The contribution of tumor and host tissue factor expression to oncogene-driven gliomagenesis

Magnus, Nathalie; Meehan, Brian; Garnier, Delphine; Hashemi, Maryam; Montermini, Laura; Lee, Tae Hoon; Milsom, Chlöe; Pawliński, Rafał; Ohlfest, John R.; Anderson, G. Mark; Mackman, Nigel; Rak, Janusz

doi:10.1016/j.bbrc.2014.10.041

Cited by 20 publications

(15 citation statements)

References 32 publications

(66 reference statements)

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“…The concept that TF-PAR2 signaling is linked to integrin association emerged from the inhibitory properties of a unique monoclonal antibody, 10H10, that has minimal effects on FVIIa binding or TF procoagulant activity, but abolishes constitutive and FVIIa-induced interaction of TF with integrins (49). This antibody potently inhibits TF-FVIIa induction of proangiogenic cytokines and consistently blocks, unlike anti-coagulant anti-TF antibodies, angiogenesis and tumor growth of aggressive breast cancer, melanoma, and glioblastoma xenograft tumors (49;72;73). Genetic studies in spontaneously developing breast cancer in mice furthermore showed that PAR2 and TF cytoplasmic domain signaling have overlapping functions in tumor progression from adenoma to invasive carcinoma (53;54), a process requiring macrophage recruitment and angiogenesis.…”

Section: Tf Signaling In Tumorcells and Angiogenesismentioning

confidence: 99%

“…The distinct contributions of extravascular coagulation activation in the TME may limit efficacy of plasma protease inhibitor-dependent anticoagulants, like heparin, and make cancer-associated thrombosis more approachable with oral small molecular target selective anticoagulants. Although certain prostate cancer cells may utilize contact pathway activation for cancer-associated thrombosis (8), redundant coagulation activation by stromal cell TF (72) likely limits the utility of selective targeting the contact pathway as primary therapy for cancer-associated thrombosis.…”

Section: Targeting the Coagulant Pathways In Cancermentioning

confidence: 99%

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Targeting clotting proteins in cancer therapy – progress and challenges

Ruf

Rothmeier

Graf

2016

Thrombosis Research

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Cancer-associated thrombosis remains a significant complication in the clinical management of cancer and interactions of the hemostatic system with cancer biology continue to be elucidated. Here, we review recent progress in our understanding of tissue factor (TF) regulation and procoagulant activation, TF signaling in cancer and immune cells, and the expanding roles of the coagulation system in stem cell niches and the tumor microenvironment. The extravascular functions of coagulant and anti-coagulant pathways have significant implications not only for tumor progression, but also for the selection of appropriate target specific anticoagulants in the therapy of cancer patients.

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Section: Tf Signaling In Tumorcells and Angiogenesismentioning

confidence: 99%

Section: Targeting the Coagulant Pathways In Cancermentioning

confidence: 99%

Targeting clotting proteins in cancer therapy – progress and challenges

Ruf

Rothmeier

Graf

2016

Thrombosis Research

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“…To explore whether overexpression of BTG2 proteins represses the formation and growth of HCC cell xenografts in vivo, we transplanted hepatoma cells into nude mice as previously described (24). Our data revealed that overexpression of BTG2 per se did not have a notable effect on tumor growth in nude mice 21 days after tumor injection (Fig.…”

Section: Btg2 Overexpression Sensitizes Huh7 Cells To Radiation-inducmentioning

confidence: 90%

Expression of B-cell translocation gene 2 is associated with favorable prognosis in hepatocellular carcinoma patients and sensitizes irradiation-induced hepatocellular carcinoma cell apoptosis in vitro and in nude mice

Chen¹,

Chen²,

Zhang³

et al. 2017

Oncology Letters

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Abstract. B-cell translocation gene 2 (BTG2) proteins have been reported to be putative tumor suppressors in various cancer types. The present study first assessed BTG2 expression in 44 human liver cancer tissue specimens, then investigated BTG2 expression in the regulation of hepatocellular carcinoma (HCC) cell apoptosis with or without radiotherapy in vitro and in vivo. The results revealed that BTG2 protein expression was significantly reduced in HCC tissues, and associated with better survival for HCC patients (P=0.05). BTG2 overexpression also sensitized Huh7 cells to radiation-induced apoptosis in vitro and in a nude mouse model, although restoration of BTG2 expression per se did not affect the viability and apoptosis of HCC cells. Future studies would confirm the role of BTG2 in hepatoma, and further develop BTG2 as a therapeutic strategy for controlling HCC.

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“…Previous studies have linked tumor cell-associated TF expression to epithelial-to-mesenchymal transition (EMT), as well as the recruitment of vascular and myeloid cells, suggesting that TF could influence the development of a supportive tumor stroma, including angiogenesis and a protumorigenic inflammatory milieu. [22][23][24][25][26][27] TF expressed by malignant cells has been proposed to promote tumorigenesis and tumor growth through coagulation-dependent and -independent mechanisms. TF initiates coagulation by binding activated factor VIIa.…”

Section: Role Of Tissue Factor In Tumorigenesis and Tumor Growthmentioning

confidence: 99%

Cancer-Associated Thrombosis: A Two-Way Street

Sharma

Flick

Palumbo

2019

Semin Thromb Hemost

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Pathological activation of the coagulation system occurs with virtually all forms of cancer, particularly epithelial malignancies. Accordingly, thrombosis is one of the most common comorbidities associated with cancer. Indeed, cancer-associated thromboembolism is the second leading cause of death for cancer patients, second only to the cancer itself. The identification of specific molecular mechanisms whereby tumor cells activate the coagulation system and drive thrombosis has been an active area of investigation for several decades. Studies in animal models and human trials have revealed that there is a bidirectional relationship between coagulation factor activity and cancer, whereby the pathological hemostatic system activation associated with cancer not only promotes thromboembolism but also drives progression of the malignancy. Numerous studies indicate that factors up and down the clotting cascade can contribute to various stages of cancer, including tumorigenesis, primary tumor growth, and metastasis. Although there are some mechanistic points of commonality, there are also clearly context-dependent contributions of coagulation components to cancer progression dependent on the type of cancer and stage of disease. It is also notable that in some instances, coagulation factors appear to contribute to cancer progression independently of their traditional roles in hemostasis and thrombosis. Here, the authors review the current state of the field with regard to hemostatic factor-driven cancer pathogenesis.

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The contribution of tumor and host tissue factor expression to oncogene-driven gliomagenesis

Cited by 20 publications

References 32 publications

Targeting clotting proteins in cancer therapy – progress and challenges

Targeting clotting proteins in cancer therapy – progress and challenges

Expression of B-cell translocation gene 2 is associated with favorable prognosis in hepatocellular carcinoma patients and sensitizes irradiation-induced hepatocellular carcinoma cell apoptosis in vitro and in nude mice

Cancer-Associated Thrombosis: A Two-Way Street

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