Phosphatidylserine is a marker of tumor vasculature and a potential target for cancer imaging and therapy

Ran, Sophia; Thorpe, Philip E.

doi:10.1016/s0360-3016(02)03928-7

Cited by 239 publications

(200 citation statements)

References 28 publications

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“…S2A). We have previously shown that phosphatidylserine-positive tumor endothelial cells seem to be viable: They lack cytoplasmic and nuclear markers of apoptosis, are morphologically intact, and the vessels transport solutes and blood (42). The percentage of phosphatidylserine-positive tumor vessels was increased markedly 48 hours after administration of a single dose of docetaxel with peak levels of 61% in PC3 tumors ( Fig.…”

Section: Exposure Of Phosphatidylserine On Tumor Blood Vessels and Ammentioning

confidence: 88%

Phosphatidylserine-Targeting Antibody Induces M1 Macrophage Polarization and Promotes Myeloid-Derived Suppressor Cell Differentiation

Yin

Huang

Lynn

et al. 2013

Cancer Immunology Research

123

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Multiple tumor-derived factors are responsible for the accumulation and expansion of immune-suppressing myeloid-derived suppressor cells (MDSC) and M2-like tumor-associated macrophages (TAM) in tumors. Here, we show that treatment of tumor-bearing mice with docetaxel in combination with the phosphatidylserine-targeting antibody 2aG4 potently suppressed the growth and progression of prostate tumors, depleted M2-like TAMs, and MDSCs, and increased the presence of M1-like TAMs and mature dendritic cells in the tumors. In addition, the antibody markedly altered the cytokine balance in the tumor microenvironment from immunosuppressive to immunostimulatory. In vitro studies confirmed that 2aG4 repolarized TAMs from an M2-to an M1-like phenotype and drove the differentiation of MDSCs into M1-like TAMs and functional dendritic cells. These data suggest that phosphatidylserine is responsible for the expansion of MDSCs and M2-like TAMs in tumors, and that bavituximab, a phosphatidylserine-targeting antibody currently in clinical trials for cancer, could reverse this process and reactivate antitumor immunity. Cancer Immunol Res; 1(4); 256-68. Ó2013 AACR.

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Section: Exposure Of Phosphatidylserine On Tumor Blood Vessels and Ammentioning

confidence: 88%

Phosphatidylserine-Targeting Antibody Induces M1 Macrophage Polarization and Promotes Myeloid-Derived Suppressor Cell Differentiation

Yin

Huang

Lynn

et al. 2013

Cancer Immunology Research

123

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“…For example, elevated production of ROS is a common feature of solid tumors. Along with hypoxic conditions, ROS can elevate cytosolic Ca 2+ levels and lead to the activation of Ca 2+ -dependent scramblases and floppases to promote the exposure of PS and, to a lesser extent, PE on the lumenal surface of tumor vascular endothelium [28][29][30] ( Figure 2d). In addition to dysregulation of phospholipid transporters, altered gene expression of multidrug-resistant proteins (ABC transporters), which can also function to outwardly transport phospholipids across the membrane, has been shown to increase PS exposure on the cell surface of certain tumor cell types.…”

Section: Alteration Of the Phospholipid Code During Tumor Progressionmentioning

confidence: 99%

The phospholipid code: a key component of dying cell recognition, tumor progression and host–microbe interactions

2015

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A significant effort is made by the cell to maintain certain phospholipids at specific sites. It is well described that proteins involved in intracellular signaling can be targeted to the plasma membrane and organelles through phospholipid-binding domains. Thus, the accumulation of a specific combination of phospholipids, denoted here as the 'phospholipid code', is key in initiating cellular processes. Interestingly, a variety of extracellular proteins and pathogen-derived proteins can also recognize or modify phospholipids to facilitate the recognition of dying cells, tumorigenesis and host-microbe interactions. In this article, we discuss the importance of the phospholipid code in a range of physiological and pathological processes.

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“…This is particularly problematic in tissue sections because tissue preparation (cutting and treatment with detergents) generates a high rate of false positives. Furthermore, PS externalization may not always be associated with cell death; it has been shown in living endothelial cells of tumor vasculature (Ran and Thorpe, 2002). PS externalization has been shown to be reversible in granulocytes and monocytes (Yang et al, 2002) and in cardiomyocytes subjected to brief episodes of ischemia (Kenis et al, 2010).…”

Section: Phosphatidylserine Exposurementioning

confidence: 99%

Visualizing Cell Death in Experimental Focal Cerebral Ischemia: Promises, Problems, and Perspectives

Zille

Farr

Przesdzing

et al. 2011

J Cereb Blood Flow Metab

121

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One of the hallmarks of stroke pathophysiology is the widespread death of many different types of brain cells. As our understanding of the complex disease that is stroke has grown, it is now generally accepted that various different mechanisms can result in cell damage and eventual death. A plethora of techniques is available to identify various pathological features of cell death in stroke; each has its own drawbacks and pitfalls, and most are unable to distinguish between different types of cell death, which partially explains the widespread misuse of many terms. The purpose of this review is to summarize the standard histopathological and immunohistochemical techniques used to identify various pathological features of stroke. We then discuss how these methods should be properly interpreted on the basis of what they are showing, as well as advantages and disadvantages that require consideration. As there is much interest in the visualization of stroke using noninvasive imaging strategies, we also specifically discuss how these techniques can be interpreted within the context of cell death.

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Phosphatidylserine is a marker of tumor vasculature and a potential target for cancer imaging and therapy

Cited by 239 publications

References 28 publications

Phosphatidylserine-Targeting Antibody Induces M1 Macrophage Polarization and Promotes Myeloid-Derived Suppressor Cell Differentiation

Phosphatidylserine-Targeting Antibody Induces M1 Macrophage Polarization and Promotes Myeloid-Derived Suppressor Cell Differentiation

The phospholipid code: a key component of dying cell recognition, tumor progression and host–microbe interactions

Visualizing Cell Death in Experimental Focal Cerebral Ischemia: Promises, Problems, and Perspectives

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