| Biomarker | NR3C1 | Full name | Nuclear receptor subfamily 3 croup C member 1 | Molecular Type | Nucleic acid (miRNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis | ||
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | DLBCL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Organizations (GEO analysis, multivariate analysis) | ||
| Pathobiological Mechanisms | High expression is associated with long survival, particularly in the CHOP treatment subgroup. | ||||
| Clinical Availability Status | Research validation phase: Retrospective analysis of 952 cases supports the need for prospective validation and stability assessment of detection. | ||||
| Notes and Dynamics | Validation of the era value of R-CHOP and development of blood sample testing methods. | ||||
| Biomarker | CD8+T cell | Full name | Cluster of differentiation8+T cell | Molecular Type | Immunological cell |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prediction of treatment response and prognosis | ||
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | DLBCL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Blood (flow cytometry) | ||
| Pathobiological Mechanisms | Baseline level association of complete response with survival in relapsed/refractory patients. | ||||
| Clinical Availability Status | Research validation phase: Validation of 78 R2-GDP protocol patients, requiring multi-protocol validation and standardized testing. | ||||
| Notes and Dynamics | Exploring the correlation between immune checkpoint inhibitors and therapeutic efficacy, standardizing flow cytometry detection strategies. | ||||
| Biomarker | BCL6 | Full name | B-cell lymphoma 6 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prediction of treatment response and drug resistance | ||
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | DLBCL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Tissues, cell lines (RNA sequencing, Western blot) | ||
| Pathobiological Mechanisms | Recruitment of HDAC inhibitors: Cidabine inhibits the effect of lenalidomide, which degrades BCL6. | ||||
| Clinical Availability Status | Validation phase: Cell line and partial tissue validation, requiring prospective trials and optimization of scoring thresholds. | ||||
| Notes and Dynamics | Conducting clinical trials of combination therapy to validate its efficacy prediction value. | ||||
| Biomarker | DnaJ heat shock protein family (Hsp40) member C9 | Full name | DnaJ heat shock protein family (Hsp40) member C9 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis | ||
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | DLBCL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Organization (immunohistochemistry, immunofluorescence) | ||
| Pathobiological Mechanisms | The nuclear staining rate of lymphoma in the marginal zone outside the spleen is significantly increased. | ||||
| Clinical Availability Status | Research Validation Phase: Validation of 40 OABL samples, requiring expanded subtype coverage and standardized detection. | ||||
| Notes and Dynamics | Provide diagnostic basis for rare subtypes and clarify multi-subtype specificity. | ||||
| Biomarker | PLA2G7 | Full name | Phospholipase A2 group VII | Molecular Type | Nucleic acid (mRNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, therapeutic targets | ||
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | DLBCL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Tissues and cell lines (GEO/TCGA analysis, in vitro experiments) | ||
| Pathobiological Mechanisms | Participates in immune and proliferative processes, with the inhibitor daunorubicin capable of suppressing cellular viability. | ||||
| Clinical Availability Status | Research validation phase: Database screening and in vitro validation, followed by large-scale diagnostic efficacy evaluation and clinical trials. | ||||
| Notes and Dynamics | Advance preclinical studies of inhibitors to validate the diagnostic value of blood samples. | ||||
| Biomarker | OR2A1-AS1 | Full name | OR2A1 antisense RNA 1 | Molecular Type | Nucleic acid |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis | ||
| Disease(or Constitution) | NHL | Disease Subtypes | DLBCL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Organizations (QRT-PCR, GEO analysis) | ||
| Pathobiological Mechanisms | Low expression is associated with poor prognosis, particularly in the germinal center B-cell-like subtype. | ||||
| Clinical Availability Status | Research validation phase: Supported by data from 98 patients and database analysis, requires prospective validation, and tissue testing is invasive. | ||||
| Notes and Dynamics | Exploring blood sample testing methods to establish a multi-marker prognostic model. | ||||
| Biomarker | miR-146a | Full name | MicroRNA-146a | Molecular Type | Nucleic acid |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis | ||
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | DLBCL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Serum (RT-qPCR) | ||
| Pathobiological Mechanisms | Progression-free survival and overall survival after treatment with the R-CHOP regimen | ||||
| Clinical Availability Status | Research validation phase: Preliminary validation of 72 patients, lacking multicenter external data, and non-unified testing procedures. | ||||
| Notes and Dynamics | Exploring the Value of Rituximab in Monitoring Minimal Residual Disease in Combination with Rituximab. | ||||
| Biomarker | STING | Full name | Stimulator of interferon genes | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnostic and therapeutic targets | ||
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | T/NK-NHL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Diagnostic biopsy specimens (immunohistochemistry), cell lines (Western blot analysis, immunohistochemistry) | ||
| Pathobiological Mechanisms | STING transcription is activated in tumor T/NK cells, while it is downregulated in B-cell NHL. | ||||
| Clinical Availability Status | Research validation: Its specific expression in T/NK cell NHL has been confirmed, and the related cGAS-STING modulators have entered clinical trials, demonstrating potential for immunotherapy applications. | ||||
| Notes and Dynamics | The positivity rates of T/NK cell subtypes in NHL vary (7.7%-95%) and are independent of the patients' clinical-pathological parameters and prognosis; all B-cell NHL cases are negative, serving as a specific marker to distinguish T/NK cell NHL from B-cell NHL. | ||||
| Biomarker | CD19 | Full name | Cluster of differentiation 19 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Therapeutic targets (alternative targets for relapsed/refractory diseases) |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | B-NHL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Biopsy specimens during recurrence (immunohistochemistry, flow cytometry) | ||
| Pathobiological Mechanisms | During relapse, CD19 expression remained stable without loss of expression, which may be related to the conservation of this marker in B-cell development and tumor phenotypes. | ||||
| Clinical Availability Status | Clinical potential/research validation: The conservation of CD19 expression during relapse supports its use as an alternative target after anti-CD19 therapy failure. | ||||
| Notes and Dynamics | All patients with CD19 positivity at relapse (14/14) maintained positive results, providing a novel basis for anti-CD19 targeted therapy in relapsed/refractory B-cell NHL. | ||||
| Biomarker | CD3 | Full name | Cluster of differentiation 3 | Molecular Type | Protein (T cell marker) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Treatment targets, diagnostics (phenotype monitoring when relapse occurs) |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | T-NHL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Tumor tissue (conventional pathological detection techniques such as immunohistochemistry) | ||
| Pathobiological Mechanisms | As a T cell marker, the loss or reduction of its expression may influence disease progression. | ||||
| Clinical Availability Status | Validation phase: Relevant studies have explored its association with prognosis, requiring larger-scale data validation | ||||
| Notes and Dynamics | It is a potential key variable for the prognostic evaluation of pediatric ALCL, and its expression status can assist in optimizing treatment strategies and stratifying recurrence risk. | ||||
| Biomarker | CD20 | Full name | Cluster of differentiation 20 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Treatment targets, diagnostics |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | B-NHL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Biopsy specimens at the time of diagnosis and recurrence (immunohistochemistry, flow cytometry) | ||
| Pathobiological Mechanisms | After treatment with anti-CD20 drugs (e.g., rituximab), some patients exhibit CD20 expression loss upon relapse, which may be associated with tumor cell phenotypic transformation. | ||||
| Clinical Availability Status | Validation phase: Relevant studies have explored its association with prognosis, requiring larger-scale data validation. | ||||
| Notes and Dynamics | It is a potential key variable for the prognostic evaluation of pediatric ALCL, and its expression status can assist in optimizing treatment strategies and stratifying recurrence risk. | ||||
| Biomarker | miR-340-5p | Full name | MicroRNA-340-5p | Molecular Type | Nucleic acid |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Predict response to therapy and prognosis |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | ENKTL | ||
| Organ | Lymphoid tissue | Test Sample / Technology Platform | Serum (miRNA sequencing, RT-qPCR) | ||
| Pathobiological Mechanisms | Regulation of PD-L1 involvement in immune evasion, low levels of miR-340-5p associated with reduced efficacy of pembrolizumab | ||||
| Clinical Availability Status | Research validation phase: Cell line and small-sample cohort validation is valid, requiring multicenter large-sample trials and standardized testing | ||||
| Notes and Dynamics | It is expected to guide immunotherapy regimens, focusing on optimizing detection sensitivity and exploring combined biomarkers. | ||||
| Biomarker | EBV-DNA | Full name | Epstein-Barr virus DNA | Molecular Type | Nucleic acid (viral DNA) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognostic assessment (EBV-positive cHL) |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | blood plasma （qPCR） | ||
| Pathobiological Mechanisms | EBV infection is associated with the onset of chronic lymphocytic leukemia (cHL), and plasma EBV-DNA levels reflect viral activity and tumor burden. | ||||
| Clinical Availability Status | Clinical validation phase: Non-invasive detection of EBV-positive chronic lymphocytic leukemia (cHL) indicates disease activity and prognosis. | ||||
| Notes and Dynamics | Combined with cfDNA grouping, patients with EBV-and SOCS1 mutations have a higher risk of treatment failure. | ||||
| Biomarker | IL-6 | Full name | Interleukin-6 | Molecular Type | Proteins (cytokines) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognostic assessment, association with neurocognitive function |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Serum（Luminex、ELISA） | ||
| Pathobiological Mechanisms | Reflects systemic inflammatory status, with high levels indicating a high risk of recurrence and associated with neurocognitive impairment in HL survivors. | ||||
| Clinical Availability Status | Clinical application/research phase: Pre-treatment high IL-6 and hs-CRP levels were associated with short RFS; hs-CRP ≥3 mg/L was correlated with poor attention and memory function. | ||||
| Notes and Dynamics | The association between IL-6-mediated pulmonary disease and visual-motor processing speed can serve as a target for intervention trials. | ||||
| Biomarker | qPET | Full name | Quantitative positron emission tomography (SUVmax/SUVpeak ratio) | Molecular Type | Imaging-molecular composite index (SUV ratio) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Treatment response prediction, risk stratification |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | PET/CT imaging (SUVpeak/SUVmean calculation) | ||
| Pathobiological Mechanisms | Quantify tumor metabolic activity to differentiate high-risk (qPET>3, EFS=47.6%) and low-risk (qPET≤3, EFS>83%) patients with vDS5. | ||||
| Clinical Availability Status | Clinical translation phase: Expansion of vDS ordinal classification to provide a basis for individualized treatment strategies for vDS5 patients. | ||||
| Notes and Dynamics | Patients with qPET<1.3 may skip radiotherapy, while those with qPET>3 require treatment regimen adjustment, as validated in pediatric cHL. | ||||
| Biomarker | PLT/PDW, PLR | Full name | Platelet count/Platelet distribution width ratio, Platelet-to-lymphocyte ratio | Molecular Type | Hematological parameters (cell ratios) |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis assessment (advanced cHL) |
| Disease(or Constitution) | Non-Hodgkin Lymphoma (NHL) | Disease Subtypes | cHL | ||
| Organ | Blood and lymphoid tissue | Test Sample / Technology Platform | Whole blood (complete blood count) | ||
| Pathobiological Mechanisms | Reflects inflammatory status and immune dysregulation, with low PLT/PDW and high PLR indicating immunosuppression and elevated risk of tumor progression. | ||||
| Clinical Availability Status | Clinical validation phase: Multivariate analysis revealed that PLT/PDW <24.5 and PLR ≥245 were independent risk factors for adverse FFP and PFS. | ||||
| Notes and Dynamics | In early-stage chronic lymphocytic leukemia (cHL), platelet-rich blood (PLR) is also a reliable prognostic indicator and can be incorporated into routine complete blood count (CBC) risk assessment. | ||||