis in pancreatic cell lines, but not in normal fibroblast cells. Both early and late apoptosis were observed in co-treated pancreatic cancer cells as indicated by Annexin V assay and the detection of polyADP ribosyl polymerase (PARP) in Western blot. Conclusion: Arginine deprivation by PEG-BCT-100 combined with CAV treatment showed a strong synergetic effect on inducing cell death in pancreatic cell lines, suggesting that the supplement of CAV could facilitate the treatment outcome of arginine deprivation by arginase. This combined treatment may serve as a treatment strategy for pancreatic cancer. Citation Format: Tsz Tung Kwong, Chi Hang Wong, Herbert Ho Fung Loong, Stephen Lam Chan. A preclinical study of the combined treatment of arginase and canavanine in pancreatic 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 1241. doi:10.1158/1538-7445.AM2017-1241
Abstract 2058: Co-treatment of NVP-BSK805 highly sensitizes drug-resistant cancer cells by increasing P-gp inhibition
Authors: Yu Jin Park, Ji Hyun Cheon, Ji Yeon Son, Sung Pil Yoon, Hyung Sik Kim
Journal: Cancer Research (2017)

Abstract The high expression of P-glycoprotein (P-gp) is consistently observed in multidrug resistance (MDR) cancer cells. The purpose of our study is to identify conditions that could increase the sensitivity of P-gp-overexpressing the drug-resistant KBV20C cancer cell line. We have used the commercially-available epigenetic library, which includes 128 compounds. Using the cellular viability test, we also identified that NVP-BSK805 is highly sensitized to KBV20C-resistant cells and vincristine treatment. However, NVP-BSK805-induced sensitization was not observed in vincristine-treated sensitive KB parent cells, suggesting that the effects are specific to resistant cancer cells. Using FACS analysis, western blot, and Annexin V staining, we identified that NVP-BSK805 sensitized vincristine-treated KBV20C cells arrest via apoptosis and G2. Furthermore, sensitization potency of NVP-BSK805, in combination with vincristine, was measured in KBV20C cells when comparing them with P-gp inhibitor verapamil or another Jak2 inhibitor CEP-33779. We further investigated the mechanisms of NVP-BSK805 against sensitization of vincristine-treated KBV20C cells. The sensitization mechanism of NVP-BSK805 was mainly dependent on the inhibition of P-gp. In addition, ATPase activity was conducted to identify its potential role in NVP-BSK805 for P-gp inhibition. Both NVP-BSK805 and CEP-33779 showed high binding affinity docking scores -9.1 and -7.4, respectively, against the ABCB1 receptor protein. Collectively, inhibition of P-gp by NVP-BSK805 can increase vincristine-sensitivity in MDR cancer cells through increased apoptosis and G2 arrest. Our findings indicate that the Jak2 inhibitor may be a promising target in the treatment of patients resistant to antimitotic drugs. Citation Format: Yu Jin Park, Ji Hyun Cheon, Ji Yeon Son, Sung Pil Yoon, Hyung Sik Kim. Co-treatment of NVP-BSK805 highly sensitizes drug-resistant cancer cells by increasing P-gp inhibition [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 2058. doi:10.1158/1538-7445.AM2017-2058