Xospata (gilteritinib) / Astellas - LARVOL DELTA

Maintenance therapy in AML: A meta-analysis and a single center retrospective study (ASH 2025) - "Therapeutic interventions were analyzed, including CC-486, sorafenib, gilteritinib, FLT3 inhibitors, azacitidine, and decitabine. The meta-analysis suggests that maintenance therapy in AML patientsis associated with improved OS, DFS, and RFS, with particularly pronounced benefits observed in MRD+ and intermediate-risk subgroups. Although maintenance therapy increases hematologic and dermatologic toxicities, its overall safety is acceptable. The retrospective analysis indicated that the VA regimen showed certain efficacy and safety in unfit or elderly AML patients, but the study is limited in number and needs more cases and a prospective cohort study to further verify."

Retrospective data • Acute Myelogenous Leukemia • Hematological Disorders • Infectious Disease • Neutropenia • Thrombocytopenia

Real-world AML survival paradox: Early escalation vs. sustained remission (ASH 2025) - "Patients were stratified into two cohorts: Cohort A (early escalation, n=1,460), comprising patients who received either second-line chemotherapy (including fludarabine, cladribine, gilteritinib, enasidinib, revumenib, olutasidenib, etoposide, or clofarabine) or hematopoietic stem cell transplant (HSCT) as salvage therapy within 6 months of completing initial therapy; and Cohort B (no escalation, n=10,540), consisting of patients who received no additional therapy during this same period. Our findings highlight the complex interplay between disease biology and treatment interventions: achieving MRD-negativity remains critical, but when MRD-positivity occurs, subsequent treatment decisions based on disease genetics prove critical. Prospective studies incorporating molecular MRD monitoring are needed to confirm these findings and further optimize post-remission therapy approaches."

Clinical • Real-world • Real-world evidence • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Hematological Malignancies • Leukemia

FLT3 testing and guideline concordance in Acute Myeloid Leukemia across an Indiana health system (ASH 2025) - "Current guidelines recommend FLT3 mutation testing at diagnosis to inform risk stratification and guide the use of FLT3 inhibitors such as midostaurin, quizartinib, and gilteritinib...The most frequently used induction therapies included venetoclax in combination with a hypomethylating agent (30%), 7+3 (15.7%), and a combination regimen consisting of fludarabine, cytarabine, idarubicin, and granulocyte colony-stimulating factor (FLAG IDA; 13.8%)... FLT3 testing was commonly performed in this cohort, yet notable variability in guideline adherence was observed. Guideline-concordant induction regimen selection was marginally higher for patients with FLT3 mutations. These findings underscore the need for institutional quality improvement initiatives aimed at enhancing the documentation of FLT3 status and optimizing the integration of guideline-directed therapies in AML management."

Discordant • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3

A modified Delphi consensus on the management of patients with relapsed or refractory FLT3-mutated acute myeloid leukemia in four Latin American countries (ASH 2025) - "Panelists agreed on ECOG performance status ≥2, high comorbidity and KPS <70 as defining criteria for unfit pts, and on the FLT3-TKI gilteritinib as the preferred first therapeutic option. Finally, panelists agreed on unacceptable toxicity and lack of tolerability as factors for discontinuing maintenance. Conclusions : While most statements reached agreement across all 4 countries, some only reached country-level agreement; including inclusion of age when defining unfit pts; HMA+venetoclax as a preferred induction choice in fit pts; whether to combine FLT3-TKI with another agent if the fit pt has suboptimal response; duration of post-HSCT treatment; and whether MRD status is a determining factor to initiate post-HSCT treatment."

Clinical • Acute Graft versus Host Disease • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Dermatology • Graft versus Host Disease • Hematological Disorders • Hematological Malignancies • Immunology • Infectious Disease • Leukemia • Neutropenia • Thrombocytopenia • FLT3

Enhanced antileukemic activity of momelotinib in combination with venetoclax and azacitidine compared to gilteritinib-based combination (ASH 2025) - "Despite extensive genomic insights, conventional chemotherapies, specifically anthracyclines and cytarabine , have remained the cornerstone of treatment for the past four decades...In contrast, selective inhibitors of JAK-STAT (ruxolitinib) or FLT3 (gilteritinib or quizartinib) alone failed to demonstrate comparable synergy, highlighting the distinct polypharmacological profile of momelotinib in mediating the cytotoxic response...Notably, while the efficacy of gilteritinib-based regimens was restricted to FLT3-mutant AML, the momelotinib combination demonstrated activity across both FLT3 mutant and FLT3 wild-type contexts. Altogether these preclinical data support clinical evaluation of momelotinib in combination with venetoclax and azacitidine as a potential effective treatment in AML."

Combination therapy • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • ACVR1 • FLT3 • IRAK1

Inhibitors of RAD51 as potential novel therapies in Acute Myeloid Leukemia (ASH 2025) - "Furthermore, these compounds often exhibit strong synergy and at least additivity in combination with both on-label and off-label use of FDA-approved compounds, as well as investigational molecularly-targeted agents, in relevant cell lines; these include FLT3 inhibitors quizartinib, gilteritinib and tuspetinib ((in MV-4-11 and HL60 cell lines) and BCR/ABL inhibitors (imatinib and regorafenib) in the K562 cell line (AACR 2025)...We have confirmed the IBRs inhibit multiple RAD51 functions including hydroxyurea-induced RAD51 focus formation, HRR by DR-GFP assay, and RS protection by RPA focus formation and a DNA fibre assay...JKYN-1 is a partially optimized (more soluble and more potent) version of IBR120 but is not resistant to degradation by liver microsomes or sufficiently capable of entry into target cells...Treatment dose and combinations will be pre-screened using a highly predictive cell line as a surrogate of human cancer stem cells for subsequently AML patient..."

Acute Myelogenous Leukemia • Colorectal Cancer • Hematological Malignancies • Leukemia • Solid Tumor • BRCA1 • BRCA2 • FLT3 • HRD • RAD51

Outcomes of umbilical cord blood transplantation for acute myeloid leukemia in the era of FLT3 inhibitors. (ASH 2025) - "Post-transplant maintenance with gilteritinib was administered in 22 patients and was associated with a trend toward improved outcomes, including a higher 1-year PFS (81.6% vs. 64.3%) and a lower relapse rate (4.5% vs. 14.3%, P < 0.05), although potential selection bias could not be excluded... In this cohort of first UCBT, FLT3-mutated AML demonstrated superior PFS and OS with a reduced relapse rate. Post-transplant FLT3 inhibitor maintenance therapy showed a potential benefit. Larger studies are warranted to validate these findings."

Acute Graft versus Host Disease • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Chronic Graft versus Host Disease • Graft versus Host Disease • Hematological Malignancies • Immunology • Infectious Disease • Leukemia • Transplantation • FLT3

Early allogeneic stem cell transplantation enhanced survival of co-expressed NUP98::NSD1 and FLT3-ITD Acute Myeloid Leukemia: An exploratory analysis. (ASH 2025) - "Only 35.7% patients achieved hematologic complete remission (CR) after induction chemotherapy, CR rates 25% (2/8) using standard "7+3" intensive chemotherapy, 75% (3/4) in Venetoclax-involved and 66.7% (2/3) in Gilteritinib-involved regimens, respectively. This exploratory study suggests that early allo-HSCT may offer survival advantages in AML patients with co-occurring NUP98::NSD1 and FLT3-ITD mutations, who exhibited poor response to chemotherapy, by avoiding toxicities from multiple cycles of intensive chemotherapy prior to transplantation. Large-scale prospective studies are required to define the optimal transplantation timing."

Acute Graft versus Host Disease • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Graft versus Host Disease • Hematological Disorders • Hematological Malignancies • Immunology • Infectious Disease • Leukemia • Transplantation • BCOR • CCND3 • CEBPA • FLT3 • IDH2 • NRAS • NSD1 • NUP98 • PAX5 • WT1

Risk of relapse and mortality after non-myeloablative allogeneic stem cell transplant for Acute Myeloid Leukemia and myelodysplastic syndrome after fludarabine, cyclophosphamide, and 200 centigray total body irradiation with gvhd prophylaxis using post-transplant cyclophosphamide, sirolimus, and mycophenolate mofetil: Impact of maintenance chemotherapy (ASH 2025) - "Oral HMA agents were decitabine/cedazuridine (dec-c) 3d/28-day cycle, and oral azacitidine (Oral-Aza) for 14 days per 28-day cycle...A total of 32 (31%) patients received post-HSCT maintenance chemotherapy: infusional HMA (n=2), recombinant-Granulocyte Colony Stimulating Factor (rhGCSF)/decitabine (n=2), gilteritinib (n=7), dec-c (n=9), oral-aza (2), and venetoclax/Azacitidine (n=8)... NMA conditioning with Flu/Cy/2Gy TBI yields low NRM. Post-transplant maintenance therapy, particularly with HMAs and targeted agents, is associated with reduced relapse in intermediate-risk and adverse-risk TP53 wt AML and MDS. However, outcomes remain poor for patients with TP53 mu t AML and MDS, indicating an urgent need for alternative or intensified maintenance strategies in these high-risk groups."

Clinical • Post-transplantation • Acute Graft versus Host Disease • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Chronic Graft versus Host Disease • Chronic Myelomonocytic Leukemia • Graft versus Host Disease • Hematological Malignancies • Immunology • Leukemia • Myelodysplastic Syndrome • Transplantation • FLT3 • TP53

Efficacy and safety of salvage therapies in relapsed/refractory Acute Myeloid Leukemia: A systematic review and network meta-analysis (ASH 2025) - "For safety, Cytarabine showed the lowest incidence of AEs (SUCRA = 0.71), while Enasidenib demonstrated the best profile in reducing mortality (SUCRA = 0.87). This NMA highlights Gilteritinib as the most effective and safest salvage therapy for R/R AML, particularly in patients with FLT3-mutated disease. Gemtuzumab Ozogamicin, Apamistamab, and Enasidenib also showed favorable outcomes, depending on molecular profiles and clinical priorities. These findings underscore the importance of individualized therapy selection based on efficacy, safety, and molecular characteristics."

Retrospective data • Review • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3

Gilteritinib maintenance therapy after allogeneic hematopoietic stem cell transplantation in FLT3-mutated AML: A systematic review and meta-analysis (ASH 2025) - "Due to a lack of uniform reporting across studies, a pooled analysis of the toxicity profile, especially of GVHD incidence, could not be performed. However, some individual studies reported a higher incidence of GVHD in the Gilteritinib arm, raising the possibility of an association that warrants further investigation and larger randomized controlled trials."

Retrospective data • Review • Acute Graft versus Host Disease • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Chronic Graft versus Host Disease • Graft versus Host Disease • Hematological Malignancies • Immunology • Leukemia • Transplantation • FLT3

Comparative safety and efficacy of first- and second-generation FLT3 inhibitors in newly diagnosed and relapsed AML: A meta-analysis stratified by molecular biomarkers (ASH 2025) - "First-generation (sorafenib and midostaurin) and second-generation (gilteritinib, quizartinib, and crenolanib) FLT inhibitors demonstrated efficacy and safety across disease stages and are now used as a standard of treatment for FLT3-mutated AML. Conclusions Second-generation FLT inhibitors exhibit enhanced efficacy in relapsed-refractory AML scenarios and comparable outcomes to first-generation inhibitors in newly diagnosed AML.Stratification using ITD allelic ratio and NPM1 co-mutation is emerging as a critical factor. In light of these findings, it's imperative to integrate second-generation inhibitors in salvage settings and Biomarker-guided treatment decisions in front-line FLT3 mutant-AML"

Biomarker • Retrospective data • Acute Myelogenous Leukemia • Cardiovascular • Hematological Disorders • Hypertension • Neutropenia • FLT3 • NPM1

Maintenance with hypomethylating agent + venetoclax after intensive induction chemotherapy in patients with newly diagnosed Acute Myeloid Leukemia (ASH 2025) - "Background Consolidative therapy with high/intermediate-dose cytarabine is standard practice for fit patients with newly diagnosed acute myeloid leukemia (ND-AML) who achieve complete remission (CR) after receiving intensive induction chemotherapy (IC). Oral azacitidine is approved as maintenance therapy in patients who achieve CR after IC but are unable to complete intensive consolidation therapy...Five patients (20%) received a FLT3 inhibitor with HMA and VEN (3 quizartinib, 2 gilteritinib), and 1 patient (4%) received an IDH-2 inhibitor (enasidenib)...These findings must be interpreted in the context of several limitations: a relatively small sample size, a median of one maintenance cycle, and the absence of scheduled repeat disease assessments. Larger, prospective studies are needed to confirm these observations and better define the role of HMA + VEN in this setting."

Clinical • Acute Graft versus Host Disease • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Chronic Graft versus Host Disease • Graft versus Host Disease • Hematological Malignancies • Immunology • Leukemia • FLT3 • IDH1 • IDH2 • TP53

Development of HPB-092: A novel dual kinase inhibitor targeting FLT3 and IRAK4 for the treatment of relapsed/refractory Acute Myeloid Leukemia (RR-AML) (ASH 2025) - "Compared to the approved FLT3 inhibitors gilteritinib and quizartinib, as well as the clinical-stage dual inhibitor CA-4948, HPB-092 displayed comparable or superior potency against mutant FLT3 and IRAK4, improved kinome selectivity (selectivity score 50 μM), and no hERG inhibition (IC50 > 10 μM), along with an excellent overall safety profile in nonclinical species. The study has been approved by the Institutional Review Board (IRB) and has also been submitted to ClinicalTrials.gov, currently pending final approval. The first patient is anticipated to be enrolled in the fourth quarter of 2025."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3 • IRAK4 • SF3B1 • U2AF1

A healthy volunteer study with lomonitinib predicts pharmacokinetics and pharmacodynamics in a relapsed refractory AML study (ASH 2025) - P1 | "Multiple in vivo studies with both xenograft and syngeneic immune competent murine models demonstrated that lomonitinib has superior efficacy to gilteritinib in ITD and gatekeeper mutation-dependent disease. The safety profile of lomonitinib enables rapid FLT3 engagement by using a loading dose (5-fold higher than the maintenance dose) which is not possible with other long half-life FLT3 inhibitors with less favorable therapeutic indices. Application of healthy volunteer studies with agents having a broad therapeutic index such as lomonitinib offer the opportunity to enter a subsequent AML patient clinical trial at a clinically effective dose identified from pre-clinical models."

Clinical • PK/PD data • Acute Myelogenous Leukemia • FLT3 • IRAK4

Dichotomy of TP53 mutant AML MRD microenvironment: Spatially segregated immunosuppressive mechanisms and niche-specific structural support (ASH 2025) - "Patients received either Aza/Ven- or Ara-C/Idarubicin-based regimens combined with magrolimab or gilteritinib. single-cell proteomics analysis of bone marrow biopsies provides a spatially resolved view of the TP53mut AML microenvironment, uncovering persistent p53+ MRD cells enriched for erythroid phenotypes. Their structural niches suggest MRD-protective roles of MSCs and adipocytes, and immunosuppressive features such as spatial separation between T-cell clusters and p53+ cells, involvement of Tregs within lymphocyte clusters and a distance-dependent TIGIT surge of T and NK-cells in proximity to p53+ cells. This comprehensive spatial analysis offers new insights into the mechanisms of immune escape and MRD persistence in TP53mut AML."

IO biomarker • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • CD14 • CD34 • FOXP3 • NPM1 • TFRC • TIGIT • TP53

Unveiling FLT3 in B-ALL: Molecular drivers and targeted treatment opportunities (ASH 2025) - "In vitro assays withincreasing concentrations of 6 FLT3i for 24, 48, 72h [Gilteritinib (Gil), Midostaurin, Crenolanib, Sorafenib,Quizartinib, Ponatinib (Pon)] and Venetoclax (Ven) were performed on primary patient samples (n=29; FLT3-mut n=5/29), 11 B-ALL wt cell lines, 2 B-ALL mut (NALM6-mut, KASUMI-10), and 4 AML cell lines (OCI-AML3 wt; MV-4-11, MOLM-13, MONO-MAC6 FLT3-mut). FLT3 alterations define a novel Ph-negative B-ALL subgroup withtherapeutic relevance. Given the responses in FLT3-wt in addition to the mutated models, FLT3i may alsobenefit patients without FLT3 muts. Thanks to: Ricerca Corrente by the Italian MoH L3P1946 andAILTreviso."

Acute Lymphocytic Leukemia • Acute Myelogenous Leukemia • B Acute Lymphoblastic Leukemia • Bone Marrow Transplantation • Hematological Malignancies • Leukemia • T Acute Lymphoblastic Leukemia • FLT3 • IKZF1 • KMT2A • PBX1 • TCF3 • TP53 • ZNF384

GB3226, a novel, orally active, first-in-class small molecule inhibitor of ENL-yeats and FLT3 kinase for the treatment of Relapsed/Refractory Acute Myeloid Leukemia (ASH 2025) - "In cell-based assays, GB3226potently inhibited proliferation of both MV4; 11 (IC50=18 nM) and MOLM13 (IC50=32 nM) cell lines andwas additive/synergistic when combined with standard-of-care agents, including venetoclax, gilteritinib,and revumenib. We have developed GB3226, a novel, oral, first-in-class, dual inhibitor of ENL-YEATS and FLT3for the treatment of AML. Preclinical studies demonstrate that GB3226 exhibits potent anti-leukemicactivity and has the potential for combination use with multiple therapeutic agents across diverse AMLgenotypes. GB3226 has shown robust in vitro and in vivo efficacy, along with a favorable preclinical safetyprofile."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • FLT3 • HOXA9 • KIT • MEIS1 • MELK • NTRK3 • TET2

Preliminary safety and efficacy of the frida study: Iadademstat and gilteritinib in FLT3-mutated relapsed/refractory acute myeloid leukemia (ASH 2025) - P1 | "Preclinically, iada is synergistic with gilteritinib in FLT3 mut AML cells and in derivedcell lines resistant to venetoclax, azacitidine or other FLT3is (Sacilotto et al., 2022 Eur J. of Cancer 174S1).More than 140 pts have been treated with iada, including treatment-naïve AML pts in the ALICE studywhere, in combination with azacitidine, iada produced rapid, durable, and deep responses with amanageable safety profile (Salamero et al., Lancet Hematol...The FRIDA Phase 1 study(NCT05546580) aims to establish the safety, tolerability, and the recommended Phase 2 dose (RP2D) ofthe combination of iada plus gilteritinib in FLT3 mut R/R AML.Adult pts with ≤ 2 prior lines of therapy (including quizartinib and gilteritinib if not refractory), receivediada PO at doses of 50 to 100 μg on a 5 days ON- 2 days OFF (5+2) schedule for 3 or 4 weeks (wks), in 28-day cycles with continuous gilteritinib PO at 120 mg/day...The combination of iada and gilteritinib at the tested doses..."

Clinical • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Febrile Neutropenia • Gene Therapies • Hematological Malignancies • Leukemia • Neutropenia • FLT3

Pre-clinical efficacy of FLT3/BRAF targeting with novel dual inhibitor PHI3 in FLT3/RAS co-mutated AML (ASH 2025) - "Introduction:In AML with FLT3 mutations, FLT3 inhibitors are routinely used in combination with inductionchemotherapy in fit patients, and with a low-intensity HMA/Venetoclax backbone in older patients. Our study demonstrates the efficacy of the novel dual BRAF/FLT3 inhibitor PHI3 in FLT3-mutated AML,including those resistant to gilteritinib due to RAS mutations. These findings suggest the potentialtherapeutic value of dual targeting of FLT3 and RAF/MAPK signaling in FLT3-mutated AML, achieved byblocking the major resistance bypass signaling pathway."

Preclinical • Acute Myelogenous Leukemia • BRAF • CASP3 • FLT3 • KRAS • NRAS

FLT3-F691L confers kinase-independent resistance via Grb2-dependent MAPK signaling in AML (ASH 2025) - "Unlike gilteritinib or a negative controlPROTAC, CRBN(FLT3)-8 robustly suppressed viability, clonogenicity, and RAF/MEK signaling in FLT3-F691LAML, indicating that FLT3-F691L retains essential non-kinase functions.To uncover pathways mediating the FLT3-F691L kinase-independent function, we performed a genome-wide CRISPR-Cas9 dropout screen in isogenic FLT3-ITD and FLT3-F691L AML cells treated with gilteritinib.Grb2, an adaptor protein that links receptor tyrosine kinases to Ras activation via SOS, emerged as a topdependency unique to gilteritinib-treated FLT3-F691L cells. Our findings support thedevelopment of FLT3 degraders or combined targeting of FLT3 and Ras/MAPK pathways to overcomeFLT3-F691L-driven resistance in relapsed/refractory AML. Importantly, this work suggests that otherrecurrent hot-spot mutations in oncogenic kinases may similarly confer kinase-independent functions incancer and should be systematically investigated as potential drivers of therapeutic..."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • CRBN • FLT3 • STAT5

Acute leukemia during pregnancy: A three-decade Mayo Clinic experience (ASH 2025) - "One patient had refractory disease and achieved partial remission after salvage,another had refractory disease and achieved CR after multiple lines of therapy, and a third achieved CRafter FLAG-idarubicin and revumenib...All receivedintensive induction: 7+3 (n=5), 7+3 + ATRA (n=1), 7+3 + gilteritinib (n=1), and 7+3 + nilotinib (n=1)...Notably, 5 (28%) of patients received chemotherapy during pregnancy. Larger,multi-institutional cohorts are warranted to further characterize the incidence and outcomes of AL inpregnancy."

Acute Lymphocytic Leukemia • Acute Myelogenous Leukemia • Acute Promyelocytic Leukemia • Hematological Malignancies • Hodgkin Lymphoma • Infectious Disease • Leukemia • Lymphoma • Pneumonia • Respiratory Diseases • T Acute Lymphoblastic Leukemia • KMT2A • NUP214

Post-transplant FLT3 inhibitor maintenance is associated with improved survival in FLT3-ITD positive acute myelogenous leukemia irrespective of pre-transplant MRD status (ASH 2025) - "Fourteen (44%) received gilteritinib, 13 (41%) received sorafenib,and 5 (16%) received midostaurin as their first TKI post-HCT. Despite limitations, including limited sample size, we observed an improvement in OS in patients whoreceived post-HCT TKIm, irrespective of pre-HCT MRD status and conditioning regimen intensity.Consistent TKIm post-HCT is challenging due to the high discontinuation rate from toxicity."

Clinical • Post-transplantation • Pre-transplantation • Acute Myelogenous Leukemia • Graft versus Host Disease • Hematological Disorders • Hematological Malignancies • Immunology • Leukemia • Transplantation • FLT3

Real-world effectiveness and safety of gilteritinib plus venetoclax and azacitidine in FLT3 mutated acute myeloid leukemia (ASH 2025) - "These real-world data indicated GVA is an efficient treatment for these FLT3 mutated AML patients, notonly limited to older/unfit or R/R patients."

Clinical • Real-world • Real-world effectiveness • Real-world evidence • Acute Myelogenous Leukemia • Bone Marrow Transplantation • FLT3

A multiarm phase 1b study of personalized oral maintenance therapy with decitabine/cedazuridine (ASTX727) plus physician's choice of venetoclax, gilteritinib, enasidenib, or ivosidenib in Acute Myeloid Leukemia (ASH 2025) - P1 | "Pts were required to have received at least 2 courses of intensive chemotherapy(intermediate to high-dose cytarabine-based) or 3 courses of low-intensity therapy (HMA or low-dosecytarabine-based) prior to enrollment. Personalized fully oral maintenance therapy is feasible in AML. Myelosuppression andinfections were the most common adverse events. Further enrollment and follow-up is needed toevaluate efficacy."

Clinical • IO biomarker • P1 data • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Febrile Neutropenia • Gastroenterology • Gastrointestinal Disorder • Hematological Disorders • Hematological Malignancies • Hypertension • Immunology • Infectious Disease • Leukemia • Leukopenia • Myelodysplastic Syndrome • Neutropenia • Novel Coronavirus Disease • Pneumonia • Respiratory Diseases • Septic Shock • Thrombocytopenia • TP53