Acute Myeloid Leukemia (AML) Patients
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Updates in Mastocytosis
Updates in Mastocytosis Tryptase PD-L1 Tracy I. George, M.D. Professor of Pathology 1 Disclosure: Tracy George, M.D. Research Support / Grants None Stock/Equity (any amount) None Consulting Blueprint Medicines Novartis Employment ARUP Laboratories Speakers Bureau / Honoraria None Other None Outline • Classification • Advanced mastocytosis • A case report • Clinical trials • Other potential therapies Outline • Classification • Advanced mastocytosis • A case report • Clinical trials • Other potential therapies Mastocytosis symposium and consensus meeting on classification and diagnostic criteria for mastocytosis Boston, October 25-28, 2012 2008 WHO Classification Scheme for Myeloid Neoplasms Acute Myeloid Leukemia Chronic Myelomonocytic Leukemia Atypical Chronic Myeloid Leukemia Juvenile Myelomonocytic Leukemia Myelodysplastic Syndromes MDS/MPN, unclassifiable Chronic Myelogenous Leukemia MDS/MPN Polycythemia Vera Essential Thrombocythemia Primary Myelofibrosis Myeloproliferative Neoplasms Chronic Neutrophilic Leukemia Chronic Eosinophilic Leukemia, NOS Hypereosinophilic Syndrome Mast Cell Disease MPNs, unclassifiable Myeloid or lymphoid neoplasms Myeloid neoplasms associated with PDGFRA rearrangement associated with eosinophilia and Myeloid neoplasms associated with PDGFRB abnormalities of PDGFRA, rearrangement PDGFRB, or FGFR1 Myeloid neoplasms associated with FGFR1 rearrangement (EMS) 2017 WHO Classification Scheme for Myeloid Neoplasms Chronic Myelomonocytic Leukemia Acute Myeloid Leukemia Atypical Chronic Myeloid Leukemia Juvenile Myelomonocytic -
The Clinical Management of Chronic Myelomonocytic Leukemia Eric Padron, MD, Rami Komrokji, and Alan F
The Clinical Management of Chronic Myelomonocytic Leukemia Eric Padron, MD, Rami Komrokji, and Alan F. List, MD Dr Padron is an assistant member, Dr Abstract: Chronic myelomonocytic leukemia (CMML) is an Komrokji is an associate member, and Dr aggressive malignancy characterized by peripheral monocytosis List is a senior member in the Department and ineffective hematopoiesis. It has been historically classified of Malignant Hematology at the H. Lee as a subtype of the myelodysplastic syndromes (MDSs) but was Moffitt Cancer Center & Research Institute in Tampa, Florida. recently demonstrated to be a distinct entity with a distinct natu- ral history. Nonetheless, clinical practice guidelines for CMML Address correspondence to: have been inferred from studies designed for MDSs. It is impera- Eric Padron, MD tive that clinicians understand which elements of MDS clinical Assistant Member practice are translatable to CMML, including which evidence has Malignant Hematology been generated from CMML-specific studies and which has not. H. Lee Moffitt Cancer Center & Research Institute This allows for an evidence-based approach to the treatment of 12902 Magnolia Drive CMML and identifies knowledge gaps in need of further study in Tampa, Florida 33612 a disease-specific manner. This review discusses the diagnosis, E-mail: [email protected] prognosis, and treatment of CMML, with the task of divorcing aspects of MDS practice that have not been demonstrated to be applicable to CMML and merging those that have been shown to be clinically similar. Introduction Chronic myelomonocytic leukemia (CMML) is a clonal hemato- logic malignancy characterized by absolute peripheral monocytosis, ineffective hematopoiesis, and an increased risk of transformation to acute myeloid leukemia. -
Philadelphia Chromosome Unmasked As a Secondary Genetic Change in Acute Myeloid Leukemia on Imatinib Treatment
Letters to the Editor 2050 The ELL/MLLT1 dual-color assay described herein entails 3Department of Cytogenetics, City of Hope National Medical Center, Duarte, CA, USA and co-hybridization of probes for the ELL and MLLT1 gene regions, 4 each labeled in a different fluorochrome to allow differentiation Cytogenetics Laboratory, Seattle Cancer Care Alliance, between genes involved in 11q;19p chromosome translocations Seattle, WA, USA E-mail: [email protected] in interphase or metaphase cells. In t(11;19) acute leukemia cases, gain of a signal easily pinpoints the specific translocation breakpoint to either 19p13.1 or 19p13.3 and 11q23. In the References re-evaluation of our own cases in light of the FISH data, the 19p breakpoints were re-assigned in two patients, underscoring a 1 Harrison CJ, Mazzullo H, Cheung KL, Gerrard G, Jalali GR, Mehta A certain degree of difficulty in determining the precise 19p et al. Cytogenetic of multiple myeloma: interpretation of fluorescence in situ hybridization results. Br J Haematol 2003; 120: 944–952. breakpoint in acute leukemia specimens in the context of a 2 Thirman MJ, Levitan DA, Kobayashi H, Simon MC, Rowley JD. clinical cytogenetics laboratory. Furthermore, we speculate that Cloning of ELL, a gene that fuses to MLL in a t(11;19)(q23;p13.1) the ELL/MLLT1 probe set should detect other 19p translocations in acute myeloid leukemia. Proc Natl Acad Sci 1994; 91: 12110– that involve these genes with partners other than MLL. Accurate 12114. molecular classification of leukemia is becoming more im- 3 Tkachuk DC, Kohler S, Cleary ML. -
Acute Myeloid Leukemia Evolving from JAK 2-Positive Primary Myelofibrosis and Concomitant CD5-Negative Mantle Cell
Hindawi Publishing Corporation Case Reports in Hematology Volume 2012, Article ID 875039, 6 pages doi:10.1155/2012/875039 Case Report Acute Myeloid Leukemia Evolving from JAK 2-Positive Primary Myelofibrosis and Concomitant CD5-Negative Mantle Cell Lymphoma: A Case Report and Review of the Literature Diana O. Treaba,1 Salwa Khedr,1 Shamlal Mangray,1 Cynthia Jackson,1 Jorge J. Castillo,2 and Eric S. Winer2 1 Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School, Brown University, Providence, RI 02903, USA 2 Division of Hematology/Oncology, The Miriam Hospital, The Warren Alpert Medical School, Brown University, Providence, RI 02904, USA Correspondence should be addressed to Diana O. Treaba, [email protected] Received 2 April 2012; Accepted 21 June 2012 Academic Editors: E. Arellano-Rodrigo, G. Damaj, and M. Gentile Copyright © 2012 Diana O. Treaba et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Primary myelofibrosis (formerly known as chronic idiopathic myelofibrosis), has the lowest incidence amongst the chronic myeloproliferative neoplasms and is characterized by a rather short median survival and a risk of progression to acute myeloid leukemia (AML) noted in a small subset of the cases, usually as a terminal event. As observed with other chronic myeloproliferative neoplasms, the bone marrow biopsy may harbor small lymphoid aggregates, often assumed reactive in nature. In our paper, we present a 70-year-old Caucasian male who was diagnosed with primary myelofibrosis, and after 8 years of followup and therapy developed an AML. -
Mirna182 Regulates Percentage of Myeloid and Erythroid Cells in Chronic Myeloid Leukemia
Citation: Cell Death and Disease (2017) 8, e2547; doi:10.1038/cddis.2016.471 OPEN Official journal of the Cell Death Differentiation Association www.nature.com/cddis MiRNA182 regulates percentage of myeloid and erythroid cells in chronic myeloid leukemia Deepak Arya1,2, Sasikala P Sachithanandan1, Cecil Ross3, Dasaradhi Palakodeti4, Shang Li5 and Sudhir Krishna*,1 The deregulation of lineage control programs is often associated with the progression of haematological malignancies. The molecular regulators of lineage choices in the context of tyrosine kinase inhibitor (TKI) resistance remain poorly understood in chronic myeloid leukemia (CML). To find a potential molecular regulator contributing to lineage distribution and TKI resistance, we undertook an RNA-sequencing approach for identifying microRNAs (miRNAs). Following an unbiased screen, elevated miRNA182-5p levels were detected in Bcr-Abl-inhibited K562 cells (CML blast crisis cell line) and in a panel of CML patients. Earlier, miRNA182-5p upregulation was reported in several solid tumours and haematological malignancies. We undertook a strategy involving transient modulation and CRISPR/Cas9 (clustered regularly interspersed short palindromic repeats)-mediated knockout of the MIR182 locus in CML cells. The lineage contribution was assessed by methylcellulose colony formation assay. The transient modulation of miRNA182-5p revealed a biased phenotype. Strikingly, Δ182 cells (homozygous deletion of MIR182 locus) produced a marked shift in lineage distribution. The phenotype was rescued by ectopic expression of miRNA182-5p in Δ182 cells. A bioinformatic analysis and Hes1 modulation data suggested that Hes1 could be a putative target of miRNA182-5p. A reciprocal relationship between miRNA182-5p and Hes1 was seen in the context of TK inhibition. -
ASTRO Bone Metastases Guideline-Full Version
1 Palliative Radiotherapy for Bone Metastases: An ASTRO Evidence-Based Guideline Stephen T. Lutz, M.D.,* Lawrence B. Berk, M.D., Ph.D.,† Eric L. Chang, M.D.,‡ Edward Chow, M.B.B.S.,§ Carol A. Hahn, M.D.,║ Peter J. Hoskin, M.D.,¶ David D. Howell, M.D.,# Andre A. Konski, M.D.,** Lisa A. Kachnic, M.D.,†† Simon S. Lo, M.B. ChB,§§ Arjun Sahgal, M.D.,║║ Larry N. Silverman, M.D.,¶¶ Charles von Gunten, M.D., Ph.D., FACP,## Ehud Mendel, M.D., FACS,*** Andrew D. Vassil, M.D.,††† Deborah Watkins Bruner, R.N., Ph.D.,‡‡‡ and William F. Hartsell, M.D.§§§ * Department of Radiation Oncology, Blanchard Valley Regional Cancer Center, Findlay, Ohio; † Department of Radiation Oncology, Moffitt Cancer Center, Tampa, Florida; ‡ Department of Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas; § Department of Radiation Oncology, Sunnybrook Odette Cancer Center, University of Toronto, Toronto, Ontario, Canada; ║ Department of Radiation Oncology, Duke University, Durham, North Carolina; ¶ Mount Vernon Centre for Cancer Treatment, Middlesex, UK; # Department of Radiation Oncology, University of Michigan, Mt. Pleasant, Michigan; ** Department of Radiation Oncology, Wayne State University, Detroit, Michigan; †† Department of Radiation Oncology, Boston Medical Center, Boston, Massachusetts; §§ Department of Radiation Oncology, Ohio State University, Columbus, Ohio; ║║ Department of Radiation Oncology, Sunnybrook Odette Cancer Center and the Princess Margaret Hospital, University of Toronto, Toronto, Ontario, Canada; ¶¶ 21st Century Oncology, Sarasota, Florida; ## The Institute for Palliative Medicine, San Diego Hospice, San Diego, California; *** Neurological Surgery, Ohio State University, Columbus, Ohio; ††† Department of Radiation Oncology, The Cleveland Clinic 2 Foundation, Cleveland, Ohio; ‡‡‡ School of Nursing, University of Pennsylvania, Philadelphia, Pennsylvania; §§§ Department of Radiation Oncology, Good Samaritan Cancer Center, Downers Grove, Illinois Reprint requests to: Stephen Lutz, M.D., 15990 Medical Drive South, Findlay, OH 45840. -
Mutations and Prognosis in Primary Myelofibrosis
Leukemia (2013) 27, 1861–1869 & 2013 Macmillan Publishers Limited All rights reserved 0887-6924/13 www.nature.com/leu ORIGINAL ARTICLE Mutations and prognosis in primary myelofibrosis AM Vannucchi1, TL Lasho2, P Guglielmelli1, F Biamonte1, A Pardanani2, A Pereira3, C Finke2, J Score4, N Gangat2, C Mannarelli1, RP Ketterling5, G Rotunno1, RA Knudson5, MC Susini1, RR Laborde5, A Spolverini1, A Pancrazzi1, L Pieri1, R Manfredini6, E Tagliafico7, R Zini6, A Jones4, K Zoi8, A Reiter9, A Duncombe10, D Pietra11, E Rumi11, F Cervantes12, G Barosi13, M Cazzola11, NCP Cross4 and A Tefferi2 Patient outcome in primary myelofibrosis (PMF) is significantly influenced by karyotype. We studied 879 PMF patients to determine the individual and combinatorial prognostic relevance of somatic mutations. Analysis was performed in 483 European patients and the seminal observations were validated in 396 Mayo Clinic patients. Samples from the European cohort, collected at time of diagnosis, were analyzed for mutations in ASXL1, SRSF2, EZH2, TET2, DNMT3A, CBL, IDH1, IDH2, MPL and JAK2. Of these, ASXL1, SRSF2 and EZH2 mutations inter-independently predicted shortened survival. However, only ASXL1 mutations (HR: 2.02; Po0.001) remained significant in the context of the International Prognostic Scoring System (IPSS). These observations were validated in the Mayo Clinic cohort where mutation and survival analyses were performed from time of referral. ASXL1, SRSF2 and EZH2 mutations were independently associated with poor survival, but only ASXL1 mutations held their prognostic relevance (HR: 1.4; P ¼ 0.04) independent of the Dynamic IPSS (DIPSS)-plus model, which incorporates cytogenetic risk. In the European cohort, leukemia-free survival was negatively affected by IDH1/2, SRSF2 and ASXL1 mutations and in the Mayo cohort by IDH1 and SRSF2 mutations. -
The AML Guide Information for Patients and Caregivers Acute Myeloid Leukemia
The AML Guide Information for Patients and Caregivers Acute Myeloid Leukemia Emily, AML survivor Revised 2012 Inside Front Cover A Message from Louis J. DeGennaro, PhD President and CEO of The Leukemia & Lymphoma Society The Leukemia & Lymphoma Society (LLS) wants to bring you the most up-to-date blood cancer information. We know how important it is for you to understand your treatment and support options. With this knowledge, you can work with members of your healthcare team to move forward with the hope of remission and recovery. Our vision is that one day most people who have been diagnosed with acute myeloid leukemia (AML) will be cured or will be able to manage their disease and have a good quality of life. We hope that the information in this Guide will help you along your journey. LLS is the world’s largest voluntary health organization dedicated to funding blood cancer research, advocacy and patient services. Since the first funding in 1954, LLS has invested more than $814 million in research specifically targeting blood cancers. We will continue to invest in research for cures and in programs and services that improve the quality of life for people who have AML and their families. We wish you well. Louis J. DeGennaro, PhD President and Chief Executive Officer The Leukemia & Lymphoma Society Inside This Guide 2 Introduction 3 Here to Help 6 Part 1—Understanding AML About Marrow, Blood and Blood Cells About AML Diagnosis Types of AML 11 Part 2—Treatment Choosing a Specialist Ask Your Doctor Treatment Planning About AML Treatments Relapsed or Refractory AML Stem Cell Transplantation Acute Promyelocytic Leukemia (APL) Treatment Acute Monocytic Leukemia Treatment AML Treatment in Children AML Treatment in Older Patients 24 Part 3—About Clinical Trials 25 Part 4—Side Effects and Follow-Up Care Side Effects of AML Treatment Long-Term and Late Effects Follow-up Care Tracking Your AML Tests 30 Take Care of Yourself 31 Medical Terms This LLS Guide about AML is for information only. -
Acute Massive Myelofibrosis with Acute Lymphoblastic Leukemia Akut Masif Myelofibrozis Ve Akut Lenfoblastik Lösemi Birlikteliği
204 Case Report Acute massive myelofibrosis with acute lymphoblastic leukemia Akut masif myelofibrozis ve akut lenfoblastik lösemi birlikteliği Zekai Avcı1, Barış Malbora1, Meltem Gülşan1, Feride Iffet Şahin2, Bülent Celasun3, Namık Özbek1 1Department of Pediatrics, Başkent University Faculty of Medicine, Ankara, Turkey 2Department of Medical Genetics, Başkent University Faculty of Medicine, Ankara, Turkey 3Department of Pathology, Başkent University Faculty of Medicine, Ankara, Turkey Abstract Acute myelofibrosis is characterized by pancytopenia of sudden onset, megakaryocytic hyperplasia, extensive bone mar- row fibrosis, and the absence of organomegaly. Acute myelofibrosis in patients with acute lymphoblastic leukemia is extremely rare. We report a 4-year-old boy who was diagnosed as having acute massive myelofibrosis and acute lym- phoblastic leukemia. Performing bone marrow aspiration in this patient was difficult (a “dry tap”), and the diagnosis was established by means of a bone marrow biopsy and immunohistopathologic analysis. The prognostic significance of acute myelofibrosis in patients with acute lymphoblastic leukemia is not clear. (Turk J Hematol 2009; 26: 204-6) Key words: Acute myelofibrosis, acute lymphoblastic leukemia, dry tap Received: April 9, 2008 Accepted: December 24, 2008 Özet Akut myelofibrozis ani gelişen pansitopeni, kemik iliğinde megakaryositik hiperplazi, belirgin fibrozis ve organomegali olmaması ile karakterize bir hastalıktır. Akut myelofibrozis ile akut lenfoblastik lösemi birlikteliği çok nadir görülmektedir. -
Myelodysplastic Syndromes Overview and Types
cancer.org | 1.800.227.2345 About Myelodysplastic Syndromes Overview and Types If you have been diagnosed with a myelodysplastic syndrome or are worried about it, you likely have a lot of questions. Learning some basics is a good place to start. ● What Are Myelodysplastic Syndromes? ● Types of Myelodysplastic Syndromes Research and Statistics See the latest estimates for new cases of myelodysplastic syndromes in the US and what research is currently being done. ● Key Statistics for Myelodysplastic Syndromes ● What's New in Myelodysplastic Syndrome Research? What Are Myelodysplastic Syndromes? Myelodysplastic syndromes (MDS) are conditions that can occur when the blood- forming cells in the bone marrow become abnormal. This leads to low numbers of one or more types of blood cells. MDS is considered a type of cancer1. Normal bone marrow 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Bone marrow is found in the middle of certain bones. It is made up of blood-forming cells, fat cells, and supporting tissues. A small fraction of the blood-forming cells are blood stem cells. Stem cells are needed to make new blood cells. There are 3 main types of blood cells: red blood cells, white blood cells, and platelets. Red blood cells pick up oxygen in the lungs and carry it to the rest of the body. These cells also bring carbon dioxide back to the lungs. Having too few red blood cells is called anemia. It can make a person feel tired and weak and look pale. Severe anemia can cause shortness of breath. White blood cells (also known as leukocytes) are important in defending the body against infection. -
Cancer Treatment and Survivorship Facts & Figures 2019-2021
Cancer Treatment & Survivorship Facts & Figures 2019-2021 Estimated Numbers of Cancer Survivors by State as of January 1, 2019 WA 386,540 NH MT VT 84,080 ME ND 95,540 59,970 38,430 34,360 OR MN 213,620 300,980 MA ID 434,230 77,860 SD WI NY 42,810 313,370 1,105,550 WY MI 33,310 RI 570,760 67,900 IA PA NE CT 243,410 NV 185,720 771,120 108,500 OH 132,950 NJ 543,190 UT IL IN 581,350 115,840 651,810 296,940 DE 55,460 CA CO WV 225,470 1,888,480 KS 117,070 VA MO MD 275,420 151,950 408,060 300,200 KY 254,780 DC 18,750 NC TN 470,120 AZ OK 326,530 NM 207,260 AR 392,530 111,620 SC 143,320 280,890 GA AL MS 446,900 135,260 244,320 TX 1,140,170 LA 232,100 AK 36,550 FL 1,482,090 US 16,920,370 HI 84,960 States estimates do not sum to US total due to rounding. Source: Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute. Contents Introduction 1 Long-term Survivorship 24 Who Are Cancer Survivors? 1 Quality of Life 24 How Many People Have a History of Cancer? 2 Financial Hardship among Cancer Survivors 26 Cancer Treatment and Common Side Effects 4 Regaining and Improving Health through Healthy Behaviors 26 Cancer Survival and Access to Care 5 Concerns of Caregivers and Families 28 Selected Cancers 6 The Future of Cancer Survivorship in Breast (Female) 6 the United States 28 Cancers in Children and Adolescents 9 The American Cancer Society 30 Colon and Rectum 10 How the American Cancer Society Saves Lives 30 Leukemia and Lymphoma 12 Research 34 Lung and Bronchus 15 Advocacy 34 Melanoma of the Skin 16 Prostate 16 Sources of Statistics 36 Testis 17 References 37 Thyroid 19 Acknowledgments 45 Urinary Bladder 19 Uterine Corpus 21 Navigating the Cancer Experience: Treatment and Supportive Care 22 Making Decisions about Cancer Care 22 Cancer Rehabilitation 22 Psychosocial Care 23 Palliative Care 23 Transitioning to Long-term Survivorship 23 This publication attempts to summarize current scientific information about Global Headquarters: American Cancer Society Inc. -
Predictors of Survival in Acute Myeloid Leukemia by Treatment Modality
ANTICANCER RESEARCH 36: 1719-1728 (2016) Predictors of Survival in Acute Myeloid Leukemia by Treatment Modality SAMIP MASTER1, RICHARD MANSOUR1, SRINIVAS S. DEVARAKONDA1, ZHENZHEN SHI2, GLENN MILLS1 and RUNHUA SHI1 1Department of Medicine & Feist-Weiller Cancer Center, Louisiana State University Health Shreveport, Shreveport, LA, U.S.A.; 2Weill Cornell Medical College, New York, NY, U.S.A. Abstract. Background/Aim: Evaluations of efficacy of distance less than 30 miles from treatment Center, diagnosis treatment modality in analyses on patients with acute myeloid and treatment at same facility, were independently associated leukemia (AML) often combine chemotherapy and stem cell with worse survival. Conclusion: Survival analysis of AML in transplantation (SCT). To account for the effect of SCT and the National Cancer Database showed multiple factors to be determine the impact of chemotherapy alone, the National independently associated with survival. Outcomes based on Cancer Data Base from 1998-2011 was analyzed. Patients and treatment suggest an improved survival when utilizing Methods: Patients with AML from 1998-2011 aged 18-64 years chemotherapy and SCT as the primary treatment modality. were included. Chi-square analysis was used to assess the association between treatment and factors investigated. The The American Cancer Society estimated there were Kaplan–Meier method was used to assess overall survival. approximately 20,830 new cases and 10,460 deaths from Log-rank methods were used to determine factors significant acute myeloid leukemia (AML) in 2015 (1). AML is for survival. Multivariable Cox regression analysis was used to generally a disease of older people and uncommon before determine the effect of chemotherapy alone, and both the age of 45 years.