2015 ADA Posters 1474-1929.Indd
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1 Evidence for Gliadin Antibodies As Causative Agents in Schizophrenia
1 Evidence for gliadin antibodies as causative agents in schizophrenia. C.J.Carter PolygenicPathways, 20 Upper Maze Hill, Saint-Leonard’s on Sea, East Sussex, TN37 0LG [email protected] Tel: 0044 (0)1424 422201 I have no fax Abstract Antibodies to gliadin, a component of gluten, have frequently been reported in schizophrenia patients, and in some cases remission has been noted following the instigation of a gluten free diet. Gliadin is a highly immunogenic protein, and B cell epitopes along its entire immunogenic length are homologous to the products of numerous proteins relevant to schizophrenia (p = 0.012 to 3e-25). These include members of the DISC1 interactome, of glutamate, dopamine and neuregulin signalling networks, and of pathways involved in plasticity, dendritic growth or myelination. Antibodies to gliadin are likely to cross react with these key proteins, as has already been observed with synapsin 1 and calreticulin. Gliadin may thus be a causative agent in schizophrenia, under certain genetic and immunological conditions, producing its effects via antibody mediated knockdown of multiple proteins relevant to the disease process. Because of such homology, an autoimmune response may be sustained by the human antigens that resemble gliadin itself, a scenario supported by many reports of immune activation both in the brain and in lymphocytes in schizophrenia. Gluten free diets and removal of such antibodies may be of therapeutic benefit in certain cases of schizophrenia. 2 Introduction A number of studies from China, Norway, and the USA have reported the presence of gliadin antibodies in schizophrenia 1-5. Gliadin is a component of gluten, intolerance to which is implicated in coeliac disease 6. -
Downloaded from the National Database for Autism Research (NDAR)
International Journal of Molecular Sciences Article Phenotypic Subtyping and Re-Analysis of Existing Methylation Data from Autistic Probands in Simplex Families Reveal ASD Subtype-Associated Differentially Methylated Genes and Biological Functions Elizabeth C. Lee y and Valerie W. Hu * Department of Biochemistry and Molecular Medicine, The George Washington University, School of Medicine and Health Sciences, Washington, DC 20037, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-202-994-8431 Current address: W. Harry Feinstone Department of Molecular Microbiology and Immunology, y Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. Received: 25 August 2020; Accepted: 17 September 2020; Published: 19 September 2020 Abstract: Autism spectrum disorder (ASD) describes a group of neurodevelopmental disorders with core deficits in social communication and manifestation of restricted, repetitive, and stereotyped behaviors. Despite the core symptomatology, ASD is extremely heterogeneous with respect to the severity of symptoms and behaviors. This heterogeneity presents an inherent challenge to all large-scale genome-wide omics analyses. In the present study, we address this heterogeneity by stratifying ASD probands from simplex families according to the severity of behavioral scores on the Autism Diagnostic Interview-Revised diagnostic instrument, followed by re-analysis of existing DNA methylation data from individuals in three ASD subphenotypes in comparison to that of their respective unaffected siblings. We demonstrate that subphenotyping of cases enables the identification of over 1.6 times the number of statistically significant differentially methylated regions (DMR) and DMR-associated genes (DAGs) between cases and controls, compared to that identified when all cases are combined. Our analyses also reveal ASD-related neurological functions and comorbidities that are enriched among DAGs in each phenotypic subgroup but not in the combined case group. -
Abstracts from the 9Th Biennial Scientific Meeting of The
International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):15 DOI 10.1186/s13633-017-0054-x MEETING ABSTRACTS Open Access Abstracts from the 9th Biennial Scientific Meeting of the Asia Pacific Paediatric Endocrine Society (APPES) and the 50th Annual Meeting of the Japanese Society for Pediatric Endocrinology (JSPE) Tokyo, Japan. 17-20 November 2016 Published: 28 Dec 2017 PS1 Heritable forms of primary bone fragility in children typically lead to Fat fate and disease - from science to global policy a clinical diagnosis of either osteogenesis imperfecta (OI) or juvenile Peter Gluckman osteoporosis (JO). OI is usually caused by dominant mutations affect- Office of Chief Science Advsor to the Prime Minister ing one of the two genes that code for two collagen type I, but a re- International Journal of Pediatric Endocrinology 2017, 2017(Suppl 1):PS1 cessive form of OI is present in 5-10% of individuals with a clinical diagnosis of OI. Most of the involved genes code for proteins that Attempts to deal with the obesity epidemic based solely on adult be- play a role in the processing of collagen type I protein (BMP1, havioural change have been rather disappointing. Indeed the evidence CREB3L1, CRTAP, LEPRE1, P4HB, PPIB, FKBP10, PLOD2, SERPINF1, that biological, developmental and contextual factors are operating SERPINH1, SEC24D, SPARC, from the earliest stages in development and indeed across generations TMEM38B), or interfere with osteoblast function (SP7, WNT1). Specific is compelling. The marked individual differences in the sensitivity to the phenotypes are caused by mutations in SERPINF1 (recessive OI type obesogenic environment need to be understood at both the individual VI), P4HB (Cole-Carpenter syndrome) and SEC24D (‘Cole-Carpenter and population level. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Japanese Delegation of Athletics Team for Doha,Qatar 2019 27 SEP-06 OCT
Japanese Delegation of Athletics Team For Doha,Qatar 2019 27 SEP-06 OCT IAAF World Championships in Athletics-Doha,Qatar 第 17 回 IAAF 世界陸上競技選手権大会 ( カタ ー ル ・ドー ハ ) ❶ Hirooki ARAI(L)& Kai KOBAYASHI(R) Play Back London 2017 [プレイバック・ロンドン大会2017] 前回の2017年ロンドン大会では男子50kmW勢が躍動。 荒井広宙が2位、小林快が3位とダブル表彰台に上り、 丸尾知司も5位に入りました。また、男子4×100mR も3位に入り、世界選手権では初のメダルを獲得。また、 サニブラウン アブデルハキームは男子100mで準決勝、 200mでは決勝に進出(7位)。日本はメダル3、入賞2 の成績を収めました。 ❷ Men’s 4×100m Relay ❸ Satoshi MARUO ❹ Abdul Hakim SANIBROWN Japanese Medalists & Prizewinners in London 2017 Silver Athlete Record Men 50kmW Hirooki ARAI ❶Left 3.41.17 Bronze Men 50kmW Kai KOBAYASHI ❶Right 3.41.19 S.TADA,S.IIZUKA, Men 4×100mR 38.04 Y.KIRYU,K.FUJIMITSU❷ 5th Men 50kmW Satoshi MARUO❸ 3.43.03 7th Men 200m Abdul Hakim SANIBROWN❹ 20.63 02 Message[メッセージ] thletes aiming at the top of the world will be gathering in the blazing city Doha. The IAAF World Athletics Championships Doha 2019 is a great stageA for you to challenge the “power and skill” of the world, and it has an important meaning as a prelude to 2020 Tokyo Olympic Games which is quickly approaching. Expand your athletic ability you have gained through competition experiences and years of hard training here in Doha and make a huge step towards the grand stage. Along with your athletic ability, human quality is also very important. Athletics is an individual sport except for relays, but it is necessary to have Team JAPAN awareness. The consciousness of competing as a team will also enhance your human quality, and that rise helps to improve individual competitiveness. For athletes and staff, I ask you to unite by respecting each other, and have the spirit of “One for All, All for One”. -
John Angelo John Angelo, 93, of Flushing, Died Saturday in Wheeling Hospital
_nim mm acnnu ain..im«uu ■ — John Angelo John Angelo, 93, of Flushing, died Saturday in Wheeling Hospital. He ^ was bom in Aielli, Italy, April 20, .J J 1898. He was a Catholic. He was preceded in death by his iP(O wife, Frances M. Bakowski Angelo; j___ one sister. Surviving arc three sons, John J. O and Richard, both of Flushing and “3 Gene of St. Clairsville; six grand- (_ x children; three great-grandchildren. Friends will be received at the O Warren Funeral Home, Flushing, to 3" day from 1 until 9 p.m. Mass of Christian Burial will be celebrated Monday at 10 a.m. in St. Paul’s Catholic Church, Flushing, with Monsignor Robert Punkc officiating. Burial in Gates of Heaven Cemetery Laffcrty. Memorial_ .,contributions may be made to Flushing or Lafferty Volun teer Fire Departments. Giovanni Angeloni oiovanni (John) Angeloni, 94 Los Angeles, Calif., formerly of Rayland, Ohio, died Tuesday April 15, 2003 in Pasadena! Calif. He was born October 19, 1908 in Aielli, Italy, the son of the late Carmine and Concetta Angeloni. He was Director of the Music Department at Hawthorne Christian Schools for 40 years. He founded Council #90 of the Sons of Columbus in Inglewood, California, and he was co- founder and first president of the Abruzzesi-Molisani di California. In addition to his parents he was preceded in death by his first wife Mary (Tedeschi) Angeloni and second wife Alma (Del Vecchio) Angeloni and a son, Ivan Angeloni. Surviving are two sons Ramon and Elvio of Los Angeles; a daughter, Vanina (Angeloni) Ruiz of Los Angeles; a brother, Olivio (Lee) Angeloni of Corona, Calif; a sister Eda Leoni of Upland Heights, Yorkville, Ohio; eight grandchildren and seven great-grandchildren. -
Anemia Is Associated with Blunted Response to Β-Blocker Therapy Using Carvedilol ― Insights from Japanese Chronic Heart Failure (J-CHF) Study ―
Circ J 2018; 82: 691 – 698 Supplementary File doi: 10.1253/circj.CJ-17-0442 Anemia Is Associated With Blunted Response to β-Blocker Therapy Using Carvedilol ― Insights From Japanese Chronic Heart Failure (J-CHF) Study ― Yuji Nagatomo, MD; Tsutomu Yoshikawa, MD; Hiroshi Okamoto, MD; Akira Kitabatake, MD; Masatsugu Hori, MD on behalf of J-CHF Investigators ——— Supplementary File 1 ——— • Haruki Musha (Yokohama City Seibu Hospital) Appendix S1. The J-CHF Program Committees and Members • Toshiaki Ebina (Yokohama City University Yokohama Seibu Executive Committee Hospital) Masatsugu Hori, Satoshi Ogawa, Ryozo Nagai, Masanori Matsuzaki, • Ichiro Michishita (Yokohama Kyosai Hospital) Yasuo Ohashi, Hitonobu Tomoike, Hiroshi Okamoto. • Tetsuo Takahashi (Yokohama City Hospital) Steering Committee • Satoshi Umemura (Yokohama City University School of Medicine) Hiroyuki Tsutsui, Iwao Yamaguchi, Ryozo Nagai, Satoshi Ogawa, • Toyoji Nemoto (National Sagamihara Hospital) Tsutomu Yoshikawa, Nobuhisa Hagiwara, Michihiro Yoshimura, • Tohru Izumi (Kitasato University School of Medicine) Katsuo Kanmatsuse, Satoshi Umemura, Minoru Takekoshi, Yoshifusa • Hideo Himeno (Fujisawa City Hospital) Aizawa, Hisayoshi Fujiwara, Masatsugu Hori, Kunio Miyatake, • Teruhisa Tanabe (Tokai University School of Medicine) Junichi Yoshikawa, Mitsuhiro Yokoyama, Toru Kita, Masanori • Hiroyuki Daida (Juntendo University) Matsuzaki, Toru Ohe, Yoshinori Doi, Takao Higaki, Imaizumi • Mitsuaki Isobe (Tokyo Medical and Dental University) Tsutomu. • Koichiro Kinugawa (Tokyo University -
Japanese Delegation of Athleticsteam for Eugene, UNITED STATES 2014 22-27 JUL
Japanese Delegation of AthleticsTeam for Eugene, UNITED STATES 2014 22-27 JUL ⓒ Alamy/ アフロ Eugene ⓒ AP/ アフロ Hayward field stadium IAAF World Junior Championships in Athletics - Eugene, UNITED STATES IAAF 世界ジュニア陸上競技選手権大会(ユージン /2014) Japan Association of Athletics Federations 2-7-1 Nishi-Shinjuku.shinjuku-ku,Tokyo,163-0717 Japan Tel 81-3-5321-6580 Official site: http://www.jaaf.or.jp/ Playback Barcelona 2012 [プレイバック・バルセロナ 2012] 1992年のバルセロナ・オリンピックのメイン 会場となったエスタディ・オリンピック・リュ イス・コンパニスで開催された第14回世界ジュ ニア陸上選手権大会。当時はまだ生まれていな かった選手たちが世界と戦い、メダル2個を含 む入賞9の成績を残した。 400mHの松本岳大(❶、加古川東高・兵庫)は、 準決勝で自己タイ(50秒76)をマークすると、決 勝でも50秒41まで記録を伸ばして、銀メダルを 獲得。男子4×100mR(❷)では大瀨戸一馬(小 倉東高・福岡)、橋元晃志(川薩清修館高・鹿児 島)、ケンブリッジ飛鳥(日本大)、金森和貴(松 江北高・島根)のゴールデン・エイジがジュニ ア日本新となる39秒01で予選を通過すると、決 勝でも39秒02と好走して銅メダルを獲得した。 メダルには届かなかったものの、10000mW の西塔拓己(❸)は40分19秒10のジュニア日本 新で4位入賞、男子10000mでは村山謙太(駒澤 大)、横手健(明治大)が6位と7位に入賞、女 子3000mの上原美幸(鹿児島女高)は8位、男子 110mHの田中新也(筑波大)は7位と力を発揮。 競歩の西塔は、翌年の世界選手権20kmWでオ リンピックを含めて競歩史上最高成績に並ぶ6 位に入賞。世界ジュニアをステップに大きく飛 躍した。 ※所属は当時のもの ❷ Japan Men 4×100mR 3rd ❶ Takahiro MATSUMOTO Men 400mH 2nd Japanese Prizewinners in World Junior Championships Barcelona 2012 バルセロナ大会日本人入賞者 Event Pos Mark Name/Team 氏名(所属) Men 10000m 6 th 29:40.56 Kenta MURAYAMA 村山 謙太(駒澤大) Men 10000m 7 th 29:41.81 Ken YOKOTE 横手 健(明治大) Men 110mH(99.1cm) 7 th 13.72 -1.0 Shinya TANAKA 田中 新也(筑波大) Men 400mH 2 nd 50.41 Takahiro MATSUMOTO(❶) 松本 岳大(加古川東高) Men 10000mW 4 th 40:19.10 Takumi SAITO(❸) 西塔 拓己(東洋大) 〔大瀨戸一馬・橋元 晃志 × (❷) Men 4 100mR 3 rd 39.02 Japan ケンブリッジ飛鳥・金森 和貴〕 〔横山 直広⇒木村 賢太 × Men 4 400mR 7 th 3:09.67 Japan 上妻 昇太⇒木村 和史〕 Women 3000m 8 th 9:21.81 Miyuki UEHARA 上原 美幸(鹿児島女高) Women 10000mW 8 th 4:04.92 Nozomi YAGI 八木 望(熊谷女高) ※所属は当時のもの ❸ Takumi SAITO Men 10000mW 4th 02 Photo/©Agence SHOT MESSAGE [メッセージ] nternational Association of Athletics Federations (IAAF) is comprised of 212 member countries/territory, and that number exceeds those of the International OlympicI Committee (IOC) and International Federation of Association Football (FIFA). -
Abstracts from the 50Th European Society of Human Genetics Conference: Electronic Posters
European Journal of Human Genetics (2019) 26:820–1023 https://doi.org/10.1038/s41431-018-0248-6 ABSTRACT Abstracts from the 50th European Society of Human Genetics Conference: Electronic Posters Copenhagen, Denmark, May 27–30, 2017 Published online: 1 October 2018 © European Society of Human Genetics 2018 The ESHG 2017 marks the 50th Anniversary of the first ESHG Conference which took place in Copenhagen in 1967. Additional information about the event may be found on the conference website: https://2017.eshg.org/ Sponsorship: Publication of this supplement is sponsored by the European Society of Human Genetics. All authors were asked to address any potential bias in their abstract and to declare any competing financial interests. These disclosures are listed at the end of each abstract. Contributions of up to EUR 10 000 (ten thousand euros, or equivalent value in kind) per year per company are considered "modest". Contributions above EUR 10 000 per year are considered "significant". 1234567890();,: 1234567890();,: E-P01 Reproductive Genetics/Prenatal and fetal echocardiography. The molecular karyotyping Genetics revealed a gain in 8p11.22-p23.1 region with a size of 27.2 Mb containing 122 OMIM gene and a loss in 8p23.1- E-P01.02 p23.3 region with a size of 6.8 Mb containing 15 OMIM Prenatal diagnosis in a case of 8p inverted gene. The findings were correlated with 8p inverted dupli- duplication deletion syndrome cation deletion syndrome. Conclusion: Our study empha- sizes the importance of using additional molecular O¨. Kırbıyık, K. M. Erdog˘an, O¨.O¨zer Kaya, B. O¨zyılmaz, cytogenetic methods in clinical follow-up of complex Y. -
(12) United States Patent (10) Patent No.: US 8.440,393 B2 Birrer Et Al
USOO8440393B2 (12) United States Patent (10) Patent No.: US 8.440,393 B2 Birrer et al. (45) Date of Patent: May 14, 2013 (54) PRO-ANGIOGENIC GENES IN OVARIAN OTHER PUBLICATIONS TUMORENDOTHELIAL CELL, SOLATES Boyd (The Basic Science of Oncology, 1992, McGraw-Hill, Inc., p. (75) Inventors: Michael J. Birrer, Mt. Airy, MD (US); 379). Tomas A. Bonome, Washington, DC Tockman et al. (Cancer Res., 1992, 52:2711s-2718s).* (US); Anil Sood, Pearland, TX (US); Pritzker (Clinical Chemistry, 2002, 48: 1147-1150).* Chunhua Lu, Missouri City, TX (US) Benedict et al. (J. Exp. Medicine, 2001, 193(1) 89-99).* Jiang et al. (J. Biol. Chem., 2003, 278(7) 4763-4769).* (73) Assignees: The United States of America as Matsushita et al. (FEBS Letters, 1999, vol. 443, pp. 348-352).* Represented by the Secretary of the Singh et al. (Glycobiology, 2001, vol. 11, pp. 587-592).* Department of Health and Human Abbosh et al. (Cancer Res. Jun. 1, 2006 66:5582-55.91 and Supple Services, Washington, DC (US); The mental Figs. S1-S7).* University of MD Anderson Cancer Zhai et al. (Chinese General Practice Aug. 2008, 11(8A): 1366 Center, Houston, TX (US) 1367).* Lu et al. (Cancer Res. Feb. 15, 2007, 64(4): 1757-1768).* (*) Notice: Subject to any disclaimer, the term of this Bagnato et al., “Activation of Mitogenic Signaling by Endothelin 1 in patent is extended or adjusted under 35 Ovarian Carcinoma Cells', Cancer Research, vol. 57, pp. 1306-1311, U.S.C. 154(b) by 194 days. 1997. Bouras et al., “Stanniocalcin 2 is an Estrogen-responsive Gene (21) Appl. -
Maternal Diabetes and Autism Spectrum Disorders in the Offspring: a Review of Epidemiological Evidence and Potential Biologic Mechanisms
North American Journal of Medicine and Science Oct 2011 Vol 4 No.4 217 Review Maternal Diabetes and Autism Spectrum Disorders in the Offspring: A Review of Epidemiological Evidence and Potential Biologic Mechanisms Katherine Bowers, PhD;* Cuilin Zhang MD, PhD* Epidemiology Branch, Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD Gestational diabetes is a common pregnancy complication whose prevalence is increasing among women of reproductive age and results in both short-and long-term adverse outcomes for the offspring. Hyperglycemia or other consequences of adverse maternal metabolic profiles in pregnancy may contribute to autism risk through several potential mediating mechanisms, such as inflammation, oxidative stress, and epigenetics. The present review aims to summarize recent studies exploring the association between maternal pre-gestational diabetes, gestational diabetes, obesity and autism spectrum disorders (ASD) in the offspring. We will also explore potential biologic mechanisms to explain the association between in utero exposure to a hyperglycemic environment and risk for ASD, including inflammation, oxidative stress and epigenetics. Considering the concurrent rise in obesity and diabetes in pregnancy, as well as the modifiable nature of these disorders, their associations with ASD and the underlying molecular mechanisms should be explored further. [N A J Med Sci. 2011;4(4):217-221.] Key Words: gestational diabetes mellitus -
Pathogenetic Subgroups of Multiple Myeloma Patients
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector ARTICLE High-resolution genomic profiles define distinct clinico- pathogenetic subgroups of multiple myeloma patients Daniel R. Carrasco,1,2,8 Giovanni Tonon,1,8 Yongsheng Huang,3,8 Yunyu Zhang,1 Raktim Sinha,1 Bin Feng,1 James P. Stewart,3 Fenghuang Zhan,3 Deepak Khatry,1 Marina Protopopova,5 Alexei Protopopov,5 Kumar Sukhdeo,1 Ichiro Hanamura,3 Owen Stephens,3 Bart Barlogie,3 Kenneth C. Anderson,1,4 Lynda Chin,1,7 John D. Shaughnessy, Jr.,3,9 Cameron Brennan,6,9 and Ronald A. DePinho1,5,9,* 1 Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115 2 Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts 02115 3 The Donna and Donald Lambert Laboratory of Myeloma Genetics, Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205 4 The Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115 5 Center for Applied Cancer Science, Belfer Institute for Innovative Cancer Science, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 6 Neurosurgery Service, Memorial Sloan-Kettering Cancer Center, Department of Neurosurgery, Weill Cornell Medical College, New York, New York 10021 7 Department of Dermatology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, 02115 8 These authors contributed equally to this work. 9 Cocorresponding authors: [email protected] (C.B.); [email protected] (J.D.S.); [email protected] (R.A.D.) *Correspondence: [email protected] Summary To identify genetic events underlying the genesis and progression of multiple myeloma (MM), we conducted a high-resolu- tion analysis of recurrent copy number alterations (CNAs) and expression profiles in a collection of MM cell lines and out- come-annotated clinical specimens.