| 1. |
- Dahl Jensen, Lasse, et al.
(author)
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Zebrafish Models to Study Hypoxia-Induced Pathological Angiogenesis in Malignant and Nonmalignant Diseases
- 2011
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In: Birth Defects Research. Part C: Embryo Today Reviews. - : John Wiley and Sons.Ltd. - 1542-975X .- 1542-9768. ; 93:2, s. 182-193
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Research review (peer-reviewed)abstract
- Most in vivo preclinical disease models are based on mouse and other mammalian systems. However, these rodent-based model systems have considerable limitations to recapitulate clinical situations in human patients. Zebrafish have been widely used to study embryonic development, behavior, tissue regeneration, and genetic defects. Additionally, zebrafish also provides an opportunity to screen chemical compounds that target a specific cell population for drug development. Owing to the availability of various genetically manipulated strains of zebrafish, immune privilege during early embryonic development, transparency of the embryos, and easy and precise setup of hypoxia equipment, we have developed several disease models in both embryonic and adult zebrafish, focusing on studying the role of angiogenesis in pathological settings. These zebrafish disease models are complementary to the existing mouse models, allowing us to study clinically relevant processes in cancer and nonmalignant diseases, which otherwise would be difficult to study in mice. For example, dissemination and invasion of single human or mouse tumor cells from the primary site in association with tumor angiogenesis can be studied under normoxia or hypoxia in zebrafish embryos. Hypoxia-induced retinopathy in the adult zebrafish recapitulates the clinical situation of retinopathy development in diabetic patients or age-related macular degeneration. These zebrafish disease models offer exciting opportunities to understand the mechanisms of disease development, progression, and development of more effective drugs for therapeutic intervention.
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| 2. |
- Cao, Yihai
(author)
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Angiogenesis and Vascular Functions in Modulation of Obesity, Adipose Metabolism, and Insulin Sensitivity
- 2013
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In: Cell Metabolism. - : CELL PRESS, 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA. - 1550-4131 .- 1932-7420. ; 18:4, s. 478-489
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Research review (peer-reviewed)abstract
- White and brown adipose tissues are hypervascularized and the adipose vasculature displays phenotypic and functional plasticity to coordinate with metabolic demands of adipocytes. Blood vessels not only supply nutrients and oxygen to nourish adipocytes, they also serve as a cellular reservoir to provide adipose precursor and stem cells that control adipose tissue mass and function. Multiple signaling molecules modulate the complex interplay between the vascular system and the adipocytes. Understanding fundamental mechanisms by which angiogenesis and vasculatures modulate adipocyte functions may provide new therapeutic options for treatment of obesity and metabolic disorders by targeting the adipose vasculature.
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| 3. |
- Cao, Yihai
(author)
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Erythropoietin in cancer: a dilemma in risk therapy
- 2013
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In: Trends in endocrinology and metabolism. - : Elsevier. - 1043-2760 .- 1879-3061. ; 24:4, s. 190-199
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Research review (peer-reviewed)abstract
- Erythropoietin (EPO) is a frequently prescribed drug for treatment of cancer-related and chemotherapy-induced anemia in cancer patients. Paradoxically, recent preclinical and clinical studies indicate that EPO could potentially accelerate tumor growth and jeopardize survival in cancer patients. In this review I critically discuss the current knowledge and broad biological functions of EPO in association with tumor growth, invasion, and angiogenesis. The emphasis is focused on discussing the complex interplay between EPO and other tumor-derived factors in angiogenesis, tumor growth, invasion, and metastasis. Understanding the multifarious functions of EPO and its reciprocal relation with other signaling pathways is crucial for developing more effective agents for cancer therapy and for minimizing risks for cancer patients.
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| 4. |
- Cao, Yihai, et al.
(author)
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Forty-Year Journey of Angiogenesis Translational Research
- 2011
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In: Science Translational Medicine. - : American Association for the Advancement of Science. - 1946-6234 .- 1946-6242. ; 3:114
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Research review (peer-reviewed)abstract
- Forty years ago, Judah Folkman predicted that tumor growth is dependent on angiogenesis and that inhibiting this process might be a new strategy for cancer therapy. This hypothesis formed the foundation of a new field of research that represents an excellent example of how a groundbreaking scientific discovery can be translated to yield benefits for patients. Today, antiangiogenic drugs are used to treat human cancers and retinal vascular diseases. Here, we guide readers through 40 years of angiogenesis research and discuss challenges of antiangiogenic therapy.
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| 5. |
- Cao, Yihai
(author)
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Future options of anti-angiogenic cancer therapy
- 2016
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In: CHINESE JOURNAL OF CANCER. - : SUN YAT SEN UNIV MED SCI WHO. - 1000-467X .- 1944-446X. ; 35:21
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Research review (peer-reviewed)abstract
- In human patients, drugs that block tumor vessel growth are widely used to treat a variety of cancer types. Many rigorous phase 3 clinical trials have demonstrated significant survival benefits; however, the addition of an anti-angiogenic component to conventional therapeutic modalities has generally produced modest survival benefits for cancer patients. Currently, it is unclear why these clinically available drugs targeting the same angiogenic pathways produce dissimilar effects in preclinical models and human patients. In this article, we discuss possible mechanisms of various anti-angiogenic drugs and the future development of optimized treatment regimens.
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| 6. |
- Cao, Yihai
(author)
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Multifarious functions of PDGFs and PDGFRs in tumor growth and metastasis
- 2013
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In: Trends in Molecular Medicine. - : Elsevier. - 1471-4914 .- 1471-499X. ; 19:8, s. 460-473
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Research review (peer-reviewed)abstract
- Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) are frequently expressed in various tumors and their expression levels correlate with tumor growth, invasiveness, drug resistance, and poor clinical outcomes. Emerging experimental evidence demonstrates that PDGFs exhibit multiple functions in modulation of tumor growth, metastasis, and the tumor microenvironment by targeting malignant cells, vascular cells, and stromal cells. Understanding PDGF PDGFR-mediated molecular signaling may provide new mechanistic rationales for optimizing current cancer therapies and the development of future novel therapeutic modalities.
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