tbuckley/cabot-search huggingface dataset:
Partnering Behavioral Modification With Bariatric Surgery
Authors: Christina A. Minami, Jonah J. Stulberg, Eric S. Hungness
Journal: JAMA (2016)

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Abstract 4045: Urban-rural disparity of overweight/obesity distribution and its potential association with breast cancer among Chinese females
Authors: Ying Gao, Yubei Huang, Hongji Dai, Peishan Wang, Haixin Li, Fengju Song, Hong Zheng, Henglei Dong, Jiali Han, Yaogang Wang, Kexin Chen
Journal: Cancer Research (2016)

Abstract Background: Disparity of overweight/obesity distribution had been investigated in developed countries, but rarely been investigated in developing countries, especially for China with rapid socio-economic development in the past decades. Methods: A total of 1 210 762 participants were recruited from the Chinese National Breast Cancer Screening Program. Overweight and obesity were defined as body mass index (BMI) ranged 24.0-27.9 kg/m2 and BMI ≥ 28.0kg/m2, respectively. Results: The prevalence of overweight/obesity for Chinese rural women (35.2%, 29.2% for overweight and 6.0% for obesity) was significantly higher than that for Chinese urban women (33.4%, 27.7% for overweight and 5.7% for obesity) (P &amp;lt;0.001). For either rural or urban women, the prevalence of overweight/obesity was highest in north region, followed by east region for rural women and north-east region for urban women. For rural women, higher prevalence of overweight/obesity was significantly positively associated with elder age, Han nationality, low level of education, no occupation, high family income, less number of family residents, insurance, and elder age at marriage. Similar positive associations were also found for urban women, except negative associations for high family income, less number of family residents, and elder age at marriage. A non-significant positive association between overweight/obesity and breast cancer was found for rural women [odds ratio (OR) = 1.06; 95% confidence interval (CI): 0.87-1.29], but a significant positive association for urban women (OR = 1.55; 95%CI: 1.19-2.02). Conclusions: There was an obvious urban-rural disparity of overweight/obesity distribution among Chinese females, which could also lead to an obvious disparity of breast cancer distribution. Citation Format: Ying Gao, Yubei Huang, Hongji Dai, Peishan Wang, Haixin Li, Fengju Song, Hong Zheng, Henglei Dong, Jiali Han, Yaogang Wang, Kexin Chen. Urban-rural disparity of overweight/obesity distribution and its potential association with breast cancer among Chinese females. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4045.
Phase 1 Trial Of Bone Marrow Stromal Cells (Bone Marrow-derived MSCS) To Treat Tissue Damage In Allogeneic Stem Cell Transplant Recipients: Biological Markers Correlate With Clinical Responses and Survival
Authors: Minoo Battiwalla, Fang Yin, Sawa Ito, Xingmin Feng, Fariba Chinian, J. Joseph Melenhorst, Eleftheria K Koklanaris, Marianna Sabatino, David Stroncek, Leigh Samsel, Jeffrey K. Klotz, Nancy F. Hensel, Pamela Robey, A. John Barrett
Journal: Blood (2013)
ALS disrupts spinal motor neuron maturation and aging pathways within gene co-expression networks
Authors: Ritchie Ho, Samuel Sances, Genevieve Gowing, Mackenzie Weygandt Amoroso, Jacqueline G O'Rourke, Anais Sahabian, Hynek Wichterle, Robert H Baloh, Dhruv Sareen, Clive N Svendsen
Journal: Nature Neuroscience (2016)
Abstract 1245: RRx-001 is effective in temozolomide-sensitive and resistant GBM
Authors: Veronica Steri, Bryan Oronsky, Jan Scicinski, Gabriele Bergers
Journal: Cancer Research (2016)

Abstract Glioblastoma Multiforme (GBM) is one of the most aggressive malignancies in humans, being highly invasive and drug-resistant, limiting the effectiveness of surgery, chemotherapy and radiotherapy. Concurrent Temozolomide (TMZ) and radiation is the standard of care for newly diagnosed GBM patients, however, patients respond poorly and prognosis remains dismal. TMZ response is limited to patients with hypermethylation of the methylguanine methyltransferase (MGMT) promoter. Despite recent advances in therapeutic strategies, treating GBM is still an unsolved clinical challenge requiring the investigation of novel approaches with better responses over approved therapies. RRx-001 is a novel ROS-mediated systemically non-toxic chemo-sensitizing epigenetic agent with vascular normalizing properties under investigation in Phase II clinical trials in brain metastases and GBM. We assessed whether RRx-001 is an effective approach for treating GBM by testing its effects alone and in combination with TMZ both in vitro as well as in GBM mouse models. RRx-001 induced cytotoxicity in human TMZ-sensitive as well as resistant patient-derived GBM cell lines. In addition, its effect in TMZ-sensitive GBM cells was greater than the one induced by TMZ alone. We then asked whether the in vitro effects of RRx-001 translated to therapeutic efficacy in vivo. To this end, we injected mice intracranially with a TMZ-resistant murine mesenchymal GBM cells, and treated tumor-bearing mice with RRx-001 alone and in combination with TMZ. RRx-001 treatment alone modestly prolonged survival compared to control cohorts, whereas the combination of RRx-001 and TMZ substantially prolonged survival compared to controls and either treatment alone. Moreover, histological evaluation of GBM tumors revealed that combination of RRx-001 and TMZ induced vessel hyperdilation and apoptosis compared to RRx-001 alone. Thus, in vivo RRx-001 combined to TMZ may also indirectly regulate tumor growth by modifying the tumor stroma. These data suggest that TMZ may still affect the microenvironment in TMZ-resistant tumors and that RRx-001 enhances these effects by both directly and indirectly restricting GBM growth, making it a promising therapeutic agent alone and in combination with TMZ. Citation Format: Veronica Steri, Bryan Oronsky, Jan Scicinski, Gabriele Bergers. RRx-001 is effective in temozolomide-sensitive and resistant GBM. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1245.
PWE-002 Cell growth is impaired in a cellular model of non-alcoholic fatty liver disease, but is unaffected by simple steatosis
Authors: E S Gilchrist, K Lockman, A Pryde, P Cowan, P Lee, J N Plevris
Journal: Gut (2010)

<h3>Introduction</h3> Non-alcoholic fatty liver disease (NAFLD) is an important cause of cirrhosis. Cirrhosis can be considered as a state where disordered growth leads to inadequate repair and a risk of malignancy. We sought to study the growth characteristics of C3A cells in an in vitro model of NAFLD. <h3>Methods</h3> C3A cells (well differentiated hepatoblastoma cells) were preconditioned for 72 h in control media, media containing oleate (which leads to steatosis, but not insulin resistance) or LPON media containing lactate (L), pyruvate (P), octanoate (O) and ammonia (N) (leading to steatosis, insulin resistance and increased reactive oxygen species). The cells were passaged and re-incubated in the appropriate media. Cells were harvested daily for cell counting and total protein estimation for 5 days. Cell cycle analysis and apoptosis estimation were performed on day 3. <h3>Results</h3> Growth curves were established, showing by both cell counting and protein estimation that growth was significantly reduced in the NAFLD model (p&lt; 0.0001) compared to control media and oleate (Abstract 002 Figure 1). Cell cycle analysis showed that cells grown in LPON did not accumulate in G0/G1, but appeared to accumulate in S phase (Abstract 002 Figure 2). Cells grown in oleate cycled normally. There was an increase in apoptosis in both oleate and LPON groups (26.1 and 27.7% cells undergoing apoptosis, compared to 13.5% of control cells, p&lt;0.0001). <h3>Conclusion</h3> NAFLD-induced cells showed significantly impaired growth compared with both control and simple steatotic cells in this model. This was not wholly attributable to an increase in apoptosis, as there was a similar increase in apoptosis with steatosis. While simple fat accumulation increased apoptosis, there was in addition, impairment of cell growth in our NAFLD model, which may be due to formation of reactive oxygen species, causing DNA damage and cell cycle arrest.
Abstract 321: S49076, a novel kinase inhibitor of MET, AXL and FGFR, demonstrates marked in vitro and in vivo efficacy in hepatocellular carcinoma
Authors: Annemilai Tijeras-Raballand, Adrien Pasteur-Rousseau, Matthieu Martinet, Philippe Bonnin, Marc Pocard, Sébastien Banquet, Valérie Cattan, Eric Raymond, Armand de Gramont
Journal: Cancer Research (2016)

Abstract Introduction: Hepatocellular carcinoma (HCC) is the second cause of cancer-related deaths worldwide. While sorafenib may improve overall survival in advanced HCC, new therapies are needed. Both preclinical and clinical data support a role of MET and AXL receptor tyrosine kinases in HCC progression. We thus evaluated S49076, a novel MET/AXL/FGFR inhibitor in HCC cell lines in vitro and in a transgenic mouse model of HCC. Materials and Methods: MET and AXL expressions were assessed in a panel of HCC cell lines by western blot. Downstream signaling pathways were investigated in the presence of HGF, GAS6 and S49076. Cell invasion was evaluated on matrigel assay. Transgenic mice developing stage-defined HCC were treated with S49076 (50mg/kg). Tumor response was evaluated measuring liver volume by echo-doppler and the number of tumor nodules at intermediary (12weeks) and final sacrifice (16 weeks). Results: Both MET and AXL are expressed in the majority of HCC lines screened. Notably, a high level of AXL was observed in the SK-HEP1 cells which were therefore selected for further investigation. MET and AXL pathways were strongly stimulated by their respective ligands, HGF and GAS6. Combination of HGF and GAS6 led to marked activation of ERK. S49076 inhibited MET and AXL pathway activation and HGF- and GAS6- induced invasion at nanomolar concentrations. In vivo anti-tumor efficacy of S49076 was demonstrated in a transgenic MET-expressing mouse model of HCC. Conclusion: S49076 displayed strong MET and AXL pathway inhibition and anti-invasive properties in SK-HEP1 HCC cells. Moreover, S49076 demonstrated antitumor activity in a mouse model of HCC. Together, these results would support development of S49076 as an innovative treatment in HCC patients. Citation Format: Annemilai Tijeras-Raballand, Adrien Pasteur-Rousseau, Matthieu Martinet, Philippe Bonnin, Marc Pocard, Sébastien Banquet, Valérie Cattan, Eric Raymond, Armand de Gramont. S49076, a novel kinase inhibitor of MET, AXL and FGFR, demonstrates marked in vitro and in vivo efficacy in hepatocellular carcinoma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 321.
Outcome Of Dose-Adjusted Decitabine Regimen Compared With FLAG Regimen In The Treatment Of Relapsed/Refractory Acute Myeloid Leukemia
Authors: Qian Wu, Guangsheng He, Wu Depei, Aining Sun, Huiying Qiu, Zhengming Jin, Miao Miao, XiaoWen Tang, Yue Han, Yiming Shen, Feng Chen, Xiaohui Hu, Song Jin, Xuhui Zhang
Journal: Blood (2013)
Interleukin-23 Drives Intestinal Inflammation through Direct Activity on T Cells
Authors: Philip P. Ahern, Chris Schiering, Sofia Buonocore, Mandy J. McGeachy, Dan J. Cua, Kevin J. Maloy, Fiona Powrie
Journal: Immunity (2011)

(Immunity 33, 279–288; August 27, 2010) In this paper, there was an error in Figure 1F . The histology panel on the left is incorrect; it is the same as the image on the right taken in a different frame. Thus, both images depict the liver of a Rag1−/− host transferred with Il23r−/− T cells. The correct image of a representative liver section of a Rag1−/− host transferred with WT T cells is published here, along with the rest of the figure. The authors regret any inconvenience this error has caused. Interleukin-23 Drives Intestinal Inflammation through Direct Activity on T CellsAhern et al.ImmunityAugust 27, 2010In BriefMutations in the IL23R gene are linked to inflammatory bowel disease susceptibility. Experimental models have shown that interleukin-23 (IL-23) orchestrates innate and T cell-dependent colitis; however, the cell populations it acts on to induce intestinal immune pathology are unknown. Here, using Il23r−/− T cells, we demonstrated that T cell reactivity to IL-23 was critical for development of intestinal pathology, but not for systemic inflammation. Through direct signaling into T cells, IL-23 drove intestinal T cell proliferation, promoted intestinal Th17 cell accumulation, and enhanced the emergence of an IL-17A+IFN-γ+ population of T cells. Full-Text PDF Open Access
Randomised, double-blind, placebo-controlled trial with azithromycin selects for anti-inflammatory microbial metabolites in the emphysematous lung
Authors: Leopoldo N Segal, Jose C Clemente, Benjamin G Wu, William R Wikoff, Zhan Gao, Yonghua Li, Jane P Ko, William N Rom, Martin J Blaser, Michael D Weiden
Journal: Thorax (2016)

Azithromycin (AZM) reduces pulmonary inflammation and exacerbations in patients with COPD having emphysema. The antimicrobial effects of AZM on the lower airway microbiome are not known and may contribute to its beneficial effects. Here we tested whether AZM treatment affects the lung microbiome and bacterial metabolites that might contribute to changes in levels of inflammatory cytokines in the airways.20 smokers (current or ex-smokers) with emphysema were randomised to receive AZM 250 mg or placebo daily for 8 weeks. Bronchoalveolar lavage (BAL) was performed at baseline and after treatment. Measurements performed in acellular BAL fluid included 16S rRNA gene sequences and quantity; 39 cytokines, chemokines and growth factors and 119 identified metabolites. The response to lipopolysaccharide (LPS) by alveolar macrophages after ex-vivo treatment with AZM or bacterial metabolites was assessed.Compared with placebo, AZM did not alter bacterial burden but reduced α-diversity, decreasing 11 low abundance taxa, none of which are classical pulmonary pathogens. Compared with placebo, AZM treatment led to reduced in-vivo levels of chemokine (C-X-C) ligand 1 (CXCL1), tumour necrosis factor (TNF)-α, interleukin (IL)-13 and IL-12p40 in BAL, but increased bacterial metabolites including glycolic acid, indol-3-acetate and linoleic acid. Glycolic acid and indol-3-acetate, but not AZM, blunted ex-vivo LPS-induced alveolar macrophage generation of CXCL1, TNF-α, IL-13 and IL-12p40.AZM treatment altered both lung microbiota and metabolome, affecting anti-inflammatory bacterial metabolites that may contribute to its therapeutic effects.NCT02557958.
Abstract 3628: Improving sequencing quality of libraries prepared from FFPE DNA
Authors: pingfang liu, Lixin Chen, Laurence Ettwiller, Christine Sumner, Fiona J. Stewart, Eileen T. Dimalanta, Theodore B. Davis, Evans C. Thomas
Journal: Cancer Research (2016)

Abstract Targeted cancer therapy based on genomic alterations can be remarkably effective, and has made significant strides with the recent advances in next-generation sequencing (NGS) technology. Although samples of blood and other bodily fluids are being actively explored for early disease diagnosis and treatment monitoring, DNA isolated from FFPE samples is currently the main source for NGS-based cancer profiling in clinical settings. Unfortunately, sequencing DNA from FFPE samples is challenging due to limited quantities and poor quality, a result of DNA damage incurred during fixation and storage. Artifacts associated with FFPE DNA have limited the mutation detection sensitivity to ≥ 5% mutant allele frequency (Frampton et al, Nature Biotechnology 2013), which would unfortunately leave many low-abundance genetic variants of clinical significance undetected. For example, clinical resistance-causing KIT and EGFR mutations can be present in tumors at levels &amp;lt;&amp;lt; 1% (Milbury et al, Clin. Chem. 2012). In this study, we investigated the effects of DNA repair and different sample handling workflows on sequencing quality of libraries prepared from FFPE samples. Careful analysis of sequencing data showed that base calling qualities for all 4 bases are improved, and aberrant G:C to A:T mutations were significantly reduced upon DNA repair. Because the large majority of mutations encountered in human tumors are G:C to A:T mutations (Greenman, C. Nature 2007), we expect that lowering the damage induced background noise of FFPE DNA would allow more reliable detection of clinically important, actionable mutations at lower abundance. In addition, we observed specific sequencing artifacts associated with the method of handling FFPE samples and have since identified effective measurements to avoid such artifacts. We expect that these improvements in sequencing quality of FFPE samples would ultimately enable more sensitive and robust detection of many low level genetic variations in clinically and biologically relevant cancer genes. Citation Format: pingfang liu, Lixin Chen, Laurence Ettwiller, Christine Sumner, Fiona J. Stewart, Eileen T. Dimalanta, Theodore B. Davis, Evans C. Thomas. Improving sequencing quality of libraries prepared from FFPE DNA. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3628.
Whole Exome Analysis Of Germline Alterations Associated With Myelodysplastic Syndrome
Authors: Sarah McMahon, Bartlomiej P Przychodzen, Hideki Makishima, Thomas LaFramboise, Kenichi Yoshida, Yuichi Shiraishi, Masashi Sanada, Yasunobu Nagata, Yusuke Sato, Kenichi Chiba, Hiroko Tanaka, Satoru Miyano, Aiko Sato-Otsubo, Seishi Ogawa, Jaroslaw P. Maciejewski
Journal: Blood (2013)
Abstract 4898: Effects of chemotherapeutic agents on the tumor immune microenvironment
Authors: Marcia P. Belvin, Shiuh-Ming Luoh, Jeanne Cheung, Erin McNamara, Rafael Cubas, Jeong Kim
Journal: Cancer Research (2016)

Abstract Immunotherapeutic agents have shown dramatic success in oncology in recent years and several have been approved in melanoma and lung cancer. One strategy for extending the benefit of immunotherapy is to evaluate these agents in combination with standard of care chemotherapy, with the goal of bringing the benefit of immunotherapy into earlier lines of treatment. We have carried out a systematic evaluation of the effects of different classes of chemotherapeutic agents (including alkylating agents, platinum based agents, and taxanes) on the tumor immune microenvironment of syngeneic murine tumor models (CT26 and MC38) in two different strains of mice (BALB/c and C57BL/6). We found that different chemotherapeutic agents caused markedly different changes in the composition and cell phenotype of the tumor immune environment. The majority of chemotherapeutic agents resulted in a mild to moderate increase in CD8+ T cells in the tumor. Some agents also altered the activation state of these CD8+ cells as measured by the level of PD-1 and IFN-gamma. A subset of the chemotherapeutic agents resulted in profound changes in the number of CD4+ cells, including regulatory T cells, as well as changes in myeloid subpopulations including monocytes, neutrophils, and macrophages. In addition to single agents studies, we carried out combination studies of selected chemo agents with simultaneous addition of anti-PD-L1. Several of these combinations caused pronounced increases in efficacy above single agent treatment. We will present the combination pharmacodynamic marker changes and efficacy of these treatments. Our findings demonstrate that chemotherapeutic agents can stimulate the tumor immune environment, at least transiently, through multiple mechanisms. Different subsets of chemotherapeutic agents display unique changes in the tumor immune infiltrate, and may require different immunotherapeutic approaches. These findings provide a rationale for testing immunotherapy-chemotherapy combinations in the clinic. Citation Format: Marcia P. Belvin, Shiuh-Ming Luoh, Jeanne Cheung, Erin McNamara, Rafael Cubas, Jeong Kim. Effects of chemotherapeutic agents on the tumor immune microenvironment. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4898.