| Biomarker | Veillonella | Full name | Veillonella spp. | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis and monitoring of disease progression | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal Adenocarcinoma (EAC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Esophageal tissues (16S rRNA sequencing) | ||
| Pathobiological Mechanisms | The abundance of EAC cascade gradually increases, which is related to the transformation of BE to EAC, and participates in the activation of inflammatory signals in the tumor microenvironment | ||||
| Clinical Availability Status | Clinical research stage: the dynamic changes in EAC progression have been verified | ||||
| Notes and Dynamics | It provides new microbial markers for the monitoring of EAC precancerous lesions and has good potential for clinical transformation | ||||
| Biomarker | Atopobium | Full name | Atopobium spp. | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis and monitoring of disease progression | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal Adenocarcinoma (EAC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Esophageal tissues (16S rRNA sequencing) | ||
| Pathobiological Mechanisms | In GERD-BE-EAC, its abundance gradually increases during the progression of GERD-BE-EAC, which is involved in the regulation of lipopolysaccharide biosynthesis and inflammatory response and promotes malignant transformation | ||||
| Clinical Availability Status | Clinical research stage: it can BE used as a potential marker to monitor the progression of BE to EAC | ||||
| Notes and Dynamics | It is a key microbial marker in the occurrence and development of EAC and provides targets for early intervention | ||||
| Biomarker | Prevotella | Full name | Prevotella spp. | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, immunomodulation | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Esophageal tissue/stool (16S rRNA sequencing, qPCR) | ||
| Pathobiological Mechanisms | Some subtype abundance anomalies associated with ESCC progress, by adjusting the indoles metabolites such as tumor microenvironment, to participate in the process of immunosuppression | ||||
| Clinical Availability Status | Clinical research stage: It has been frequently identified in ESCC microbiota studies with good diagnostic specificity | ||||
| Notes and Dynamics | The dual role of ESCC microbiota (cancer-promoting and cancer-suppressing in some subtypes) needs to be further clarified to provide a basis for precise targeting of microbiota | ||||
| Biomarker | Faecalibacterium | Full name | Faecalibacterium prausnitzii | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, Prognosis | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Stool (16S rRNA sequencing) | ||
| Pathobiological Mechanisms | As a short chain fatty acid bacteria, abundance lower will destroy the integrity of intestinal barrier, enhance intestinal permeability and inflammation, indirectly promote the development of ESCC occurs | ||||
| Clinical Availability Status | Clinical research phase: Its diagnostic and prognostic relevance has been validated in multiple ESCC cohorts | ||||
| Notes and Dynamics | The changes in their abundance can reflect the imbalance of intestinal microecology and provide ideas for the treatment of combined microecological agents | ||||
| Biomarker | Lachnospira | Full name | Lachnospira spp. | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, Prognosis | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Stool (16S rRNA sequencing) | ||
| Pathobiological Mechanisms | They belong to intestinal beneficial bacteria, and their decreased abundance is related to the occurrence of ESCC. They affect tumor progression by regulating intestinal barrier function and inflammatory response | ||||
| Clinical Availability Status | Clinical research phase: multiple fecal microbiota studies have confirmed its diagnostic value | ||||
| Notes and Dynamics | It is a key marker of intestinal microbiota imbalance in ESCC and provides a target for intestinal microecological intervention | ||||
| Biomarker | Streptococcus | Full name | Streptococcus spp. | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, Prognosis | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Esophageal tissue/stool (16S rRNA sequencing, qPCR) | ||
| Pathobiological Mechanisms | Abnormal abundance is related to the occurrence of ESCC, and the high expression of some subtypes is related to the poor prognosis of patients, which is involved in the regulation of inflammatory response in tumor microenvironment | ||||
| Clinical Availability Status | Clinical phase: As a key marker in the gut and esophageal microbiota, it has been validated in multiple cohorts | ||||
| Notes and Dynamics | It can be used as an auxiliary marker for non-invasive diagnosis, and its synergistic effect with other microorganisms deserves further study | ||||
| Biomarker | Porphyromonas gingivalis | Full name | Porphyromonas gingivalis | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, immune regulation | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Esophageal tissues (16S rRNA sequencing, qPCR, IHC) | ||
| Pathobiological Mechanisms | Activation of PI3K/Akt pathway can inhibit epithelial cell apoptosis, induce IL-6 expression to promote epithelial-mesenchymal transition and myeloid-derived suppressor cell recruitment, and enhance TGF-β/Smad signaling to promote tumor growth and metastasis | ||||
| Clinical Availability Status | Clinical research stage: it is closely related to the advanced clinical stage and poor prognosis of ESCC | ||||
| Notes and Dynamics | Its abundance changes can monitor progress ESCC, provide the basis for targeted treatment strategy of microbiota | ||||
| Biomarker | Fusobacterium nucleatum | Full name | Fusobacterium nucleatum | Molecular Type | Microbes |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, immune regulation | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Esophageal tissue/stool (16S rRNA sequencing, qPCR, IHC) | ||
| Pathobiological Mechanisms | By activating NOD1 RIPK2 / the nf-kappa B pathway, promote chemokine activation mechanism, enhance tumor invasive; It is related to the clinical stage progression, poor prognosis and immunotherapy resistance of ESCC | ||||
| Clinical Availability Status | Clinical research phase: various clinical studies verify the value of his as a prognostic marker | ||||
| Notes and Dynamics | It is a key pathogenic microorganism in the tumor microenvironment of ESCC and can be used as a potential target for non-invasive diagnosis and prognostic evaluation | ||||
| Biomarker | GNRH2 | Full name | Gonadotropin-releasing hormone 2 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Risk prediction, cancer suppression | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Tissue/plasma (MR Analysis, qPCR) | ||
| Pathobiological Mechanisms | It is widely distributed in the central nervous system and peripheral tissues and plays a tumor suppressor role by inhibiting tumor cell proliferation, migration and ribosomal phosphorylation protein expression. SNP rs6051545 has a negative regulatory effect on ESCC | ||||
| Clinical Availability Status | Clinical research stage: Mendelian randomization analysis confirmed its causal relationship with ESCC, and no direct targeted drugs were available | ||||
| Notes and Dynamics | In a wide variety of tumor has antiproliferative and its effect on promoting apoptosis, provide a new potential target for ESCC targeted treatment | ||||
| Biomarker | KLK13 | Full name | Kallikrein-related peptidase 13 | Molecular Type | Proteins |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis and disease progression monitoring | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Tissue (IHC, qPCR) | ||
| Pathobiological Mechanisms | It belongs to the serine protease family and participates in the proteolytic process of tumorigenesis. Its high expression is related to the tumor progression, advanced stage and poor prognosis of ESCC, and its expression change can predict disease progression | ||||
| Clinical Availability Status | Clinical study phase: multiple clinical cohorts were used to verify its correlation with ESCC prognosis | ||||
| Notes and Dynamics | It can be used as a unique molecule to monitor the progression of ESCC, and its regulatory mechanism and targeting strategy deserve further exploration | ||||
| Biomarker | CEL | Full name | Carboxyl ester lipase | Molecular Type | protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Risk prediction, metabolic regulation | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Tissue/plasma (MR Analysis, IHC) | ||
| Pathobiological Mechanisms | It participates in lipid metabolism and affects tumor microenvironment and inflammatory response by regulating fatty acid metabolism. High expression associated with poor prognosis of ESCC, taurocholic acid can activate its function | ||||
| Clinical Availability Status | Clinical research phase: has clear its causal relationship with ESCC, related mechanism of activator is preliminary already clarify | ||||
| Notes and Dynamics | Is closely related to the metabolism of bile acid, provide theory basis for metabolic reprogramming related target therapy | ||||
| Biomarker | ST3GAL1 | Full name | ST3 beta-galactoside alpha-2,3-sialyltransferase 1 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Risk prediction, therapeutic targets | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Organization/plasma (MR analysis, Western blotting) | ||
| Pathobiological Mechanisms | It catalyzes the α-2,3 sialylation modification of glycoproteins and glycolipids, changes cell adhesion properties, enhances immune escape and tumor invasion and metastasis, and plays a role by regulating immune checkpoint molecules such as PD-L1 | ||||
| Clinical Availability Status | Clinical study phase: Mendelian randomization analysis confirmed that its high expression increased the risk of ESCC | ||||
| Notes and Dynamics | As key member of the family of sialic acid transaminase, targeted for ESCC glycosylation modification treatment provides a new direction | ||||
| Biomarker | HPSE | Full name | Heparanase | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, therapeutic targets | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Tissue/plasma (IHC, qPCR, MR Analysis) | ||
| Pathobiological Mechanisms | As a key enzyme, it degrades extracellular matrix and participates in tumor invasion, metastasis and angiogenesis. The low expression associated with adverse outcomes in patients with ESCC, through the Wnt/beta - catenin pathway regulating tumor progression | ||||
| Clinical Availability Status | Clinical research phase: The causal relationship with ESCC was verified by Mendelian randomization analysis, and the existing drugs (heparin, dalteparin) could be targeted | ||||
| Notes and Dynamics | It is a therapeutic target with great translational value, and further clinical verification of targeting efficacy is needed | ||||
| Biomarker | SECTM1 | Full name | Secreted and transmembrane protein 1 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, immune regulation | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal squamous cell carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Tissue/cell (qPCR, Western blotting, IHC) | ||
| Pathobiological Mechanisms | Promote the proliferation, migration and invasion of ESCC cells; By inducing the expression of chemokine CCL5, it can promote the polarization of macrophages to M2 phenotype and enhance the tumor immunosuppressive microenvironment | ||||
| Clinical Availability Status | Clinical research phase: A prognostic model based on SECTM1 has been constructed to verify its correlation with the poor prognosis of patients | ||||
| Notes and Dynamics | It is a key immune-related tumor promoting factor of ESCC, which provides new ideas for immunotherapy combined targeting strategy | ||||
| Biomarker | circNF1 | Full name | Circular RNA Neurofibromin 1 | Molecular Type | Nucleic acid (circRNA) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Diagnosis, prognosis, and immunotherapy efficacy prediction | ||
| Disease(or Constitution) | Esophageal Carcinoma | Disease Subtypes | Esophageal Squamous Cell Carcinoma (ESCC) | ||
| Organ | Esophagus | Test Sample / Technology Platform | Organization/serum (ddPCR, qRT - PCR) | ||
| Pathobiological Mechanisms | Through the dual regulation of PD - L1 role: on one hand driven JAK induced by IL - 6 - STAT3 pathway activation of cancer, promote the combination of p - STAT3 and PD - L1 promoter; On the other hand, it binds to ANXA1 to block USP7-mediated deubiquitination of ANXA1, enhance the interaction between USP7 and PD-L1 and the stability of PD-L1, and finally promote tumor proliferation, metastasis and immune escape | ||||
| Clinical Availability Status | Clinical research phase: was validated in a number of clinical queue with the correlation, the efficacy of immunotherapy is potential immune treatment response prediction markers | ||||
| Notes and Dynamics | To provide new targets for ESCC immunotherapy, unite against PD - L1 treatment can significantly improve curative effect, is expected to enter the clinical practice | ||||
| Biomarker | Uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) | Full name | UDP-glucuronosyltransferase 1-1 | Molecular Type | Proteins |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Treatment prediction | ||
| Disease(or Constitution) | Colorectal Cancer (CRC) | Disease Subtypes | Colorectal cancer | ||
| Organ | Colorectal | Test Sample / Technology Platform | Blood (genotyping, enzyme activity testing) | ||
| Pathobiological Mechanisms | It is involved in irinotecan metabolism, and its genetic polymorphisms affect drug toxicity and efficacy | ||||
| Clinical Availability Status | Clinical can be used as a guide (treatment), have been used to CRC, stand for kang chemotherapy dose adjustment basis | ||||
| Notes and Dynamics | It is the first biomarker for individualized dose adjustment of CRC chemotherapy, which can effectively reduce the risk of serious adverse reactions | ||||