| Biomarker | SASP factors (IL-6, IL-8, MMP3) | Full name | Senescence-associated secretory phenotype factors (Interleukin-6, Interleukin-8, Matrix metalloproteinase 3) | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | IL-6:21 kDa; IL-8:8 kDa; MMP3:54 kDa | Core Functional Dimensions | Prognosis, Monitoring | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Senescent cells, tumor microenvironment | Test Sample / Technology Platform | Serum (ELISA, SIMOA) | ||
| Pathobiological Mechanisms | Secreted by senescent cells, which promote inflammation and tumor progression | ||||
| Clinical Availability Status | Study validation: indicators for monitoring disease progression | ||||
| Notes and Dynamics | Synergized with PAI-1 to regulate the tumor microenvironment, the serum levels of non-responders were significantly increased | ||||
| Biomarker | NLR | Full name | Neutrophil/lymphocyte ratio | Molecular Type | Protein (cell count derived) |
| Molecular Formula | Molecular Weight | Core Functional Dimensions | Prognosis, treatment prediction | ||
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Immune system | Test Sample / Technology Platform | Peripheral blood (routine blood test) | ||
| Pathobiological Mechanisms | It reflects the systemic inflammatory state, and a high ratio suggests immunosuppression | ||||
| Clinical Availability Status | Clinically available: indicators for prognostic evaluation | ||||
| Notes and Dynamics | High NLR is associated with poor response to chemotherapy and poor prognosis, which can be monitored noninvasively | ||||
| Biomarker | CD8+ T cells / TILs | Full name | CD8-positive T cells / Tumor-infiltrating lymphocytes | Molecular Type | Proteins (cell surface markers) |
| Molecular Formula | Molecular Weight | CD8:34 kDa | Core Functional Dimensions | Prognosis, treatment prediction | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Immune system, tumor microenvironment | Test Sample / Technology Platform | Tissue (IHC, flow cytometry) | ||
| Pathobiological Mechanisms | It mediates anti-tumor immune response and enhances the effect of immunotherapy | ||||
| Clinical Availability Status | Study validation: Immunotherapy predictors | ||||
| Notes and Dynamics | TILs infiltration was higher in UV-related and radiation-related AS and positively correlated with ICIs response | ||||
| Biomarker | PD-L1 | Full name | Programmed death-ligand 1 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | 33 kDa | Core Functional Dimensions | Therapeutic targets, and prognosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells, immune cells | Test Sample / Technology Platform | Organization (IHC) | ||
| Pathobiological Mechanisms | The tumor cell surface molecules, inhibit T cell activity, mediated immune escape | ||||
| Clinical Availability Status | Clinical validation: predictive markers for ICIs treatment | ||||
| Notes and Dynamics | The expression is heterogeneous, which is related to CD8+ T cell infiltration, and the patients with high expression are more sensitive to ICIs | ||||
| Biomarker | PAI-1 | Full name | Plasminogen activator inhibitor-1 | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | 43 kDa | Core Functional Dimensions | Prognosis, therapeutic targets | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells, endothelial cells, hepatocytes | Test Sample / Technology Platform | Organization/serum (IHC, ELISA) | ||
| Pathobiological Mechanisms | Promote angiogenesis, immune suppression and tumor microenvironment remodeling | ||||
| Clinical Availability Status | Cutting-edge research: inhibitors in clinical trials | ||||
| Notes and Dynamics | And SASP factor synergy, TM5614 joint nivolumab in resistance against PD-1 AS effective | ||||
| Biomarker | p-AKT / p-S6K / p-4EBP1 | Full name | Phosphorylated AKT / Phosphorylated S6 kinase / Phosphorylated 4E-binding protein 1 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | p-AKT:60 kDa; p-S6K:70 kDa; p-4EBP1:15 kDa | Core Functional Dimensions | Therapeutic targets | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells | Test Sample / Technology Platform | Tissue (IHC) | ||
| Pathobiological Mechanisms | PI3K/Akt/mTOR pathway activation markers, the regulation of protein synthesis and cell growth | ||||
| Clinical Availability Status | The validation: pathway inhibitors in clinical trials | ||||
| Notes and Dynamics | P-AKT expression rate is 85%, p-4EBP1 expression rate is 88%, the pathway activation is associated with poor prognosis | ||||
| Biomarker | p-ERK1/2 | Full name | Phosphorylated extracellular signal-regulated kinase 1/2 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | ERK1:44 kDa; ERK2:42 kDa | Core Functional Dimensions | Therapeutic targets | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells | Test Sample / Technology Platform | Organization (IHC) | ||
| Pathobiological Mechanisms | MAPK/ERK pathway activation markers, promote cell proliferation and survival | ||||
| Clinical Availability Status | Validation: subtypes heterogeneity expression | ||||
| Notes and Dynamics | Expression rate of 54% (31% 95%), and provide the basis for MEK inhibitor treatment | ||||
| Biomarker | TIE1 / TIE2 (TEK) | Full name | Tyrosine kinase with immunoglobulin-like and EGF-like domains 1 / TEK receptor tyrosine kinase | Molecular Type | protein |
| Molecular Formula | Molecular Weight | TIE1:125 kDa; TIE2:125 kDa | Core Functional Dimensions | Targets for Treatment | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells, tumor cells | Test Sample / Technology Platform | Organization (IHC) | ||
| Pathobiological Mechanisms | The specific receptors of endothelial cells, activate the PI3K/Akt/mTOR pathway, steady state regulation of blood vessels | ||||
| Clinical Availability Status | Validation: TIE2 inhibitors in development | ||||
| Notes and Dynamics | The expression rate of TIE2 is 98%, which is the core target of ANGPT-TIE pathway | ||||
| Biomarker | ANG1 / ANG2 | Full name | Angiopoietin 1 / Angiopoietin 2 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | ANG1:55 kDa; ANG2:55 kDa | Core Functional Dimensions | Prognosis, therapeutic targets | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells, stromal cells | Test Sample / Technology Platform | Organization/serum (IHC, ELISA) | ||
| Pathobiological Mechanisms | Regulation ANGPT-TIE pathway, ANG1 to maintain stable blood vessels, ANG2 promote vascular remodeling | ||||
| Clinical Availability Status | ANG2 was identified as a potential target | ||||
| Notes and Dynamics | The high expression of ANG1 is associated with a good prognosis, and the serum level of ANG2 is increased in advanced AS | ||||
| Biomarker | VEGFR1 / VEGFR2 / VEGFR3 | Full name | Vascular endothelial growth factor receptor 1 / 2 / 3 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | VEGFR1:180 kDa; VEGFR2:150 kDa; VEGFR3:195 kDa | Core Functional Dimensions | Therapeutic targets, prognosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Vascular/lymphatic endothelial cells, tumor cells | Test Sample / Technology Platform | Organization (IHC) | ||
| Pathobiological Mechanisms | Combined with VEGF ligand, activate the downstream PI3K/Akt/mTOR and MAPK pathways | ||||
| Clinical Availability Status | Clinical validation/therapeutic targets: TKIs main targets | ||||
| Notes and Dynamics | Expression rate was 78%, 84%, 84% respectively, VEGFR2 lower expression is associated with poor prognosis | ||||
| Biomarker | VEGF-C / VEGF-D | Full name | Vascular endothelial growth factor C / Vascular endothelial growth factor D | Molecular Type | protein |
| Molecular Formula | Molecular Weight | VEGF-C: 40 kDa; VEGF-D: 45 kDa | Core Functional Dimensions | Therapeutic targets, prognosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells, stromal cells | Test Sample / Technology Platform | Tissue/serum (IHC, ELISA) | ||
| Pathobiological Mechanisms | Lymph angiogenesis regulation, the promotion of tumor lymphatic metastasis | ||||
| Clinical Availability Status | Validation: late subtypes enrichment | ||||
| Notes and Dynamics | The expression of VEGF-C was heterogeneous (12%-88%), and the serum level of VEGF-D increased with the stage | ||||
| Biomarker | VEGF-A | Full name | Vascular endothelial growth factor A | Molecular Type | Protein |
| Molecular Formula | Molecular Weight | 45 kDa | Core Functional Dimensions | Therapeutic targets, prognosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Tumor cells, macrophages, endothelial cells | Test Sample / Technology Platform | Tissue/serum (IHC, ELISA) | ||
| Pathobiological Mechanisms | Promote vascular endothelial cell proliferation, migration and vascular permeability increase | ||||
| Clinical Availability Status | Clinical validation/therapeutic targets: VEGF inhibitors targets | ||||
| Notes and Dynamics | 86% (85% 94%) AS expression, serum level and positively related to the tumor stage | ||||
| Biomarker | FLI-1 | Full name | Friend leukemia integration 1 transcription factor | Molecular Type | protein |
| Molecular Formula | Molecular Weight | 48 kDa | Core Functional Dimensions | diagnosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells, hematopoietic cells | Test Sample / Technology Platform | Organization (IHC) | ||
| Pathobiological Mechanisms | Transcription factors, involved in vascular endothelial cell proliferation and differentiation | ||||
| Clinical Availability Status | Clinical validation: Auxiliary diagnosis | ||||
| Notes and Dynamics | With ERG expression, improve the AS diagnostic specificity | ||||
| Biomarker | vWF | Full name | Von Willebrand factor | Molecular Type | Proteins |
| Molecular Formula | Molecular Weight | 250 kDa | Core Functional Dimensions | diagnosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells, megakaryocytes | Test Sample / Technology Platform | Tissue (IHC) | ||
| Pathobiological Mechanisms | Endothelial cells secrete proteins involved in hemostasis and vascular homeostasis | ||||
| Clinical Availability Status | Clinical validation: auxiliary diagnosis | ||||
| Notes and Dynamics | AS tissue specific expression, can distinguish between source sex tumor vascular source sex, and the blood vessels | ||||
| Biomarker | CD34 | Full name | Hematopoietic progenitor cell antigen CD34 | Molecular Type | protein |
| Molecular Formula | Molecular Weight | 110 kDa | Core Functional Dimensions | diagnosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Hematopoietic progenitors, vascular endothelial cells | Test Sample / Technology Platform | Tissue (IHC) | ||
| Pathobiological Mechanisms | Endothelial cell surface markers that regulate angiogenesis and cell migration | ||||
| Clinical Availability Status | Clinical available: auxiliary diagnostic markers | ||||
| Notes and Dynamics | Most of AS were positive, and some subtypes showed heterogeneous expression | ||||
| Biomarker | CD31 | Full name | Platelet endothelial cell adhesion molecule 1 | Molecular Type | Proteins |
| Molecular Formula | Molecular Weight | 130 kDa | Core Functional Dimensions | diagnosis | |
| Disease(or Constitution) | Angiosarcoma | Disease Subtypes | / | ||
| Organ | Vascular endothelial cells, platelets | Test Sample / Technology Platform | Organization (IHC) | ||
| Pathobiological Mechanisms | Endothelial cell surface markers involved in cell adhesion and angiogenesis | ||||
| Clinical Availability Status | Clinically available: one of the gold standards for diagnosis | ||||
| Notes and Dynamics | Almost all AS is positively expressed and is a key differential marker for epithelial tumors | ||||