tbuckley/cabot-search huggingface dataset:
Digitizing the cancer care continuum: Electronic, shareable survivorship care plans.
Authors: Jeremy Warner, Suzanne E Maddux, Jeff Brown, John Turner Hamm, John C. Krauss, Deborah Mayer, Ruth Rechis, Anna E. Schorer, Charles L. Shapiro, Lawrence N. Shulman, Neeta K. Venepalli, Edward P. Ambinder
Journal: Journal of Clinical Oncology (2016)

10101 Background: Cancer survivorship care planning was recognized as critical in a seminal 2005 Institute of Medicine report, From Cancer Patient to Cancer Survivor. Recently, the Commission on Cancer (CoC) instituted a requirement that Stage I-III patients treated with curative intent receive a treatment summary and a survivorship care plan (SCP; CoC Standard 3.3). By 2019, > 75% of eligible patients must receive a SCP. In 2015, ASCO’s Health Information Technology Work Group began transforming ASCO’s paper-based SCP template, published in the Journal of Oncology Practice (Mayer et al. 2014), into an electronic, shareable format. We report on the digital SCP and issues that needed resolution. Methods: The content and structure of ASCO’s SCP template were analyzed and translated, when possible, into unambiguous coded concepts. Subject matter experts were engaged to expand ASCO’s existing Health Level Seven International (HL7) Implementation Guide, the Clinical Oncology Treatment Plan and Summary (COTPS) Release 2.1, with the SCP elements. Results: For the SCP, six new sections and 26 data elements were created. The elements identified for computable value sets included the long-term toxicities of chemotherapy, cancer-specific surgeries, and details of radiation therapy. This led to discussions with the CDC, CoC, the FORDS Steering Committee, and the NCI Enterprise Vocabulary Services. The COTPS Release 3 was balloted through HL7, and all comments were resolved. Publication will take place in 2016. Conclusions: Data sharing is critical for the complex and multidisciplinary cancer care continuum. The process of creating an SCP interoperability standard exposed data gaps for the oncology community as a whole. For example, the CTCAE was identified as the best value set for acute chemotherapy toxicities, but it and others were not designed to expressively capture long-term toxicities. A shareable digital SCP allows cancer survivors to move forward with their lives, easing transitions of care to new geographic locations or other healthcare environments. Vendor implementations of COTPS that enable auto-population of data elements will help oncologists meet the CoC SCP standard to the benefit of patients and all care team members.
GW28-e0155 Decrease Lean Mass and Increase Fat Mass of SGA Adult Rats Associated with Down-Regulation of the mTOR/S6K Pathway in Skeletal Muscle
Authors: Muxue Yu, Chuyi Guo, Linxia Deng, Zhenyu Shen, Xiaoshan Qiu
Journal: Journal of the American College of Cardiology (2017)
Activity of sorafenib used singly or in combination with other cytotoxic drugs in gastric cancer cell lines: a preclinical study
Authors: Anna Tesei, Giovanni Brigliadori, Paola Ulivi, Francesco Fabbri, Chiara Arienti, Dino Amadori, Rosella Silvestrini, Wainer Zoli
Journal: Cancer Research (2008)

2810    Aims . To evaluate the cytotoxic effect of sorafenib used as single agent or in combination with taxanes in human cell lines derived from gastric cancers.   Experimental procedures . The experiments were performed on three cell lines (GK2, AKG, and KKP) established in our laboratory from human gastric adenocarcinoma. The effect on tumor growth was evaluated by sulforhodamine B assay and drug interaction studies were performed according to the Chou Talalay method. Cell cycle perturbations, apoptosis and the presence of mitotic catastrophe were evaluated by flow cytometric analysis and by microscopic examination of typical morphological features. Apoptosis- and chemoresistance- or chemosensitivity-related markers were evaluated by western-blot technique.   Results.  Sorafenib induced a cytotoxic effect, with IG 50  (drug concentrations inhibiting cell growth by 50%)  values ranging from 3.4 to 5.4 μM. A 48-h exposure to sorafenib caused a significant increase in cells in G2-M phase in GK2 and AKG cell lines and also in S phase in AKG line. Moreover, after a 48-h exposure to sorafenib 10 µM, a downregulation of MAP-K/ERK phosphorylation was observed. Furthermore, a decrease in Mcl-1 expression was observed in all cell lines, in parallel with a downregulation of antiapoptotic protein P-Bad. These changes were accompanied by caspase-3 cleavage, most evident in KKP cell line in which the highest percentage of apoptotic cells was recorded. The drug combination studies highlighted an antagonistic effect when exposure to sorafenib preceded that of a taxane and only an additive effect when cells were exposed simultaneously to the two drugs. Conversely, a synergistic interaction was obtained when taxane exposure preceded that of sorafenib, and was highly dependent on the time interval between exposure to the two drugs. Synergism was observed in all 3 cell lines after an interval of 24 h, in 2 cell lines after 48 h and in only 1 cell line after 72h. The efficacy of the two drugs was much lower when docetaxel was substituted by paclitaxel. A plausible explanation for the synergistic interaction observed could be that complementary targets exist along the same apoptotic pathways, e.g. downregulation of anti-apoptotic proteins belonging to bcl-2 family, P-Bad and MCL-1 by sorafenib, and phosphorylation of bcl-2 protein by docetaxel. Furthermore, the induction of an anomalous multidiploid G 0 -G 1  cell cycle phase and the triggering of the mitotic catastrophe process by a short exposure to low concentrations of docetaxel could make the cells more sensitive to subsequent exposure to sorafenib.   Conclusions.  An empirical schedule for the  association of sorafenib with taxanes may produce either  positive synergistic or undesirable antagonistic effects, highlighting the need  to identify  the most effective  clinical treatments through preclinical studies.
Downregulation of NMI promotes tumor growth and predicts poor prognosis in human lung adenocarcinomas
Authors: Jingshu Wang, Kun Zou, Xu Feng, Miao Chen, Cong Li, Ranran Tang, Yang Xuan, Meihua Luo, Wangbing Chen, Huijuan Qiu, Ge Qin, Yixin Li, Changlin Zhang, Binyi Xiao, Lan Kang, Tiebang Kang, Wenlin Huang, Xinfa Yu, Xiaojun Wu, Wuguo Deng
Journal: Molecular Cancer (2017)

N-myc (and STAT) interactor (NMI) plays vital roles in tumor growth, progression, and metastasis. In this study, we identified NMI as a potential tumor suppressor in lung cancer and explored its molecular mechanism involved in lung cancer progression.Human lung cancer cell lines and a mouse xenograft model was used to study the effect of NMI on tumor growth. The expression of NMI, COX-2 and relevant signaling proteins were examined by Western blot. Tissue microarray immunohistochemical analysis was performed to assess the correlation between NMI and COX-2 expression in lung cancer patients.NMI was highly expressed in normal lung cells and tissues, but lowly expressed in lung cancer cells and tissues. Overexpression of NMI induced apoptosis, suppressed lung cancer cell growth and migration, which were mediated by up-regulation of the cleaved caspase-3/9 and down-regulation of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin, and COX-2/PGE2. In contrast, knockdown of NMI promoted lung cancer cell colony formation and migration, which were correlated with the increased expression of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin and COX-2/PGE2. Further study showed that NMI suppressed COX-2 expression through inhibition of the p50/p65 NF-κB acetylation mediated by p300. The xenograft lung cancer mouse models also confirmed the NMI-mediated suppression of tumor growth by inhibiting COX-2 signaling. Moreover, tissue microarray immunohistochemical analysis of lung adenocarcinomas also demonstrated a negative correlation between NMI and COX-2 expression. Kaplan-Meier analysis indicated that the patients with high level of NMI had a significantly better prognosis.Our study showed that NMI suppressed tumor growth by inhibiting PI3K/AKT, MMP2/MMP9, COX-2/PGE2 signaling pathways and p300-mediated NF-κB acetylation, and predicted a favorable prognosis in human lung adenocarcinomas, suggesting that NMI was a potential tumor suppressor in lung cancer.
Loss of SWI/SNF chromatin remodelling complex is linked to advanced urinary bladder cancer
Authors: M. Szymanski, E. Sarnowska, A. Ornoch, N. Rusetska, S. Abramowicz, A. Chrzan, M. Ligaj, A. Maassen, J. Siedlecki, T. Sarnowski
Journal: Annals of Oncology (2017)
First-line panitumumab (P) plus capecitabine (C) for the treatment of elderly patients (pts) with wild-type KRAS metastatic colorectal cancer (mCRC): Preliminary results of the phase II, PANEL GITuD-2011-01 study
Authors: J.C. Méndez Méndez, M. Ramos, J.C. De la Cámara Gómez, M.L. Pellón, M. Covela, G.A. Quintero Aldana, M. Salgado Fernandez, A. Fernández-Montes, M. Reboredo, M. Valladares-Ayerbes, M. Jorge Fernandez, P. González Villarroel, C. Romero Reinoso
Journal: Annals of Oncology (2017)
Considering Bone Marrow Blasts from Nonerythroid Cells Improves the Prognostic Evaluation of Myelodysplastic Syndromes with Ring Sideroblasts
Authors: Leonor Arenillas, Xavier Calvo, Elisa Luño, Leonor Senent, Ester Alonso, Fernando Ramos, Maria Teresa Ardanaz, Carme Pedro, Mar Tormo, Victor Marco, Julia Montoro, María Díez-Campelo, Salut Brunet, Beatriz Arrizabalaga, Blanca Xicoy, Rafael Andreu, Santiago Bonanad, Andres Jerez, Meritxell Nomdedeu, Ana Ferrer, Guillermo Sanz, Lourdes Florensa
Journal: Blood (2016)
Pembrolizumab as second or further line treatment in relapsed malignant pleural mesothelioma: A Swiss registry
Authors: L.A. Mauti, D. Klingbiel, S. Schmid, H. Bouchaab, T. Bartnick, O. Gautschi, S.I. Rothschild, M. Loeffler, P. Froesch, U. Petrausch, S. Wolleb Schild, W. Mingrone, S. Pratsch Peter, S. Savic Prince, M. Pless, R. von Moos, Y. Metaxas
Journal: Annals of Oncology (2017)
Local control following resection of primary retroperitoneal sarcoma with and without preoperative radiotherapy.
Authors: Carol Jane Swallow, Amanda Cannell, Brendan Dickson, Sally Burtenshaw, Peter W. M. Chung, Rebecca Anne Gladdy, Brian O'Sullivan, Charles N Catton
Journal: Journal of Clinical Oncology (2015)

10572 Background: Retroperitoneal sarcoma (RPS) represents a therapeutic challenge due to its typically advanced stage at presentation, with local failure a harbinger of death from sarcoma following resection of primary RPS. Preoperative external beam radiotherapy (Pre-op RT) offers the potential for sterilization of margins and better local control. We present mature outcomes according to histologic subtype and treatment of patients with primary RPS managed at our center. Methods: All patients presenting with primary RPS between 01/96 and 06/11 identified from a prospective database were eligible. Distant metastases or unresectability at presentation, receipt of pre-op chemotherapy or post-op radiotherapy were exclusion criteria. All biopsy and resection specimens were re-analysed by an expert pathologist and mdm2 status used to facilitate histologic subtyping. Cumulative-incident rate curves were constructed for local and distant recurrence (LR, DR). Results: All 120 included patients underwent total gross resection. In this cohort, overall survival was 75% and 64% at 5 and 10 yrs, median 206 mos, and disease specific survival was 85% and 76% at 5 and 10 yrs, median 209 mos. Pre-op RT was given to 101 patients while 19 had surgery alone. Surgical approach, histologic subtype (80% liposarcoma, LPS) and follow-up (median 59 mos) did not differ between treatment groups; median size was larger (28 vs. 19 cm) and histologic grade lower in the surgery alone group. For the 120 patients, DR occured in 12 at a median 23 mos (range 2-131) postoperatively and varied significantly by histology (4/65 DD-LPS; 0/31 WD-LPS; 7/17 LMS; 1/7 other; p < 0.01), but not treatment group. LR occured in 24 at a median 22.5 mos (range 2-103) and varied significantly by histology (22/65 DD-LPS; 2/31 WD-LPS; 0/24 other; p = 0.01). For the entire cohort, LR rate was 20% and 28% at 5 and 10 yrs. LR at 5 yrs varied significantly by treatment group (16% for pre-op RT, 51% for surgery alone, p < 0.01). Conclusions: Pre-op RT was associated with improved local control compared with a contemporaneous control. Participation in the EORTC randomized trial of pre-opRT vs. surgery alone is essential to determine the true benefit of pre-op RT in primary RPS.
Phase II dose titration study of regorafenib for patients with unresectable metastatic colorectal cancer who are progressed after standard chemotherapy
Authors: T. Kudo, T. Kato, Y. Kagawa, K. Murata, H. Ohta, S. Noura, J. Hasegawa, H. Tamagawa, K. Ohta, M. Ikenaga, S. Miyazaki, T. Komori, J. Nishimura, T. Hata, C. Matsuda, T. Satoh, T. Mizushima, H. Yamamoto, Y. Doki, M. Mori
Journal: Annals of Oncology (2017)
Abstract 18695: Signs, Symptoms, and Treatment Patterns Across Serial Ambulatory Cardiology Visits in Patients With Heart Failure: Insights From the PINNACLE Registry
Authors: Larry A Allen, Fengming Tang, Philip Jones, Tracie Breeding, Angelo Ponirakis, Stuart J Turner
Journal: Circulation (2016)

Introduction: Heart failure (HF) guidelines recommend titration of diuretics to optimize volume status, as well as intensification of neurohoromonal antagonists as tolerated in certain patients. Ho...
REGOMA: A randomized, multicenter, controlled open-label phase II clinical trial evaluating regorafenib activity in relapsed glioblastoma patients
Authors: G. Lombardi, G.L. De Salvo, A.A. Brandes, M. Eoli, R. Rudà, M. Faedi, I. Lolli, A. Pace, S. Rizzato, D. Germano, F. Pasqualetti, M. Farina, G. Magni, A. Pambuku, E. Bergo, G. Cabrini, S. Indraccolo, M.P. Gardiman, V. Zagonel
Journal: Annals of Oncology (2017)
A critical epithelial survival axis regulated by MCL-1 maintains thymic function in mice
Authors: Reema Jain, Julie M. Sheridan, Antonia Policheni, Melanie Heinlein, Luke C. Gandolfo, Grant Dewson, Gordon K. Smyth, Stephen N. Sansom, Nai Yang Fu, Jane E. Visvader, Georg A. Holländer, Andreas Strasser, Daniel H. D. Gray
Journal: Blood (2017)
Ethics and the Legalization of Physician-Assisted Suicide: An American College of Physicians Position Paper
Authors: Lois Snyder Sulmasy, Paul S. Mueller
Journal: Annals of Internal Medicine (2017)

Calls to legalize physician-assisted suicide have increased and public interest in the subject has grown in recent years despite ethical prohibitions. Many people have concerns about how they will die and the emphasis by medicine and society on intervention and cure has sometimes come at the expense of good end-of-life care. Some have advocated strongly, on the basis of autonomy, that physician-assisted suicide should be a legal option at the end of life. As a proponent of patient-centered care, the American College of Physicians (ACP) is attentive to all voices, including those who speak of the desire to control when and how life will end. However, the ACP believes that the ethical arguments against legalizing physician-assisted suicide remain the most compelling. On the basis of substantive ethics, clinical practice, policy, and other concerns articulated in this position paper, the ACP does not support legalization of physician-assisted suicide. It is problematic given the nature of the patient–physician relationship, affects trust in the relationship and in the profession, and fundamentally alters the medical profession's role in society. Furthermore, the principles at stake in this debate also underlie medicine's responsibilities regarding other issues and the physician's duties to provide care based on clinical judgment, evidence, and ethics. Society's focus at the end of life should be on efforts to address suffering and the needs of patients and families, including improving access to effective hospice and palliative care. The ACP remains committed to improving care for patients throughout and at the end of life.
Management of infusion-related reactions (IRRs) in patients (pts) receiving daratumumab plus standard of care for the treatment of multiple myeloma (MM) in the phase 3 studies CASTOR and POLLUX
Authors: P. Moreau, N. Rabin, T. Plesner, K. Weisel, P. Sonneveld, M-V. Mateos, J.M. Schecter, H. Amin, S. Trivedi, M.A. Dimopoulos
Journal: Annals of Oncology (2017)
Transpancreatic precut papillotomy versus double-guidewire technique in difficult biliary cannulation: prospective randomized study
Authors: Harutoshi Sugiyama, Toshio Tsuyuguchi, Yuji Sakai, Rintaro Mikata, Shin Yasui, Yuto Watanabe, Dai Sakamoto, Masato Nakamura, Takao Nishikawa
Journal: Endoscopy (2017)

Abstract Background and study aims Difficult biliary cannulation and unintentional pancreatic duct cannulation are thought to be important contributors to pancreatitis occurring after endoscopic retrograde cholangiopancreatography. Our aim was to compare and evaluate the rates of success and complications of transpancreatic precut papillotomy (TPPP) and the double-guidewire technique (DGT), both with prophylactic pancreatic stenting. Patients and methods From April 2011 to March 2014, patients with difficult biliary cannulation, in whom we planned to first position a guidewire in the pancreatic duct, were enrolled, and 68 patients were prospectively randomly allocated to two groups (TPPP 34, DGT 34). We evaluated the rates of success and complications for each group. Results TPPP had a significantly higher success rate (94.1 %) than DGT (58.8 %). The rate of post-ERCP pancreatitis was 2.9 % in both groups. There was no significant difference between the two groups in the overall rate of complications related to cannulation. Conclusion If biliary cannulation cannot be achieved, TPPP should be selected first after unintentional pancreatic duct cannulation. University Hospital Medical Information Network identifier: UMIN000008200
Programa ICU-HELICS: Hacia una vigilancia europea de las infecciones nosocomiales contraídas en las unidades de cuidados intensivos
Authors: C Suetens, A Savey, J Labeeuw, I Morales
Journal: Eurosurveillance (2002)

La creacion de una base de datos destinada al analisis comparativo de las tasas de infecciones nosocomiales en los 15 paises de la Union Europea es uno de los objetivos de la red HELICS (Red de Hospitales Europeos para el Control de Infecciones mediante la Vigilancia; Hospitals in Europe Link for Infection Control through Surveillance).
Ischemic stroke as cancer predecessor and associated predictors
Authors: J. Rogado, V. Pacheco, R. Mondejar, S. Quintas, P. Gullón, J. Dotor, M.D. Fenor de la Maza, B. Obispo, G. Reig-Roselló, T. Pascual, A.I. Ballesteros Garcia, O. Donnay, J.M. Sánchez-Torres, R. López Ruiz, J. Vivancos, R. Colomer Bosch
Journal: Annals of Oncology (2017)
Nickel render anti-apoptotic effect by induction of COX-2 through IKKβ/p65-dependent pathway
Authors: Jin Ding, Jinlong Jian, jingxia li, lun song, weiming ouyang, Dongyun Zhang, chuanshu huang
Journal: Cancer Research (2007)

4259   Nickel Compounds Render Anti-apoptotic Effect to Human Bronchial Epithelial Beas-2B Cells by Induction of COX-2 through IKKβ/p65-dependent, and IKKα- and p50-independent Pathway  Jin Ding, Jinlong Jian, Jingxia Li, Lun Song,  Weiming Ouyang, Dongyun Zhang, and Chuanshu Huang  Nelson Institute of Environmental Medicine, New York University School of Medicine,  57 Old Forge Road, Tuxedo, NY 10987  #  Summary  The carcinogenicity of nickel compounds has been well documented both  in vivo  and  in vivo , however the molecular mechanisms by which nickel compounds cause cancers are far from understood yet. Since suppression of apoptosis is thought to contribute to carcinogenesis, current studies investigated the mechanisms implicated in nickel-induced anti-apoptotic effect in human bronchial epithelial (Beas-2B) cells. We found that exposure of Beas-2B cells to nickel compounds resulted in an increased COX-2 expression, and knockdown of COX-2 expression with its small interfering RNA (siCOX-2) resulted in the cell more sensitivity to nickel-triggered cell apoptosis, demonstrating that COX-2 induction renders the anti-apoptotic effect to Beas-2B cells. Overexpression of IKKβ-KM, a kinase inactive mutant of IKKβ, blocked NF-κB activation and COX-2 induction by nickel compounds, indicating that activated NF-κB may be a mediator for COX-2 induction. To further explore the implication of the NF-κB pathway in COX-2 induction and anti-apoptotic effect upon nickel exposure, mouse embryonic fibroblasts (MEFs) deficient with IKKβ, IKKα, p65 and p50, were employed. Abortion of IKKβ in IKKβ-/- cells impaired COX-2 induction by nickel exposure, whereas knockout of IKKα only showed a marginal effect. Moreover, p65, and not p50 of NF-κB subunit, was critical for nickel-induced COX-2 expression. In addition, a deficiency of IKKβ or p65 renders cells more sensitive to nickel-induced apoptosis as compared to those in wild type cells. Finally, it was shown that reactive oxygen species H 2 O 2  were involved in both NFκB activation and COX-2 expression. Collectively, our results demonstrate that COX-2 induction by nickel compounds via IKKβ/p65 NF-κB-dependent, and IKKα- and p50-independent pathway, plays a crucial role in antagonizing nickel-induced cell apoptosis in Beas-2B cells.
Potential advantage of studying preoperative sentinel node mapping with three-dimensional images by a hybrid single photon emission CT (SPECT)/CT system for breast cancer
Authors: M. Ibusuki, Y. Yamamoto, T. Kawasoe, K. Kai, S. Shiraishi, S. Tomiguchi, H. Iwase
Journal: Journal of Clinical Oncology (2007)

601 Background: Lymph node status is one of the key factors in determining the stage, appropriate therapy and outcome in patients with breast cancer. Accurate identification of sentinel nodes (SNs) has clinical importance for each patients before surgery. The purpose of this study was to assess the role of Single-photon emission computed tomography (SPECT)/CT lymphoscintigraphy in SN identification for patients with breast cancer, and to analyze the impact of such information on estimating metastases to SNs. Methods: Two hundred and twenty-three clinically node-negative patients were underwent SN biopsy between July 2002 and November 2006. CT and SPECT images were obtained after injection of subcutaneal 1mCi (99m)Tc-nanocolloid, allowing identification of SN. Target and non-target structures, including lymph nodes identified by SPECT, were drawn by SPECT/CT combined system, which was comprised of a two-detector SPECT system and a multiple-detector CT at the same platform. We compared the anatomical location of SNs demonstrated on the 3D SPECT/CT images and correlation to SN positivity. Results: SPECT/CT uptake was detected in 221 cases (99.1%). 3D SPECT/CT images visualized accurate localization of SNs in each cases. Total number of biopsied SNs were 315 , and the most frequent locations of SN were trapezoid area in the upper side of axilla. We defined this area as ‘Pectoral area (PA)’. In SN negative (SN-) patients, 228 (98.3%) SNs were found in PA, and 4 (1.7%) SNs were out of this area such as parasternal area. In SN positive (SN+) patients, 65(78.3%) SNs were in the PA, and 18(21.7%)SNs were out of PA ,respectively. Significant differences (p&lt;0.01 ,chi-square test) were found in SNs distribution whether in or out of PA between SN+ and SN- patients. Conclusions: SN biopsy navigated by 3D-SPECT/CT can clarify the preoperative anatomical localization of SNs in patients with breast cancer. Atypical distribution of SNs out of PA may suggest SN positivity as a reflection of the failure of lymphatic drainage systems. No significant financial relationships to disclose.