| Biomarker | TFF2 | Full name | Trefoil factor 2 | Molecular Type | Proteins |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Precancerous lesion surveillance | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Intraductal papillary mucinous neoplasm (IPMN) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissue, pancreatic juice (immunoassay, mass spectrometry) | ||
| Pathobiological Mechanisms | A member of trefoil factor family, it is involved in the maintenance of pancreatic ductal epithelial homeostasis, and its deficiency is associated with the accelerated development of IPMN | ||||
| Clinical Availability Status | Clinical research phase: abnormal expression in IPMN organizations, to evaluate risk of malignant transformation | ||||
| Notes and Dynamics | There are heterogeneous molecular forms of IPMN with tumor suppressive effects, and their expression status can assist in judging the malignant potential of IPMN | ||||
| Biomarker | ANXA10 | Full name | Annexin A10 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Precancerous lesion progression monitoring | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic intraepithelial neoplasia (PanIN) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissues (immunohistochemistry) | ||
| Pathobiological Mechanisms | A member of the annexin family, it is involved in the regulation of cell proliferation and differentiation, and its expression is closely related to the progression of PanIN to PDAC | ||||
| Clinical Availability Status | Clinical research phase: the expression of PanIN tissues gradually increased, which can predict the risk of malignant transformation | ||||
| Notes and Dynamics | Is progress PanIN potential prediction markers for PDAC, helps to screening high-risk patients with precancerous lesions for close monitoring | ||||
| Biomarker | LAMC2+PTX3 | Full name | Laminin subunit gamma-2 + Pentraxin 3 | Molecular Type | Protein combination |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnostic aid | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (immunoassay, mass spectrometry) | ||
| Pathobiological Mechanisms | LAMC2 participate in extracellular matrix formation, PTX3 involved in inflammation and angiogenesis, were KRAS G12V related proteins, expressed in PDAC early rise | ||||
| Clinical Availability Status | Clinical research phase: It can improve the diagnostic sensitivity of CA19-9, and has supplementary value for patients with low expression of CA19-9 | ||||
| Notes and Dynamics | It is related to KRAS mutation status and can be detected in the circulation of patients with early PDAC, which provides a basis for molecular typing | ||||
| Biomarker | KRASmut/p53mut (combined detection) | Full name | KRAS mutant + TP53 mutant | Molecular Type | Nucleic acid combination (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Plasma (single-cell exosome analysis, ctDNA sequencing) | ||
| Pathobiological Mechanisms | KRAS and p53 mutation is the most common PDAC, joint detection can cover the key drivers of the tumor | ||||
| Clinical Availability Status | Clinical research phase: in patients with stage I PDAC detection rate is high, the molecular evidence for early diagnosis | ||||
| Notes and Dynamics | Through the analysis of the single cell secrete outside body can be detected in patients with early, overcome the ctDNA limitations in the early days of low concentration | ||||
| Biomarker | APOE+ITIH3+APOA1+APOL1+CA19-9 (joint panel) | Full name | Apolipoprotein E + Inter-alpha-trypsin inhibitor heavy chain H3 + Apolipoprotein A1 + Apolipoprotein L1 + CA19-9 | Molecular Type | Protein combination |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Protein combination | ||
| Disease(or Constitution) | Protein combination | Disease Subtypes | Adenocarcinoma of the pancreatic duct (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (Mass spectrometry, immunoassay) | ||
| Pathobiological Mechanisms | It includes members of the apolipoprotein and protease inhibitors family, which are involved in the regulation of lipid metabolism and inflammatory response. The combination of these two proteins can improve the diagnostic specificity and sensitivity | ||||
| Clinical Availability Status | Clinical research phase: validation in multiple populations, diagnostic sensitivity 95%, specificity 94.1% | ||||
| Notes and Dynamics | It can effectively distinguish early PDAC from pancreatitis, solve the problem of insufficient specificity of single marker, and is suitable for high-risk population screening | ||||
| Biomarker | LYVE1 + REG1A + TFF1 joint (panel) | Full name | Lymphatic vessel endothelial hyaluronan receptor 1 + Regenerating islet-derived 1A + Trefoil factor 1 | Molecular Type | Protein combinations |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Adenocarcinoma of the pancreatic duct (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Urine (immunoassay, mass spectrometry) | ||
| Pathobiological Mechanisms | LYVE1 participate in lymph angiogenesis, REG1A regulate pancreatic secretion, TFF1 participate in mucosal protection and cell proliferation, combined can reflect the PDAC early molecular changes | ||||
| Clinical Availability Status | Clinical research phase: a urine sample is convenient, suitable for mass screening | ||||
| Notes and Dynamics | It has been verified by case-control studies and has a high level of AUC for the diagnosis of early PDAC, with obvious advantages of non-invasiveness | ||||
| Biomarker | Leucine-rich alpha-2-glycoprotein 1 + TIMP metallopeptidase inhibitor 1 + CA19-9 | Full name | LRG1+TIMP1+CA19-9 (combined panel) | Molecular Type | Protein combinationsProtein combinations |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (mass spectrometry, immunoassay) | ||
| Pathobiological Mechanisms | LRG1 involved in tumor matrix remodeling, TIMP1 regulating the activity of matrix metalloproteinases, and CA19-9 can cover different pathological process of molecular changes | ||||
| Clinical Availability Status | Clinical research phase: It has been validated in multi-center studies and is significantly superior to single markers | ||||
| Notes and Dynamics | Sensitivity and specificity to the diagnosis of early PDAC are higher than used alone CA19-9, is potential joint diagnosis scheme | ||||
| Biomarker | METTL14 | Full name | Methyltransferase-like 14 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Regulation of tumorigenesis | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Organize, cell line (immunohistochemical, mass spectrometry) | ||
| Pathobiological Mechanisms | Participate in m6A RNA methylation process, interact with piRNA - 14633, enhance METTL14 and CYP1B1 is expressed, promotes tumorigenesis | ||||
| Clinical Availability Status | Basic research phase: has clear its role in the tumorigenesis, provide ideas for epigenetic therapy | ||||
| Notes and Dynamics | Abnormal expression in PDAC, affect gene expression, through regulating the RNA methylation is potential targeted therapeutic targets | ||||
| Biomarker | hnRNPU | Full name | Heterogeneous nuclear ribonucleoprotein U | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Regulation of tumor progression | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Adenocarcinoma of the pancreatic duct (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissues and cell lines (immunoprecipitation, mass spectrometry) | ||
| Pathobiological Mechanisms | As RNA binding protein, combined with piRNA - 1742, regulating the USP8 mRNA stability, suppress MUC12 ubiquitin, promote the development of tumor | ||||
| Clinical Availability Status | Basic research phase: the experiment validate its effect on promoting carcinoma in vivo and in vitro, provide targets for mechanism study | ||||
| Notes and Dynamics | Abnormal expression in PDAC, involved in regulating cell proliferation and tumor, and its related pathways is expected to become targets for intervention | ||||
| Biomarker | GPC1⁺ exosomes | Full name | Glypican-1 positive exosomes | Molecular Type | Protein (secrete related) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis and prognosis evaluation | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Adenocarcinoma of the pancreatic duct (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (outside secrete separation flow cytometry) + | ||
| Pathobiological Mechanisms | Outside GPC1 body surface protein secretion, and by the PDAC cells secrete, participate in tumor microenvironment niche form before regulation and distant metastasis | ||||
| Clinical Availability Status | Clinical research phase: diagnostic sensitivity and specificity are close to 100%, which has been verified in large-scale samples | ||||
| Notes and Dynamics | Can distinguish between PDAC and chronic pancreatitis and healthy people, is independent of disease specific prognostic markers, and prognostic value is better than that of CA19-9 | ||||
| Biomarker | Deletion of CDKN2A/p16 | Full name | Cyclin-dependent kinase inhibitor 2A deletion | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Subtype identification, prognostic evaluation | ||
| Disease(or Constitution) | Disease Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreatic ductal adenocarcinoma (PDAC) | Test Sample / Technology Platform | Organization (next-generation sequencing, immunohistochemical) | ||
| Pathobiological Mechanisms | CDKN2A gene deletion leads to loss of p16 protein expression, lift its regulation of cell cycle, promoting tumor cell proliferation, associated with invasive tumor | ||||
| Clinical Availability Status | Clinical research phase: used to identify aggressive subtype, assess the risk of disease progression | ||||
| Notes and Dynamics | 30% to 40% of patients with PDAC is missing, is a key driver events of PDAC, lack of tumor in patients with malignant degree is higher | ||||
| Biomarker | SMAD4 mutant | Full name | SMAD family member 4 mutant | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognostic prediction and therapeutic targets | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Tissues (Next generation sequencing) | ||
| Pathobiological Mechanisms | SMAD4 is a key molecule in TGF-β signaling pathway. Mutation of Smad4 leads to loss of tumor suppressor function and promotes tumor invasion and metastasis | ||||
| Clinical Availability Status | Clinical research phase: used for prognostic evaluation, its absence is associated with poor prognosis | ||||
| Notes and Dynamics | Mutations are present in 30%-40% of patients with PDAC, and patients with mutated PDAC are more likely to have distant metastasis, which can be used as a prognostic stratification marker | ||||
| Biomarker | KRAS mutant (G12D/V/R) | Full name | Kirsten rat sarcoma viral oncogene homolog mutant | Molecular Type | Nucleic acid (DNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Treatment options and prognosis assessment | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Organization, ctDNA (next-generation sequencing) | ||
| Pathobiological Mechanisms | Is the most common PDAC KRAS mutations drive events (> 90%), lead to protein activation, drive MAPK signaling pathways such as promoting tumor proliferation and metabolic reprogramming | ||||
| Clinical Availability Status | Clinical can be used as a guide (treatment) : used for screening of targeted therapy, such as KRAS G12C inhibitors for patients | ||||
| Notes and Dynamics | It is a key event in the early development of PDAC and has been detected in precancerous lesions (PanIN). Its mutation status can guide precise treatment strategies | ||||
| Biomarker | EphA2 | Full name | Ephrin type-A receptor 2 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prediction of chemotherapy resistance | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic Cancer | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum secrete body separation + immunoassay () | ||
| Pathobiological Mechanisms | Ephrin type A receptor 2, by participating in tumor cells of epithelial mesenchymal (EMT) and signaling pathways that control, its expression is associated with gemcitabine resistance | ||||
| Clinical Availability Status | Clinical research phase: it is used to predict the response to chemotherapy and guide the adjustment of treatment regimens | ||||
| Notes and Dynamics | Exosome-derived EphA2 can be used as a minimally invasive predictive marker, and its high expression indicates an increased risk of chemotherapy resistance | ||||
| Biomarker | EPS8 | Full name | Epidermal growth factor receptor pathway substrate 8 | Molecular Type | Proteins |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis and recurrence monitoring | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Pancreatic ductal adenocarcinoma (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (Exosome isolation + Mass spectrometry) | ||
| Pathobiological Mechanisms | The epidermal growth factor receptor pathway substrate 8, involved in tumor cell migration, invasion, and signal transduction, in PDAC secrete in the body can be detected early | ||||
| Clinical Availability Status | Clinical research phase: It has been validated in patients with early PDAC and is expected to be used for recurrence monitoring | ||||
| Notes and Dynamics | Combination with GPRC5C can improve the accuracy of early diagnosis, and its expression changes are synchronized with tumor progression | ||||
| Biomarker | GPRC5C | Full name | G protein-coupled receptor class C group 5 member C | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Early diagnosis | ||
| Disease(or Constitution) | Pancreatic Cancer | Disease Subtypes | Adenocarcinoma of the pancreatic duct (PDAC) | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (Exosome isolation + Mass spectrometry) | ||
| Pathobiological Mechanisms | It belongs to the G protein-coupled receptor family, which is specifically expressed in PDAC associated exosomes and participates in the regulation of tumor cell signaling and proliferation | ||||
| Clinical Availability Status | Serum (Exosome isolation + Mass spectrometry) It belongs to the G protein-coupled receptor family, which is specifically expressed in PDAC associated exosomes and participates in the regulation of tumor cell signaling and proliferation | ||||
| Notes and Dynamics | Is the secrete body outside circulating tumor related markers, for detecting early PDAC has specificity, biopsy candidate markers can be used as a liquid | ||||