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Additional file 1. Supplementary figures and tables.

Platelet transfusion refractoriness (PTR) is an intractable issue in hematological patients, which increases bleeding risks and hospitalization costs to a great extent. We reviewed 108 patients with hematological diseases including acute leukemia, myelodysplastic syndrome, aplastic anemia, and others who received allogeneic hematopoietic stem cell transplantation (HSCT) from January 2019 through December 2020. After multivariable logistic regression, we found that splenomegaly (odds ratio [OR] = 26.98, p < .001) and JAK mutation (OR = 17.32, p = .024) were independent risk factors for PTR. During the period of transplantation, patients in the PTR group had a significantly higher platelet transfusion demand, which was reflected in the increased number of platelet transfusions (10.23 ± 6.696 vs. 5.06 ± 1.904, p < .001). After multivariate adjustment, PTR turned out to be independently associated with worse overall survival (hazard ratio = 2.794, 95% confidence interval = 1.083–7.207, p = .034). In conclusion, we found that splenomegaly and JAK gene mutation were independent risk factors for PTR in patients with hematological diseases. A history of PTR prior to allo-HSCT indicates a poor prognosis. What is the context?Platelet transfusion refractoriness is a critical issue, and it greatly increases bleeding risks and hospitalization costs.Patients with hematological diseases tend to develop PTR.PTR results from immune and nonimmune factors and the latter account for 80–90%.At present, there are few studies focused on the inducing factors of PTR, and the specific mechanism is not clear. Platelet transfusion refractoriness is a critical issue, and it greatly increases bleeding risks and hospitalization costs. Patients with hematological diseases tend to develop PTR. PTR results from immune and nonimmune factors and the latter account for 80–90%. At present, there are few studies focused on the inducing factors of PTR, and the specific mechanism is not clear. What is new?In this study, we investigated 108 patients with hematological disorders who received allogeneic HSCT from January 2019 to December 2020.We found that splenomegaly and JAK gene mutation were independent risk factors for PTR in patients with hematological diseases.PTR had a passive effect on the prognosis of patients after HSCT, as indicated by worse OS and a trend toward lower platelets after transplantation.PTR might affect megakaryocyte reconstitution after transplantation. In this study, we investigated 108 patients with hematological disorders who received allogeneic HSCT from January 2019 to December 2020. We found that splenomegaly and JAK gene mutation were independent risk factors for PTR in patients with hematological diseases. PTR had a passive effect on the prognosis of patients after HSCT, as indicated by worse OS and a trend toward lower platelets after transplantation. PTR might affect megakaryocyte reconstitution after transplantation. What is the impact?This study provides evidence that hematological patients with splenomegaly should be alert to the occurrence of PTR, which often indicates a worse prognosis of transplantation.Spleen reduction and JAK inhibitors in the treatment of PTR are worth exploring. This study provides evidence that hematological patients with splenomegaly should be alert to the occurrence of PTR, which often indicates a worse prognosis of transplantation. Spleen reduction and JAK inhibitors in the treatment of PTR are worth exploring. Abbreviations PLT: platelets; PTR: platelet transfusion refractoriness; HSCT: hematopoietic stem cell transplantation; OR: odds ratio; HR: hazard ratio; CI: confidence interval; IQR: interquartile range; SD: standard deviation; HLA: human leukocyte antigen; HPA: human platelet antigen; OS: overall survival; RFS: relapse free survival; PI: post-transfusion increment; PPR: percentage platelet recovery; CCI: corrected count increment; ICU: intensive care unit; AA: aplastic anemia; MDS: myelodysplastic syndrome; AML: acute myeloid leukemia; ALL: acute lymphocytic leukemia; CML: chronic myeloid leukemia; CMML: chronic myelomonocytic leukemia; MPN: myeloproliferative neoplasm; SI: splenic irradiation; Abs: antibodies; CR: complete remission; DAC: decitabine; GVHD: graft-versus-host disease; BM: bone marrow; PB: peripheral blood

Prolonged isolated thrombocytopenia (PT) is a common complication affecting the outcome of stem cell transplantation. In this study, we undertook a real-world study of 303 myelodysplastic syndrome (MDS) patients who received allogeneic hematopoietic stem cell transplantation (HSCT) between December 2007 and June 2018. 28.4% of MDS patients suffered from PT after HSCT. Survival analysis indicated that PT was associated with worse overall survival (OS) in MDS patients. The 2-year and 5-year OS in MDS patients with PT after HSCT were 49% and 47%, significantly worse than that of 68% and 60% in patients without PT (P=0.005). For RFS, patients with PT did not have an increased risk of disease relapse (P=0.964). After multivariate adjustment, PT was proved to be the independent risk factor associated with the worse OS (HR 1.49, 95% CI 1.00-2.21, P =0.048). We further analyzed risk factors associated with the occurrence of PT in MDS patients. Multiple logistic regression identified grade II-IV aGVHD, extensive chronic GVHD, hemorrhagic cystitis, and CMV activation as significant risk factors for developing PT. Among these variables, the Odds Ratio (OR) of grade II-IV aGVHD was the highest (P =0.001, OR: 2.65, 95% CI: 1.51-4.64). These data indicated the prognostic value of PT in MDS after HSCT. The identification of risk factors for PT may help improve patient management and lead to the design of effective treatment strategies.

Additional file 2: Figure S2. A Venn diagram shows the overlap of 22 optimal hub genes between GEO differential genes and WGCNA grey gene set.

Additional file 1: Figure S1. Correlation between gene significance and related module membership. A. The correlation between gene significance and module membership in the gray module. B. The correlation between gene significance and module membership in the blue module. *p < 0.05, **p < 0.01, ***p < 0.001.

Additional file 3: Figure S3. Identification of candidate hub genes to predict prognosis for AML patients. A. Partial likelihood deviance for different numbers of variables revealed by the LASSO regression model. Red dots represent the partial likelihood deviance values. Gray lines represent the partial likelihood deviance ± standard error. B. Fourteen candidate genes with minimum lambda values were obtained by LASSO regression with tenfold cross-validation. C. Candidate genes were filtrated from SVM-RFE algorithms. D. Five optimal hub genes overlapped between LASSO and SVM-RFE algorithm were shown by Venn diagram. Abbreviations: LASSO, least absolute shrinkage and selection operator; SVM-RFE, support vector machine recursive feature elimination.

Additional file 6: Table S1. Clinical characteristics of 48 AML patients. Table S2. Basic information for the included GEO databases.

Additional file 4: Figure S4. The expression levels of DLC1, NFIB, DENND5B, TANC2, and ELAVL4 in AML patients with different survival status. Scatter plots of the five gene’s expression level in AML patients with different survival status based on GEO dataset. *p < 0.05, **p < 0.01, ***p < 0.001. Abbreviations: GEO, Gene Expression Omnibus.

Additional file 5: Figure S5. Kaplan-Meier survival curve according to the DLC1 expression level for 48 AML patients in our center. Kaplan-Meier plots was used to visualize the overall survival probability of 48 patients based on the expression of DLC1 at diagnosis in our center.