Five Cancer Types to Be Added to Medical Oncology

Total Page：16

File Type：pdf, Size：1020Kb

Posted on NaviNet Plan Central page 2-1-2017 FIVE CANCER TYPES TO BE ADDED TO MEDICAL ONCOLOGY PATHWAYS PROGRAM 4/1/17 Beginning April 1, 2017, the Highmark Medical Oncology Management Pathways Program will expand to include five additional cancer types. Providers can expect to see the new content in the Clear Value PlusSM decision support tool starting April 1, 2017. All decisions made on or after April 1, 2017, for the new cancers will be calculated in the practice’s concordance score. All other program components remain the same. The following cancer types will be added to the Pathways Program starting April 1, 2017: • Bladder cancer • Esophageal and esophageal junction cancers • Gastric cancer • Kidney cancer • Myelodysplastic syndrome Benefits of this Pathways Program expansion include: • Access to clinical decision support for five additional cancers • Ability to provide high-quality, cost-effective care to a greater number of Highmark and non- Highmark members • Increased opportunity to improve or maintain high concordance by selecting Value Pathways for the new cancers Effective April 1, 2017, the complete list of cancer types in the Highmark Medical Oncology Management Pathways Program will be as follows: • Breast cancer • Chronic myelogenous leukemia (CML) • Colon cancer • Fallopian tube cancer • Head and neck cancer: (oropharyngeal, laryngeal, hypopharyngeal) • Hodgkin’s lymphoma • Melanoma • Multiple myeloma • Non-Hodgkin's lymphomas: (DLBCL, Follicular, CLL, SLL, Mantle Cell) • Ovarian cancer • Pancreatic adenocarcinoma • Primary peritoneal cancer • Prostate cancer • Rectal cancer (continued) • Small cell lung cancer • Non-small cell lung cancer • Esophageal and esophagogastric junction cancers (starting 4-1-17) • Gastric cancer (starting 4-1-17) • Kidney cancer (starting 4-1-17) • Myelodysplastic syndrome (starting 4-1-17) • Bladder cancer (starting 4-1-17) .

Copy Link

Recommended publications

Nidogen-1 Expression Is Associated with Overall Survival and Temozolomide Sensitivity in Low-Grade Glioma Patients
www.aging-us.com AGING 2021, Vol. 13, No. 6 Research Paper Nidogen-1 expression is associated with overall survival and temozolomide sensitivity in low-grade glioma patients Baiwei Zhang1,*, Cheng Xu2,3,*, Junfeng Liu1, Jinsheng Yang4, Qinglei Gao2,3, Fei Ye1 1Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China 2Cancer Biology Research Center, Key Laboratory of the Ministry of Education, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China 3Department of Gynecology and Obstetrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China 4Department of Neurosurgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, China *Equal contribution Correspondence to: Fei Ye; email: [email protected] Keywords: NID1, glioma, basement membrane, apoptosis, temozolomide Received: August 8, 2020 Accepted: February 16, 2021 Published: March 18, 2021 Copyright: © 2021 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT We investigated the prognostic significance of nidogen-1 (NID1) in glioma. Oncomine, GEPIA, UALCAN, CCGA database analyses showed that NID1 transcript levels were significantly upregulated in multiple cancer types, including gliomas. Quantitative RT-PCR analyses confirmed that NID1 expression was significantly upregulated in glioma tissues compared to paired adjacent normal brain tissue samples (n=9). NID1 silencing enhanced in vitro apoptosis and the temozolomide sensitivity of U251 and U87-MG glioma cells.
[Show full text]
Rare Cancers Are Not So Rare: the Rare Cancer Burden in Europe
EUROPEANJOURNALOFCANCER47 (2011) 2493– 2511 Available at www.sciencedirect.com journal homepage: www.ejconline.com Rare cancers are not so rare: The rare cancer burden in Europe Gemma Gatta a,*, Jan Maarten van der Zwan b, Paolo G. Casali c, Sabine Siesling b, Angelo Paolo Dei Tos d, Ian Kunkler e, Rene´e Otter b, Lisa Licitra f, Sandra Mallone g, Andrea Tavilla g, Annalisa Trama a, Riccardo Capocaccia g, The RARECARE working group a Department of Preventive and Predictive Medicine, Fondazione IRCSS, Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy b North East Netherlands Cancer Registry, Comprehensive Cancer Centre North East, P.O. Box 330, 9700 AH Groningen, The Netherlands c Department of Cancer Medicine, Fondazione IRCSS, Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy d Department of Pathology, General Hospital of Treviso, Via Borgo Cavalli 42, 31100 Treviso, Italy e Department of Clinical Oncology, Western General Hospital, Crewe Road South, Edinburgh EH4 2XU, UK f Head and Neck Cancer Medical Oncology Unit, Fondazione IRCSS, Istituto Nazionale dei Tumori, Via Venezian 1, 20133 Milan, Italy g Department of Cancer Epidemiology, Istituto Superiore di Sanita` , Viale Regina Elena 299, Rome, Italy ARTICLE INFO ABSTRACT Keywords: Purpose: Epidemiologic information on rare cancers is scarce. The project Surveillance of Rare cancers Rare Cancers in Europe (RARECARE) provides estimates of the incidence, prevalence and Cancer registries survival of rare cancers in Europe based on a new and comprehensive list of these diseases. Incidence Materials and methods: RARECARE analysed population-based cancer registry (CR) data on Prevalence European patients diagnosed from 1988 to 2002, with vital status information available Survival up to 31st December 2003 (latest date for which most CRs had veriﬁed data).
[Show full text]
Hamdan Medical Journal 2012; 5:79–82
Hamdan Medical Journal 2012; 5:79–82 LETTER TO THE EDITOR Cancers in Arab populations: concise notes http://dx.doi.org/10.2174/HMJ201201 Sir, social customs followed in Arab populations result in delayed patient presentation to the physician. Rapid improvements in the field of health care and dramatic socioeconomic changes resulting in Prostate cancer lies at the other end of the spectrum. modified lifestyles are believed to have contributed The incidence of clinical prostate cancer in Arabs to the increased incidence of cancers in Arab is among the lowest in the world. This is despite populations.1 For example, the UAE is experiencing a the increased prevalence of risk factors, including continually increasing proportion of cancer burden, the intake of high-caloric food rich in animal fat.7 imposing itself as the third leading cause of death Interestingly, mean serum prostate-specific antigen after cardiovascular diseases and accidents.2 Very (PSA) levels are also known to be low in Arab men. preliminary data from the CTGA (Catalogue for In fact, several studies have pointed towards the Transmission Genetics in Arabs) database for genetic necessity of establishing Arab-specific serum PSA disorders in Arab populations indicate the presence reference levels for early diagnosis of prostate cancer.8 of at least 55 cancer types in Arab people (Table 1). Although these types of cancers vary with regard to Despite the fact that heredity plays little part in their incidence and frequency, strong indicators show the aetiology of most cancer types, studies of clearly that cancers of the lung and prostate are the the molecular genetics of cancers are becoming most common among males whereas breast and invaluable tools to provide insights into the thyroid cancers are the most common among females pathways leading to individual tumours and to in the region (reviewed in reference 4).
[Show full text]
Text-Mining Clinically Relevant Cancer Biomarkers for Curation Into the Civic Database
bioRxiv preprint doi: https://doi.org/10.1101/500686; this version posted December 20, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Text-mining clinically relevant cancer biomarkers for curation into the CIViC database Jake Lever1,2, Martin R. Jones1, Arpad M. Danos3, Kilannin Krysiak3,5, Melika Bonakdar1, Jasleen Grewal1,2, Luka Culibrk1,2, Obi L. Griffith3,4,5,6,*, Malachi Griffith3,4,5,6,*, and Steven J.M. Jones1,2,7,* 1Canada’s Michael Smith Genome Sciences Centre, Vancouver, BC, Canada. 2University of British Columbia, Vancouver, BC, Canada. 3McDonnell Genome Institute, Washington University School of Medicine, St. Louis, MO, USA. 4Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO, USA. 5Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA. 6Department of Genetics, Washington University School of Medicine, St. Louis, MO, USA. 7Simon Fraser University, Burnaby, BC, Canada. * co-corresponding author Abstract Precision oncology involves analysis of individual cancer samples to understand the genes and pathways involved in the development and progression of a cancer. To improve patient care, knowledge of diagnostic, prognostic, predisposing and drug response markers is essential. Several knowledgebases have been created by different groups to collate evidence for these associations. These include the open-access Clinical Interpretation of Variants in Cancer (CIViC) knowledgebase. These databases rely on time-consuming manual curation from skilled experts who read and interpret the relevant biomedical literature.
[Show full text]
Role of IQGAP1 in Carcinogenesis
cancers Review Role of IQGAP1 in Carcinogenesis Tao Wei and Paul F. Lambert * McArdle Laboratory for Cancer Research, Department of Oncology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA; [email protected] * Correspondence: [email protected] Simple Summary: IQ motif-containing GTPase-activating protein 1 (IQGAP1) is a signal scaffolding protein that regulates a range of cellular activities by facilitating signal transduction in cells. IQGAP1 is involved in many cancer-related activities, such as proliferation, apoptosis, migration, invasion and metastases. In this article, we review the different pathways regulated by IQGAP1 during cancer development, and the role of IQGAP1 in different types of cancer, including cancers of the head and neck, breast, pancreas, liver, colorectal, stomach, and ovary. We also discuss IQGAP10s regulation of the immune system, which is of importance to cancer progression. This review highlights the signiﬁcant roles of IQGAP1 in cancer and provides a rationale for pursuing IQGAP1 as a drug target for developing novel cancer therapies. Abstract: Scaffolding proteins can play important roles in cell signaling transduction. IQ motif- containing GTPase-activating protein 1 (IQGAP1) inﬂuences many cellular activities by scaffolding multiple key signaling pathways, including ones involved in carcinogenesis. Two decades of studies provide evidence that IQGAP1 plays an essential role in promoting cancer development. IQGAP1 is overexpressed in many types of cancer, and its overexpression in cancer is associated with lower survival of the cancer patient. Here, we provide a comprehensive review of the literature regarding the oncogenic roles of IQGAP1. We start by describing the major cancer-related signaling pathways Citation: Wei, T.; Lambert, P.F.
[Show full text]
WO 2009/080437 Al
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (43) International Publication Date (10) International Publication Number 2 July 2009 (02.07.2009) PCT WO 2009/080437 Al (51) International Patent Classification: Copenhagen N (DK). LITMAN, Thomas [DK/DK]; C12Q 1/68 (2006.01) Rosen AlIe 8, Hareskovby, DK-3500 Vaeløse (DK). M0LLER, Søren [DK/DK]; Ved Furesøen 9, DK-2840 (21) International Application Number: Holte (DK). PCT/EP2008/066239 (74) Agent: INSPICOS A/S; P.O. Box 45, Kogle AlIe 2, (22) International Filing Date: DK-2970 Hørsholm (DK). 26 November 2008 (26.1 1.2008) (81) Designated States (unless otherwise indicated, for every (25) Filing Language: English kind of national protection available): AE, AG, AL, AM, (26) Publication Language: English AO, AT,AU, AZ, BA, BB, BG, BH, BR, BW, BY,BZ, CA, CH, CN, CO, CR, CU, CZ, DE, DK, DM, DO, DZ, EC, EE, (30) Priority Data: EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, PA 2007 01843 2 1 December 2007 (21.12.2007) DK IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, KZ, LA, LC, LK, 61/015,797 21 December 2007 (21.12.2007) US LR, LS, LT, LU, LY,MA, MD, ME, MG, MK, MN, MW, PA 2008 00535 11 April 2008 (11.04.2008) DK MX, MY,MZ, NA, NG, NI, NO, NZ, OM, PG, PH, PL, PT, (71) Applicant (for all designated States except US): EXIQON RO, RS, RU, SC, SD, SE, SG, SK, SL, SM, ST, SV, SY,TJ, A/S [DK/DK]; Skelstedet 16, DK-2950 VEDB^K (DK).
[Show full text]
Cancer Genomic Research at the Crossroads: Realizing the Changing Genetic Landscape As Intratumoral Spatial and Temporal Heterogeneity Becomes a Confounding Factor
UC Irvine ICTS Publications Title Cancer genomic research at the crossroads: realizing the changing genetic landscape as intratumoral spatial and temporal heterogeneity becomes a confounding factor Permalink https://escholarship.org/uc/item/4k16x50j Journal Cancer Cell International, 14(1) ISSN 1475-2867 Authors Li, Shengwen Calvin Tachiki, Lisa May Ling Kabeer, Mustafa H et al. Publication Date 2014-11-12 DOI 10.1186/s12935-014-0115-7 License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Li et al. Cancer Cell International 2014, 14:115 http://www.cancerci.com/content/14/1/115 REVIEW Open Access Cancer genomic research at the crossroads: realizing the changing genetic landscape as intratumoral spatial and temporal heterogeneity becomes a confounding factor Shengwen Calvin Li1,5,6*, Lisa May Ling Tachiki1,2, Mustafa H Kabeer1,7,8, Brent A Dethlefs1, Michael J Anthony9 and William G Loudon1,3,4,6 Abstract The US National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI) created the Cancer Genome Atlas (TCGA) Project in 2006. The TCGA’s goal was to sequence the genomes of 10,000 tumors to identify common genetic changes among different types of tumors for developing genetic-based treatments. TCGA offered great potential for cancer patients, but in reality has little impact on clinical applications. Recent reports place the past TCGA approach of testing a small tumor mass at a single time-point at a crossroads. This crossroads presents us with the conundrum of whether we should sequence more tumors or obtain multiple biopsies from each individual tumor at different time points.
[Show full text]
Development and Characterization of Monoclonal Antibodies to GDF-15 for Potential Use in Cancer Therapy
Development and characterization of monoclonal antibodies to GDF-15 for potential use in cancer therapy Die Entwicklung und Charakterisierung monoklonaler Antikörper gegen GDF-15 zur potenziellen Anwendung in der Krebstherapie Doctoral thesis for a doctoral degree at the Graduate School of Life Sciences, Julius-Maximilians-Universität Würzburg, Section: Infection and Immunity Submitted by Markus Erich Junker from Ludwighshafen/Rhein, Germany Würzburg 2015 Submitted on:……………………………………………………………………………... Office stamp Members of the Promotionskomitee: Chairperson: Professor Dr. Caroline Kisker Primary Supervisor: Professor Dr. Roland Benz (Since 29th July 2015) (From 3rd November 2008 - 20th July 2015 Professor Dr. Jörg Wischhusen) Supervisor (Second): Professor Dr. Roland Benz (Until 29th July 2015) Supervisor (Third): Professor Dr. Thomas Hünig Date of Public Defence:…………………………………………………………………... Date of Receipt of Certificates:…………………………………………………………... Table of contents Table of contents Table of contents ........................................................................................................................ 4 Zusammenfassung ...................................................................................................................... 8 Abstract .................................................................................................................................... 11 1 Introduction ..........................................................................................................................
[Show full text]
Surveillance of Rare Cancers Jan Maarten Van Der Zw an 2016
Surveillance of cancers rare Uitnodiging voor het bijwonen van de openbare verdediging van mijn proefschrift Surveillance of rare cancers vrijdag 20 mei 2016 Surveillance 12.30 uur Prof. dr. G. Berkhoffzaal of rare cancers Gebouw Waaier Jan Maarten van der Zwan Jan Maarten van der Zwan van Maarten Jan 2016 Aansluitend aan de verdediging is er ter plaatse een receptie waar u van harte voor bent uitgenodigd Jan Maarten van der Zwan Harmonieplein 59 3603 BR Maarssen Paranimfen Vincent Ho | Jan Willem Hoorn [email protected] SURVEILLANCE of RARE CANCERS Jan Maarten van der Zwan Surveillance of rare cancers Thesis, University of Twente, the Netherlands, 2016 © Jan Maarten van der Zwan ISBN: 978-94-6233-282-9 Cover design: J.M. van der Zwan Layout: Marja van Vliet Printed by: Gildeprint, Enschede Financial support for printing of this thesis was kindly provided by: Netherlands comprehensive cancer organisation Disclosure: The author wishes to thank the RARECARE project and their contributors for providing cancer registry data used for this thesis. This thesis is in line with the RARECARE publication plan, approved by the RARECARE project management. Ethical approval for access to the data was not required. In the different chapters the author is responsible for the analysis, interpretation of the data and for writing of the manuscripts. RARECARE Surveillance of Rare Cancers in Europe SURVEILLANCE OF RARE CANCERS PROEFSCHRIFT ter verkrijging van de graad van doctor aan de Universiteit Twente, op gezag van de rector magnificus, prof. dr. H. Brinksma, volgens besluit van het College voor Promoties in het openbaar te verdedigen op vrijdag 20 mei 2016 om 12.45 uur door Johannes Martinus van der Zwan Geboren op 8 juli 1981 te Amsterdam Promotiecommissie Promotoren Prof.
[Show full text]
Lynch Syndrome-Associated Ultra-Hypermutated Pediatric Glioblastoma Mimicking a Constitutional Mismatch Repair Deficiency Syndrome
Downloaded from molecularcasestudies.cshlp.org on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press Lynch syndrome-associated ultra-hypermutated pediatric glioblastoma mimicking a constitutional mismatch repair deficiency syndrome Chen Yang1, Frances Austin2, Hope Richard1, Michael Idowu1, Vernell Williamson1, Fernanda Sabato1, Andrea Ferreira-Gonzalez1, Scott A. Turner1* 1Department of Pathology, 2Department of Pediatrics, Virginia Commonwealth University, Richmond, VA * Scott Turner: [email protected] Running title: Ultra-hypermutated pediatric glioblastoma in Lynch syndrome Downloaded from molecularcasestudies.cshlp.org on October 1, 2021 - Published by Cold Spring Harbor Laboratory Press ABSTRACT Pediatric glioblastoma multiforme (GBM) has a poor prognosis due to recurrence after treatment of surgery and radiochemotherapy. A small subset of pediatric GBMs presenting with an ultra- high tumor mutational burden (TMB) may be sensitive to immune checkpoint inhibition. Here we report a 16-year-old male with an ultra-hypermutated GBM. After incomplete surgical resection, molecular analysis of the tumor identified unusually high numbers of mutations and intra-tumor heterogeneity by a hotspot NGS panel. Further comprehensive molecular profiling identified a TMB of 343 mutations/Mb. An ultra-hypermutation genotype in pediatric GBMs is suggestive of a constitutive mismatch repair deficiency syndrome (CMMRD), which often acquires additional somatic driver mutations in replicating DNA polymerase genes. Tumor sequencing identified two MSH6 nonsense variants, a hotspot POLE mutation, and a mutational signature supportive of a germline MMR deficiency with a somatic POLE mutation. However, constitutional testing identified only one nonsense MSH6 variant consistent with a Lynch syndrome diagnosis. This case represents the first confirmed Lynch syndrome case mimicking CMMRD by manifesting as an ultra-hypermutated pediatric GBM, following somatic mutations in MSH6 and POLE.
[Show full text]
Pan-Cancer Analysis of Immune Complement Signature C3/C5/C3AR1/C5AR1 in Association with Tumor Immune Evasion and Therapy Resistance
cancers Article Pan-Cancer Analysis of Immune Complement Signature C3/C5/C3AR1/C5AR1 in Association with Tumor Immune Evasion and Therapy Resistance Bashir Lawal 1,2,† , Sung-Hui Tseng 3,4,†, Janet Olayemi Olugbodi 5, Sitthichai Iamsaard 6 , Omotayo B. Ilesanmi 7 , Mohamed H. Mahmoud 8 , Sahar H. Ahmed 9, Gaber El-Saber Batiha 10 and Alexander T. H. Wu 11,12,13,14,15,* 1 PhD Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei 11031, Taiwan; [email protected] 2 Graduate Institute for Cancer Biology & Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan 3 Department of Physical Medicine and Rehabilitation, Taipei Medical University Hospital, Taipei 11031, Taiwan; [email protected] 4 Department of Physical Medicine and Rehabilitation, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan 5 Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA; [email protected] 6 Department of Anatomy, Faculty of Medicine and Research Institute for Human High Performance and Citation: Lawal, B.; Tseng, S.-H.; Health Promotion (HHP&HP), Khon Kaen University, Khon Kaen 40002, Thailand; [email protected] 7 Department of Biochemistry, Faculty of Science, Federal University Otuoke, Olugbodi, J.O.; Iamsaard, S.; Ilesanmi, Ogbia 23401, Bayelsa State, Nigeria; [email protected] O.B.; Mahmoud, M.H.; Ahmed, S.H.; 8 Department
[Show full text]
Download.Php?File=/Images/ Publication/128393883472.Pdf, Accessed: May 2012] References 23
Estimating the returns to UK publicly funded cancer-related research in terms of the net value of improved health outcomes Glover et al. Glover et al. BMC Medicine 2014, 12:99 http://www.biomedcentral.com/1741-7015/12/99 Glover et al. BMC Medicine 2014, 12:99 http://www.biomedcentral.com/1741-7015/12/99 RESEARCH ARTICLE Open Access Estimating the returns to UK publicly funded cancer-related research in terms of the net value of improved health outcomes Matthew Glover1, Martin Buxton1, Susan Guthrie2, Stephen Hanney1, Alexandra Pollitt2 and Jonathan Grant2,3* Abstract Background: Building on an approach developed to assess the economic returns to cardiovascular research, we estimated the economic returns from UK public and charitable funded cancer-related research that arise from the net value of the improved health outcomes. Methods: To assess these economic returns from cancer-related research in the UK we estimated: 1) public and charitable expenditure on cancer-related research in the UK from 1970 to 2009; 2) net monetary benefit (NMB), that is, the health benefit measured in quality adjusted life years (QALYs) valued in monetary terms (using a base-case value of a QALY of GB£25,000) minus the cost of delivering that benefit, for a prioritised list of interventions from 1991 to 2010; 3) the proportion of NMB attributable to UK research; 4) the elapsed time between research funding and health gain; and 5) the internal rate of return (IRR) from cancer-related research investments on health benefits. We analysed the uncertainties in the IRR estimate using sensitivity analyses to illustrate the effect of some key parameters.
[Show full text]