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16-September-2008 16:15:15 - lymphoblastic leukemia Acute lymphoblastic leukemia Classification and external resources ICD-10 C91.0 ICD-9 204.0 ICD-O: 9821/3 DiseasesDB 195 eMedicine med/3146 ped/2587 MeSH D054198 Acute lymphoblastic leukemia ALL, is a form of leukemia, or cancer of the white blood cells. Malignant, immature white blood cells continuously multiply and are overproduced in the bone marrow. ALL causes damage and death by crowding out normal cells in the bone marrow, and by spreading metastasizing to other organs. ALL is most common in childhood and young adulthood with a peak incidence at 4-5 years of age, and another peak in old age. The overall cure rate in children is 85%, and about 50% of adults have long-term disease-free survival.1 'Acute' refers to the undifferentiated, immature state of the circulating lymphocytes blasts, and to the rapid progression of disease, which can be fatal in weeks to months if left untreated. Contents 1 Symptoms 2 Diagnosis 3 Pathophysiology 4 Cytogenetics 5 Classification 5.1 The FAB classification 5.2 WHO proposed classification of acute lymphoblastic leukemia 5.3 Variant Features of ALL 5.4 Immunophenotyping in the diagnosis and classification of ALL 6 Treatment 6.1 Chemotherapy 6.2 Radiation therapy 7 Epidemiology 8 Prognosis 9 Additional images 10 References 11 External links Symptoms Initial symptoms are not specific to ALL, but worsen to the point that medical help is sought. The signs and symptoms of ALL are variable but follow from bone marrow replacement and/or organ infiltration. Generalised weakness and fatigue Anemia Frequent or unexplained fever and infections Weight loss and/or loss of appetite Excessive and unexplained bruising Bone pain, joint pains caused by the spread of blast cells to the surface of the bone or into the joint from the marrow cavity Breathlessness Enlarged lymph nodes, liver and/or spleen The signs and symptoms of ALL result from the lack of normal and healthy blood cells because they are crowded out by malignant and immature leukocytes white blood cells. Therefore, people with ALL experience symptoms from malfunctioning of their erythrocytes red blood cells, leukocytes, and platelets not functioning properly. Laboratory tests which might show abnormalities include blood count tests, renal function tests, electrolyte tests and liver enzyme tests. Diagnosis Diagnosing ALL begins with a medical history and physical examination, complete blood count, and blood smears. Because the symptoms are so general, many other diseases with similar symptoms must be excluded. Typically, the higher the white blood cell count, the worse the prognosis. 2 Blast cells are seen on blood smear in 90% of cases. A bone marrow biopsy is conclusive proof of ALL.3 A spinal tap will tell if the spinal column and brain has been invaded. Pathological examination, cytogenetics particularly the presence of Philadelphia chromosome and immunophenotyping, establish whether the blast cells began from the B lymphocytes or T lymphocytes. DNA testing can establish how aggressive the disease is; different mutations have been associated with shorter or longer survival. Medical imaging such as ultrasound or CT scanning can find invasion of other organs commonly the lung, liver, spleen, lymph nodes, brain, kidneys and reproductive organs. 4 Pathophysiology The cause of most ALL is not known. In general, cancer is caused by damage to DNA that leads to uncontrolled cellular growth and spread throughout the body, either by increasing chemical signals that cause growth, or interrupting chemical signals that control growth. Damage can be caused through the formation of fusion genes, as well as the dysregulation of a proto-oncogene via juxtaposition of it to the promotor of another gene, e.g. the T-cell receptor gene. This damage may be caused by environmental factors such as chemicals, drugs or radiation. ALL is associated with exposure to radiation and chemicals in animals and humans. The association of radiation and leukemia in humans has been clearly established in studies of victims of the Chernobyl nuclear reactor and atom bombs in Hiroshima and Nagasaki. In animals, exposure to benzene and other chemicals can cause leukemia. Epidemiological studies have associated leukemia with workplace exposure to chemicals, but these studies are not as conclusive. Patients who are treated for other cancers with radiation and chemotherapy often develop leukemias as a result of that treatment.citation needed Cytogenetics Cytogenetic translocations associated with specific molecular genetic abnormalities in ALL Cytogenetic translocation Molecular genetic abnormality t9;22q34;q11 BCR-ABL fusionP185 t12;21CRYPTIC TEL-AML1fusion t1;19q23;p13 E2A-PBX fusion t4;11q21;q23 MLL-AF4 fusion t8;14q24;q32 IGH-MYC fusion t11;14p13;q11 TCR-RBTN2 fusion Cytogenetics, the study of characteristic large changes in the chromosomes of cancer cells, has been increasingly recognized as an important predictor of outcome in ALL.5 Some cytogenetic subtypes have a worse prognosis than others. These include: A translocation between chromosomes 9 and 22, known as the Philadelphia chromosome, occurs in about 20% of adult and 5% in pediatric cases of ALL. A translocation between chromosomes 4 and 11 occurs in about 4% of cases and is most common in infants under 12 months. Not all translocations of chromosomes carry a poorer prognosis. Some translocations are relatively favorable. For example, Hyperdiploidy 50 chromosomes is a good prognostic factor. Cytogenetic change Risk category Philadelphia chromosome Poor prognosis t4;11q21;q23 Poor prognosis t8;14q24.1;q32 Poor prognosis Complex karyotype more than four abnormalities Poor prognosis Low hypodiploidy or near triploidy Poor prognosis High hyperdiploidy Good prognosis del9p Good prognosis Classification As ALL is not a solid tumour, the TxNxMx notation as used in solid cancers is of little use. The FAB classification Subtyping of the various forms of ALL used to be done according to the French-American-British FAB classification,6 which was used for all acute leukemias including acute myelogenous leukemia, AML. ALL-L1: small uniform cells ALL-L2: large varied cells ALL-L3: large varied cells with vacuoles bubble-like features Each subtype is then further classified by determining the surface markers of the abnormal lymphocytes, called immunophenotyping. There are 2 main immunologic types: pre-B cell and pre-T cell. The mature B-cell ALL L3 is now classified as Burkitt's lymphoma/leukemia. Subtyping helps determine the prognosis and most appropriate treatment in treating ALL. WHO proposed classification of acute lymphoblastic leukemia The recent WHO International panel on ALL recommends that the FAB classification be abandoned, since the morphological classification has no clinical or prognostic relevance. It instead advocates the use of the immunophenotypic classification mentioned below. 1- Acute lymphoblastic leukemia/lymphoma Synonyms:Former Fab L1/L2 i. Precursor B acute lymphoblastic leukemia/lymphoma. Cytogenetic subtypes:7 t12;21p12,q22 TEL/AML-1 t1;19q23;p13 PBX/E2A t9;22q34;q11 ABL/BCR TV,11V;q23 V/MLL ii. Precursor T acute lymphoblastic leukemia/lymphoma 2- Burkitt's leukemia/lymphoma Synonyms:Former FAB L3 3- Biphenotypic acute leukemia Variant Features of ALL 1- Acute lymphoblastic leukemia with cytoplasmic granules 2- Aplastic presentation of ALL 3- Acute lymphoblastic leukemia with eosinophilia 4- Relapse of lymphoblastic leukemia 5- Secondary AML Immunophenotyping in the diagnosis and classification of ALL The use of a TdT assay and a panel of monoclonal antibodies MoAbs to T cell and B cell associated antigens will identify almost all cases of ALL. Immunophenotypic categories of acute lymphoblastic leukemia ALL Types FAB Class Tdt T cell associate antigen B cell associate antigen c Ig s Ig Precursor B L1,L2 + - + -/+ - Precursor T L1,L2 + + - - - B-cell L3 - - + - + Treatment The earlier acute lymphocytic leukemia is detected, the more effective the treatment. The aim is to induce a lasting remission, defined as the absence of detectable cancer cells in the body usually less than 5% blast cells on the bone marrow. Treatment for acute leukemia can include chemotherapy, steroids, radiation therapy, intensive combined treatments including bone marrow or stem cell transplants, and growth factors. Chemotherapy Chemotherapy is the initial treatment of choice. Most ALL patients end up receiving a combination of different treatments. There are no surgical options, due to the body-wide distribution of the malignant cells. A newly developed study for the treatment of Acute Lymphoblastic leukemia, known as COALL 03-07 is underway in Hamburg. This new study compares chemotherapeutic regimes to discover which therapy better suits patients with ALL. As the chemotherapy regimens can be intensive and protracted often about 2 years in case of the GMALL UKALL, HyperCVAD or CALGB protocols; about 3 years for males on COG protocols, many patients have an intravenous catheter inserted into a large vein termed a central venous catheter or a Hickman line, or a Portacath a cone-shaped port with a silicone nose that is surgically planted under the skin, usually near the collar bone, and the most effective product available, due to low infection risks and the long-term viability of a portacath. Since ALL cells sometimes penetrate the Central Nervous System CNS, most protocols include delivery of chemotherapy into the CNS fluid. More advanced centers deliver the drug through Ommaya reservoir a device surgically placed under the scalp and used to deliver drugs to the CNS fluid and to extract CNS fluid for various tests. More traditional centers would perform multiple lumbar punctures as needed for testing and treatment delivery. Radiation therapy Radiation therapy or radiotherapy is used on painful bony areas, in high disease burdens, or as part of the preparations for a bone marrow transplant total body irradiation. Radiation in the form of whole brain radiation is also used for central nervous system prophylaxis, to prevent recurrence of leukemia in the brain. Whole brain prophylaxis radiation used to be a common method in treatment of children's ALL. Recent studies showed that CNS chemotherapy provided results as favorable but with less developmental side effects. As a result, the use of whole brain radiation has been more limited. Epidemiology The number of annual ALL cases in the US is roughly 4000, 3000 of which inflict children. ALL accounts for approximately 80 percent of all childhood leukemia cases, making it the most common type of childhood cancer. It has a peak incident rate of 2-5 years old, decreasing in incidence with increasing age before increasing again at around 50 years old. ALL is slightly more common in males than females. There is an increased incidence in people with Down Syndrome, Fanconi anemia, Bloom syndrome, Ataxia telangiectasia, X-linked agammaglobulinemia and Severe combined immunodeficiency. Prognosis Advancements in medical technology and research over the past four decades in the treatment of ALL has improved the overall prognosis significantly from a zero to 20-75 percent survival rate, largely due to the continuous development of clinical trials and improvements in bone marrow transplantation BMT and stem cell transplantation SCT technology. It is worth noting that medical advances in recent years, both through matching the best treatment to the genetic characteristics of the blast cells and through the availability of new drugs, are not fully reflected in statistics that usually refer to five-year survival rates. The prognosis for ALL differs between individuals depending on a wide variety of factors: Sex: females tend to fare better than males. Ethnicity: Caucasians are more likely to develop acute leukemia than African-Americans, Asians and Hispanics and tend to have a better prognosis than non-Caucasians. Age at diagnosis: children between 1-10 years of age are most likely to develop ALL and to be cured of it. Cases in older patients are more likely to result from chromosomal abnormalities e.g. the Philadelphia chromosome that make treatment more difficult and prognoses poorer. White blood cell count at diagnosis of less than 50,000/µl Whether the cancer has spread to the brain or spinal cord Morphological, immunological, and genetic subtypes Response of patient to initial treatment Genetic disorders such as Down's Syndrome Correlation of prognosis with bone marrow cytogenetic finding in acute lymphoblastic leukemia Prognosis Cytogenetic findings Favorable Hyperdiploidy 50 ; t 12;21 Intermediate Hyperdioloidy 47 -50; Normaldiploidy; del 6q; Rearrangements of 8q24 Unfavorable Hypodiploidy-near haploidy; Near tetraploidy; del 17p; t 9;22; t 11q23 Additional images acute lymphoblastic leukemia ALL, peripheral blood of a child, Pappenheim stain, magnification x100 bone marrow smear large magnification from a patient with acute lymphoblastic leukemia bone marrow smear from a patient with acute lymphoblastic leukemia References ^ Harrison's Principles of Internal Medicine, 16th ion, Chapter 97. Malignancies of Lymphoid Cells. Clinical Features, Treatment, and Prognosis of Specific Lymphoid Malignancies. ^ Collier, J.A.B 1991. Oxford Handbook of Clinical Specialties, Third ion. Oxford, 810. ISBN 0-19-262116-5. ^ Harrison's Principles of Internal Medicine, 16th ioN, Chapter 97. Malignancies of Lymphoid Cells. Clinical Features, Treatment, and Prognosis of Specific Lymphoid Malignancies. ^ Merck Manualcitation needed ^ Moorman A, Harrison C, Buck G, Richards S, Secker-Walker L, Martineau M, Vance G, Cherry A, Higgins R, Fielding A, Foroni L, Paietta E, Tallman M, Litzow M, Wiernik P, Rowe J, Goldstone A, Dewald G 2007. Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia ALL: analysis of cytogenetic data from patients treated on the Medical Research Council MRC UKALLXII/Eastern Cooperative Oncology Group ECOG 2993 trial. Blood 109 8: 3189-97. doi:10.1182/blood-2006-10-051912. PMID 17170120. ^ ACS :: How Is Acute Lymphocytic Leukemia Classified?. ^ Advances in Acute Lymphoblastic Leukemia. External links Information about ALL from the Leukemia Lymphoma Society Information about ALL from Cancer Research UK Directory of children's cancer-related resources from Children's Cancer Web Information about ALL from the Centre for Cancer and Blood Disorders at Sydney Children's Hospital Information about ALL from European LeukemiaNet Information on childhood ALL from ACOR's Ped-Onc Resource Center, including disease details MRD, phenotypes, molecular characterization, a layman's list of current and past clinical trials, a collection of articles on the possible causes of ALL, a bibliography of journal articles, and links to sources of support for parents of children with ALL. Association of Cancer Online Resource ACOR Leukemia Links - provides links to information on leukemia, including ALL, primarily in adults. v d e Pathology: hematology, myeloid hematologic disease primarily D50-D77, 280-289 RBCs/ hemoglobinopathy + Polycythemia - Macrocytosis - Anemia Nutritional Iron deficiency anemia, Plummer-Vinson syndrome, Megaloblastic anemia Pernicious anemia Hemolytic Herary enzyme disorders G6PD Deficiency, Pyruvate kinase deficiency,Triosephosphate isomerase deficiency other: Thalassemia, Sickle-cell disease/trait, Herary spherocytosis, Herary elliptocytosis, Herary stomatocytosis Acquired Autoimmune Warm, Cold, HUS, MAHA, PNH, PCH, Myelophthisic Aplastic Acquired PRCA, Diamond-Blackfan anemia, Fanconi anemia, Sideroblastic anemia Blood tests Normocytic - Microcytic - Macrocytic - Normochromic - Hypochromic Other Methemoglobinemia Coagulation/platelets/ coagulopathy/ bleeding diathesis + Hypercoagulability primary: Antithrombin III deficiency - Protein C deficiency/Activated protein C resistance/Protein S deficiency/Factor V Leiden - Hyperprothrombinemia acquired: DIC Congenital afibrinogenemia, Purpura fulminans - autoimmune Antiphospholipid Other Essential thrombocytosis - clotting factor: Hemophilia A/VIII, B/IX, C/XI Von Willebrand disease Hypoprothrombinemia/II - XIII platelet function: Bernard-Soulier syndrome - Glanzmann's thrombasthenia - Gray platelet syndrome - May Hegglin anomaly - Pelger-Huet anomaly Purpura: Henoch-Schönlein, ITP Evans syndrome, TTP Thrombocytopenia Heparin-induced thrombocytopenia Monocytes/ macrophages + Histiocytosis WHO-I Langerhans cell histiocytosis WHO-II/non-Langerhans-cell Juvenile xanthogranuloma, Hemophagocytic lymphohistiocytosis WHO-III/malignant Acute monocytic leukemia, Malignant histiocytosis, Erdheim-Chester disease Other Chronic granulomatous disease -cytosis: Monocytosis - -penia: Monocytopenia Granulocytes + -cytosis: granulocytosis Neutrophilia, Eosinophilia, Basophilia - -penia: Granulocytopenia/agranulocytosis Neutropenia, Kostmann syndrome See also hematological malignancy and immune disorders v d e Hematological malignancy/leukemia histology ICD-O 9590-9989, C81-C96, 200-208 Lymphoid/ Lymphoproliferative Lymphomas/ Lymphoid leukemias 9590-9739, 9800-9839 B cell lymphoma, leukemia most CD19, CD20 TdT+ ALL Precursor B acute lymphoblastic leukemia/lymphoma CD5+ SLL/CLL - mantle zone Mantle cell CD22+ Prolymphocytic - Hairy cell leukemia CD79a+ marginal zone Splenic marginal zone, MALT, Nodal marginal zone germinal center Follicular, Burkitt's, Diffuse large Other B Primary effusion - Lymphomatoid granulomatosis Plasma cells Plasmacytoma - Multiple myeloma - Waldenström macroglobulinemia T cell/NK cell lymphoma, leukemia most CD3, CD4, CD8 TdT+ ALL Precursor T acute lymphoblastic leukemia/lymphoma TdT- Cutaneous - Mycosis fungoides/Sézary's disease, Angioimmunoblastic - Anaplastic large cell - Hepatosplenic - Lymphomatoid papulosis Adult - Large granular lymphocyte - Prolymphocytic - Acute lymphoblastic Aggressive NK-cell leukemia Other Hodgkin's lymphoma usually B cell - Post-transplant lymphoproliferative disorder - Acute biphenotypic leukaemia Myeloid Myeloid leukemias 9840-9939 AML: Acute myeloblastic leukemia M1, M2 - APL/M3 - monocyte M4, AMoL/M5 - Erythroleukemia/M6 - AMKL/M7 - megakaryoblast - granulocyte Acute basophilic, Acute eosinophilic, Mast cell leukemia CML: CMoL, Philadelphia chromosome - Myeloid sarcoma Myelodysplastic- myeloproliferative 9945-9946 Juvenile myelomonocytic leukemia - Chronic myelomonocytic leukemia Myeloproliferative 9950-9964 Polycythemia vera - Essential thrombocytosis - Myelofibrosis - granulocyte CNL, Chronic eosinophilic leukemia/Hypereosinophilic syndrome Myelodysplastic 9980-9989 Sideroblastic anemia - Paroxysmal nocturnal hemoglobinuria Mast cell tumor 9740-9749 Mast-cell sarcoma - Malignant mastocytosis - Malignant histiocytosis - Langerhans cell histiocytosis See also hematology and immune disorders Retrieved from http://en..org/wiki/Acute_lymphoblastic_leukemia Categories: Hematology | Blood disorders | Types of cancerHidden categories: All articles with statements | Articles with statements since September 2007 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية Deutsch Italiano ‪Norsk bokmÃ¥l‬ ‪Norsk nynorsk‬ Polski Português СрпÑ?ки / Srpski Suomi Svenska This page was last modified on 6 August 2008, at 02:50
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