A5072872655- Acute Myeloid Leukemia Research
- Cancer Genomics and Diagnostics
- Sarcoma Diagnosis and Treatment
- Chronic Myeloid Leukemia Treatments
- Acute Lymphoblastic Leukemia research
- Single-cell and spatial transcriptomics
- Epigenetics and DNA Methylation
- Hematopoietic Stem Cell Transplantation
- RNA modifications and cancer
- Immune Cell Function and Interaction
- Cancer-related gene regulation
- Immune cells in cancer
- Complement system in diseases
- Inflammatory Biomarkers in Disease Prognosis
- Prenatal Screening and Diagnostics
- SARS-CoV-2 and COVID-19 Research
- IL-33, ST2, and ILC Pathways
- Cardiac Fibrosis and Remodeling
- Histone Deacetylase Inhibitors Research
- T-cell and B-cell Immunology
- Childhood Cancer Survivors' Quality of Life
- Hematological disorders and diagnostics
- Transplantation: Methods and Outcomes
- Long-Term Effects of COVID-19
- CAR-T cell therapy research
Institute of Hematology & Blood Diseases Hospital
2020-2024
Chinese Academy of Medical Sciences & Peking Union Medical College
2020-2024
Southern Medical University
2017-2020
Nanfang Hospital
2017-2020
National Clinical Research
2020
Macrophage-orchestrated chronic inflammation plays an important role in cardiovascular disease, including accelerating the development of calcific aortic valve disease (CAVD). M1 and M2 macrophage polarization imbalances can alter intensity inflammatory responses. Recombinant human interleukin 37 (IL-37) could be involved regulating immune cell function to attenuate inflammation. This study aimed identify IL-37 specifically modulates investigate underlying mechanism. Compared with normal...
Abstract Purpose: Patient-tailored minimal residual disease (MRD) monitoring based on circulating tumor DNA (ctDNA) sequencing of leukemia-specific mutations enables early detection relapse for pre-emptive treatment, but its utilization in pediatric acute myelogenous leukemia (AML) is scarce. Thus, we aim to examine the role ctDNA as a prognostic biomarker response treatment AML. Experimental Design: A prospective longitudinal study with 50 children AML was launched, and sequential bone...
Abstract ETV6 :: RUNX1 is the most common fusion gene in childhood acute lymphoblastic leukaemia (ALL) and associated with favorable outcomes, especially low‐risk children. However, as many 10% of children relapse within 3 years, such early relapses have poor survival. Identifying at risk for an important challenge. We interrogated data from 87 ‐positive B‐cell ALL available preserved bone marrow samples (discovery cohort). profiled somatic point mutations a panel 559 genes genome‐wide...
Non-Down's syndrome acute megakaryocytic leukemia (non-DS-AMKL) is a subtype of childhood myeloid (AML), whose prognosis, prognostic factors and treatment recommendations have not yet to be defined in children. We conducted retrospective study with 65 newly diagnosed non-DS-AMKL children from August 2003 June 2020 investigate the clinical impact outcome. Among all patients, 47 them were treated at our center who received three different regimens due time point admission (CAMS-another,...
Relapse of childhood AML1-ETO (AE) acute myeloid leukemia is the most common cause treatment failure. Optimized minimal residual disease monitoring methods required to prevent relapse. In this study, we used next-generation sequencing identify breakpoints in fusion gene and DNA-based droplet digital PCR (ddPCR) method was for dynamic AE-DNA. The ddPCR technique provides more sensitive precise quantitation AE during progression Quantification by further contributes improved prognosis. Our...
<div>AbstractPurpose:<p>Patient-tailored minimal residual disease (MRD) monitoring based on circulating tumor DNA (ctDNA) sequencing of leukemia-specific mutations enables early detection relapse for pre-emptive treatment, but its utilization in pediatric acute myelogenous leukemia (AML) is scarce. Thus, we aim to examine the role ctDNA as a prognostic biomarker response treatment AML.</p>Experimental Design:<p>A prospective longitudinal study with 50 children AML was...
<p>Figure S3. Kaplan-Meier plot showed the PFS of patients diagnosed as CBF and non-CBF AML underwent dynamic monitoring mutations by ctDNA from admission to last cycle chemotherapy. PFS, progression-free survival. CBF, core binding factor</p>
<p>Figure S2. Comparison of CIR stratified by the different timepoint post treatment residual status either plasma ctDNA (A-C) or mutation in BM (D-F). according to (A) (D) at C2D1 treatment; (B) (E) C3D1 (C) (F) C4D1 treatment. A higher was associated with patients DNA positive results any point (all p<0.001). BM, bone marrow; CIR, cumulative incidence relapse; C2D1, Cycle 2 day 1; C3D1, 3 C4D1, 4 1</p>
<p>Figure S1. Flowchart of patient selection and enrollment. In total, 50 patients 195 paired samples (ctDNA BM DNA) from this population can be analyzed. the last row, plasma included at separate timepoint were depicted. BM, bone marrow; C2D1, Cycle 2 day 1; C3D1, 3 C4D1, 4 1</p>
<p>Figure S4. The correlation of the VAFs in patient-specific tumor mutation site detected plasma ctDNA and matched MFC based MRD. Scatter plot 195 individual mutations by both methods (r=0.586, p<0.001).</p>
<div>AbstractPurpose:<p>Patient-tailored minimal residual disease (MRD) monitoring based on circulating tumor DNA (ctDNA) sequencing of leukemia-specific mutations enables early detection relapse for pre-emptive treatment, but its utilization in pediatric acute myelogenous leukemia (AML) is scarce. Thus, we aim to examine the role ctDNA as a prognostic biomarker response treatment AML.</p>Experimental Design:<p>A prospective longitudinal study with 50 children AML was...
<p>Figure S3. Kaplan-Meier plot showed the PFS of patients diagnosed as CBF and non-CBF AML underwent dynamic monitoring mutations by ctDNA from admission to last cycle chemotherapy. PFS, progression-free survival. CBF, core binding factor</p>
<p>Figure S5. Comparison of PFS stratified by the different timepoint post-treatment residual status either plasma ctDNA or MFC at (A) C2D1, (B) C3D1 and (C) C4D1 post-treatment. neg-MFC neg was defined as VAF mutation being negative for MRD each timepoint. pos-MFC >0.01% pos immunophenotype ≥10−4 myeloblasts MFC, multiparameter flow cytometry; Cycle 2 day 1; C3D1, 3 C4D1, 4 1</p>
<p>Figure S2. Comparison of CIR stratified by the different timepoint post treatment residual status either plasma ctDNA (A-C) or mutation in BM (D-F). according to (A) (D) at C2D1 treatment; (B) (E) C3D1 (C) (F) C4D1 treatment. A higher was associated with patients DNA positive results any point (all p<0.001). BM, bone marrow; CIR, cumulative incidence relapse; C2D1, Cycle 2 day 1; C3D1, 3 C4D1, 4 1</p>
<p>Figure S5. Comparison of PFS stratified by the different timepoint post-treatment residual status either plasma ctDNA or MFC at (A) C2D1, (B) C3D1 and (C) C4D1 post-treatment. neg-MFC neg was defined as VAF mutation being negative for MRD each timepoint. pos-MFC >0.01% pos immunophenotype ≥10−4 myeloblasts MFC, multiparameter flow cytometry; Cycle 2 day 1; C3D1, 3 C4D1, 4 1</p>
<p>Figure S4. The correlation of the VAFs in patient-specific tumor mutation site detected plasma ctDNA and matched MFC based MRD. Scatter plot 195 individual mutations by both methods (r=0.586, p<0.001).</p>
<p>Figure S1. Flowchart of patient selection and enrollment. In total, 50 patients 195 paired samples (ctDNA BM DNA) from this population can be analyzed. the last row, plasma included at separate timepoint were depicted. BM, bone marrow; C2D1, Cycle 2 day 1; C3D1, 3 C4D1, 4 1</p>