| Biomarker | MicroRNA (MiR-31) | Full name | MicroRNA-31 | Molecular Type | Nucleic acid（DNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis |
| Disease(or Constitution) | Endometrial Cancer | Disease Subtypes | All subtypes | ||
| Organ | Endometrium | Test Sample / Technology Platform | Organization, Serum (qRT-PCR) | ||
| Pathobiological Mechanisms | It affects the proliferation, invasion and chemosensitivity of tumor cells by regulating downstream target genes (such as SATB2). | ||||
| Clinical Availability Status | Research stage: Demonstrates potential as a prognostic marker and for predicting chemotherapy response. | ||||
| Notes and Dynamics | High expression is associated with poor prognosis and may serve as a potential biomarker for liquid biopsy. | ||||
| Biomarker | TP53 | Full name | Tumor protein p53 | Molecular Type | Nucleic acid（DNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Endometrial Cancer | Disease Subtypes | Serous carcinoma, endometrioid carcinoma | ||
| Organ | Endometrium | Test Sample / Technology Platform | Organization (IHC, NGS) | ||
| Pathobiological Mechanisms | Tumor suppressor genes, when mutated, lead to the loss of function of the p53 protein, which is unable to regulate the cell cycle and apoptosis, promoting malignant transformation. | ||||
| Clinical Availability Status | Clinical recommendation (classification / prognosis): The mutation rate of serous carcinoma exceeds 80%, which is a core biomarker for the high-risk subtype. | ||||
| Notes and Dynamics | The mutant patients are mostly of the high-risk type, with a high risk of recurrence after surgery, and thus require intensified adjuvant therapy. | ||||
| Biomarker | CTNNB1 | Full name | Catenin beta 1 | Molecular Type | Nucleic acid（DNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Endometrial Cancer | Disease Subtypes | Endometrioid carcinoma, serous carcinoma | ||
| Organ | Endometrium | Test Sample / Technology Platform | Organization (IHC, NGS) | ||
| Pathobiological Mechanisms | The β-catenin encoding protein, when mutated, leads to the obstruction of protein degradation and its accumulation in the nucleus, activating the Wnt/β-catenin pathway and driving tumor formation. | ||||
| Clinical Availability Status | Study verification (subtype classification): Mutations are more commonly found in low-grade endometrioid carcinomas and are associated with high differentiation and low invasiveness. | ||||
| Notes and Dynamics | It can serve as an auxiliary indicator for differentiating endometrioid carcinoma from other subtypes, and patients with the mutant type have a better prognosis. | ||||
| Biomarker | PIK3CA | Full name | Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha | Molecular Type | Nucleic acid（DNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Endometrial Cancer | Disease Subtypes | All subtypes | ||
| Organ | Endometrium | Test Sample / Technology Platform | Whole blood / Tumor tissue (NGS, ARMS-PCR) | ||
| Pathobiological Mechanisms | The oncogene is mutated to activate the PI3K/AKT signaling pathway, thereby promoting the survival, proliferation and drug resistance of tumor cells. | ||||
| Clinical Availability Status | Clinically applicable (target-guided): The mutation rate is approximately 20%-30%. Mutant patients are sensitive to PI3K inhibitors. | ||||
| Notes and Dynamics | MTOR inhibitors (such as everolimus) have shown therapeutic potential in patients with PIK3CA mutations. | ||||
| Biomarker | PTEN | Full name | Phosphatase and tensin homolog | Molecular Type | Nucleic acid（DNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Endometrial Cancer | Disease Subtypes | Endometrioid carcinoma, serous carcinoma | ||
| Organ | Endometrium | Test Sample / Technology Platform | Whole blood / Tumor tissue (NGS, Sanger sequencing) | ||
| Pathobiological Mechanisms | Tumor suppressor genes, when mutated, cause the protein to lose its function and fail to inhibit the PI3K/AKT pathway, thereby promoting tumor formation and invasion. | ||||
| Clinical Availability Status | Clinical validation (classification / prognosis): Approximately 30% - 40% of endometrial cancer cases have mutations, and patients with mutated genes have a relatively better prognosis. | ||||
| Notes and Dynamics | It is a core driver mutation of endometrioid carcinoma, which can serve as a screening marker for targeted PI3K pathway therapy. | ||||
| Biomarker | HE4 | Full name | Human epididymis protein 4 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis |
| Disease(or Constitution) | Endometrial Cancer | Disease Subtypes | All subtypes | ||
| Organ | Endometrium | Test Sample / Technology Platform | Serum / Plasma (ELISA, electrochemiluminescence method) | ||
| Pathobiological Mechanisms | Abnormally highly expressed during tumor progression, it participates in tumor cell invasion, adhesion and angiogenesis. Its level is related to tumor burden and is involved in cell proliferation, anti-apoptosis and epithelial-mesenchymal transition. It is specifically higher than CA-125 in endometrial cancer. | ||||
| Clinical Availability Status | Clinical recommendation (diagnosis / stratification): Incorporate the endometrial cancer risk assessment model. The AUC for early diagnosis is superior to that of CA-125. | ||||
| Notes and Dynamics | Combined with CA-125 testing, the sensitivity of early diagnosis can be increased to over 85%, and it is applicable for screening of post-menopausal women. | ||||
| Biomarker | CA-125 | Full name | Cancer antigen 125 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, monitoring, prognosis |
| Disease(or Constitution) | Endometrial Cancer | Disease Subtypes | Endometrioid carcinoma, serous carcinoma | ||
| Organ | Endometrium | Test Sample / Technology Platform | Serum / Plasma (ELISA, CLIA) | ||
| Pathobiological Mechanisms | Abnormally highly expressed during tumor progression, it participates in tumor cell invasion, adhesion and angiogenesis. Its level is related to the tumor burden. | ||||
| Clinical Availability Status | Clinically commonly used (routine test): Widely used for postoperative monitoring and recurrence warning; combined with HE4 can enhance the efficacy of early diagnosis. | ||||
| Notes and Dynamics | A single indicator has insufficient sensitivity for patients in stage I. Benign gynecological diseases (such as pelvic inflammation) may lead to false positives. | ||||
| Biomarker | ZEB1 | Full name | Zinc finger E-box-binding homeobox 1 | Molecular Type | Protein / Nucleic acid（RNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | All subtypes | ||
| Organ | Breast | Test Sample / Technology Platform | Tumor tissues (IHC, qPCR, NGS) | ||
| Pathobiological Mechanisms | ZEB1 is a key transcription factor in EMT. It induces EMT by inhibiting the expression of E-cadherin, and enhances the invasive, metastatic and drug-resistant capabilities of tumor cells. | ||||
| Clinical Availability Status | Research verification: High expression of ZEB1 is associated with an increased risk of distant metastasis and poor prognosis in breast cancer. | ||||
| Notes and Dynamics | ZEB1 inhibitors can reverse the EMT phenotype and restore the sensitivity of tumor cells to chemotherapy. The related drugs are currently in the preclinical development stage. | ||||
| Biomarker | Beclin 1 | Full name | Beclin 1 autophagy related | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | All subtypes | ||
| Organ | Breast | Test Sample / Technology Platform | Tumor tissues (IHC, Western Blot) | ||
| Pathobiological Mechanisms | Beclin 1 is a key protein for initiating autophagy. In breast cancer, the expression of Beclin 1 is abnormal (either high or low expression is possible), and it affects the survival of tumor cells and chemotherapy resistance through regulating autophagy. | ||||
| Clinical Availability Status | Research verification: The expression status of Beclin 1 is correlated with the chemosensitivity of breast cancer. Low expression may indicate chemotherapy resistance. | ||||
| Notes and Dynamics | The use of autophagy inhibitors (such as hydroxychloroquine) in combination with chemotherapy to explore therapeutic value in patients with abnormal Beclin 1 expression. | ||||
| Biomarker | Beclin 1 | Full name | Beclin 1 autophagy related | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | All subtypes | ||
| Organ | Breast | Test Sample / Technology Platform | Tumor tissues (IHC, Western Blot) | ||
| Pathobiological Mechanisms | Beclin 1 is a key protein for initiating autophagy. In breast cancer, the expression of Beclin 1 is abnormal (either high or low expression is possible), and it affects the survival of tumor cells and chemotherapy resistance through regulating autophagy. | ||||
| Clinical Availability Status | Research verification: The expression status of Beclin 1 is correlated with the chemosensitivity of breast cancer. Low expression may indicate chemotherapy resistance. | ||||
| Notes and Dynamics | The use of autophagy inhibitors (such as hydroxychloroquine) in combination with chemotherapy to explore therapeutic value in patients with abnormal Beclin 1 expression. | ||||
| Biomarker | GRP | Full name | Gastrin-releasing peptide | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | Neuroendocrine subtype | ||
| Organ | Breast | Test Sample / Technology Platform | Tumor tissues (IHC, radioimmunoassay RIA) | ||
| Pathobiological Mechanisms | GRP is a neuropeptide hormone. In some breast cancers (especially the neuroendocrine subtype), GRP is highly expressed. It promotes cell proliferation and metastasis by binding to the GRP receptor. | ||||
| Clinical Availability Status | Research verification: GRP testing is used for the diagnosis of neuroendocrine subtypes of breast cancer, and drugs targeting the GRP receptor are in preclinical research. | ||||
| Notes and Dynamics | The combined detection of GRP with other neuroendocrine markers (such as Syn and CgA) can enhance the accuracy of neuroendocrine subtype diagnosis. | ||||
| Biomarker | CTLA-4 | Full name | Cytotoxic T-lymphocyte-associated protein 4 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | Triple-negative | ||
| Organ | Breast | Test Sample / Technology Platform | CTLA tumor tissue (IHC), peripheral blood T cells (flow cytometry) | ||
| Pathobiological Mechanisms | CTLA-4 is expressed on the surface of activated T cells. By inhibiting T cell activation, it negatively regulates anti-tumor immunity and leads to tumor immune escape. | ||||
| Clinical Availability Status | Clinical application (immunotherapy guidance): CTLA-4 inhibitors (such as ipilimumab) have been approved for the treatment of advanced triple-negative breast cancer (in combination with PD-1 inhibitors) | ||||
| Notes and Dynamics | The expression level of CTLA-4 can predict the response to immunotherapy. Patients with high expression are more likely to benefit from immunotherapy combined treatment. | ||||
| Biomarker | GLUT1 | Full name | Glucose transporter 1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | All subtypes | ||
| Organ | Breast | Test Sample / Technology Platform | Tumor tissue (IHC, PET-CT: functional imaging) | ||
| Pathobiological Mechanisms | GLUT1 is a key protein for glucose transmembrane transport. Tumor cells highly express GLUT1 to enhance glucose uptake, meeting the energy demands for rapid proliferation. | ||||
| Clinical Availability Status | Research verification: High expression of GLUT1 is associated with poor prognosis of breast cancer and can serve as a metabolic treatment target. | ||||
| Notes and Dynamics | GLUT1 inhibitors (such as STF-31) when used in combination with chemotherapy and immunotherapy, have shown a synergistic anti-tumor effect in preclinical models. | ||||
| Biomarker | E-cadherin | Full name | Cadherin-1 | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Monitoring, prognosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | All subtypes | ||
| Organ | Breast | Test Sample / Technology Platform | Tumor tissue (IHC, IF) | ||
| Pathobiological Mechanisms | E-cadherin mediates the adhesion between epithelial cells. Its expression being downregulated or lost leads to the disruption of cell-cell connections, promoting tumor epithelial-mesenchymal transition (EMT) and metastasis. | ||||
| Clinical Availability Status | Research verification / Clinical reference: Low expression of E-cadherin is associated with an increased risk of lymph node metastasis and distant metastasis in breast cancer. | ||||
| Notes and Dynamics | The expression status of E-cadherin can serve as an indicator for risk stratification of metastasis, guiding the intensity of postoperative adjuvant therapy. | ||||
| Biomarker | microRNA (miR-21, miR-155) | Full name | MicroRNA-21 / MicroRNA-155 | Molecular Type | Nucleic acid（miRNA） |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Monitoring, prognosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | All subtypes | ||
| Organ | Breast | Test Sample / Technology Platform | Serum / Plasma / Tumor Tissue (Real-time Fluorescence Quantitative PCR qPCR, NGS) | ||
| Pathobiological Mechanisms | miR-21 promotes cell proliferation by inhibiting tumor suppressor genes (such as PTEN); miR-155 regulates inflammatory pathways and the immune microenvironment, facilitating tumor progression. | ||||
| Clinical Availability Status | Research verification: Liquid biopsy (serum miRNA) shows potential in early diagnosis and prognosis stratification, but has not yet been widely used clinically. | ||||
| Notes and Dynamics | miR-21 and miR-155 can serve as combined markers to enhance diagnostic accuracy; drugs targeting miRNAs are currently in preclinical research. | ||||
| Biomarker | CEA | Full name | Carcinoembryonic antigen | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Monitoring, prognosis |
| Disease(or Constitution) | Breast Cancer | Disease Subtypes | All subtypes | ||
| Organ | Breast | Test Sample / Technology Platform | Serum (ELISA, CLIA) | ||
| Pathobiological Mechanisms | CEA is an embryonic antigen. Breast cancer cells express it abnormally and release it into the bloodstream, which is associated with tumor metastasis and poor prognosis. | ||||
| Clinical Availability Status | Clinical assistance (for monitoring recurrence): Commonly used for recurrence monitoring in advanced or metastatic breast cancer. The specificity and sensitivity for early diagnosis are relatively low. | ||||
| Notes and Dynamics | An increase in CEA can also be observed in gastrointestinal tumors, inflammatory conditions, etc. It is necessary to combine with imaging examinations to confirm recurrence. | ||||