| Biomarker | BCL-2 | Full name | B-cell lymphoma 2 | Molecular Type | Protein (Apoptosis regulatory protein) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Therapeutic targets, prognostic evaluation |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Tumor tissue (immunohistochemistry, Western blot) | ||
| Pathobiological Mechanisms | Regulates apoptosis, is highly expressed in cHL, and is associated with tumor cell survival. Venetoclax can induce apoptosis in its positive cells. | ||||
| Clinical Availability Status | Research/Drug Development Phase: Venetoclax exhibits cytotoxicity against cHL cell lines, providing a basis for novel targeted therapy. | ||||
| Notes and Dynamics | Research/Drug Development Phase: Venetoclax exhibits cytotoxicity against cHL cell lines, providing a basis for novel targeted therapy. | ||||
| Biomarker | S-TK1 | Full name | Serum thymidine kinase 1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, disease status assessment |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Serum (Novel antibody detection method) | ||
| Pathobiological Mechanisms | Participates in DNA synthesis, with elevated levels during tumor cell proliferation and higher baseline levels compared to healthy controls. | ||||
| Clinical Availability Status | Research phase: Limited sample size and short follow-up period, reliability of conclusions remains to be validated. | ||||
| Notes and Dynamics | Larger-scale studies are required to confirm its value as a diagnostic and prognostic biomarker. | ||||
| Biomarker | sPD-L1 | Full name | Soluble programmed death-ligand 1 | Molecular Type | Protein (soluble immune checkpoint molecule) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Assessment of disease status |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Plasm (ELISA、Luminex) | ||
| Pathobiological Mechanisms | High expression of PD-L1 in the tumor microenvironment leads to its release into the plasma, reflecting an immunosuppressive state, but is not directly correlated with total PD-L1 expression in tissues. | ||||
| Clinical Availability Status | Research phase: Significantly elevated compared to the healthy control group, and correlated with clinical indicators. | ||||
| Notes and Dynamics | It does not reflect tissue PD-L1 expression and requires analysis in conjunction with biopsy samples; future studies should explore its association with ICB treatment response. | ||||
| Biomarker | ctDNA | Full name | Circulating tumor DNA | Molecular Type | Nucleic acid (DNA from tumor tissue) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognostic assessment, minimal residual disease monitoring, and clonal evolution analysis |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Plasma (LyV4.0 ctDNA CAPP-seq, whole-genome low coverage sequencing, targeted NGS) | ||
| Pathobiological Mechanisms | DNA fragments released by tumor cells reflect tumor burden and genetic mutation status, with high levels prior to treatment indicating poor prognosis and being highly correlated with PET/CT findings. | ||||
| Clinical Availability Status | Research validation/clinical translation phase: The 3-year PFS prediction C-index was 64.9%, which improved to 69.8% when combined with IPS, enabling the identification of high-risk patients. | ||||
| Notes and Dynamics | The most frequently mutated gene is STAT6, with significant differences in mutation profiles across subtypes; it enables dynamic tracking of disease progression and complements imaging assessments. | ||||
| Biomarker | TARC（CCL17） | Full name | Thymus and activation-regulated chemokine (C-C motif chemokine ligand 17) | Molecular Type | Protein (chemokines) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Treatment response monitoring, prognosis evaluation, and diagnostic triage. |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Serum/plasma (ELISA, electrochemical biosensors, Luminex) | ||
| Pathobiological Mechanisms | HRS cells secrete and recruit CCR4-positive immune cells, participating in tumor microenvironment regulation, with their levels decreasing after treatment. | ||||
| Clinical Availability Status | Clinical validation/partial application: Differentiation between patients with chronic Hodgkin lymphoma (cHL) and healthy individuals before treatment, with post-treatment levels correlating to event-free survival (EFS). | ||||
| Notes and Dynamics | The TARC level at the end of treatment in pediatric chronic lymphocytic leukemia (cHL) can be used to assess remission status; combining with EV-miRNA may improve predictive accuracy, and blocking its signaling pathway could become a therapeutic strategy. | ||||
| Biomarker | phospho-PD-1 | Full name | Phosphorylated programmed cell death protein 1 | Molecular Type | Protein (phosphorylated protein) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Response prediction to treatment, functional abnormal T cell markers |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Tumor-infiltrating lymphocytes (TILs) (monoclonal antibody detection, flow cytometry) | ||
| Pathobiological Mechanisms | The phosphorylation of the intracellular ITSM motif in PD-1 reflects the signaling activity of PD-1, marking activated T cells susceptible to PD-1 inhibition. After PD-1 blockade, its levels decrease. | ||||
| Clinical Availability Status | Research validation phase: Identification of PD-1 signal-activated T cells provides molecular basis for PD-1 immune checkpoint blockade (ICB) therapy response. | ||||
| Notes and Dynamics | The phosphorylation level of PD-1 is prominent in PD-1-positive and TIM-3-positive TILs, while in CD8-positive TILs, the phosphorylation level of PD-1 can serve as an evaluation indicator for ICB efficacy. | ||||
| Biomarker | CD20 | Full name | Cluster of differentiation 20 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Auxiliary diagnosis |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Immunohistochemistry (IHC) | ||
| Pathobiological Mechanisms | It is a surface marker of B cells, expressed by normal B cells and some B-cell lymphomas. CD30-positive Hodgkin lymphoma tumor cells often do not express it or exhibit only weakly positive expression. | ||||
| Clinical Availability Status | Clinical validation/Routine application: Primarily used to exclude non-Hodgkin lymphomas of B-cell origin such as diffuse large B-cell lymphoma, and to assist in determining the disease type. | ||||
| Notes and Dynamics | Only a minority of CD30-positive Hodgkin lymphoma cases exhibit weak CD20 positivity, requiring comprehensive evaluation in conjunction with other markers to avoid misdiagnosis based on a single indicator. | ||||
| Biomarker | CD30 | Full name | Cluster of differentiation 30 | Molecular Type | Protein (transmembrane glycoprotein) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Targeted Therapy Targets |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Immunohistochemistry (IHC) | ||
| Pathobiological Mechanisms | Belongs to the tumor necrosis factor receptor superfamily, normally expressed in activated T cells, B cells, and NK cells; in CD30-positive Hodgkin lymphoma, tumor cells exhibit high expression of CD30, serving as a disease-specific marker. | ||||
| Clinical Availability Status | Clinical validation/guideline recommendation: It is the core biomarker for the diagnosis of CD30-positive Hodgkin lymphoma and also serves as a key target for anti-CD30 targeted therapy. | ||||
| Notes and Dynamics | The efficacy of anti-CD30 monoclonal antibodies (e.g., Brentuximab Vedotin) depends on the expression level of tumor cell CD30, and the expression status must be confirmed by immunohistochemistry (IHC) to guide the selection of targeted therapy regimens. | ||||
| Biomarker | KMT2D | Full name | Lysine Methyltransferase 2D | Molecular Type | Nucleic acid (gene) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | TKI resistance prediction, therapeutic targets. |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Cell line/patient sample (siRNA-mediated knockdown, gene expression analysis) | ||
| Pathobiological Mechanisms | Mutation-induced imatinib resistance can be reduced by knockdown, and the expression can be restored to reverse the resistance. | ||||
| Clinical Availability Status | Research validation: Associated with upregulated CCNE2 expression. | ||||
| Notes and Dynamics | Histone modification enzyme-related markers provide novel strategies for overcoming drug resistance. | ||||
| Biomarker | ENO1 | Full name | Enolase 1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prediction of TKI treatment response, therapeutic targets. |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Cell line/patient sample (metabolomics analysis, Western blot) | ||
| Pathobiological Mechanisms | Drug-resistant cells exhibit greater dependence on their mediated glycolysis, and downregulation can induce autophagic degradation and ferroptosis of GPX4. | ||||
| Clinical Availability Status | Research validation: exhibits negative correlation with TMEM164, and the combination of inhibitors enhances TKI sensitivity. | ||||
| Notes and Dynamics | Regulating ferroptosis through the AMPK/mTOR pathway provides a basis for combination therapy. | ||||
| Biomarker | MDM2 gene variants (SNP309) | Full name | Mouse Double Minute 2 Homolog gene variants (Single Nucleotide Polymorphism 309) | Molecular Type | Nucleic acid (gene) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Response prediction and prognosis |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Whole blood (genotyping) | ||
| Pathobiological Mechanisms | The SNP309 G/G genotype is associated with the risk of molecular response failure and interacts with the TP53 SNP215 combination to influence prognosis | ||||
| Clinical Availability Status | Study validation: Specific genotype combinations are associated with treatment response and survival rates. | ||||
| Notes and Dynamics | Provide reference for individualized TKI treatment regimen formulation. | ||||
| Biomarker | miR-495-3p | Full name | microRNA-495-3p | Molecular Type | Nucleic acid (miRNA) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Drug resistance prediction, therapeutic targets |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Cell models/patient samples (expression level detection, functional experiments) | ||
| Pathobiological Mechanisms | Downregulation of expression leads to TKI resistance, and drug efflux is inhibited by regulating MDR1. | ||||
| Clinical Availability Status | Research verification: overexpression inhibits the growth of drug-resistant cells. | ||||
| Notes and Dynamics | May serve as a therapeutic target to reverse TKI resistance. | ||||
| Biomarker | HOXA4 gene methylation | Full name | Homeobox A4 gene methylation | Molecular Type | Nucleic acid (DNA methylation) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Drug resistance prediction, disease progression prediction |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Patient sample (methylation-sensitive high-resolution melting technique) | ||
| Pathobiological Mechanisms | High methylation is associated with imatinib resistance and disease progression to advanced stages, and is correlated with transcription type, smoking, and high Sokal score. | ||||
| Clinical Availability Status | Study verification: The methylation level in the drug-resistant group was significantly higher than that in the well-responsive group. | ||||
| Notes and Dynamics | Epigenetic biomarkers provide a basis for risk stratification. | ||||
| Biomarker | ASXL1 mutation | Full name | Additional Sex Combs Like 1 gene mutation | Molecular Type | Nucleic acid (gene) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis and prediction of treatment response |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Patient samples (direct sequencing, qRT-PCR) | ||
| Pathobiological Mechanisms | Mutant patients exhibit significantly increased risks of drug resistance and disease progression, which are correlated with the Sokal risk score. | ||||
| Clinical Availability Status | Research verification: 11.25% of patients exhibited mutations, which were associated with ABL1 KD mutations. | ||||
| Notes and Dynamics | Can assist in formulating the optimal TKI regimen to prevent disease progression. | ||||
| Biomarker | ASF1A | Full name | Anti-Silencing Function 1A Histone Chaperone | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Disease progression prediction, therapeutic targets |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Bone marrow samples (expression level detection, functional experiments) | ||
| Pathobiological Mechanisms | Mediates cell differentiation arrest, promotes the transformation of CML into the acute phase, and activates the Notch signaling pathway | ||||
| Clinical Availability Status | Research verification: abnormally elevated levels in patients during the acute phase. | ||||
| Notes and Dynamics | Targeting ASF1A May Become a Novel Strategy for CML Treatment | ||||
| Biomarker | CCAT2 | Full name | Colon Cancer Associated Transcript 2 | Molecular Type | Nucleic acid (lncRNA) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Imatinib treatment response prediction |
| Disease(or Constitution) | Chronic Myeloid Leukemia(CML) | Disease Subtypes | / | ||
| Organ | Blood, bone marrow | Test Sample / Technology Platform | Peripheral blood mononuclear cells (real-time reverse transcription PCR) | ||
| Pathobiological Mechanisms | Highly expressed in CML patients, associated with treatment response, spleen volume, and EUTOS score | ||||
| Clinical Availability Status | Research verification: High expression associated with imatinib resistance. | ||||
| Notes and Dynamics | Can serve as a molecular biomarker for predicting treatment response in chronic-phase CML patients. | ||||