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Absolon N.S.A.,British Columbia Cancer Agency BCCA | Balneaves L.G.,University of Toronto | Truant T.L.O.,University of British Columbia | Cashman R.L.,BCCA | And 3 more authors.
Clinical Journal of Oncology Nursing | Year: 2016

Background: Sleep-wake disturbances are experienced by as many as 75% of patients with cancer and are associated with poor symptom management, lower functionality, and decreased quality of life. Although promising sleep interventions exist, they require extensive resources and time. Objectives: The objectives of this study were to develop a brief, self-administered sleep intervention and to evaluate the feasibility and potential efficacy of its implementation with adult patients with cancer who were about to receive, were receiving, or had received radiation therapy in an ambulatory cancer care setting. Methods: Pre- and postintervention surveys and qualitative interviews were conducted with patients with cancer experiencing insomnia (N = 28) and receiving radiation treatment within the past six months. Patients received instruction on breathing, visualization, and intonation. Adherence and sleep quality were primary study outcomes. Analyses included descriptive statistics and repeated measure regression analysis. Thematic analysis was conducted on qualitative data. Findings: Adherence to the sleep intervention was high (75%), and significant improvement was found in global sleep quality (p < 0.0001) regardless of level of adherence. Sleep onset latency (p = 0.0005), sleep duration (p = 0.0016), and sleep quality (p < 0.0001) were significantly improved. Age was significantly correlated with sleep quality (p = 0.0094), with older participants reporting greater benefit from the intervention. Participants reported that the intervention was easy to learn and implement and that it “calmed the mind.”. © 2016 by the Oncology Nursing Society. Source

Pinheiro H.,University of Porto | Carvalho J.,University of Porto | Oliveira P.,University of Porto | Ferreira D.,University of Porto | And 11 more authors.
Human Molecular Genetics | Year: 2012

Disruption of E-cadherin (CDH1 gene) expression, subcellular localization or function arises during initiation and progression of almost 90% of all epithelial carcinomas. Nevertheless, the mechanisms through which this occurs are largely unknown. Previous studies showed the importance of CDH1 intron 2 sequences for proper gene and protein expression, supporting these as E-cadherin cis-modulators. Through RACE and RT-PCR, we searched for transcription events arising from CDH1 intron 2 and discovered several new transcripts. One, named CDH1a, with high expression in spleen and absent from normal stomach, was demonstrated to be translated into a novel isoform, differing from canonical E-cadherin in its N-terminal, as determined by mass spectrometry. Quantitative and functional assays showed that when overexpressed in an E-cadherin negative context, CDH1a replaced canonical protein interactions and functions. However, when co-expressed with canonical E-cadherin, CDH1a increased cell invasion and angiogenesis. Further, interferon-induced gene IFITM1 and IFI27 levels were increased upon CDH1a overexpression. Effects on invasion and IFITM1 and IFI27 expression were reverted upon CDH1a-specific knockdown. Importantly, CDH1a was de novo expressed in gastric cancer cell lines. This study presents a new mechanism by which E-cadherin functions are impaired by cis-regulatory mechanisms possibly with the involvement of inflammatory machinery. If confirmed in other cancer models, our data enclose potential for designing targeted therapies to rescue E-cadherin function. © The Author 2012. Published by Oxford University Press. All rights reserved. Source

Banerjee D.,Applied Genomics | Banerjee D.,University of British Columbia | Banerjee D.,British Columbia Cancer Agency BCCA
Cancers | Year: 2010

Human cancers are still diagnosed and classified using the light microscope. The criteria are based upon morphologic observations by pathologists and tend to be subject to interobserver variation. In preoperative biopsies of non-small cell lung cancers, the diagnostic concordance, even amongst experienced pulmonary pathologists, is no better than a coin-toss. Only 25% of cancer patients, on average, benefit from therapy as most therapies do not account for individual factors that influence response or outcome. Unsuccessful first line therapy costs Canada CAN$1.2 billion for the top 14 cancer types, and this extrapolates to $90 billion globally. The availability of accurate drug selection for personalized therapy could better allocate these precious resources to the right therapies. This wasteful situation is beginning to change with the completion of the human genome sequencing project and with the increasing availability of targeted therapies. Both factors are giving rise to attempts to correlate tumor characteristics and response to specific adjuvant and neoadjuvant therapies. Static cancer classification and grading systems need to be replaced by functional classification systems that not only account for intra- and intertumor heterogeneity, but which also allow for the selection of the correct chemotherapeutic compounds for the individual patient. In this review, the examples of lung and breast cancer are used to illustrate the issues to be addressed in the coming years, as well as the emerging technologies that have great promise in enabling personalized therapy. © 2010 by the authors; licensee MDPI, Basel, Switzerland. Source

Ali R.H.,Vancouver General Hospital | Lee C.-H.,Vancouver General Hospital | Hayes M.M.,British Columbia Cancer Agency BCCA
Diagnostic Cytopathology | Year: 2014

We report the fine-needle aspiration cytology of a case of metastatic small cell osteosarcoma to the liver with rosette formation, originating from distal femur, in a 36-year-old female. The aspirate of the liver metastases revealed a relatively monomorphic population of mitotically active small blue round cells arranged in clusters with prominent rosette formation simulating a neuroendocrine carcinoma or other rosette-forming small round cell tumors such as Ewing sarcoma. No extracellular mineralized matrix material was present. Comparison of the liver aspirate with the biopsy from the distal femoral lesion was crucial in reaching the correct diagnosis of metastatic small cell osteosarcoma with rosette formation. This is a potential diagnostic pitfall, particularly if interpreted without the knowledge of a suspected primary bone tumor. Copyright © 2012 Wiley Periodicals, Inc. Source

Mager D.E.,State University of New York at Buffalo | Mody V.,State University of New York at Buffalo | Xu C.,State University of New York at Buffalo | Forrest A.,State University of New York at Buffalo | And 7 more authors.
Pharmaceutical Research | Year: 2012

Purpose To characterize temporal exposure and elimination of 5 gold/dendrimer composite nanodevices (CNDs) (5 nm positive, negative, and neutral, 11 nm negative, 22 nm positive) in mice using a physiologically based mathematical model. Methods 400 ug of CNDs is injected intravenously to mice bearing melanoma cell lines. Gold content is determined from plasma and tissue samples using neutron activation analysis. A physiologically based pharmacokinetic (PBPK) model is developed for 5 nm positive, negative, and neutral and 11 nm negative nanoparticles and extrapolated to 22 nm positive particles. A global sensitivity analysis is performed for estimated model parameters. Results Negative and neutral particles exhibited similar distribution profiles. Unique model parameter estimates and distribution profiles explain similarities and differences relative to positive particles. The model also explains mechanisms of elimination by kidney and reticuloendothelial uptake in liver and spleen, which varies with particle size and charge. Conclusion Since the PBPK model can capture the diverse temporal profiles of non-targeted nanoparticles, we propose that when specific binding ligands are lacking, size and charge of nanodevices govern most of their in vivo interactions. © Springer Science+Business Media, LLC 2012. Source

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