| Biomarker | miRNA-155 | Full name | microRNA-155 | Molecular Type | microrna |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, and treatment resistance | ||
| Disease(or Constitution) | Colorectal Cancer (CRC) | Disease Subtypes | Colorectal Cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Tumor tissue/blood/stool (qRT-PCR, RNA sequencing) | ||
| Pathobiological Mechanisms | Targeted SOCS1, FOXO3a gene, the activation of PI3K/AKT, the nf-kappa B pathway, promote cell proliferation, EMT and chemotherapy drug resistance; At the same time, it can affect the tumor microenvironment by regulating the function of immune cells | ||||
| Clinical Availability Status | Clinical research phase: its diagnostic and prognostic value has been verified in multi-center clinical samples, and it has not entered routine clinical practice | ||||
| Notes and Dynamics | antisense oligonucleotides targeting miRNA-155 have been shown to be effective in preclinical studies, which are both tumor promoters and potential therapeutic targets | ||||
| Biomarker | Microsatellite instability (MSI-H) | Full name | Microsatellite Instability-High | Molecular Type | Genomic Signatures |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, treatment prediction | ||
| Disease(or Constitution) | Colorectal Cancer (CRC) | Disease Subtypes | Colorectal cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Tumor tissue/blood (NGS, PCR, IHC) | ||
| Pathobiological Mechanisms | DNA mismatch repair defects lead to microsatellite sequence instability, increased tumor mutation burden, and enhanced immunogenicity | ||||
| Clinical Availability Status | Clinically available (treatment options) : It has been included in CRC practice guidelines and used as a marker for predicting the benefit of immunotherapy | ||||
| Notes and Dynamics | It is the first cross-cancer immunotherapy predictive marker, and FDA approved pan-cancer immunotherapy indications based on MSI-H status | ||||
| Biomarker | Clostridium symbiosum (C. symbiosum) | Full name | Clostridium symbiosum | Molecular Type | Bacteria |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, Prognosis | ||
| Disease(or Constitution) | Colorectal Cancer (CRC) | Disease Subtypes | Colorectal cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Stool/tumor tissue (qPCR, metagenomic sequencing) | ||
| Pathobiological Mechanisms | The production of branched-chain amino acids activates the mTORC1 pathway, which promotes cholesterol synthesis and cancer stem cell properties | ||||
| Clinical Availability Status | Study validation: Stool test showed diagnostic value and was in the stage of clinical transformation research | ||||
| Notes and Dynamics | Its abundance gradually increases with the adenoma-carcinoma sequence, which can be used as a non-invasive early diagnostic marker. Combined with FIT, it can improve the screening sensitivity | ||||
| Biomarker | Anaerobic Peptostreptococcus (P. anaerobius) | Full name | Peptostreptococcus anaerobius | Molecular Type | Bacteria |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, treatment resistance | ||
| Disease(or Constitution) | Colorectal Cancer (CRC) | Disease Subtypes | Colorectal cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Tumor tissue/stool (qPCR, metagenomic sequencing) | ||
| Pathobiological Mechanisms | PCWBR2 binds integrin α2β1 to activate PI3K-Akt-NF-κB pathway, generate IDA to inhibit ferroptosis, recruit MDSCs and lead to immunotherapy resistance | ||||
| Clinical Availability Status | Research validation: its cancer-promoting effect in CRC has been identified and it is in the early clinical research stage | ||||
| Notes and Dynamics | It is a key mediator of chemotherapy and immunotherapy resistance in CRC, and targeting its metabolites IDA or adhesin proteins has therapeutic potential | ||||
| Biomarker | Colistin damage characteristics can be used as a molecular fingerprint for early diagnosis of CRC, and combined detection with Fn can improve the diagnostic accuracy Enterotoxigenic Bacteroides fragilis (ETBF) | Full name | Enterotoxigenic Bacteroides fragilis | Molecular Type | Bacteria |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, Prognosis | ||
| Disease(or Constitution) | Colorectal Cancer (CRC) | Disease Subtypes | Colorectal cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Tumor tissue/feces (qPCR, ELISA) | ||
| Pathobiological Mechanisms | The production of BFT toxin clefts E-cadherin to release β-catenin, activates the expression of c-Myc, and inhibits miR-149-3p to promote inflammation and proliferation | ||||
| Clinical Availability Status | Research validation: It has been confirmed to be associated with CRC progression in clinical samples and is in the preclinical transformation stage | ||||
| Notes and Dynamics | Downregulation of FXR can promote its colonization, and targeting FXR or ETBF is expected to become a preventive and therapeutic strategy for CRC | ||||
| Biomarker | pks+ E. coli | Full name | Polyketide synthase-positive Escherichia coli | Molecular Type | Bacteria |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, susceptibility | ||
| Disease(or Constitution) | Colorectal Cancer (CRC) | Disease Subtypes | Colorectal cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Tumor tissue/stool (qPCR, metagenomic sequencing) | ||
| Pathobiological Mechanisms | Colicin production leads to DNA double-strand breaks and genomic instability, promoting tumorigenesis | ||||
| Clinical Availability Status | Research validation: The enrichment phenomenon has been verified in clinical samples and has not entered routine clinical application | ||||
| Notes and Dynamics | Colistin damage characteristics can be used as a molecular fingerprint for early diagnosis of CRC, and combined detection with Fn can improve the diagnostic accuracy | ||||
| Biomarker | Fusobacterium nucleatum (Fn) | Full name | Fusobacterium nucleatum | Molecular Type | Bacteria |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, and treatment resistance | ||
| Disease(or Constitution) | Diagnosis, prognosis, and treatment resistance Colorectal Cancer (CRC) | Disease Subtypes | Colorectal cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Tumor tissue/stool/blood (qPCR, NGS, ELISA) | ||
| Pathobiological Mechanisms | FadA binds E-cadherin to activate the β-catenin signaling pathway, Fap2 binds TIGIT to inhibit NK/T cell function, produce succinate to inhibit the cGAS-STING pathway, and promote immunosuppression, EMT, and chemotherapy resistance | ||||
| Clinical Availability Status | Research validation/early clinical: Stool and tumor tissue tests have been widely used in research; Blood tests are being validated on a large scale | ||||
| Notes and Dynamics | F. animalis C2 clade is the core biomarker of CRC, and its subtype F. animalis C2 clade is the most associated with CRC. The multi-dimensional stool panel has great potential for clinical transformation | ||||
| Biomarker | Bilirubin (including total Bilirubin, direct bilirubin, and indirect bilirubin) | Full name | Bilirubin (total, direct, indirect) | Molecular Type | Metabolites (hemoglobin metabolites) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Assessment of liver function, determination of cholestasis, and grading of disease severity | ||
| Disease(or Constitution) | Liver Cirrhosis | Disease Subtypes | Compensated, Decompensated | ||
| Organ | Liver | Test Sample / Technology Platform | Serum (biochemical analyzer, using diazo method, vanadate oxidation method, etc.) | ||
| Pathobiological Mechanisms | Bilirubin is mainly derived from the metabolism of hemoglobin after the destruction of red blood cells. It needs to be taken up, combined (converted to direct bilirubin) and excreted by the liver. In liver cirrhosis, on the one hand, liver cell damage leads to the decrease of bilirubin uptake and binding function and the increase of indirect bilirubin. On the other hand, intrahepatic bile ducts are compressed, bile excretion pathway is blocked (such as cirrhosis with intrahepatic cholestasis), and direct bilirubin excretion is impaired, resulting in increased direct bilirubin, and ultimately often manifested as increased total bilirubin (direct bilirubin and indirect bilirubin can be elevated at the same time or a dominant type). Bilirubin level is one of the important indicators Child - Pugh, grading, continue to rise prompted increased risk of liver failure. | ||||
| Clinical Availability Status | Clinical routine use: as a core marker for liver function assessment, disease classification and prognosis judgment of liver cirrhosis, it is included in the Child-Pugh scoring system, and the clinical detection and interpretation system is mature. | ||||
| Notes and Dynamics | Bilirubin can comprehensively reflect the metabolic function and biliary excretion of liver cells in patients with liver cirrhosis, and is an important indicator to judge the severity of liver function damage and prognosis, especially for patients with decompensated liver cirrhosis (such as jaundice). It has irreplaceable value in monitoring the disease. However, it should be noted that non-cirrhotic factors such as hemolytic diseases, biliary stones/tumors may also lead to elevated bilirubin, which should be combined with hepatobiliary imaging examinations (such as abdominal ultrasound, CT) and other liver function indicators for comprehensive identification. | ||||
| Biomarker | Prothrombin Time (PT) | Full name | Prothrombin Time / International Normalized Ratio (INR) | Molecular Type | Proteins (coagulation factor related indicators, reflecting coagulation function) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Liver function assessment, bleeding risk prediction, prognosis judgment | ||
| Disease(or Constitution) | Liver Cirrhosis | Disease Subtypes | Compensated, Decompensated | ||
| Organ | Liver | Test Sample / Technology Platform | Plasma (coagulation analyzer, by coagulation method) | ||
| Pathobiological Mechanisms | Prothrombin (coagulation factor Ⅱ) and coagulation factors Ⅴ, Ⅶ, and Ⅹ are synthesized by hepatocytes. PT mainly reflects the function of exogenous coagulation pathway. In liver cirrhosis, the damage of liver cells leads to the reduction of the synthesis of the above coagulation factors, and may be accompanied by vitamin K malabsorption (intestinal congestion caused by cirrhosis portal hypertension, affecting the absorption of fat-soluble vitamins), which further aggravates the deficiency of coagulation factor synthesis and eventually leads to prolonged PT. PT extend the degree and scope of liver cell injury, severe liver function damage degree, also direct the patient bleeding risk (e.g., ruptured esophageal gastric varices bleeding). | ||||
| Clinical Availability Status | Clinical routine use: it is a key indicator for liver function assessment, bleeding risk stratification and prognosis judgment in patients with liver cirrhosis. It is included in the Child-Pugh scoring system, and is widely used in clinical practice and recommended by guidelines. | ||||
| Notes and Dynamics | PT can sensitively reflect the synthesis function of hepatocytes and coagulation status in patients with liver cirrhosis, which is of great value in predicting the risk of bleeding and guiding clinical intervention (such as preoperative evaluation and prophylactic use of hemostatic drugs). But need vitamin K deficiency, use of anticoagulant drugs (such as warfarin), diffuse intravascular coagulation (DIC), and other factors of cirrhosis of the liver specificity on the result of PT, avoid misjudgment liver function. | ||||
| Biomarker | CK-18 | Full name | Cytokeratin-18 | Molecular Type | Cellular structural proteins (intermediate filament proteins) |
| Molecular Formula | Varies by species (human CK-18: C₄₇₉H₇₄₃N₁₂₅O₁₄₀S₃) | Molecular Weight | ~53 kDa | Core Functional Dimensions | Assessment of hepatocyte apoptosis and liver injury |
| Disease(or Constitution) | Metabolic Associated Fatty Liver Disease (MASLD) | Disease Subtypes | Non-Alcoholic Steatohepatitis (NASH), Simple fatty liver (differential diagnosis) | ||
| Organ | Liver | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | Three serum markers (HA, PIIINP, TIMP-1) were calculated by the algorithm. HA reflects the function of hepatic sinusoidal endothelial cells and the degree of fibrosis. PIIINP reflects the rate of collagen synthesis, which is related to the early formation of liver fibrosis. TIMP-1 inhibits matrix metalloproteinase activity, inhibits collagen degradation, and promotes the progression of fibrosis. The ELF score can quantify the degree of liver fibrosis, and the higher the value, the more severe the fibrosis CK-18 is the main cytoskeletal protein in the cytoplasm of hepatocytes, which maintains the structural integrity of hepatocytes. When hepatocyte apoptosis occurs in MASLD patients, caspases cleave CK-18 to produce M30 fragment. Intact CK-18 (M65 fragment) was released in necrotic hepatocytes. In NASH, hepatocyte apoptosis is the core pathological feature. The level of M30 fragment is positively correlated with the degree of hepatic steatosis, lobular inflammation and fibrosis, and can specifically reflect the activity of hepatocyte apoptosis. M65 fragment can reflect the total hepatocyte injury of apoptosis and necrosis comprehensively | ||||
| Clinical Availability Status | In the clinical research stage, serum has been widely used in disease stratification, prognosis evaluation and drug clinical trials of MASLD (especially NASH). For example, evaluating the inhibitory effect of drugs such as toagliflozin and pioglitazone on hepatocyte apoptosis is also used to distinguish simple fatty liver from NASH | ||||
| Notes and Dynamics | CK-18 (M30 fragment) is a specific biomarker reflecting hepatocyte apoptosis, which makes up for the deficiency of ALT/AST and other traditional indicators that are difficult to distinguish the types of hepatocyte injury (apoptosis/necrosis), and can indicate the occurrence and progression risk of NASH at an early stage. The detection is convenient and minimally invasive, but the current detection methods have not been fully standardized, and there are differences in the reference ranges of different laboratories. In the severe stage of liver fibrosis, the level may be false negative due to the reduction of the number of hepatocytes, which needs to be comprehensively interpreted in combination with ELF score, LSM and other indicators | ||||
| Biomarker | ELF Score | Full name | Enhanced Liver Fibrosis Score | Molecular Type | Multi-molecule combination score (containing hyaluronic acid, procollagen type III N-terminal peptide, tissue inhibitor of metalloproteinase-1) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Assessment of LIVER fibrosis | ||
| Disease(or Constitution) | Metabolic Associated Fatty Liver Disease (MASLD) | Disease Subtypes | Simple fatty liver, Non-Alcoholic Steatohepatitis (NASH), Liver fibrosis/cirrhosis | ||
| Organ | Liver | Test Sample / Technology Platform | Serum | ||
| Pathobiological Mechanisms | It was calculated by the formula (FIB-4 = age ×AST/(platelet count ×√ALT)). Age reflects the cumulative effect of liver disease; AST/ALT ratio reflects the degree of liver cell injury. Platelet count is associated with portal hypertension and fibrosis (thrombocytopenia in fibrosis). FIB-4 can quickly assess the risk of fibrosis in patients with MASLD by simple clinical parameters Three serum markers (HA, PIIINP, TIMP-1) were calculated by the algorithm. HA reflects the function of hepatic sinusoidal endothelial cells and the degree of fibrosis. PIIINP reflects the rate of collagen synthesis, which is related to the early formation of liver fibrosis. TIMP-1 inhibits matrix metalloproteinase activity, inhibits collagen degradation, and promotes the progression of fibrosis. The ELF score can quantify the degree of liver fibrosis, and the higher the value, the more severe the fibrosis | ||||
| Clinical Availability Status | Non-invasive fibrosis screening markers are widely used in clinical practice and recommended by many guidelines for initial fibrosis stratification of MASLD, such as screening high-risk patients who need further liver biopsy or LSM testing Clinical biomarkers have been recommended by NICE and other guidelines for the screening of advanced fibrosis in MASLD patients and the evaluation of prognosis, such as the evaluation of the improvement effect of liraglutide on fibrosis | ||||
| Notes and Dynamics | FIB-4 is simple to calculate and has a high negative predictive value (>90%) for advanced fibrosis, which can effectively exclude low-risk patients. However, its accuracy decreases in middle-aged people (40-65 years old) and patients complicated with thrombocytopenia (such as other hematological diseases), so it needs to be interpreted with caution The ELF score combines the information of multiple fibrosis-related molecules and has a high diagnostic accuracy for advanced fibrosis (AUROC 0.80-0.90), which is convenient to detect and can reduce unnecessary liver biopsy. However, the accuracy is slightly lower in mild fibrosis stage, and it needs to be combined with LSM and other indicators | ||||
| Biomarker | FIB-4 | Full name | Fibrosis-4 Index | Molecular Type | Scoring measures (based on age, AST, ALT, platelet count) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Assessment OF LIVER FIBROSIS | ||
| Disease(or Constitution) | Metabolic Associated Fatty Liver Disease (MASLD) | Disease Subtypes | Simple fatty liver, Non-Alcoholic Steatohepatitis (NASH), Liver fibrosis/cirrhosis | ||
| Organ | Liver | Test Sample / Technology Platform | Serum (combined with age and platelet count should be considered | ||
| Pathobiological Mechanisms | It was calculated by the formula (FIB-4 = age ×AST/(platelet count ×√ALT)). Age reflects the cumulative effect of liver disease; AST/ALT ratio reflects the degree of liver cell injury. Platelet count is associated with portal hypertension and fibrosis (thrombocytopenia in fibrosis). FIB-4 can quickly assess the risk of fibrosis in patients with MASLD by simple clinical parameters | ||||
| Clinical Availability Status | Non-invasive fibrosis screening markers are widely used in clinical practice and recommended by many guidelines for initial fibrosis stratification of MASLD, such as screening high-risk patients who need further liver biopsy or LSM testing | ||||
| Notes and Dynamics | FIB-4 is simple to calculate and has a high negative predictive value (>90%) for advanced fibrosis, which can effectively exclude low-risk patients. However, its accuracy decreases in middle-aged people (40-65 years old) and patients complicated with thrombocytopenia (such as other hematological diseases), so it needs to be | ||||
| Biomarker | miR-214 / miR-126 | Full name | MicroRNA-214 / MicroRNA-126 | Molecular Type | Nucleic acid (RNA) |
| Molecular Formula | Molecular Weight | 6.6 kDa | Core Functional Dimensions | Diagnosis and prognosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells, vascular endothelial cells | Test Sample / Technology Platform | Tissue/serum (qRT-PCR, NGS) | ||
| Pathobiological Mechanisms | Tumor-promoting miRNA, which promotes the proliferation of malignant endothelial cells | ||||
| Clinical Availability Status | Study validation: Markers of disease progression | ||||
| Notes and Dynamics | Overexpression is positively correlated with the malignant degree of angiosarcoma | ||||
| Biomarker | miR-497 / miR-497-5p | Full name | MicroRNA-497 / MicroRNA-497-5p | Molecular Type | Nucleic acid (RNA) |
| Molecular Formula | Molecular Weight | 6.6 kDa | Core Functional Dimensions | Therapeutic targets | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells | Test Sample / Technology Platform | Tissue/serum (qRT-PCR, NGS) | ||
| Pathobiological Mechanisms | Tumor suppressor miRNA targeting CCND2, CDK6, KCa3.1 and other genes | ||||
| Clinical Availability Status | Study validation: Multi-target regulation | ||||
| Notes and Dynamics | Overexpression reduced tumor cell migration and formation, while miR-497-5p inhibited cell proliferation and invasion | ||||
| Biomarker | miR-340 | Full name | MicroRNA-340 | Molecular Type | Nucleic acid (RNA) |
| Molecular Formula | Molecular Weight | 6.6 kDa | Core Functional Dimensions | Targets for Treatment | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells | Test Sample / Technology Platform | Tissue/serum (qRT-PCR, NGS) | ||
| Pathobiological Mechanisms | Tumor suppressor miRNA, which inhibits SIRT7 expression, inhibits tumor growth and invasion | ||||
| Clinical Availability Status | Research validation: potential therapeutic targets | ||||
| Notes and Dynamics | Overexpression can inhibit the proliferation and metastasis of angiosarcoma cells | ||||
| Biomarker | miR-210 | Full name | MicroRNA-210 | Molecular Type | Nucleic acid (RNA) |
| Molecular Formula | Molecular Weight | 6.6 kDa | Core Functional Dimensions | Prognosis and therapeutic targets | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells, immune cells | Test Sample / Technology Platform | Tissue/serum (qRT-PCR, NGS) | ||
| Pathobiological Mechanisms | Tumor suppressor miRNA, down-regulation promotes the proliferation of angiosarcoma cells | ||||
| Clinical Availability Status | Study validation: Subtype-specific expression | ||||
| Notes and Dynamics | Targeting E2F3 and ephrin A3, downregulation is associated with poor prognosis | ||||