The newly published European Society of Medical Oncology (ESMO) Guidelines for Myelodysplastic Syndromes (MDS): ESMO Clinical Practice Guidelines for Diagnosis, Treatment, and Follow-up (hereinafter referred to as the Guidelines) are not fully consistent with the previously updated National Comprehensive Cancer Network (NCCN) Guidelines (2nd edition, 2014), and China’s medical and health insurance policies, patients’ subjective willingness to treat the disease The medical and health insurance policies and patients’ subjective willingness to treat their diseases in China are also different from those in Western countries such as Europe and the United States. In accordance with the principle of “use it for me”, the ESMO clinical practice guidelines are interpreted here. Diagnosis] The most basic tests required to confirm the diagnosis of MDS include peripheral blood count and leukocyte count, morphologic analysis of blood cells on bone marrow aspiration smear and peripheral blood smear, bone marrow biopsy and cytogenetic analysis of bone marrow cells. Morphologic abnormalities of the erythroid lineage, granulocyte lineage, and megakaryocyte developmental abnormalities on bone marrow and/or peripheral blood smears, as well as analysis of primitive cell ratios, are particularly important in the diagnosis of MDS. Peripheral blood smears should be categorized by 200 cells and bone marrow aspirate smears by 500 cells, emphasizing that “primitive cells” do not include promyelocytes. The diagnosis of hypoproliferative MDS and MDS with myelofibrosis depends on a bone marrow biopsy. To avoid missing the identification of small abnormal clones, 20-25 mid-life images should be analyzed, if possible. If the karyotype is normal or if not enough schizonts are available for analysis, further fluorescence in situ hybridization (FISH) including probes for 5q31, cen7, 7q31, cen8, TP53, 20q, and cenY should be performed. Other laboratory tests include lactate dehydrogenation (LDH), serum ferritin, transferrin saturation, reticulocyte count, vitamin B12 and folate levels, binding bead protein, endogenous erythropoietin (EPO), and creatinine level measurements. After the diagnosis of MDS, LDH and serum ferritin are of prognostic value, and EPO levels may be useful in making decisions about EPO therapy. In those patients with a high suspicion of MDS, flow cytometry immunophenotyping and acquired mutations, especially epigenetic regulation and chromatin remodeling (TET2, DNMT3a, ASXL1, IDH1/2, EZH2), premRNA shears (SF3B1, SRSF2, U2AF1), transcription factors (RUNX1, P53) and signaling (NRAS, CBL) were detected to help in the identification of clonal disease. Other laboratory tests that can help in the differential diagnosis and outcome prediction of MDS, such as human immunodeficiency virus (HIV) and microvirus19, HLA-DR15, thyroid function, and exclusionary flow cytometry analysis for large granular lymphocytic leukemia and paroxysmal sleep hemoglobinuria (PNH), are not recommended in this guideline. The World Health Organization (WHO) 2008 edition criteria were used for staging and diagnosis. After the diagnosis of MDS, the prognosis and risk grouping should be based on the International Prognostic Score System for MDS (IPSS-R) (table on the next page), which was revised in 2012. The low and intermediate risk of IPSS or the very low, low and intermediate risk of IPSS-R are generally grouped into the lower risk group, while other patients are grouped into the higher risk group, which is an important basis for the treatment strategy of MDS grouping (lower and higher risk). Patient-related factors, such as age, general status score and evaluation of comorbidities, are also important for prognosis and treatment selection, which should be given adequate attention by our colleagues in China. The efficacy criteria were based on the MDS International Working Group’s efficacy criteria (2006). Treatment of higher-risk MDS patients] For higher-risk patients aged <65~70 years, human leukocyte antigen (HLA) matching should be performed, and HLA-matched (or single unmatched) siblings or matched unrelated donors should be actively sought. scores, cytogenetics, and other factors. Patients <55 years of age are generally treated with a clear myeloablative pretreatment regimen. There is no consensus on the need to use AML-like chemotherapy or demethylating agents (HMA) to reduce progenitor cells prior to transplantation, but it is generally considered for patients with >10% progenitor cells who are to be pretreated with reduced doses. Treatment options for higher-risk patients who are not candidates for allo-HSCT include HMA, AML-like chemotherapy, and low-dose chemotherapy. Because decitabine is not approved for marketing in Europe, only azacitidine (a cytosine nucleoside analog) is recommended in this guideline. The recommended dose is 75 mg/(m2・d) administered subcutaneously for 7 days, 28 days for at least 6 courses of AML-like chemotherapy for younger patients (generally <60-65 years) with good karyotype grouping and >10% primitive cells, as a bridging therapy before allo-HSCT. Ticam. Low-dose cytarabine remains an appropriate option for higher-risk patients with normal karyotype who are not candidates for AML-like chemotherapy or allo-HSCT, especially those who are unlikely (including for financial reasons) to receive azacitidine or decitabine. The recommended dose is 20 mg/(m2・d) for 14 to 21 days in a 4-week course. The primary therapeutic goals for patients with lower-risk MDS are to increase peripheral blood counts and to improve the patient’s quality of life (QoL). First-line treatment for patients with anemia: EPO (30,000 units/week to 80,000 units/week) is preferred for non-5q-syndrome patients, and the combination with granulocyte colony-stimulating factor (G-CSF) can further improve the efficacy, with a median onset of action of 8-12 weeks and a median duration of maintenance of efficacy of about 2 years. Patients with p53 mutations may require more intense therapy. Second-line therapy in patients with anemia: non-5q-syndrome patients who fail EPO therapy (primary failure or relapse after initiation) may be treated with anti-thymocyte globulin (ATG) ± cyclosporine, HMA or lenalidomide. Treatment of neutropenia and thrombocytopenia: patients with neutropenic fever may be treated with anti-infective drugs in addition to G Symptomatic thrombocytopenia may be treated with clinical trials such as thrombopoietin (TPO) agonists, ATG or azacitidine. Prophylactic platelet transfusion is generally not recommended for patients with neutropenia, nor is prophylactic antibiotics and/or G-CSF recommended for patients with neutropenia. lower-risk patients with red blood cell transfusions exceeding 40 to 120 units, or serum ferritin exceeding 1000 mg/L to 2500 mg/L, or Significantly reduced cardiac T2 on magnetic resonance imaging (MRI) should be treated with iron removal. In addition, patients with iron overload who are proposed for allo-HSCT should receive iron removal therapy as soon as possible. Desferrioxamine mesylate or Deferasirox may be the drug of choice for iron removal therapy.