| Biomarker | BCAT1 | Full name | Branched-Chain Amino Acid Transaminase 1 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, therapeutic targets | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Bone marrow (RNA sequencing, qRT-PCR) | ||
| Pathobiological Mechanisms | Promoting the development of AML through the FLT3-ITD/BCAT1/MYC pathway | ||||
| Clinical Availability Status | Research validation: High expression in the NPM1+FLT3-ITD+ subtype. | ||||
| Notes and Dynamics | The predictive prognostic ability is superior to the FLT3-ITD allele ratio, and FLT3 inhibitors can downregulate its expression. | ||||
| Biomarker | FLVCR2 | Full name | Feline Leukemia Virus Subgroup C Receptor 2 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, immune infiltration-related | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Bone marrow (qRT-PCR, Western blot) | ||
| Pathobiological Mechanisms | Influence tumor microenvironment immune cell infiltration and regulate AML progression | ||||
| Clinical Availability Status | Frontier research: Negatively correlated with activated NK cells and CD8+ T Cell infiltration. | ||||
| Notes and Dynamics | Silencing can inhibit the growth of AML cells and promote apoptosis. | ||||
| Biomarker | CYTH4 | Full name | Cytohesin 4 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, therapeutic targets | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Bone marrow (RNA sequencing, in vitro functional validation) | ||
| Pathobiological Mechanisms | Participates in immune regulation, promotes cell growth, and inhibits apoptosis. | ||||
| Clinical Availability Status | Research validation: High expression is associated with high white blood cell count and high-risk status. | ||||
| Notes and Dynamics | Transplantation can significantly improve survival in patients with high expression, providing a basis for risk stratification. | ||||
| Biomarker | NT-proBNP | Full name | N-terminal pro-brain natriuretic peptide | Molecular Type | Proteins |
| Molecular Formula | / | Molecular Weight | 10 kDa | Core Functional Dimensions | Prognosis, Monitoring |
| Disease(or Constitution) | Myocarditis | Disease Subtypes | / | ||
| Organ | Myocardium | Test Sample / Technology Platform | Serum/plasma (ELISA) | ||
| Pathobiological Mechanisms | BNP precursor fragment is more stable than BNP and reflects the state of cardiac function | ||||
| Clinical Availability Status | Clinically available | ||||
| Notes and Dynamics | It is more significant in severe myocarditis and its prognostic value is better than that of BNP | ||||
| Biomarker | ARHGAP43 | Full name | Rho GTPase Activating Protein 43 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Bone marrow (RNA sequencing, qRT-PCR) | ||
| Pathobiological Mechanisms | Participates in inflammatory and immune responses, promoting cell proliferation | ||||
| Clinical Availability Status | Research validation: High expression indicates poor prognosis.. | ||||
| Notes and Dynamics | Hematopoietic stem cell transplantation improves outcomes in patients with high expression. | ||||
| Biomarker | DNMT3A mutation | Full name | DNA Methyltransferase 3 Alpha gene mutation | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Susceptibility, prognosis, therapeutic Targets | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood/bone marrow (genomic sequencing) | ||
| Pathobiological Mechanisms | Catalyze de novo DNA methylation, mutations lead to hypomethylation of hematopoietic stem cell-specific genes, thereby blocking cell differentiation. | ||||
| Clinical Availability Status | Clinically validated/Targeted therapy: Common mutations in normal karyotype AML. | ||||
| Notes and Dynamics | R882 site mutation is the most common, indicating poor prognosis; demethylating agents such as decitabine show better therapeutic response. | ||||
| Biomarker | BNP | Full name | Brain natriuretic peptide | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | 4 kDa | Core Functional Dimensions | Prognosis, Monitoring |
| Disease(or Constitution) | Myocarditis | Disease Subtypes | / | ||
| Organ | Myocardium | Test Sample / Technology Platform | Serum/Plasma (ELISA) | ||
| Pathobiological Mechanisms | Myocardium is released during stretching or cardiac insufficiency, reflecting ventricular load | ||||
| Clinical Availability Status | Clinically available | ||||
| Notes and Dynamics | Assist in assessing cardiac function and predicting the risk of heart failure | ||||
| Biomarker | TET2 mutation | Full name | Ten-Eleven Translocation 2 gene mutation | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Susceptibility, prognosis | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood/bone marrow (genomic sequencing) | ||
| Pathobiological Mechanisms | The encoding methylenecylenine di-oxidase (MCD) gene, when mutated, leads to high DNA methylation, which affects hematopoietic cell differentiation. | ||||
| Clinical Availability Status | Research validation: Coexistence with multiple gene mutations, the prognostic value remains controversial. | ||||
| Notes and Dynamics | Mutations are mutually exclusive with IDH1/2; the mutation may represent an early event in leukemia development, influencing disease progression. | ||||
| Biomarker | cTnI / cTnT | Full name | Cardiac troponin I / Cardiac troponin T | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | cTnI: 24 kDa; cTnT: 37 kDa | Core Functional Dimensions | Diagnosis, Prognosis |
| Disease(or Constitution) | Myocarditis | Disease Subtypes | / | ||
| Organ | Myocardium | Test Sample / Technology Platform | Serum/plasma (ELISA, SIMOA) | ||
| Pathobiological Mechanisms | Myocardial cells are released after injury, reflecting the degree of myocardial necrosis | ||||
| Clinical Availability Status | Clinically available (recommended by guidelines) | ||||
| Notes and Dynamics | Core myocarditis diagnostic markers, high specificity and sensitivity, is one of the gold standard | ||||
| Biomarker | RUNX1-RUNX1T1/CBFβ-MYH11 | Full name | RUNX1-RUNX1 Translocation Partner 1/Core Binding Factor Beta-Myosin Heavy Chain 11 fusion gene | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood/bone marrow (FISH, RT-qPCR) | ||
| Pathobiological Mechanisms | t(8;21) or inv(16) generates fusion proteins, suppresses hematopoietic gene transcription, and blocks cell differentiation. | ||||
| Clinical Availability Status | Clinical validation/guideline recommendation: ELN guideline for favorable prognosis group indicators. | ||||
| Notes and Dynamics | Monotherapy yields favorable prognosis, while cases with c-Kit mutation are classified as intermediate-risk. The conventional '3+7' chemotherapy regimen demonstrates high response rates. | ||||
| Biomarker | Lactate | Full name | Lactic acid | Molecular Type | Metabolites |
| Molecular Formula | / | Molecular Weight | 90.08 Da | Core Functional Dimensions | Diagnosis and Prognosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | All cells (anaerobic metabolism), liver (gluconeogenesis) | Test Sample / Technology Platform | Serum/plasma (colorimetry, enzymatic method, blood gas analyzer) | ||
| Pathobiological Mechanisms | During myocardial ischemia, anaerobic metabolism is enhanced and lactic acid accumulates. It reflects the degree of tissue hypoxia and the disorder of energy metabolism of myocardial cells | ||||
| Clinical Availability Status | Clinical available (emergency evaluation) : in the emergency treatment of chest pain rapid screening process, used for patients with suspected AMI emergency stratification, lactic acid > 2 tendency for prompt severe myocardial ischemia, L need to priority intervention | ||||
| Notes and Dynamics | Within 24 h of the level associated with AMI mortality is (lactate > 4 tendency when L mortality increased 5 times); High negative predictive value (95% accuracy for ruling out critical ischemia at <1mmol/L) | ||||
| Biomarker | biCEBPA | Full name | Biallelic CCAAT/Enhancer Binding Protein Alpha gene mutation | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood/bone marrow (genomic sequencing) | ||
| Pathobiological Mechanisms | The key transcription factor for hematopoietic myeloid cell differentiation, double allele mutations affect cell differentiation regulation. | ||||
| Clinical Availability Status | Clinical validation/guideline recommendation: WHO defines independent subtypes, and the ELN guidelines incorporate prognostic stratification. | ||||
| Notes and Dynamics | Single mutations are associated with a favorable prognosis, whereas the presence of a TET2 mutation is associated with a poorer prognosis; the related immunophenotype holds promise for disease screening. | ||||
| Biomarker | TMAO | Full name | Trimethylamine N-oxide | Molecular Type | metabolites |
| Molecular Formula | / | Molecular Weight | 75.11 Da | Core Functional Dimensions | Susceptibility, prognosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Liver (metabolism of gut microbiota-derived TMA) | Test Sample / Technology Platform | Serum/plasma (LC-MS and GC-MS) | ||
| Pathobiological Mechanisms | Metabolites of gut microbiota (derived from choline and L-carnitine); Promote macrophage foaming, inhibit endothelial function, and accelerate atherosclerosis | ||||
| Clinical Availability Status | Research validation (risk) : large-scale cohort (n = 1273) confirmed that TMAO > 5 μmol/L 62% increased risk of coronary heart disease, in patients with AMI were significantly higher than stable coronary heart disease (p < 0.01); It is not included in clinical guidelines, but only used as an indicator for scientific research and screening of high-risk populations | ||||
| Notes and Dynamics | It is greatly affected by diet (the intake of red meat and egg yolk can increase), so standardized diet is needed before testing; It is related to the composition of intestinal flora, which can guide the "diet-microbiota" intervention treatment | ||||
| Biomarker | TP53 mutation | Full name | Tumor Protein P53 gene mutation | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood/bone marrow (genomic sequencing) | ||
| Pathobiological Mechanisms | The encoded cell cycle regulatory transcription factor exhibits abnormal DNA repair function after mutation, leading to uncontrolled cell proliferation. | ||||
| Clinical Availability Status | Clinical validation/Advanced therapies: ELN guidelines recommend early screening; targeted drugs under development. | ||||
| Notes and Dynamics | The results indicate a poor prognosis, with low complete response rate (CRR) and high recurrence rate. The combination of APR-246 and azacitidine demonstrated synergistic therapeutic effects and was granted orphan drug designation. | ||||
| Biomarker | miR-208a/b / miR-499 | Full name | MicroRNA-208a / MicroRNA-208b / MicroRNA-499 | Molecular Type | Non-coding RNA (miRNA) |
| Molecular Formula | / | Molecular Weight | 22 nt | Core Functional Dimensions | Early diagnosis and prognosis |
| Disease(or Constitution) | Coronary heart disease (CHD) | Disease Subtypes | / | ||
| Organ | Myocardium | Test Sample / Technology Platform | Serum/plasma (RT-PCR, microfluidic chip) | ||
| Pathobiological Mechanisms | Myocardial high specificity (miR-208-a expression in myocardial only); Mir-208a is rapidly released after AMI and regulates myocardial contractile function related genes | ||||
| Clinical Availability Status | Clinical validation (key direction of early diagnosis) : the detection rate of miR-208a was 100% within 4 hours of AMI onset, the specificity was 100% (negative in non-AMI patients), and Mir-208a was listed as a "potential early marker" in the Diagnosis and Treatment Pathway of Acute chest Pain. The AUC of miR-499 in diagnosis of AMI was 0.994, which was positively correlated with infarct size | ||||
| Notes and Dynamics | The half-life of miR-208a is short (2h), which requires rapid detection. Joint miR-499 can improve prognosis evaluation effectiveness, both negative hint 30 d risk of adverse events < 1% | ||||
| Biomarker | FLT3 mutation (ITD/TKD) | Full name | Fms-Like Tyrosine Kinase 3 gene mutation (Internal Tandem Duplication/Tyrosine Kinase Domain) | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, therapeutic targets | ||
| Disease(or Constitution) | Acute Myeloid Leukemia (AML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood/bone marrow (gene sequencing, DNA fragment analysis) | ||
| Pathobiological Mechanisms | Type III receptor tyrosine kinase, upon mutation, activates pathways such as STAT5 and RAS/MAPK, driving abnormal proliferation of hematopoietic cells. | ||||
| Clinical Availability Status | Clinically available/under targeted therapy: key prognostic stratification indicators, with targeted drugs already approved. | ||||
| Notes and Dynamics | ITD mutations are associated with poorer prognosis than TKD, and the higher the allele ratio, the worse the prognosis. Inhibitors such as sorafenib and midostaurin require combination with chemotherapy to improve resistance. | ||||