{"id":3210,"date":"2020-12-22T18:07:14","date_gmt":"2020-12-22T16:07:14","guid":{"rendered":"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/blood-cancers\/acute-leukemias\/"},"modified":"2020-12-23T00:10:59","modified_gmt":"2020-12-22T22:10:59","slug":"acute-leukemias","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/blood-cancers\/acute-leukemias\/","title":{"rendered":"Acute leukemias"},"content":{"rendered":"\n

Leukemias are tumors of the bone marrow. In acute leukemias, the neoplastic cells are early hematopoietic cells (-blasts).<\/div><\/p>\n\n\n\n
\n\n\n\n

Description<\/h4>\n<\/span>\n\n\n

In healthy individuals, the number of precursor (-blast) cells in the bone marrow stays at a normal range (since cells maturate and new -blast cells are formed).<\/p>\n\n\n\n

  • In acute leukemias, precursor cells (-blasts) lose the ability to maturate, and these cells start proliferating and pile up in the bone marrow<\/li>
  • This may affect hematopoiesis and cause cytopenia<\/strong> (cell number decrease in the blood) of other cell lineages (thrombocytopenia<\/strong>, anemia<\/strong>, leukopenia<\/strong>)
    • The patient may present with symptoms that fit one of the cytopenia types (bleeding, hypoxia, or infections)<\/li><\/ul><\/li>
    • Precursor cells usually reach the circulation
      • They will seem polymorphic: larger, with and a big, pale nucleolus<\/li>
      • This may result in an increased count of the specific cell lineage<\/li><\/ul><\/li>
      • Acute leukemias have a sudden onset, they can arise on their own or as a progression of chronic leukemia<\/li>
      • Progress quickly, but are curable<\/li>
      • Mostly affect younger patients.<\/li><\/ul>\n\n\n<\/span>\n

        Acute myeloid leukemias and myelodysplastic syndromes<\/h2>\n<\/span>\n\n<\/span>\n

        Acute myeloid leukemias<\/h3>\n<\/span>\n\n\n

        In AML, we will see an increase in the number of myeloblasts<\/strong>.<\/p>\n\n\n\n

        • Presents within weeks or months<\/strong> with symptoms related to the cytopenia
          • Fatigue<\/li>
          • Fever<\/li>
          • Spontaneous bleeding<\/li>
          • Opportunistic infections<\/li><\/ul><\/li>
          • Appears mostly in adults (median age is 50)<\/li><\/ul>\n\n\n<\/span>\n

            Risk factors<\/h4>\n<\/span>\n\n\n
            • Trisomy 21 (Down syndrome)<\/li>
            • Exposure to benzene<\/li><\/ul>\n\n\n<\/span>\n

              Characteristics<\/h4>\n<\/span>\n\n\n
              • Over 20% <\/strong>of cells in the bone-marrow are myeloblasts (normal is about 5%)<\/li>
              • Bone marrow is usually hypercellular<\/li>
              • Myeloblasts usually do not maturate<\/strong><\/li>
              • May be associated with dysplasia in other lineages<\/li><\/ul>\n\n\n<\/span>\n

                Clinical manifestations<\/h4>\n<\/span>\n\n\n
                • Thrombocytopenia, anemia, and sometimes leukopenia<\/li><\/ul>\n\n\n<\/span>\n

                  Classification<\/h4>\n<\/span>\n\n\n

                  There was an old French-American-British classification with 7 classes (M0-M7) thas has been replaced with 4 major classes defined by WHO. We’ll cover the most classic subtype — Acute promyelocytic leukemia<\/strong>.<\/p>\n\n\n\n

                  • Class I — AML with recurrent chromosomal translocations<\/strong>
                    • Acute promyelocytic leukemia<\/strong><\/li><\/ul><\/li>
                    • Class II — AML with multilineage dysplasia<\/li>
                    • Class III — Therapy-relayed AML<\/li>
                    • Class IV — Non-specific<\/li><\/ul>\n\n\n<\/span>\n

                      Acute promyelocytic leukemia<\/h4>\n<\/span>\n\n\n
                      • Caused by a translocation in chromosomes 15 and 17 — or t(15;17)<\/strong><\/li>
                      • Promyelocytes accumulate<\/li>
                      • RAR receptors are disrupted<\/li>
                      • A high number of Auer rods
                        • Increased risk for DIC — medical emergency<\/li><\/ul><\/li>
                        • Prophylaxis includes all-trans retinoic acid (ARTA) to help promyelocytes to mature (this is not a cure, but rather a short-term solution)<\/li>
                        • Good prognosis<\/li><\/ul>\n\n\n<\/span>\n

                          Myelodysplastic Syndromes (MDS)<\/h3>\n<\/span>\n\n\n

                          A group of stem-cell disorders characterized by defective maturation, associated with a high risk (10-40%) of transformation to AML.<\/p>\n\n\n\n

                          • Partial or complete replacement of the cells in the bone marrow by transformed cells
                            • These cells have inefficient and disordered differentiation and proliferation<\/li><\/ul><\/li>
                            • Patients present with symptoms similar to AML (related to thrombocytopenia, anemia, and neutropenia)<\/li>
                            • Relatively rare, affecting older patients (ages 50-70)<\/li>
                            • Most cases are idiopathic
                              • Some can develop due to exposure to alkalizing agents and radiotherapy<\/li><\/ul><\/li>
                              • Variable prognosis<\/li><\/ul>\n\n\n<\/span>\n

                                Characteristics<\/h4>\n<\/span>\n\n\n
                                • A normal<\/strong> or increased<\/strong> amount of myeloblasts, but lower than 20% <\/strong>(recall over 20% is AML)<\/li>
                                • Bone marrow is hypercellular<\/li>
                                • Inefficient myeloblast maturation<\/li>
                                • May be associated with dysplasia in other lineages<\/li><\/ul>\n\n\n<\/span>\n

                                  Clinical manifestations<\/h4>\n<\/span>\n\n\n
                                  • Pancytopenia<\/li><\/ul>\n\n\n<\/span>\n

                                    Pathogenesis<\/h4>\n<\/span>\n\n\n

                                    The genetic alterations causing MDS can be classified into 3 categories:<\/p>\n\n\n\n

                                    • Epigenetic factors<\/strong> (histone modification)<\/li>
                                    • RNA splicing factors<\/strong> (RNA splicing machinery)<\/li>
                                    • Transcription factors<\/strong> (TF controlling normal myelopoiesis)<\/li><\/ul>\n\n\n\n

                                      In 10% of MDS cases, p53 mutations were present, leading to a worse prognosis.<\/p>\n\n\n<\/span>\n

                                      Comparison of AML and MDS<\/h3>\n<\/span>\n\n\n
                                      Disease<\/strong><\/td>Myeloblast count<\/strong><\/td>Bone marrow cellularity<\/strong><\/td>Maturation<\/strong><\/td>May be associated with dysplasia<\/strong><\/td>Blood count<\/strong><\/td><\/tr>
                                      AML<\/td>Over 20%<\/td>Usually hypercellular<\/td>Usually none<\/td>Yes<\/td>Anemia, thrombocytopenia, sometimes leukopenia<\/td><\/tr>
                                      MDS<\/td>5-20%<\/td>Hypercellular<\/td>Yes, inefficient<\/td>Yes<\/td>Cytopenia<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n<\/span>\n

                                      Precursor Lymphoblastic Lymphomas and Leukemias<\/h2>\n<\/span>\n\n<\/span>\n

                                      Description<\/h4>\n<\/span>\n\n\n

                                      Malignant tumor of precursor lymphoid cells (lymphoblasts).<\/p>\n\n\n<\/span>\n

                                      Classification<\/h4>\n<\/span>\n\n\n

                                      Can be either lymphoblastic leukemia (known as acute lymphoblastic leukemia<\/strong> or ALL<\/strong>), or lymphoblastic lymphoma.<\/p>\n\n\n\n

                                      • Acute Lymphoblastic Leukemia (ALL)
                                        • Much more common than lymphoblastic lymphomas<\/li>
                                        • “Acute” demarcates that it involves precursor cells (lymphoblasts<\/strong>)<\/li>
                                        • The letter before “ALL” is related to which cell type is affected
                                          • T-ALL is for T-cells<\/li>
                                          • B-ALL is for B-cells<\/li>
                                          • NK-ALL is for NK-cells<\/li><\/ul><\/li><\/ul><\/li>
                                          • Lymphoblastic Lymphoma
                                            • Much less common than ALL<\/li>
                                            • When the tumor involves the lymph nodes (much more common in T-cells)<\/li><\/ul><\/li><\/ul>\n\n\n<\/span>\n

                                              Characteristics<\/h4>\n<\/span>\n\n\n

                                              In ALL, we’ll see an increase in the number of lymphoblasts<\/strong>.<\/p>\n\n\n\n

                                              • Presents within weeks<\/strong> with the following:
                                                • Symptoms related to cytopenia<\/li>
                                                • Pain in the bones<\/li>
                                                • Headaches, vomiting<\/li><\/ul><\/li>
                                                • Generally, has a good prognosis<\/li>
                                                • Mediastinal masses appear in most cases of T-ALL
                                                  • The masses are referred to as lymphoblastic lymphoma (see above)<\/li><\/ul><\/li><\/ul>\n\n\n<\/span>\n

                                                    Risk factors<\/h4>\n<\/span>\n\n\n
                                                    • Trisomy 21 (Down syndrome)<\/li><\/ul>\n\n\n<\/span>\n

                                                      Genetic background<\/h4>\n<\/span>\n\n\n
                                                      • Most patients show a gain-of-function of NOTCH1<\/strong> gene<\/li>
                                                      • The usual translocations are t(12;21) and t(9;22)<\/strong>
                                                        • t(12;21) has a good prognosis, mostly seen in children<\/strong><\/li>
                                                        • t(9;22) has a bad prognosis, mostly seen in adults (Philadelphia chromosome)<\/strong><\/li><\/ul><\/li><\/ul>\n\n\n<\/span>\n

                                                          Epidemiology<\/h4>\n<\/span>\n\n\n
                                                          • Appears mostly in young patients<\/li>
                                                          • B-ALL is much more common than T-ALL<\/li><\/ul>\n<\/span>

                                                            Description<\/h4>

                                                            Acute myeloid leukemias and myelodysplastic syndromes<\/h2>

                                                            Acute myeloid leukemias<\/h3>

                                                            Risk factors<\/h4>

                                                            Characteristics<\/h4>

                                                            Clinical manifestations<\/h4>

                                                            Classification<\/h4>

                                                            Acute promyelocytic leukemia<\/h4>

                                                            Myelodysplastic Syndromes (MDS)<\/h3>

                                                            Characteristics<\/h4>

                                                            Clinical manifestations<\/h4>

                                                            Pathogenesis<\/h4>

                                                            Comparison of AML and MDS<\/h3>

                                                            Precursor Lymphoblastic Lymphomas and Leukemias<\/h2>

                                                            Description<\/h4>

                                                            Classification<\/h4>

                                                            Characteristics<\/h4>

                                                            Risk factors<\/h4>

                                                            Genetic background<\/h4>

                                                            Epidemiology<\/h4><\/div>","protected":false},"excerpt":{"rendered":"

                                                            Description In healthy individuals, the number of precursor (-blast) cells in the bone marrow stays at a normal range (since cells maturate and new -blast cells are formed). In acute leukemias, precursor cells (-blasts) lose the ability to maturate, and these cells start proliferating and pile up in the bone marrow This may affect hematopoiesis […]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":3209,"menu_order":1,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-3210","page","type-page","status-publish","hentry"],"yoast_head":"\nAcute leukemias – Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/pre-clinical\/pathology\/blood-cancers\/acute-leukemias\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"4 minutes\" \/>\n<script type=\"application\/ld+json\" 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