| Biomarker | CD203c | Full name | Ectonucleotide Pyrophosphatase/Phosphodiesterase Family Member 3 | Molecular Type | Protein (surface antigen) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, treatment, and monitoring |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Peripheral blood (flow cytometry) | ||
| Pathobiological Mechanisms | Specifically expressed in basophils, overexpressed in CML patients, and significantly reduced after treatment. | ||||
| Clinical Availability Status | Research Verification: Associated with disease risk characteristics, upregulated IgE receptor cross-linking. | ||||
| Notes and Dynamics | The changes in the number of basophils can be evaluated during the diagnostic and treatment phases. | ||||
| Biomarker | miR-486-5p | Full name | microRNA-486-5p | Molecular Type | Nucleic acid (miRNA) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis, and prediction of treatment response |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Peripheral blood leukocytes/K562 cells (qRT-PCR) | ||
| Pathobiological Mechanisms | Downregulated in newly diagnosed patients, upregulated after imatinib treatment, with better prognosis and more significant therapeutic response in high-expression patients. | ||||
| Clinical Availability Status | Research validation: Correlated with the Sokar score, enabling early diagnosis of CML. | ||||
| Notes and Dynamics | Exhibits tumor-suppressive effects and regulates the downstream signaling pathway of BCR-ABL. | ||||
| Biomarker | MALAT1 | Full name | Metastasis-Associated Lung Adenocarcinoma Transcript 1 | Molecular Type | Nucleic acid (lncRNA) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Dassatinib resistance prediction |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Patient samples (bioinformatics analysis, differential expression gene screening) | ||
| Pathobiological Mechanisms | May exert tumor-suppressive effects and be associated with the development of dafatinib resistance in CML | ||||
| Clinical Availability Status | Research validation: Predicting their functions by constructing lncRNA-miRNA-mRNA networks. | ||||
| Notes and Dynamics | To provide guidance for the research on the resistance mechanism of dasatinib and the development of therapeutic targets. | ||||
| Biomarker | RPL13 | Full name | Ribosomal Protein L13 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Imatinib resistance prediction |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Plasma (ultracentrifugation, LC-MS/MS, Western blot, PRM) | ||
| Pathobiological Mechanisms | Imatinib-resistant patients exhibit significantly upregulated exosomes in plasma, which are involved in protein synthesis regulation | ||||
| Clinical Availability Status | Research validation: Differentially expressed genes have been confirmed through multiple technical validations. | ||||
| Notes and Dynamics | To provide new insights into the mechanism of imatinib resistance, it serves as a potential biomarker for drug resistance. | ||||
| Biomarker | miR-20/miR-106/miR-222 | Full name | microRNA-20/microRNA-106/microRNA-222 | Molecular Type | Nucleic acid (miRNA) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Plasma (real-time quantitative RT-PCR) | ||
| Pathobiological Mechanisms | Significantly upregulated in newly diagnosed CML patients, targeting the regulation of cell cycle, MAPK and other related pathways. | ||||
| Clinical Availability Status | Research verification: upregulated by 17.4-fold, 19-fold, and 74.95-fold respectively, with statistical significance. | ||||
| Notes and Dynamics | Provide a theoretical basis for the diagnosis and prognosis evaluation of CML. | ||||
| Biomarker | LDH | Full name | Lactate Dehydrogenase | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis, and treatment monitoring |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Peripheral blood (GeneXpert RT-PCR, ROC curve analysis) | ||
| Pathobiological Mechanisms | Strongly positively correlated with BCR-ABL transcription levels, with a significant decrease observed post-treatment | ||||
| Clinical Availability Status | Clinical validation: AUC of 0.881, superior to indicators such as uric acid and platelets. | ||||
| Notes and Dynamics | Economically viable, it can serve as an alternative diagnostic marker, prognostic biomarker, and potential therapeutic target. | ||||
| Biomarker | BCR-ABL (p210) fusion gene (13a2/e14a2 subtype) | Full name | Breakpoint Cluster Region - Abelson murine leukemia viral oncogene homolog 1 (p210) fusion gene (13a2/e14a2 subtype) | Molecular Type | Nucleic acid (fusion gene) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, subtype differentiation |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Leukemic cell/patient sample (nanocluster beacon fluorescence technology) | ||
| Pathobiological Mechanisms | The chromosomal translocation t(9;22) is the cause, with significant differences in clinical manifestations, treatment efficacy, and prognosis between the two subtypes. | ||||
| Clinical Availability Status | Technical validation: Subtype identification can be completed within 40 minutes, with detection limits of 16pM (e13a2) and 9pM (e14a2), respectively. | ||||
| Notes and Dynamics | Achieve high-efficiency single-tube detection to provide subtype-based evidence for precision therapy. | ||||
| Biomarker | Tregs/eTregs | Full name | Regulatory T cells/effector Regulatory T cells | Molecular Type | Immunocyte |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Monitoring and prognosis of treatment-free response (TFR) |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Clinical samples (flow cytometry) | ||
| Pathobiological Mechanisms | Maintaining TFR, with a transient increase in eTregs after discontinuation followed by return to baseline, and CD8(+) T cells in an activated state. | ||||
| Clinical Availability Status | Research validation: Characteristic changes were observed in patients with 3-year TFR maintenance. | ||||
| Notes and Dynamics | As a biomarker for TFR, high concentrations of imatinib exposure may exert immunosuppressive effects. | ||||
| Biomarker | CIP2A | Full name | Cancerous Inhibitor of Protein Phosphatase 2A | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis, prediction of treatment failure |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Diagnostic sample (protein level detection) | ||
| Pathobiological Mechanisms | Overexpression is associated with disease progression and treatment failure, with this effect observed only in patients treated with dasatinib. | ||||
| Clinical Availability Status | Research validation: Clinical trials have confirmed its association with progression-free survival and treatment failure rate. | ||||
| Notes and Dynamics | It can serve as a simple and feasible diagnostic biomarker, providing a reference for the formulation of therapeutic strategies. | ||||
| Biomarker | Anti-RoSSA antibody | Full name | Anti-Ro/SSA antibody (Ro52/Tripartite Motif Containing 21, Ro60/SSA) | Molecular Type | Protein (autoantibody) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, disease association |
| Disease(or Constitution) | Autoimmune Disease (AD) | Disease Subtypes | pSS | ||
| Organ | Spleen, thymus, lymphoid tissue | Test Sample / Technology Platform | Serum (immunological assay) | ||
| Pathobiological Mechanisms | Participates in immune regulation; target of autoimmune response in salivary glands. | ||||
| Clinical Availability Status | Clinically available; positive rate reaches 60%-80% in pSS cases, sensitivity of 75%-85% for early screening, and specificity >88%. | ||||
| Notes and Dynamics | Core serological marker; associated with extraglandular manifestations. | ||||
| Biomarker | Anti-La/SSB antibodies | Full name | Anti-La/SSB antibodies | Molecular Type | Protein (autoantibody) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, disease association |
| Disease(or Constitution) | Autoimmune Disease (AD) | Disease Subtypes | pSS | ||
| Organ | Spleen, thymus, lymphoid tissue | Test Sample / Technology Platform | Serum (immunological assay) | ||
| Pathobiological Mechanisms | Participates in immune regulation and RNA metabolism. | ||||
| Clinical Availability Status | Clinically available; in pSS patients, positive rate is 30%-60%, with specificity >90% for differentiating from other autoimmune diseases.. | ||||
| Notes and Dynamics | Often co-occurs with Anti-Ro/SSA; aids in diagnosis. | ||||
| Biomarker | LA | Full name | Lupus Anticoagulant | Molecular Type | Protein (abnormal antibody function) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, thrombosis risk assessment |
| Disease(or Constitution) | Autoimmune Disease (AD) | Disease Subtypes | APS | ||
| Organ | Spleen, thymus, lymphoid tissue | Test Sample / Technology Platform | Serum (APTT corrected test, RVVT, etc.) | ||
| Pathobiological Mechanisms | Prolonged clotting time, detected by functional tests | ||||
| Clinical Availability Status | Clinically available: Strongly associated with thrombosis. | ||||
| Notes and Dynamics | It exhibits a higher positivity rate in patients with venous thrombosis, serving as a critical thrombotic risk indicator. | ||||
| Biomarker | anti-β2-GPⅠ antibodies | Full name | Anti-beta-2-Glycoprotein Ⅰ antibodies | Molecular Type | Protein (autoantibody) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, thrombosis risk assessment |
| Disease(or Constitution) | Autoimmune Disease (AD) | Disease Subtypes | APS | ||
| Organ | Spleen, thymus, lymphoid tissue | Test Sample / Technology Platform | Serum (ELISA) | ||
| Pathobiological Mechanisms | The target antigen is β2-glycoprotein I, which participates in coagulation/anticoagulation regulation. | ||||
| Clinical Availability Status | Clinically available: higher specificity than aCL. | ||||
| Notes and Dynamics | It has significant supplementary diagnostic value for aCL-negative suspected APS patients. | ||||
| Biomarker | aCL | Full name | Anti-Cardiolipin Antibodies | Molecular Type | Protein (autoantibody) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Thrombosis/acute pregnancy risk assessment |
| Disease(or Constitution) | Autoimmune Disease (AD) | Disease Subtypes | APS | ||
| Organ | Spleen, thymus, lymphoid tissue | Test Sample / Technology Platform | Serum (ELISA) | ||
| Pathobiological Mechanisms | The target antigen is cardiolipin, with subtypes including IgG, IgM, and IgA. | ||||
| Clinical Availability Status | Clinically available: Persistent positivity at medium to high titers is a critical diagnostic criterion for APS. | ||||
| Notes and Dynamics | IgG subtypes show strongest association with thrombosis and adverse pregnancy outcomes. | ||||
| Biomarker | SHP2 | Full name | Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase 2 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis and pathogenesis-related |
| Disease(or Constitution) | Autoimmune Disease (AD) | Disease Subtypes | SLE | ||
| Organ | Spleen, thymus, lymphoid tissue | Test Sample / Technology Platform | Plasma (ELISA) | ||
| Pathobiological Mechanisms | Elevated plasma levels, associated with clinical laboratory features, promote lupus progression。 | ||||
| Clinical Availability Status | Research verification: Inhibitors can improve tissue damage and immune dysfunction in lupus mice | ||||
| Notes and Dynamics | Closely associated with the pathogenesis of SLE, it also holds potential as a diagnostic and therapeutic target. | ||||
| Biomarker | Sema5A | Full name | Semaphorin 5A | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Pathogenesis-related, therapeutic targets |
| Disease(or Constitution) | Autoimmune Disease (AD) | Disease Subtypes | SLE | ||
| Organ | Spleen, thymus, lymphoid tissue | Test Sample / Technology Platform | Serum and peripheral blood mononuclear cells (ELISA, qRT-PCR, Western Blot) | ||
| Pathobiological Mechanisms | Elevated serum levels promote Th17 differentiation through the Sema5A-PlexinA1 axis and the PI3K-Akt-mTOR pathway. | ||||
| Clinical Availability Status | Research validation: Positively correlated with SLEDAI, lupus nephritis, and IL-17A levels. | ||||
| Notes and Dynamics | A novel therapeutic target for SLE, which also reflects immune dysregulation. | ||||