Drug delivery strategies in maximizing anti-angiogenesis and anti-tumor immunity

Lai, Victoria; Neshat, Sarah Y.; Rakoski, Amanda; Pitingolo, James; Doloff, Joshua C.

doi:10.1016/j.addr.2021.113920

Cited by 25 publications

(16 citation statements)

References 146 publications

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“…It is well acknowledged that the tumor angiogenesis and the tumor microenvironment share a strong correlation. As tumor growth depends on tumor angiogenesis, metronomic chemotherapy has also been shown to irritate the antitumor immune response and inhibit the tumor angiogenesis [ 46 ]. It is necessary to evaluate the antiangiogenetic effect of MCL in a dose-dependent manner.…”

Section: Resultsmentioning

confidence: 99%

Mecheliolide elicits ROS-mediated ERS driven immunogenic cell death in hepatocellular carcinoma

Sun

et al. 2022

Redox Biology

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Section: Resultsmentioning

confidence: 99%

Mecheliolide elicits ROS-mediated ERS driven immunogenic cell death in hepatocellular carcinoma

Sun

et al. 2022

Redox Biology

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“…In murine glioma models, CPA can induce immunogenic cell death when administered on a metronomic, medium-dose intermittent chemotherapy (MEDIC) schedule (24,25), leading to elimination of GL261 gliomas implanted in syngeneic mice and activation of long-term antitumor immunity (26). Other CPA treatment schedules are much less effective at inducing immune cell recruitment in glioma models (27), a finding that was recently validated in breast cancer models (28).…”

Section: Aacrjournalsorgmentioning

confidence: 99%

Type-I Interferon Signaling Is Essential for Robust Metronomic Chemo-Immunogenic Tumor Regression in Murine Breast Cancer

Vergato

Doshi

Roblyer

et al. 2022

Cancer Research Communications

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Many patients with breast cancer have a poor prognosis with limited therapeutic options. Here, we investigated the potential of chemo-immunogenic therapy as an avenue of treatment. We utilized two syngeneic mouse mammary tumor models, 4T1 and E0771, to examine the chemo-immunogenic potential of cyclophosphamide and the mechanistic contributions of cyclophosphamide-activated type-I interferon (IFN) signaling to therapeutic activity. Chemically-activated cyclophosphamide induced robust IFNα/β receptor-1-dependent signaling linked to hundreds of IFN-stimulated gene responses in both cell lines. Further, in 4T1 tumors, cyclophosphamide given on a medium-dose, 6-day intermittent metronomic schedule induced strong IFN signaling but comparatively weak immune cell infiltration associated with long-term tumor growth stasis. Induction of IFN signaling was somewhat weaker in E0771 tumors but was followed by widespread downstream gene responses, robust immune cell infiltration and extensive, prolonged tumor regression. The immune dependence of these effective anti-tumor responses was established by CD8 T-cell immunodepletion, which blocked cyclophosphamide-induced E0771 tumor regression and led to tumor stasis followed by regrowth. Strikingly, IFNα/β receptor-1 antibody blockade was even more effective in preventing E0771 immune cell infiltration and blocked the major tumor regression induced by cyclophosphamide treatment. Type-I IFN signaling is thus essential for the robust chemo-immunogenic response of these tumors to cyclophosphamide administered on a metronomic schedule.

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“…Tumor development, invasion and metastasis are highly dependent on neovascularization ( Goncalves et al, 2021 ; Rimini and Casadei-Gardini, 2021 ). Under physiological conditions, angiogenesis is intricately and precisely regulated by multiple molecules and mechanisms that allow the formation of highly tissue-specific, structured and hierarchical vascular networks to sustain the physiological processes of embryonic development, growth and tissue repair ( Lai et al, 2021 ; Martin and Gurevich, 2021 ; Narasimhan et al, 2021 ). However, tumor cells are able to release large amounts of vascular endothelial growth factor (VEGF) and inhibit the secretion of angiogenesis inhibitory factor, which unbalances the regulatory mechanism of angiogenesis, resulting in rapid, uncontrolled proliferation of tumor neovascularization and a large, abnormally disordered replenishment network ( Liu Y. et al, 2021 ; Uemura et al, 2021 ; Zhu et al, 2021 ).…”

Section: Biological Function and Molecular Mechanism Of Circular Rnas In Glioblastomamentioning

confidence: 99%

Research Progress of circRNAs in Glioblastoma

Guo

Piao

2021

Front. Cell Dev. Biol.

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Circular RNAs (circRNAs) are a class of single-stranded covalently closed non-coding RNAs without a 5′ cap structure or 3′ terminal poly (A) tail, which are expressed in a variety of tissues and cells with conserved, stable and specific characteristics. Glioblastoma (GBM) is the most aggressive and lethal tumor in the central nervous system, characterized by high recurrence and mortality rates. The specific expression of circRNAs in GBM has demonstrated their potential to become new biomarkers for the development of GBM. The specific expression of circRNAs in GBM has shown their potential as new biomarkers for GBM cell proliferation, apoptosis, migration and invasion, which provides new ideas for GBM treatment. In this paper, we will review the biological properties and functions of circRNAs and their biological roles and clinical applications in GBM.

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Drug delivery strategies in maximizing anti-angiogenesis and anti-tumor immunity

Cited by 25 publications

References 146 publications

Mecheliolide elicits ROS-mediated ERS driven immunogenic cell death in hepatocellular carcinoma

Mecheliolide elicits ROS-mediated ERS driven immunogenic cell death in hepatocellular carcinoma

Type-I Interferon Signaling Is Essential for Robust Metronomic Chemo-Immunogenic Tumor Regression in Murine Breast Cancer

Research Progress of circRNAs in Glioblastoma

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