Disparities in registration and use of an online patient portal among older adults: findings from the LitCog cohort

(C) The Author 2015. Published by Oxford University Press on behalf of the American Medical Informatics Association. All rights reserved.Financial disclosure: This project was supported by the National Institute on Aging (R01 AG030611), the National Center for Research Resources (5UL1RR025741), and the National Center for Advancing Translational Sciences (Grant 8UL1TR000150). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Smith is currently supported by a Cancer Research UK Fellowship

Canvass: a crowd-sourced, natural-product screening library for exploring biological space

NCATS thanks Dingyin Tao for assistance with compound characterization. This research was supported by the Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH). R.B.A. acknowledges support from NSF (CHE-1665145) and NIH (GM126221). M.K.B. acknowledges support from NIH (5R01GM110131). N.Z.B. thanks support from NIGMS, NIH (R01GM114061). J.K.C. acknowledges support from NSF (CHE-1665331). J.C. acknowledges support from the Fogarty International Center, NIH (TW009872). P.A.C. acknowledges support from the National Cancer Institute (NCI), NIH (R01 CA158275), and the NIH/National Institute of Aging (P01 AG012411). N.K.G. acknowledges support from NSF (CHE-1464898). B.C.G. thanks the support of NSF (RUI: 213569), the Camille and Henry Dreyfus Foundation, and the Arnold and Mabel Beckman Foundation. C.C.H. thanks the start-up funds from the Scripps Institution of Oceanography for support. J.N.J. acknowledges support from NIH (GM 063557, GM 084333). A.D.K. thanks the support from NCI, NIH (P01CA125066). D.G.I.K. acknowledges support from the National Center for Complementary and Integrative Health (1 R01 AT008088) and the Fogarty International Center, NIH (U01 TW00313), and gratefully acknowledges courtesies extended by the Government of Madagascar (Ministere des Eaux et Forets). O.K. thanks NIH (R01GM071779) for financial support. T.J.M. acknowledges support from NIH (GM116952). S.M. acknowledges support from NIH (DA045884-01, DA046487-01, AA026949-01), the Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program (W81XWH-17-1-0256), and NCI, NIH, through a Cancer Center Support Grant (P30 CA008748). K.N.M. thanks the California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board for support. B.T.M. thanks Michael Mullowney for his contribution in the isolation, elucidation, and submission of the compounds in this work. P.N. acknowledges support from NIH (R01 GM111476). L.E.O. acknowledges support from NIH (R01-HL25854, R01-GM30859, R0-1-NS-12389). L.E.B., J.K.S., and J.A.P. thank the NIH (R35 GM-118173, R24 GM-111625) for research support. F.R. thanks the American Lebanese Syrian Associated Charities (ALSAC) for financial support. I.S. thanks the University of Oklahoma Startup funds for support. J.T.S. acknowledges support from ACS PRF (53767-ND1) and NSF (CHE-1414298), and thanks Drs. Kellan N. Lamb and Michael J. Di Maso for their synthetic contribution. B.S. acknowledges support from NIH (CA78747, CA106150, GM114353, GM115575). W.S. acknowledges support from NIGMS, NIH (R15GM116032, P30 GM103450), and thanks the University of Arkansas for startup funds and the Arkansas Biosciences Institute (ABI) for seed money. C.R.J.S. acknowledges support from NIH (R01GM121656). D.S.T. thanks the support of NIH (T32 CA062948-Gudas) and PhRMA Foundation to A.L.V., NIH (P41 GM076267) to D.S.T., and CCSG NIH (P30 CA008748) to C.B. Thompson. R.E.T. acknowledges support from NIGMS, NIH (GM129465). R.J.T. thanks the American Cancer Society (RSG-12-253-01-CDD) and NSF (CHE1361173) for support. D.A.V. thanks the Camille and Henry Dreyfus Foundation, the National Science Foundation (CHE-0353662, CHE-1005253, and CHE-1725142), the Beckman Foundation, the Sherman Fairchild Foundation, the John Stauffer Charitable Trust, and the Christian Scholars Foundation for support. J.W. acknowledges support from the American Cancer Society through the Research Scholar Grant (RSG-13-011-01-CDD). W.M.W.acknowledges support from NIGMS, NIH (GM119426), and NSF (CHE1755698). A.Z. acknowledges support from NSF (CHE-1463819). (Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH); CHE-1665145 - NSF; CHE-1665331 - NSF; CHE-1464898 - NSF; RUI: 213569 - NSF; CHE-1414298 - NSF; CHE1361173 - NSF; CHE1755698 - NSF; CHE-1463819 - NSF; GM126221 - NIH; 5R01GM110131 - NIH; GM 063557 - NIH; GM 084333 - NIH; R01GM071779 - NIH; GM116952 - NIH; DA045884-01 - NIH; DA046487-01 - NIH; AA026949-01 - NIH; R01 GM111476 - NIH; R01-HL25854 - NIH; R01-GM30859 - NIH; R0-1-NS-12389 - NIH; R35 GM-118173 - NIH; R24 GM-111625 - NIH; CA78747 - NIH; CA106150 - NIH; GM114353 - NIH; GM115575 - NIH; R01GM121656 - NIH; T32 CA062948-Gudas - NIH; P41 GM076267 - NIH; R01GM114061 - NIGMS, NIH; R15GM116032 - NIGMS, NIH; P30 GM103450 - NIGMS, NIH; GM129465 - NIGMS, NIH; GM119426 - NIGMS, NIH; TW009872 - Fogarty International Center, NIH; U01 TW00313 - Fogarty International Center, NIH; R01 CA158275 - National Cancer Institute (NCI), NIH; P01 AG012411 - NIH/National Institute of Aging; Camille and Henry Dreyfus Foundation; Arnold and Mabel Beckman Foundation; Scripps Institution of Oceanography; P01CA125066 - NCI, NIH; 1 R01 AT008088 - National Center for Complementary and Integrative Health; W81XWH-17-1-0256 - Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program; P30 CA008748 - NCI, NIH, through a Cancer Center Support Grant; California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board; American Lebanese Syrian Associated Charities (ALSAC); University of Oklahoma Startup funds; 53767-ND1 - ACS PRF; PhRMA Foundation; P30 CA008748 - CCSG NIH; RSG-12-253-01-CDD - American Cancer Society; RSG-13-011-01-CDD - American Cancer Society; CHE-0353662 - National Science Foundation; CHE-1005253 - National Science Foundation; CHE-1725142 - National Science Foundation; Beckman Foundation; Sherman Fairchild Foundation; John Stauffer Charitable Trust; Christian Scholars Foundation)Published versionSupporting documentatio

Application of a RE-AIM framework to assess the impact of the Southwest American Indian Collaborative Network

In response to a Request for Proposals from the National Cancer Institute (NCI), the Inter Tribal Council of Arizona (ITCA) along with health care partners from the Phoenix Indian medical Center (PIMC) and academic partners from the Arizona Cancer Center (ACC) at the University of Arizona (UA), and the University of Nevada Las Vegas (UNLV) established a Community Network Program entitled the Southwest American Indian Collaborative Network (SAICN). The ultimate goal of the SAICN project was to “eliminate cancer health disparities by closing the gap between the health needs of the community and cancer prevention and control made possible by a responsive health delivery and research system.” At the close of the 5-year funding period for the SAICN project, a RE-AIM framework provided an important evaluative tool for identifying areas of potential long term impact

Cancer Causes Control

IntroductionIn the early 1990s, a comprehensive cancer control (CCC) approach was developed in the United States (US). In 2003, the US-Affiliated Pacific Islands (USAPI) adopted the CCC approach through a regional coalition, the Cancer Council of the Pacific Islands (CCPI). Using the CCC approach, the CCPI developed jurisdiction-specific cancer coalitions and initiated their respective cancer plans.MethodsThe evolution of the CCC approach and the history of the CCPI regional coalition are reviewed. The outcomes of the regional approach for cancer control in the USAPI are described to illustrate the possibilities, value-added and innovation of using a CCC strategy in a multi-national coalition based in a resource-limited environment.ResultsThe CCC approach enabled the CCPI to (1) harmonize cancer control efforts between the six USAPI jurisdictions, (2) represent the USAPI cancer needs as a single voice, and (3) develop a regional cancer control strategy. Outcomes include (1) a regional cancer registry, (2) three sequential regional CCC plans, (3) leveraged resources for the USAPI, (4) enhanced on-site technical assistance and training, (5) improved standards for cancer screening, (6) evidence-based cancer control interventions adapted for the USAPI.ConclusionThe regional CCPI coupled with the CCC approach is an effective engine of change. The CCC strategies enabled navigation of the political, geographic, cultural, and epidemiologic Pacific environment. The regional partners have been able to harmonize cancer control efforts in resource-limited settings. Regional cancer coalitions may be effective in the global arena for cancer control between communities, states, or countries.NU58DP006336/National Center for Chronic Disease Prevention and Health Promotion/DP000777/National Center for Chronic Disease Prevention and Health Promotion/NU58DP006269/National Center for Chronic Disease Prevention and Health Promotion/DP003906/National Center for Chronic Disease Prevention and Health Promotion/DP000779/National Center for Chronic Disease Prevention and Health Promotion/2U54CA143727/National Cancer Institute/DP000826/National Center for Chronic Disease Prevention and Health Promotion/17NU58DP006312/National Center for Chronic Disease Prevention and Health Promotion/NU58DP006348/National Center for Chronic Disease Prevention and Health Promotion/DP000976/National Center for Chronic Disease Prevention and Health Promotion/NU58DP005810/National Center for Chronic Disease Prevention and Health Promotion/DP00847/National Center for Chronic Disease Prevention and Health Promotion/U58 DP000835/DP/NCCDPHP CDC HHS/United StatesDP003939/National Center for Chronic Disease Prevention and Health Promotion/NU58DP006335/National Center for Chronic Disease Prevention and Health Promotion/U58 DP003906/DP/NCCDPHP CDC HHS/United StatesDP000781/National Center for Chronic Disease Prevention and Health Promotion/NU58DP006303/National Center for Chronic Disease Prevention and Health Promotion/NU58DP006289/National Center for Chronic Disease Prevention and Health Promotion/2018-12-29T00:00:00Z30535525PMC6311141vault:3129

The landscape of somatic copy-number alteration across human cancers

available in PMC 2010 August 18.A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-κΒ pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P50CA90578)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109038))National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109467)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA085859)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA 098101)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, K08CA122833

Talking Glossary of Genomics Terminology: A Genomics Education Module for American Indian Communities

This paper describes the development of an audio visual genomics glossary that was designed as an education tool for American Indian communities. This “Talking Glossary of Genomics Terminology” is a multimedia DVD that was modeled on the “Talking Glossary of Genetics,” which was developed by the National Human Genome Research Institute (NHGRI). The NHGRI Glossary was modified and expanded with content designed to increase awareness among American Indians about cancer, genomics, and personalized medicine. Partners on the project include the Inter Tribal Council of Arizona, Inc., Phoenix Indian Medical Center, Arizona Cancer Center at the University of Arizona, the Translational Genomics Research Institute, as well as Arizona State University and University of Arizona graduate students

Novel role of VMP1 as modifier of the pancreatic tumor cell response to chemotherapeutic drugs

We hypothesized that inhibiting molecules that mediate the adaptation response to cellular stress can antagonize the resistance of pancreatic cancer cells to chemotherapeutic drugs. Toward this end, here, we investigated how VMP1, a stress-induced autophagy-associated protein, modulate stress responses triggered by chemotherapeutic agents in PDAC. We find that VMP1 is particularly over-expressed in poorly differentiated human pancreatic cancer. Pharmacological studies show that drugs that work, in part, via the endoplasmic reticulum stress response, induce VMP1 expression. Similarly, VMP1 is induced by known endoplasmic reticulum stress activators. Genetic inactivation of VMP1 using RNAi-based antagonize the pancreatic cancer stress response to antitumoral agents. Functionally, we find that VMP1 regulates both autophagy and chemotherapeutic resistance even in the presence of chloroquin, ATG5 or Beclin 1 siRNAs, or a Beclin 1-binding VMP1 mutant. In addition, VMP1 modulates endoplasmic reticulum stress independently of its coupling to the molecular and cellular autophagy machinery. Preclinical studies demonstrate that xenografts expressing an inducible and tractable form of VMP1 show increased resistance to the gemcitabine treatment. These results underscore a novel role for VMP1 as a potential therapeutic target for combinatorial therapies aimed at sensitizing pancreatic cancer cells to chemotherapeutic agents as well as provide novel molecular mechanisms to better understand this phenomenon.Fil: Gilabert, Mariana. Cancer Research Center of Marseille; Francia. Aix-Marseille University; Francia. Centre National de la Recherche Scientifique; FranciaFil: Vaccaro, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Fernandez Zapico, Martín E.. Mayo Clinic Cancer Center; Estados UnidosFil: Calvo, Ezequiel L.. Molecular Endocrinology and Oncology Research Center; CanadáFil: Turrini, Olivier. Cancer Research Center of Marseille; Francia. Aix-Marseille University; Francia. Centre National de la Recherche Scientifique; FranciaFil: Secq, Véronique. Cancer Research Center of Marseille; Francia. Aix-Marseille University; Francia. Centre National de la Recherche Scientifique; FranciaFil: Garcia, Stéphanie. Cancer Research Center of Marseille; Francia. Aix-Marseille University; Francia. Centre National de la Recherche Scientifique; FranciaFil: Moutardier, Vincent. Cancer Research Center of Marseille; Francia. Aix-Marseille University; Francia. Centre National de la Recherche Scientifique; FranciaFil: Lomberk, Gwen. Mayo Clinic; Estados UnidosFil: Dusetti, Nelson. Cancer Research Center of Marseille; Francia. Aix-Marseille University; Francia. Centre National de la Recherche Scientifique; FranciaFil: Urrutia, Raul. Mayo Clinic; Estados UnidosFil: Iovanna, Juan L.. Cancer Research Center of Marseille; Francia. Aix-Marseille University; Francia. Centre National de la Recherche Scientifique; Franci

Sensitization of renal carcinoma cells to TRAIL-induced apoptosis by rocaglamide and analogs

Rocaglamide has been reported to sensitize several cell types to TRAIL-induced apoptosis. In recent years, advances in synthetic techniques have led to generation of novel rocaglamide analogs. However, these have not been extensively analyzed as TRAIL sensitizers, particularly in TRAIL-resistant renal cell carcinoma cells. Evaluation of rocaglamide and analogs identified 29 compounds that are able to sensitize TRAIL-resistant ACHN cells to TRAIL-induced, caspase-dependent apoptosis with sub-µM potency which correlated with their potency as protein synthesis inhibitors and with loss of cFLIP protein in the same cells. Rocaglamide alone induced cell cycle arrest, but not apoptosis. Rocaglates averaged 4–5-fold higher potency as TRAIL sensitizers than as protein synthesis inhibitors suggesting a potential window for maximizing TRAIL sensitization while minimizing effects of general protein synthesis inhibition. A wide range of other rocaglate effects (e.g. on JNK or RAF-MEK-ERK signaling, death receptor levels, ROS, ER stress, eIF4E phosphorylation) were assessed, but did not contribute to TRAIL sensitization. Other than a rapid loss of MCL-1, rocaglates had minimal effects on mitochondrial apoptotic pathway proteins. The identification of structurally diverse/mechanistically similar TRAIL sensitizing rocaglates provides insights into both rocaglate structure and function and potential further development for use in RCC-directed combination therapy.This project has been funded in whole or in part with Federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. HHSN261200800001E. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. This research was supported [in part] by the Intramural Research Program of NIH, Frederick. National Lab, Center for Cancer Research. Research performed at Boston University was supported in part by NIH R35 GM118173. Work at the BU-CMD is supported by R24 GM111625. (HHSN261200800001E - National Cancer Institute, National Institutes of Health; Intramural Research Program of NIH, Frederick. National Lab, Center for Cancer Research; R35 GM118173 - NIH; R24 GM111625)Published versio

Promotion of Skin Protection in Children in Waterbury, VT

Background: Vermont has among the highest rates of skin cancer in the nation. Between 2001 and 2005, Vermont had the highest incidence of melanoma of any state, 63% higher than the national average. It is also estimated that if children under 18 regularly used sunscreen of at least SPF 15, the incidence of squamous and basal cell carcinomas would decrease by 78%. Modeling by the EPA and CDC suggests that recommended sun protection measures could prevent 11,000 cases of skin cancer, 50 deaths, and $30 million in cancer treatment costs nationwide. Intervention: To create an information sheet on skin protection and skin cancer prevention to be included in well-child visits at the Waterbury Health Center. Method: I integrated state-specific data, national data, and epidemiologic facts about the risks of sun exposure and other risks for skin cancer with recommendations made by the UVM Dermatology residents who I interviewed, in order to create a brief yet fairly comprehensive fact sheet on skin protection in children.https://scholarworks.uvm.edu/fmclerk/1281/thumbnail.jp

Jefferson Cancer Center Officially Recognized the National Cancer Institute

No abstract available