P1, N=78, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Dec 2024 --> Dec 2025

P1/2, N=215, Recruiting, 4D Molecular Therapeutics | N=150 --> 215 | Trial completion date: Nov 2025 --> Nov 2026 | Trial primary completion date: Nov 2024 --> Nov 2025

The interaction behaviour between VEGF in the solution and the immobilise DNA aptamer/Ppy-based structure was analysed using Langmuir isotherm model. The developed electrochemical biosensor in promising for in vitro applications in early cancer diagnostics and treatment monitoring, enabling rapid screening of patient samples.

The current results demonstrated the applicability of the HerboChip platform and systematically elucidated the activity of selected TCMs on angiogenesis and its related signal transduction mechanisms.

These data suggest that autocrine VEGF-B mediates a signal to coordinate lipid synthesis and mitochondrial fitness with T cell activation for survival and immune response. Moreover, autocrine VEGF-B signaling in T cells provides a therapeutic target against infection and tumors as well as an avenue for the treatment of autoimmune diseases.

In conclusion, this study provides a detailed examination of the relationship between FDI-6 and both the molecular interactions and protein expressions of VEGF-B. Our findings support FDI-6 as a potential therapeutic agent in pathological processes associated with angiogenesis.

We examined the anti-VEGF-B-specific monoclonal antibody 2H10 in preclinical xenograft models of breast and colorectal cancer, in comparison with the anti-VEGF-A antibody bevacizumab...Accordingly, treatment resulted in partial inhibition of tumor growth, and significantly improved the response to chemotherapy. Our studies indicate the importance of VEGF-B in tumor growth, and the potential of specific anti-VEGF-B treatment to inhibit tumor development, alone or in combination with established chemotherapies.

Functionally, suppressing VEGFB expression successfully mitigated the oncogenic effects induced by CHPF overexpression. Collectively, these findings suggest that CHPF may act as a tumour promoter in CRC, operating in a VEGFB-dependent manner and could be a potential target for therapeutic interventions in CRC treatment.

P2, N=32, Recruiting, H. Lee Moffitt Cancer Center and Research Institute | Initiation date: Oct 2023 --> Feb 2024

This demonstrates the potential of leveraging deep learning for accurate VEGF prediction as a powerful tool to accelerate research, streamline drug discovery and uncover novel therapeutic targets. This insightful approach holds promise for expanding our knowledge of VEGF's role in health and disease.Communicated by Ramaswamy H. Sarma.

The combination of sapanisertib and ziv-aflibercept was generally tolerable and demonstrated anti-tumor activity in heavily pre-treated patients with advanced malignancies.

P1, N=83, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: Jan 2025 --> Jan 2024

P1, N=83, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2024 --> Jan 2025

P=N/A, N=140, Completed, Sanofi | Active, not recruiting --> Completed

Although limited by sample size and follow-up, these findings highlight the potential of the combination of ziv-aflibercept antiangiogenic therapy with pembrolizumab in patients with advanced melanoma resistant to anti-PD-1 treatment and the need for further research to improve outcomes in anti-PD-1-resistant melanoma.

P1, N=78, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2023 --> Dec 2024 | Trial primary completion date: Dec 2023 --> Dec 2024

P1, N=30, Recruiting, Panolos Bioscience

P2, N=114, Completed, CSL Behring | Phase classification: P2a --> P2

P2, N=32, Recruiting, H. Lee Moffitt Cancer Center and Research Institute

P3, N=202, Active, not recruiting, GCS IHFB Cognacq-Jay | Recruiting --> Active, not recruiting | Trial completion date: Aug 2023 --> Jun 2024 | Trial primary completion date: Oct 2022 --> Jun 2023

P1, N=30, Recruiting, Panolos Bioscience | Not yet recruiting --> Recruiting

P1, N=30, Not yet recruiting, Panolos Bioscience

P2, N=19, Completed, Dana-Farber Cancer Institute | Active, not recruiting --> Completed

This review summarizes the regulatory role of VEGFB in the onset and development of NAFLD and illustrates its underlying molecular mechanism. In conclusion, the signaling pathway mediated by VEGFB in the liver may provide an innovative approach to the diagnosis and treatment of NAFLD.

The apoptotic effects of C-VGB3 on HUVE and 4T1 MCT cells were inferred from annexin-PI and TUNEL staining and activation of P53, caspase-3, caspase-7, and PARP1, which mechanistically occurred through the intrinsic pathway mediated by Bcl2 family members, cytochrome c, Apaf-1 and caspase-9, and extrinsic pathway via death receptors and caspase-8. These data indicate that binding regions shared by VEGF family members may be important in developing novel pan-VEGFR inhibitors that are highly relevant in the pathogenesis of angiogenesis-related diseases.

GSK3β regulatory role is mediated by the reperfusion injury salvage kinase (RISK) pathway, and its inhibition by Akt activation blocks mitochondrial permeability transition pore (mPTP) opening and enhances myocardial survival. The present article discusses the involvement of the PI3K/Akt/GSK3β pathway in cardioprotective effects of natural products against MIRI.

P1, N=83, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2023 --> Jan 2024

NEAT2 downregulation inhibited cell proliferation and EMT through VEGFB and TGF-β/Smad3 pathway in vitro, disclosing a new regulatory mechanism in OSCC. In addition, downregulation of NEAT2 could inhibit the tumor growth and metastasis.

To conclude, TARDBP was found to regulate the alternative splicing of VEGF via SRSF1, induce the formation of VEGF but inhibit that of VEGFb, and promote OC angiogenesis. Hence, TARDBP can serve as an independent prognostic factor and new target for OC cancer therapy.

P2, N=19, Active, not recruiting, Dana-Farber Cancer Institute | N=43 --> 19 | Trial completion date: Dec 2021 --> Dec 2022

In addition, it reduced the metastatic capacity in a 4T1 breast cancer model in vivo. Collectively, our conclusions reveal that Russelioside A is an attractive natural compound for treating triple-negative breast cancer growth and metastasis through regulating NF-κB activation.

There is a significant difference in overall survival between HCC patients with high and low expression of ANGPT2, PGF, VEGFA, and VEGFD. Disease free survival (DFS) is significantly shorter in HCC patients with high ANGPT2, PGF, and VEGFA expression than in those with low ANGPT2, PGF, and VEGFA expression.

Furthermore, non-tumor adjacent tissue presented an increase of the inflammatory status that could be the basis for future tumor progression. In conclusion, these proteins could be useful as biomarkers of diagnosis for CRC at early stages.

In addition, the developed phage-based EIS immunosensor was applied to satisfactorily detect VEGF165 in human serum samples. Considering its ultra-sensitivity, good selectivity, batch reproducibility and stability, the screened selective phage-based EIS sensor is envisioned potential application in diagnosis and therapy.

Enhanced therapeutic efficacy was achieved when two agents ([Lu]Lu-cG250 RIT and sunitinib) that on their own did not induce satisfactory response levels, are combined. Our findings provide a promising new therapeutic strategy for patients with advanced RCC.

However, there was a negative correlation between the expression of RUNX3 gene and the ratio of VEGF-positive cells in sorafenib group (R=0.509 7). Sorafenib may inhibit the PDX angiogenesis and the growth of hepatocellular carcinoma by regulating the RUNX3-VEGF pathway.

Free aflibercept in excess of the VEGF-bound form was not maintained at this dose level. The dose limiting toxicity (DLT) of aflibercept combined with docetaxel was febrile neutropenia, which occurred in 2 of 3 Japanese patients at the lowest aflibercept dose level (2 mg/kg) combined with docetaxel (60 mg/m) and therapeutic G-CSF use. A recommended dose for further studies was not determined because of the DLT at the starting dose.

TNFSF11 (or RANKL) shows high expression in CAFs and osteoblastic OS cells in OS, and osteoblasts in GCTB. This study investigates pro-angiogenic genes in GCTB and OS and suggests that these genes and their expression patterns are cell-type specific and could provide potential prognostic biomarkers and cell type target treatment for GCTB and OS.

The angiogenic characteristics of meningiomas may be suppressed by using antiangiogenic drugs to prevent neovascularization, thus improving prognosis.

Taken together, the above data indicates that XIST serves as an oncogenic factor to enhance the growth and invasion of OSCC cells by targeting the miR-133a/VEGFB axis.

In a phase II window study of Olaparib alone or with Cisplatin or with Durvalumab or no treatment, we performed transcriptomic profiling to evaluate the modulation of tumor microenvironment post- treatment. Conclusions Our results uncover macrophage-mediated immune suppression as a liability of PARP inhibitor treatment. These results are consistent with data showing that targeting immunosuppressive macrophages overcomes PARP inhibitor resistance in BRCA1-associated triple-negative breast cancer.

NDRG1-induced VEGFA exerts protective effects in GBM via the VEGFA/VEGFR2 pathway. Therefore, targeting both NDRG1 and VEGFA may represent a novel therapy for the treatment of GBM.