| Biomarker | Aquaporin family (AQP1, AQP3, etc.) | Full name | Aquaporin family (AQP1, AQP3, etc.) | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis treatment guidance |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | Tumor tissue, urine, and prostate cancer cell lines (IHC, real-time PCR, Western blot) | ||
| Pathobiological Mechanisms | The p38MAPK pathway (AQP1), ERK1/2 pathway (AQP3, AQP9), and RalA/PKA/cAMP pathway (AQP3 membrane localization) collectively drive prostate cancer progression, stem cell maintenance, and metastasis by integrating into complex cellular signaling networks. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | Due to the lack of large-scale, prospective clinical trials for validation, there is currently insufficient evidence to systematically use AQP for risk stratification. | ||||
| Biomarker | CgA | Full name | Chromogranin A | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis treatment guidance |
| Disease(or Constitution) | PCa | Disease Subtypes | Neuroendocrine carcinoma | ||
| Organ | Prostate | Test Sample / Technology Platform | Serum/plasma (IHC) | ||
| Pathobiological Mechanisms | In prostate cancer, elevated CgA levels directly reflect the differentiation of tumor cells into a neuroendocrine phenotype. Following treatment, the neuroendocrine subpopulation undergoes clonal expansion, leading to increased CgA secretion, while PSA levels may decrease rather than rise, resulting in a clinical-biological dissociation. High CgA levels are associated with more aggressive disease phenotypes and poor prognosis. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | Its level is influenced by multiple factors; therefore, interpretation should be combined with clinical context, with greater emphasis on dynamic trends rather than single absolute values. | ||||
| Biomarker | LncRNA (HOTAIR, NEAT1, etc.) | Full name | Long non-coding RNA (HOTAIR, NEAT1, etc.) | Molecular Type | Nucleic acid |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis, transfer, therapeutic response |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | Tissues, cell lines, urine (RNA-seq, RT-qPCR) | ||
| Pathobiological Mechanisms | Regulation of AR signaling, transcriptional programs, and drug sensitivity. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | Most are in the research phase, and HOTAIR holds potential in the diagnosis and treatment of prostate cancer. | ||||
| Biomarker | Histone modifications (H3K4me1, etc.) | Full name | Histone modifications (H3K4me1, etc.) | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis, treatment resistance |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | Tumor tissue (ChIP-seq, IHC, WB) | ||
| Pathobiological Mechanisms | Histone methylation/acetylation alters chromatin state, influencing AR signaling, cell cycle, etc. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | Further extensive research is required to validate the study of histones. | ||||
| Biomarker | DNA methylation (GSTP1, RASSF1, etc.) | Full name | DNA methylation (GSTP1, RASSF1, etc.) | Molecular Type | Nucleic acid |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | Urine, serum, plasma, tissues (MSRE-PCR, qPCR, whole-genome methylation sequencing) | ||
| Pathobiological Mechanisms | The hypermethylation of gene promoter leads to the silencing of tumor suppressor gene, which leads to the loss of antioxidant function, and affects the cell cycle and apoptosis. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | Large-scale clinical validation is required. GSTP1 demonstrates high potential for clinical translation. | ||||
| Biomarker | Ψ | Full name | Pseudouridine | Molecular Type | Nucleic acid |
| Molecular Formula | C9H12N2O6 | Molecular Weight | 244.20 g/mol | Core Functional Dimensions | Diagnosis, prognosis |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | blood, urine, tumor tissue (ELISA, IHC, flow cytometry, H-NMR) | ||
| Pathobiological Mechanisms | The rapid proliferation and metabolism of cancer cells lead to increased RNA metabolism and elevated pseudouridine concentration. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | Large-scale clinical validation is currently underway. | ||||
| Biomarker | SPDEF | Full name | SAM Pointed Domain-containing ETS Transcription Factor | Molecular Type | Nucleic acid |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnose |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | Serum and plasma (MSRE-PCR, qPCR) | ||
| Pathobiological Mechanisms | A specific CpG site in the promoter region of SPDEF gene was significantly hypomethylated in the blood leukocyte DNA of PCa patients, and the hypomethylation degree was positively correlated with the malignancy of the tumor. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | The specific molecular mechanisms by which low SPDEF methylation drives prostate cancer progression require experimental validation | ||||
| Biomarker | RAGE | Full name | Receptor for Advanced Glycation End-products | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis, therapeutic targets |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | Tumor tissue (IHC, WB) imaging (targeting RAGE multimodal nanoprobes) | ||
| Pathobiological Mechanisms | RAGE, a cell surface receptor, binds to various ligands (e.g., AGEs, HMGB1, and S100 proteins), activating the PI3K/Akt/NF-κB signaling pathway. This activation drives chronic inflammation, thereby promoting tumor growth, invasion, and treatment resistance. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | RAGE possesses multifaceted potential in diagnosis, prognosis assessment, and therapeutic targeting. Current research is advancing the clinical validation of RAGE diagnostics and the clinical translation of targeted imaging technologies. | ||||
| Biomarker | Citrate | Full name | Citrate | Molecular Type | Organic salt |
| Molecular Formula | C6H5O7-3 | Molecular Weight | 189.1 g/mol | Core Functional Dimensions | Diagnose |
| Disease(or Constitution) | PCa | Disease Subtypes | / | ||
| Organ | Prostate | Test Sample / Technology Platform | urine, semen, prostatic secretions (proton nuclear magnetic resonance spectrum H-NMR) | ||
| Pathobiological Mechanisms | The zinc level in cancer cells decreases, and the TCA cycle is restored, with citrate being utilized for energy production and lipid synthesis. This results in a significant reduction of citrate levels in tumor tissues. | ||||
| Clinical Availability Status | Research verification | ||||
| Notes and Dynamics | The diagnostic efficacy of citrate combined with PSA requires further clinical validation to facilitate its clinical application. | ||||
| Biomarker | HMGA2 | Full name | High mobility group AT-hook 2 | Molecular Type | protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | The prognosis |
| Disease(or Constitution) | Pituitary Adenoma | Disease Subtypes | Prolactin tumor (PRLPA) | ||
| Organ | Pituitary | Test Sample / Technology Platform | Organization (immunohistochemical IHC) | ||
| Pathobiological Mechanisms | Regulation of E2F1 activity, promote the tumor proliferation | ||||
| Clinical Availability Status | Clinical validation: invasive PRLPA higher expression, positively related to the tumor size, risk of recurrence | ||||
| Notes and Dynamics | With miR - let - 7 joint detection risk stratification can be optimized | ||||
| Biomarker | PRL | Full name | Prolactin | Molecular Type | Hormones |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Monitoring |
| Disease(or Constitution) | Pituitary Adenoma | Disease Subtypes | Prolactinoma (PRLPA) | ||
| Organ | Pituitary | Test Sample / Technology Platform | Serum (immune analysis method, chemiluminescence method) | ||
| Pathobiological Mechanisms | Excessive secretion by tumor cells regulates mammary gland development and lactation | ||||
| Clinical Availability Status | Clinical routine application: diagnostic gold standard, the sensitivity of + 95%, specificity 90% +; Effect for recurrence of monitoring and early warning, need to eliminate interference factors such as pregnancy, drugs | ||||
| Notes and Dynamics | Associated with imaging diagnosis, dopamine agonist levels drop hints curative effect after treatment | ||||
| Biomarker | miR-125b | Full name | microRNA-125b | Molecular Type | Microrna (miRNA) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis, |
| Disease(or Constitution) | Adrenocortical Carcinoma | Disease Subtypes | Non-functional/functional | ||
| Organ | Adrenal Cortex | Test Sample / Technology Platform | Serum/organization (RT - qPCR, NGS) | ||
| Pathobiological Mechanisms | Targeting inhibition of tumor suppressor gene expression, and promote the proliferation and metastasis of tumor cells | ||||
| Clinical Availability Status | Study phase: Low expression in adrenocortical carcinoma, diagnostic AUC of 0.82, correlated with overall survival | ||||
| Notes and Dynamics | Secrete body outside miR - 125 - b testing is expected to become a noninvasive diagnostic and monitoring samples | ||||
| Biomarker | β-catenin (nuclear) | Full name | Nuclear β-catenin protein | Molecular Type | Protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Prognosis |
| Disease(or Constitution) | Adrenocortical Carcinoma | Disease Subtypes | Non-functional/functional | ||
| Organ | Adrenal Cortex | Test Sample / Technology Platform | Organization (immunohistochemical IHC) | ||
| Pathobiological Mechanisms | CTNNB1 gene expression product, check and ratify a hint pathways activated, to participate in the development of tumor | ||||
| Clinical Availability Status | Clinical auxiliary application: nuclear positive expression of support adrenal cortical carcinoma diagnosis and negatively related to the degree of tumor differentiation | ||||
| Notes and Dynamics | It can be used as a marker for protein level verification of CTNNB1 mutation and auxiliary molecular typing | ||||
| Biomarker | p53 (mutant) | Full name | Mutant p53 protein | Molecular Type | Protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Prognosis |
| Disease(or Constitution) | Adrenocortical Carcinoma | Disease Subtypes | Non-functional/functionality | ||
| Organ | Adrenal Cortex | Test Sample / Technology Platform | Tissue (immunohistochemical IHC) | ||
| Pathobiological Mechanisms | TP53 gene expression product of mutant p53, loss of tumor suppressor function, to promote tumor progression | ||||
| Clinical Availability Status | Clinical routine application: IHC testing mutant p53 expression, positive suggests high malignant degree, used for prognosis evaluation | ||||
| Notes and Dynamics | Combined detection with Ki-67 can improve the screening efficiency of high-risk patients | ||||
| Biomarker | SF1 (NR5A1) | Full name | Steroidogenic factor 1 | Molecular Type | Protein/nucleic acid |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis and typing |
| Disease(or Constitution) | Adrenocortical Carcinoma | Disease Subtypes | Nonfunctional/functional | ||
| Organ | Adrenal Cortex | Test Sample / Technology Platform | Tissue (IHC, NGS) | ||
| Pathobiological Mechanisms | Transcription factors regulate adrenocortical cell differentiation and hormone synthesis, and their abnormal expression drives tumorigenesis | ||||
| Clinical Availability Status | Clinical auxiliary application: IHC positive identifiable source of adrenal cortex, used to identify other metastatic tumors | ||||
| Notes and Dynamics | In poorly differentiated carcinoma expression rate is high, can be used as the key to the origin of tumor diagnosis markers | ||||
| Biomarker | TERT | Full name | Telomerase reverse transcriptase | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Prognosis, Monitoring |
| Disease(or Constitution) | Adrenocortical Carcinoma | Disease Subtypes | Non-functional/functional | ||
| Organ | Adrenal Cortex | Test Sample / Technology Platform | Tissue/serum cfDNA (NGS, FISH) | ||
| Pathobiological Mechanisms | Telomerase reverse transcriptase, promoter mutation or amplification elongates telomeres, promoting tumor immortalization | ||||
| Clinical Availability Status | Clinical validation: TuBianZhe tumor invasive strong, high recurrence rate, cfDNA detection dynamically monitoring of disease progression | ||||
| Notes and Dynamics | TERT mutation detection by liquid biopsy is the frontier of non-invasive recurrence monitoring | ||||