Myelodysplastic Syndromes Fact Sheet

Total Page：16

File Type：pdf, Size：1020Kb

Myelodysplastic Syndromes Myelodysplastic Syndromes (MDS) are a group of hematologic malignancies in which mutations prevent the bone marrow from properly making blood stem cells that form healthy blood cells. What is MDS? Global Incidence Three types of blood cells are needed for dierent functions in the body. All three are aected by MDS: Approximately 87,000 new cases of In healthy people, bone MDS are diagnosed every year marrow is responsible for making blood stem cells, which eventually form into healthy blood cells. Low blood cell counts, known as Red blood cells (RBCs) White blood cells Platelets cytopenias, are known as a work to bring oxygen (WBCs) help the help the blood Median age at diagnosis: defining feature of MDS. from the lungs to the body fight off clot after an injury approximately 70 years old rest of the body infections Symptoms Overall incidence of MDS is slightly higher in males than in females Many symptoms of MDS can be life-threatening: However, the incidence of MDS is considered to be underestimated due to lack of reporting and under-diagnosis Prognosis Anemia Neutropenia Thrombocytopenia (low RBC count) can cause (low WBC count) can cause (low platelet cell count) can fatigue, weakness and recurring infections, fevers cause easy bruising, bleeding shortness of breath and sore mouth from the nose and mouth and a rash of small red dots on For the most severe forms of MDS: the skin ~5 months Due to this lack of mature RBCs, many patients with MDS experience severe chronic anemia, eventually requiring frequent red blood cell transfusions For lower risk MDS: Risk Factors ~6 years Older Prior cancer Family History of Exposure to high dose age treatment history smoking radiation or workplace benzene Treatment >30% Treatment options depend on the needs of the individual patient. Some treatment options include: Supportive care such as For >30% of patients with MDS, their disease blood transfusions and Chemotherapy Stem cell may progress to a deadly blood cancer called erythropoiesis-stimulating transplant agent (ESA) therapy Acute Myeloid Leukemia (AML). It is important for people with MDS to understand the symptoms of their disease and to talk to a healthcare professional about appropriate treatment options. © 2020 Bristol Myers Squibb.

Copy Link

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
[Show full text]
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.
[Show full text]
Bone Marrow (Stem Cell) Transplant for Sickle Cell Disease Bone Marrow (Stem Cell) Transplant
Bone Marrow (Stem Cell) Transplant for Sickle Cell Disease Bone Marrow (Stem Cell) Transplant for Sickle Cell Disease 1 Produced by St. Jude Children’s Research Hospital Departments of Hematology, Patient Education, and Biomedical Communications. Funds were provided by St. Jude Children’s Research Hospital, ALSAC, and a grant from the Plough Foundation. This document is not intended to take the place of the care and attention of your personal physician. Our goal is to promote active participation in your care and treatment by providing information and education. Questions about individual health concerns or speciﬁ c treatment options should be discussed with your physician. For more general information on sickle cell disease, please visit our Web site at www.stjude.org/sicklecell. Copyright © 2009 St. Jude Children’s Research Hospital How did bone marrow (stem cell) transplants begin for children with sickle cell disease? Bone marrow (stem cell) transplants have been used for the treatment and cure of a variety of cancers, immune system diseases, and blood diseases for many years. Doctors in the United States and other countries have developed studies to treat children who have severe sickle cell disease with bone marrow (stem cell) transplants. How does a bone marrow (stem cell) transplant work? 2 In a person with sickle cell disease, the bone marrow produces red blood cells that contain hemoglobin S. This leads to the complications of sickle cell disease. • To prepare for a bone marrow (stem cell) transplant, strong medicines, called chemotherapy, are used to weaken or destroy the patient’s own bone marrow, stem cells, and infection ﬁ ghting system.
[Show full text]
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.
[Show full text]
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.
[Show full text]
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.
[Show full text]
Your Blood Cells
Page 1 of 2 Original Date The Johns Hopkins Hospital Patient Information 12/00 Oncology ReviseD/ RevieweD 6/14 Your Blood Cells Where are Blood cells are made in the bone marrow. The bone marrow blood cells is a liquid that looks like blood. It is found in several places of made? the body, such as your hips, chest bone and the middle part of your arm and leg bones. What types of • The three main types of blood cells are the red blood cells, blood cells do the white blood cells and the platelets. I have? • Red blood cells carry oxygen to all parts of the body. The normal hematocrit (or percentage of red blood cells in the blood) is 41-53%. Anemia means low red blood cells. • White blood cells fight infection. The normal white blood cell count is 4.5-11 (K/cu mm). The most important white blood cell to fight infection is the neutrophil. Forty to seventy percent (40-70%) of your white blood cells should be neutrophils. Neutropenia means your neutrophils are low, or less than 40%. • Platelets help your blood to clot and stop bleeding. The normal platelet count is 150-350 (K/cu mm). Thrombocytopenia means low platelets. How do you Your blood cells are measured by a test called the Complete measure my Blood Count (CBC) or Heme 8/Diff. You may want to keep track blood cells? of your blood counts on the back of this sheet. What When your blood counts are low, you may become anemic, get happens infections and bleed or bruise easier.
[Show full text]
Automatic Blood Cell and CRP Counter with Three-Part Differential
FEATURE ARTICLE Automatic Blood Cell and CRP Counter with Three-Part Differential Measurement of White Blood Cells The LC-170 CRP FEATURE ARTICLE Automatic Blood Cell and CRP Counter with Three-Part Differential Measurement of White Blood Cells, The LC-170 CRP Yasuo Yamao WBC, RBC, Hct Electrical impedance method Hgb CRP Cyanmethemoglobin method Latex immunoturbidmetry WBC (White blood cells) LYM% MON% GRA% CRP quantitative LC-170CRP (Lymphocyte %) (Monocyte %) (Granulocyte %) analysis LYM# MON# GRA# (C-reactive protein) (Lymphocyte No.) (Monocyte No.) (Granulocyte No.) RBC (Red blood cells) PLT (Platelets) Hgb(Hemoglobin) Pct (Plateletcrit) Hct (Hematocrit) MPV (Mean Platelet Volume) MCV (Mean Corpuscular Volume) PDW (Platelet Distribution Width) MCH (Mean Corpuscular Hemoglobin) MCHC (Mean Corpuscular Hemoglobin Concentration) RDW (Red Blood Cell Distribution Width) Example of results Abstract The LC-l70 CRP automatic blood cell and CRP counter, developed by Horiba, is capable of simultaneously measuring all 19 C-reactive protein (CRP) density parameters and counting red blood cells, platelets, and three types of white blood cell: lymphocytes, monocytes, and granulocytes. As clinicians demand ever-higher precision measurements, a need has developed for clinical test machines having excellent operational and cost performance. This compact machine should make a powerful tool for initial diagnosis of inflammatory and infectious diseases, especially at small- and mid-size medical institutions. 20 Technical Reports 1 Introduction 2 Measurement Principles To prevent an explosion of medical costs as Japanese The LC-170 CRP uses the electrical impedance method society ages and fewer children are born, the Ministry of to count blood cells, the cyanmethemoglobin method to Health, Labor, and Welfare is pursuing a thorough reform measure hemoglobin concentration, and latex of the medical insurance system, including “preventing immunoturbidimetry to measure CRP concentration.
[Show full text]
Chronic Myeloid Leukemia Mimicking Primary Myelofibrosis: a Case Report
ISSN: 2640-7914 DOI: https://dx.doi.org/10.17352/ahcrr CLINICAL GROUP Received: 02 November, 2020 Case Report Accepted: 01 February, 2021 Published: 02 February, 2021 *Corresponding author: Anju S, Junior Resident, Gov- Chronic myeloid leukemia ernment Medical College, Kottayam, Kerala, India, Tel: 91 9496057350; E-mail: mimicking primary Keywords: Chronic myeloid leukemia; Primary myelo- fi brosis; Blast crisis; Myeloproliferative neoplasms myelofi brosis: A case report https://www.peertechz.com Anju S*, Jayalakshmy PL and Sankar Sundaram Junior Resident, Government Medical College, Kottayam, Kerala, India Abstract Bone marrow fi brosis leading to dry tap aspiration and often associated with blast crisis has previously been reported in both Chronic myeloid leukemia and Primary myelofi brosis. The similarities between these two conditions in terms of clinical presentation and morphology can really create a diagnostic dilemma. Here we present a case of Chronic myeloid leukemia in fi brosis and blast crisis in a 32 year old lady which closely resembled Primary myelofi brosis in transformation. All myeloproliferative neoplasms can undergo blast transformation. In this case, the detection of Philadelphia chromosome helped to distinguish Chronic myeloid leukemia from other myeloproliferative neoplasms. Introduction diffi cult to distinguish the different MPNs especially those in blast crisis and fi brosis. The treatment of CML involves targeted Myeloproliferative Neoplasm (MPN) results from therapy namely, Imatinib mesylate, which is a tyrosine kinase unchecked proliferation of the cellular elements in the bone inhibitor. Also, JAK1/2 inhibitors administered in PMF patients marrow characterized by panmyelosis and accompanied by show clinical improvement [2]. So, it is Important to distinguish erythrocytosis, granulocytosis, and/or thrombocytosis in every MPNs even in their blastic phase as they have different the peripheral blood.
[Show full text]
Essential Thrombocythemia Facts No
Essential Thrombocythemia Facts No. 12 in a series providing the latest information for patients, caregivers and healthcare professionals www.LLS.org • Information Specialist: 800.955.4572 Introduction Highlights Essential thrombocythemia (ET) is one of several l Essential thrombocythemia (ET) is one of a related “myeloproliferative neoplasms” (MPNs), a group of closely group of blood cancers known as “myeloproliferative related blood cancers that share several features, notably the neoplasms” (MPNs) in which cells in the bone “clonal” overproduction of one or more blood cell lines. marrow that produce the blood cells develop and All clonal disorders begin with one or more changes function abnormally. (mutations) to the DNA in a single cell; the altered cells in l ET begins with one or more acquired changes the marrow and the blood are the offspring of that one (mutations) to the DNA of a single blood-forming mutant cell. Other MPNs include polycythemia vera and cell. This results in the overproduction of blood cells, myelofibrosis. especially platelets, in the bone marrow. The effects of ET result from uncontrolled blood cell l About half of individuals with ET have a mutation production, notably of platelets. Because the disease arises of the JAK2 (Janus kinase 2) gene. The role that this from a change to an early blood-forming cell that has the mutation plays in the development of the disease, capacity to form red cells, white cells and platelets, any and the potential implications for new treatments, combination of these three cell lines may be affected – and are being investigated. usually each cell line is affected to some degree.
[Show full text]
Neutrophils (A.K.A
Neutrophils (a.k.a. leukocyte, granulocyte, white blood cell, WBC) blood cells on a microscope slide showing the lobed nucleus of two neutrophils a 3-d drawing of a neutrophil This chart shows how blood cells are produced in the bone marrow from “stem cells” and how we organize them into groups. By Mikael Häggström The Mul(faceted Func(ons of Neutrophils Tanya N. Mayadas,1 Xavier Cullere,1 and Clifford A. Lowell2 “Neutrophils and neutrophil-like cells are the major pathogen-fighKng immune cells in organisms ranging from slime molds to mammals. Central to their funcKon is their ability to be recruited to sites of infecKon, to recognize and phagocytose (eang foreign objects like bacteria) microbes, and then to kill pathogens through a combinaon of cytotoxic mechanisms.” Form • average diameter of 12-15 micrometers (µm) in peripheral blood smears • in suspension, neutrophils have an average diameter of 8.85 µm • mulK-lobed shape nucleus • survive for only 8–12 h in the circulaon and up to 1–2 days in Kssues • Neutrophils will show increasing segmentaon (many segments of nucleus) as they mature. A normal neutrophil should have 3-5 segments. • Neutrophils account for approximately 50-70% of all white blood cells (leukocytes) Func(on • first line of host defense against a wide range of infecKous pathogens including bacteria, fungi, and protozoa • Neutrophils are generated at a rate of 1011 per day, which can increase to 1012 per day during bacterial infection. • Researchers once believed that neutrophils were present only during the most acKve phase of an infecKon, funcKoning as pathogen killers.
[Show full text]
How Are White Blood Cells Classified?
How are white blood cells classified? Copyright 2017 by the Rector and Visitors of the University of Virginia How are white blood cells classified? Types of White Blood Cells: Neutrophil Eosinophil Basophil Lymphocyte Monocyte . The types of white blood cells are shown above. The next page will describe lymphocytes in further detail. A healthy individual has all of these white blood cells types, but within specific ranges. Deviation from these ranges can indicate acute illness or a chronic disease. A mnemonic that is often used to remember the relative amount of each white blood cell that should be present is “Never Let Monkeys Eat Bananas.” Never Neutrophil Highest amounts Let Lymphocyte Monkeys Monocyte Eat Eosinophil Bananas Basophil Lowest amounts . In other words, neutrophils should always be present in higher amounts compared to the other cell types. This will be described further in “A first step in diagnosing LGL leukemia: The blood smear.” Copyright 2017 by the Rector and Visitors of the University of Virginia How are white blood cells classified? Introduction: White blood cells are blood cells that fight infection and disease. Lymphocytes are a type of white blood cell. They can identify antigens (substances foreign to the body) and cause an immune response. There are three types of lymphocytes: T-cell, NK-cell, and B-cell. In healthy adults, 10-15% of the lymphocytes are large granular lymphocytes (LGLs). To learn more about LGL cells, see “A first step in diagnosing LGL leukemia: The blood smear.” A person is diagnosed with LGL leukemia if there is a clonal (copied) population of T-cells or NK-cells present.
[Show full text]