tbuckley/cabot-search huggingface dataset:
Long-term non-invasive ventilation therapies in children: A scoping review
Authors: Maria L. Castro-Codesal, Kristie Dehaan, Robin Featherstone, Prabhjot K. Bedi, Carmen Martinez Carrasco, Sherri L. Katz, Elaine Y. Chan, Glenda N. Bendiak, Fernanda R. Almeida, Deborah L. Olmstead, Rochelle Young, Vicki Woolf, Karen A. Waters, Colin Sullivan, Lisa Hartling, Joanna E. MacLean
Journal: Sleep Medicine Reviews (2017)

Long-term non-invasive ventilation (NIV) is a common modality of breathing support used for a range of sleep and respiratory disorders. The aim of this scoping review was to provide a summary of the literature relevant to long-term NIV use in children. We used systematic methodology to identify 11,581 studies with final inclusion of 289. We identified 76 terms referring to NIV; the most common term was NIV (22%). Study design characteristics were most often single center (84%), observational (63%), and retrospective (54%). NIV use was reported for 73 medical conditions with obstructive sleep apnea and spinal muscular atrophy as the most common conditions. Descriptive data, including NIV incidence (61%) and patient characteristics (51%), were most commonly reported. Outcomes from sleep studies were reported in 27% of studies followed by outcomes on reduction in respiratory morbidity in 19%. Adverse events and adherence were reported in 20% and 26% of articles respectively. Authors reported positive conclusions for 73% of articles. Long-term use of NIV has been documented in a large variety of pediatric patient groups with studies of lower methodological quality. While there are considerable data for the most common conditions, there are fewer data to support NIV use for many additional conditions.
Comparison of the sensitivity to endocrine therapy of PR+/ER- patients and ER+/PR- patients with HER2+ breast cancer
Authors: X. Hao, Y. Liu, R. Hui, J. Zhang
Journal: Journal of Clinical Oncology (2009)

e11558 Background: Her2 and PR expression are important indicators for prognosis of breast cancer. Aslo, it's proved that their expression could guide chemotherapy, endocrine therapy and targeted therapy in many studies. Methods: Collected 3,677 primary breast cancer cases from 2002 to 2004 in Tianjin University Cancer Hospital. All of the cases were confirmed by pathohistological method. All patients are female, aged from 15 to 92 years old, with median age 50 years old. Median follow-up time is 40 months. Her-2, PR and ER expression were detected by immunohistochemical methods. Results: 1. With Her2+ breast cancer, 168 patients are PR+/ER- and 211 patients are ER+/PR-. 2. All patients treated with anthracycline-based adjuvant chemotherapy with 6 cycles and then given endocrine therapy: Pre-menopausal patients were given TAM (10mg P.O Bid); Post-menopausal patients were given AI (letrozole 2.5m po. bid or anastrozole 1 mg P.O Qd). Median follow-up time is 45 months. With Her2+ BC, 3-year DFS(disease-free survival rate) of PR+/ER- patients is 94.53%, higher than that of PR-/ER+ ones (91.81%).With Her2- BC, 3-year DFS of PR+/ER- patients is lower than that of PR-/ER+ (p&lt;0.05). 3. Total of 1853 cases with 5-year followed up, and 1297 cases have been given endocrine therapy. 5-year overall survival rate was 83.41%. With Her2+ BC, it's significant difference that 5-year OS of PR+/ER- patients is higher than that of PR-/ER+ ones. However, there's no difference of 5- year OS between them with Her2- BC. Conclusions: With Her2+ breast cancer, 3-year DFS of PR+/ER- patients is higher than ER+/PR- and also PR+/ER- patients may more sensitive to endocrine therapy than ER+/PR- patients. No significant financial relationships to disclose.
Integrated Genome Sequencing Reveals Frequent Loss of Function Alterations of ARID1A and Other Epigenetic Modifiers in Sezary Syndrome
Authors: Mark Kiel, Anagh A Sahasrabuddhe, Thiru Velusamy, Fuzon Chung, Nathanael G. Bailey, Bryan L Betz, David W Bahler, Roberto N. Miranda, L. Jeffrey Medeiros, Megan S Lim, Kojo S.J. Elenitoba-Johnson
Journal: Blood (2014)
High prevalence of metabolic syndrome features in patients previously treated for non-functioning pituitary macroadenoma
Authors: Sjoerd D. Joustra, Kim M.J.A. Claessen, Natasha M. Appelman-Dijkstra, Olaf M. Dekkers, Andre P. Van Beek, Bruce H.R. Wolffenbuttel, Alberto M. Pereira, Nienke R. Biermasz
Journal: Endocrine Reviews (2013)

Introduction Patients treated for non-functioning pituitary macroadenoma (NFMA) have alterations in sleep characteristics and circadian rhythmicity. These symptoms may be related to dysfunction of the suprachiasmatic nucleus of the hypothalamus, since a vast majority experienced compression of the adjacent optic chiasm. In accordance, structural hypothalamic damage is associated with increased prevalence of the metabolic syndrome. However, metabolic sequelae in patients treated for NFMA are not well established, since these patients are usually studied in the setting of growth hormone deficiency (GHD) of heterogeneous origin. Aim To study the prevalence of (features) of the metabolic syndrome in patients with NFMA. Methods The metabolic syndrome (NCEP-ATP III criteria) was studied in an unselected cohort of patients in long-term remission after treatment for NFMA, receiving adequate substitution for any pituitary deficiencies. Population based normative data of 63,995 Dutch inhabitants were derived from the LifeLines cohort study. Standardized morbidity ratios (SMR) were calculated after indirect standardization of data stratified for age and gender. Results We included 145 patients (mean age 64 ± 12 yrs, 56% male) in remission at least 1 year postoperatively (mean 12 ± 9 yrs). Visual field defects before surgery were present in 86%, and 47% had received adjuvant radiotherapy. Any pituitary deficiency was present in 92%, and GHD in 75% (of which 75% used rhGH therapy). Patients had an increased risk for reduced HDL-cholesterol (SMR 1.59 (95% CI 1.13-2.11)), raised triglycerides (SMR 2.31 (95% CI 1.78-2.90)) and the metabolic syndrome (SMR 1.60 (95% CI 1.22-2.02)). Visual field defects at baseline were independently associated with increased blood pressure (OR 6.8 (95% CI 1.9-24.0)). Presence of GHD or rhGH therapy showed a BMI-dependent relation with the metabolic syndrome and reduced HDL-cholesterol, but not with increased triglycerides. Cortisol substitution and radiotherapy were of no influence. Conclusion Patients treated for NFMA have an increased prevalence of the metabolic syndrome, and visual field defects were associated with increased blood pressure. Hypothalamic dysfunction may explain these metabolic abnormalities, in addition to intrinsic imperfections of hormone replacement therapy or untreated GHD. Additional research is required to explore the relation between derangements in circadian rhythmicity and metabolic syndrome in this patients group.
Abstract 15: Remote Ischemic Preconditioning Confers Late Protection Against Myocardial Ischemia-Reperfusion Injury in Mice by Upregulating Interleukin-10
Authors: Zheqing Cai, Nirmal Parajuli, Xiaoxu Zheng, Lewis Becker
Journal: Circulation Research (2012)

Remote ischemic preconditioning (RIPC) induces a prolonged late phase of multi-organ protection against ischemia-reperfusion (IR) injury. In the present study, we tested the hypothesis that RIPC confers late protection against myocardial IR injury by upregulating expression of IL-10. Mice were exposed to lower limb RIPC or sham leg ischemia. After 24 h, mice with RIPC demonstrated decreased myocardial infarct size and improved cardiac contractility following 30-min ischemia and 120-min reperfusion (I-30/R-120), accompanied by increased phosphorylation of Akt and eNOS in the heart. These effects of RIPC were completely blocked by anti-IL-10 receptor antibodies. Moreover, in IL-10 KO mice, RIPC was no longer able to provide cardioprotection against IR injury. IL-10 receptors were expressed in cardiomyocytes under basal conditions. Stimulation with exogenous IL-10 increased Akt phosphorylation and decreased myocardial infarct size after I-30/R-120 in isolated perfused hearts. Wildtype mice with RIPC demonstrated increased plasma IL-10 levels, while in the preconditioned gastrocnemius muscle, the phosphatase PTEN was inactivated and expression of IL-10 was increased through Stat3. Myocyte-specific PTEN inactivation led to increased Stat3 phosphorylation and IL-10 protein expression in the gastrocnemius muscle. Taken together, these results suggest that RIPC induces late protection against myocardial IR injury by increasing expression of IL-10 in the remote muscle, followed by release of IL-10 into the circulation, and activation of protective signaling pathways in the heart. This study provides a scientific basis for the use of RIPC to confer systemic protection against IR injury.
Erratum: Mammalian target of rapamycin activator RHEB is frequently overexpressed in human carcinomas and is critical and sufficient for skin epithelial carcinogenesis (Cancer Research (2010) 70, (3287-3298) DOI:10.1158/0008-5472. CAN-09-3467)
Authors: Z. H. Lu, M. B. Shvartsman, A. Y. Lee, J. M. Shao, M. M. Murray, R. D. Kladney, D. Fan, S. Krajewski, G. G. Chiang, Gordon B Mills, J. M. Arbeit
Journal: Cancer Research (2010)
Abstract P4-09-01: Tumor suppressor control of the cancer stem cell angiogenic niche
Authors: D Crowe, K Kramer, J Wu
Journal: Cancer Research (2017)

Abstract Mammary stem cells (MSC) expansion is associated with aggressive human breast cancer. The nuclear receptor peroxisome proliferator activated receptor γ (PPARγ) is a breast cancer tumor suppressor, but the mechanisms of this suppression are not completely characterized. To determine if PPARγ regulates MSC expansion in mammary cancer, we deleted PPARγ expression in the mammary epithelium of an in vivo model of basal breast cancer. Loss of PPARγ expression reduced tumor latency, and expanded the CD24+/CD49fhi MSC population. PPARγ null mammary tumors exhibited increased angiogenesis which was detected in human breast cancer. In vivo inhibition of a PPARγ regulated miR-15a/angiopoietin-1 pathway blocked increased angiogenesis and MSC expansion. PPARγ bound and activated a canonical response element in the miR-15a gene. PPARγ null tumors were sensitive to the targeted anti-angiogenic drug sunitinib but resistant to cytotoxic chemotherapy. Normalization of tumor vasculature with sunitinib resulted in objective response to cytotoxic chemotherapy. Chemotherapy treated PPARγ null mammary tumors exhibited luminal phenotype and expansion of unipotent CD61+ luminal progenitor cells. Transplantation of chemotherapy treated luminal progenitor cells recapitulated the luminal phenotype. These results have important implications for anti-angiogenic therapy in breast cancer patients. Citation Format: Crowe D, Kramer K, Wu J. Tumor suppressor control of the cancer stem cell angiogenic niche [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-09-01.
Efficacy of High-Dose Sequential Chemotherapy and Autograft for Transformed Non Hodgkin’s B Cell Lymphoma: Results of a Retrospective Analysis from GITIL (Gruppo Italiano Terapie Innovative nei Linfomi).
Authors: Massimo Di Nicola, Liliana Devizzi, Alessandro Rambaldi, Manuela Zanni, Fabio Benedetti, Caterina Patti, Tiziano Barbui, Corrado Tarella, Alessandro M. Gianni
Journal: Blood (2007)
Abstract P3-03-08: A large-scale functional screen to identify resistance mechanisms to selective estrogen receptor degraders fulvestrant and GDC-810 in ER+ breast cancer
Authors: P Mao, Q Quartey, O Cohen, F Piccioni, N Wagle
Journal: Cancer Research (2017)

Abstract Therapies that target the estrogen receptor provide clinical benefit and improved survival for patients with estrogen receptor-positive (ER+) breast cancer, yet drug resistance remains a challenging problem, leading to disease relapse and mortality. In recent years, the selective estrogen receptor degrader (SERD) fulvestrant has become an important therapeutic option for patients with resistant ER+ metastatic breast cancer, and newer oral SERDs such as GDC-810 are currently being tested in clinical trials. The mechanisms of intrinsic and acquired resistance to SERDs remain to be fully elucidated. We conducted a large-scale lentiviral open reading frame (ORF) screen to identify genes whose overexpression confers drug resistance to either fulvestrant or GDC-810 in the ER+ breast cancer cell line T47D. The lentivral ORF expression library used in this study consists of 16,544 barcoded ORFs, including 2,767 ORFs with mutations. The initial screen yielded 72 genes resulting in resistance to fulvestrant and 85 genes resulting in resistance to GDC-0810, with 44 genes overlapping. The top ranked-genes included multiple genes belonging to the PI3K/Akt, ERbB/HER, and FGF/FGFR pathways as well as genes involved in cell cycle progression. Fibroblast growth factor receptor 1 (FGFR1) amplifications are frequently observed in patients with ER+ breast cancer, and have previously been implicated in resistance to endocrine therapies. Several FGFs (FGF3, FGF6, FGF10, and FGF22) were among the top-ranked resistance genes for both fulvestrant and GDC-0810, suggesting that activation of the FGFR signaling pathway may render cells resistant to fulvestrant and GDC-810. In the presence of FGF2, overexpression of FGFR1 in ER+ breast cancer cells resulted in resistance to both fulvestrant and GDC-0810. The ability of an FGFR inhibitor to overcome FGFR-mediated resistance to SERDs is being tested. Additional potential resistance genes identified in the ORF screen are also being validated. In summary, a whole-genome functional resistance screen has identified several candidate genes and pathways that may cause resistance to fulvestrant and GDC-810. Several of these candidates, such as FGFR1, are also found in patients who develop resistance to SERDs, suggesting rational combination therapies to overcome or preempt SERD resistance. Citation Format: Mao P, Quartey Q, Cohen O, Piccioni F, Wagle N. A large-scale functional screen to identify resistance mechanisms to selective estrogen receptor degraders fulvestrant and GDC-810 in ER+ breast cancer [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P3-03-08.
EXTERNALIZATION OF CONDUCTOR CABLES IN QUICKSITE AND QUICKFLEX LEFT VENTRICULAR LEADS
Authors: Madhu Reddy, Moustapha Atoui, Jayasree Pillarisetti, Sampath Gunda, Donita Atkins, Sudharani Bommana, Pramod Janga, Raghuveer Dendi, Rhea Pimentel, Martin Emert, Loren Berenbom, Dhanunjaya Lakkireddy
Journal: Journal of the American College of Cardiology (2015)
The Proteomic Landscape of Human Ex Vivo Regulatory and Conventional T Cells Reveals Specific Metabolic Requirements
Authors: Claudio Procaccini, Fortunata Carbone, Dario Di Silvestre, Francesca Brambilla, Veronica De Rosa, Mario Galgani, Deriggio Faicchia, Gianni Marone, Donatella Tramontano, Marco Corona, Carlo Alviggi, Antonio Porcellini, Antonio La Cava, Pierluigi Mauri, Giuseppe Matarese
Journal: Immunity (2016)

(Immunity 44, 406–421, February 16, 2016) In the originally published version of this article, Tables S1–S5 were accidentally omitted from the online version. They have been added to the online version, and the journal regrets this error. The Proteomic Landscape of Human Ex Vivo Regulatory and Conventional T Cells Reveals Specific Metabolic RequirementsProcaccini et al.ImmunityFebruary 16, 2016In BriefThe proteomic signature of human Treg and Tconv cells and their functional specialization is poorly understood. Matarese and colleagues identified metabolic pathway signatures that suggest a highly-tuned balance between glucose and fatty-acid oxidation impacting functions of in vitro versus ex vivo human Treg and Tconv cells. Full-Text PDF Open Access
The Learning Healthcare System and Cardiovascular Care: A Scientific Statement From the American Heart Association
Authors: Thomas M. Maddox, Nancy M. Albert, William B. Borden, Lesley H. Curtis, T. Bruce Ferguson, David P. Kao, Gregory M. Marcus, Eric D. Peterson, Rita Redberg, John S. Rumsfeld, Nilay D. Shah, James E. Tcheng
Journal: Circulation (2017)

The learning healthcare system uses health information technology and the health data infrastructure to apply scientific evidence at the point of clinical care while simultaneously collecting insights from that care to promote innovation in optimal healthcare delivery and to fuel new scientific discovery. To achieve these goals, the learning healthcare system requires systematic redesign of the current healthcare system, focusing on 4 major domains: science and informatics, patient-clinician partnerships, incentives, and development of a continuous learning culture. This scientific statement provides an overview of how these learning healthcare system domains can be realized in cardiovascular disease care. Current cardiovascular disease care innovations in informatics, data uses, patient engagement, continuous learning culture, and incentives are profiled. In addition, recommendations for next steps for the development of a learning healthcare system in cardiovascular care are presented.
Incidence and Risk Factors for Thrombosis in Patients with Acute Promyelocytic Leukemia. Experience of the PETHEMA LPA96 and LPA99 Protocols.
Authors: Pau Montesinos, Javier de la Serna, Edo Vellenga, Consuelo Rayon, Juan Bergua, Ricardo Parody, Jordi Esteve, Marcos Gonzalez, Salud Brunet, Miguel Sanz
Journal: Blood (2006)
Pralatrexate Is An Effective Treatment for Heavily Pretreated Patients with Relapsed/Refractory Transformed Mycosis Fungoides (tMF)
Authors: Francine M Foss, Steven M Horwitz, Lauren Pinter-Brown, Andre Goy, Barbara Pro, Bertrand Coiffier, Leslie Popplewell, Kerry Joanne Savage, Andrei Shustov, Jasmine M. Zain, Tony Koutsoukos, Steven M. Fruchtman, Owen A O'Connor
Journal: Blood (2010)
Clinical Efficacy and Safety of Combined Thalidomide and Fludarabine Therapy in B-Cell Chronic Lymphocytic Leukemia Patients.
Authors: Anna Dmoszynska, Krzysztof Giannopoulos, Malgorzata Kowal, Monika Podhorecka, Paulina Wlasiuk, Agnieszka Bojarska-Junak, Wioletta Trzesniewska, Jacek Rolinski
Journal: Blood (2006)
Blinatumomab versus Chemotherapy for Advanced Acute Lymphoblastic Leukemia
Authors: Hagop Kantarjian, Anthony Stein, Nicola Gökbuget, Adele K Fielding, Andre C Schuh, Josep-Maria Ribera, Andrew Wei, Hervé Dombret, Robin Foà, Renato Bassan, Önder Arslan, Miguel A Sanz, Julie Bergeron, Fatih Demirkan, Ewa Lech-Maranda, Alessandro Rambaldi, Xavier Thomas, Heinz-August Horst, Monika Brüggemann, Wolfram Klapper, Brent L Wood, Alex Fleishman, Dirk Nagorsen, Christopher Holland, Zachary Zimmerman, Max S Topp
Journal: New England Journal of Medicine (2017)

Blinatumomab, a bispecific monoclonal antibody construct that enables CD3-positive T cells to recognize and eliminate CD19-positive acute lymphoblastic leukemia (ALL) blasts, was approved for use in patients with relapsed or refractory B-cell precursor ALL on the basis of single-group trials that showed efficacy and manageable toxic effects.In this multi-institutional phase 3 trial, we randomly assigned adults with heavily pretreated B-cell precursor ALL, in a 2:1 ratio, to receive either blinatumomab or standard-of-care chemotherapy. The primary end point was overall survival.Of the 405 patients who were randomly assigned to receive blinatumomab (271 patients) or chemotherapy (134 patients), 376 patients received at least one dose. Overall survival was significantly longer in the blinatumomab group than in the chemotherapy group. The median overall survival was 7.7 months in the blinatumomab group and 4.0 months in the chemotherapy group (hazard ratio for death with blinatumomab vs. chemotherapy, 0.71; 95% confidence interval [CI], 0.55 to 0.93; P=0.01). Remission rates within 12 weeks after treatment initiation were significantly higher in the blinatumomab group than in the chemotherapy group, both with respect to complete remission with full hematologic recovery (34% vs. 16%, P<0.001) and with respect to complete remission with full, partial, or incomplete hematologic recovery (44% vs. 25%, P<0.001). Treatment with blinatumomab resulted in a higher rate of event-free survival than that with chemotherapy (6-month estimates, 31% vs. 12%; hazard ratio for an event of relapse after achieving a complete remission with full, partial, or incomplete hematologic recovery, or death, 0.55; 95% CI, 0.43 to 0.71; P<0.001), as well as a longer median duration of remission (7.3 vs. 4.6 months). A total of 24% of the patients in each treatment group underwent allogeneic stem-cell transplantation. Adverse events of grade 3 or higher were reported in 87% of the patients in the blinatumomab group and in 92% of the patients in the chemotherapy group.Treatment with blinatumomab resulted in significantly longer overall survival than chemotherapy among adult patients with relapsed or refractory B-cell precursor ALL. (Funded by Amgen; TOWER ClinicalTrials.gov number, NCT02013167 .).
Molecular Ontogeny of Donor-Derived Lymphomas Occurring After Transplantation,
Authors: Oliver Weigert, Nadja Kopp, Andrew A. Lane, Akinori Yoda, Suzanne E. Dahlberg, Donna Neuberg, Anita Y Bahar, Bjoern Chapuy, Frank Kuo, Terry Haley, Timothy J Sullivan, Edward Fox, Scott J. Rodig, Joseph H Antin, David M Weinstock
Journal: Blood (2011)
Pancreatic Cancer Progression Relies upon Mutant p53-Induced Oncogenic Signaling Mediated by NOP14
Authors: Yongxing Du, Ziwen Liu, Lei You, Pengjiao Hou, Xiaoxia Ren, Tao Jiao, Wenjing Zhao, Zongze Li, Hong Shu, Changzheng Liu, Yupei Zhao
Journal: Cancer Research (2017)

Mutant p53 (mutp53) proteins promote tumor invasion and metastasis in pancreatic ductal adenocarcinoma (PDAC). However, the mechanism underlying sustained activation of mutp53 oncogenic signaling is currently unclear. In this study, we report that NOP14 nucleolar protein (NOP14) expression is upregulated in PDAC tumors and metastatic tissue specimens. NOP14 overexpression promoted cell motility, whereas NOP14 inhibition decreased invasive capacity of PDAC cells. In vivo invasion assays conducted on established subcutaneously, orthotopically, and intravenously injected tumor mouse models also indicated NOP14 as a promoter of PDAC metastasis. Mechanistically, mutp53 was validated as a functional target of NOP14; NOP14 primed tumor invasion and metastasis by increasing the stability of mutp53 mRNA. The NOP14/mutp53 axis suppressed p21 expression at both the transcriptional and posttranscriptional levels via induction of miR-17-5p in PDAC cells. In vivo, high NOP14 expression in PDAC patient tumors correlated with local metastasis and lymph invasion. Overall, our findings define a novel mechanism for understanding the function of NOP14 in the metastatic cascade of PDAC. Targeting NOP14 allows for effective suppression of tumor invasion in a mutp53-dependent manner, implicating NOP14 inhibition as a potential approach for attenuating metastasis in p53-mutant tumors. Cancer Res; 77(10); 2661-73. ©2017 AACR.