Biology of Angiogenesis and Invasion in Glioma

Tate, Matthew C.; Aghi, Manish K.

doi:10.1016/j.nurt.2009.04.001

Cited by 193 publications

(158 citation statements)

References 127 publications

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“…Such phenomena may be due to findings from the dataset demonstrating that loss of NPAS3 expression increases expression of angiogenesis-promoting factors including FGFR2 and VEGFA, which are well characterized in the progression of astrocytomas. 47,48 Increased levels of vascular endothelial growth factor A are prominently identified in high-grade astrocytomas, 47,48 which correlate well with absence of NPAS3 expression observed in these lesions.…”

Section: Discussionmentioning

confidence: 80%

NPAS3 Demonstrates Features of a Tumor Suppressive Role in Driving the Progression of Astrocytomas

Moreira

Kiehl

et al. 2011

The American Journal of Pathology

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Malignant astrocytomas, the most common primary brain tumors, are predominantly fatal. Improved treatments will require a better understanding of the biological features of high-grade astrocytomas. To better understand the role of neuronal PAS 3 (NPAS3) in diseases in human beings, it was investigated as a candidate for astrocytomagenesis based on the presence of aberrant protein expression in greater than 70% of a human astrocytoma panel (n ‫؍‬ 433) and most notably in surgically resected malignant lesions. In subsequent functional studies, it was concluded that NPAS3 exhibits features of a tumor-suppressor, which drives the progression of astrocytomas by modulating the cell cycle, proliferation, apoptosis, and cell migration/invasion and has a further influence on the viability of endothelial cells. Of clinical importance, absence of NPAS3 expression in glioblastomas was a significantly negative prognostic marker of survival. In addition, malignant astrocytomas lacking NPAS3 expression demonstrated loss of function mutations, which were associated with loss of heterozygosity. While overexpressed NPAS3 in malignant glioma cell lines significantly suppressed transformation, the converse decreased expression considerably induced more aggressive growth. In addition, knockdown NPAS3 expression in a human astrocyte cell line in concert with the human papillomavirus E6 and E7 oncogenes induced growth of malignant astrocytomas. In conclusion, NPAS3 drives the progression of human malignant astrocytomas as a tumor suppressor and is a negative prognostication marker for survival.

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Section: Discussionmentioning

confidence: 80%

NPAS3 Demonstrates Features of a Tumor Suppressive Role in Driving the Progression of Astrocytomas

Moreira

Kiehl

et al. 2011

The American Journal of Pathology

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“…Vasculogenesis involves the de novo formation of blood vessels that utilize bone marrow-derived endothelial progenitor cells (Jain et al, 2007). Angiogenesis is the production of new blood vessels by endothelial cells from pre-existing vessels and is considered to be the primary mode of vessel formation in gliomas (Tate and Aghi, 2009). Endothelial cells play a major role in brain tumor angiogenesis.…”

Section: Brain Tumor Stem-like Cellsmentioning

confidence: 99%

“…Endothelial cells play a major role in brain tumor angiogenesis. During the angiogenic process, degradation of the vessel membrane and extracellular matrix (ECM) facilitates endothelial cell activation and migration toward tumor cells expressing proangiogenic factors (Tate and Aghi, 2009). Activated endothelial cells up-regulate factors involved in cell surface adhesion and migration to ultimately promote cell adhesion, migration, and survival (Brooks et al, 1994;Gladson, 1996).…”

Section: Brain Tumor Stem-like Cellsmentioning

confidence: 99%

The brain tumor microenvironment

Charles

Holland

Gilbertson

et al. 2011

Glia

693

327

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High-grade brain tumors are heterogeneous with respect to the composition of bona fide tumor cells and with respect to a range of intermingling parenchymal cells. Glioblastomas harbor multiple cell types, some with increased tumorigenicity and stem cell-like capacity. The stem-like cells may be the cells of origin for tumor relapse. However, the tumor-associated parenchymal cells such as vascular cells, microglia, peripheral immune cells, and neural precursor cells also play a vital role in controlling the course of pathology. In this review, we describe the multiple interactions of bulk glioma cells and glioma stem cells with parenchymal cell populations and highlight the pathological impact as well as signaling pathways known for these types of cell-cell communication. The tumor-vasculature not only nourishes glioblastomas, but also provides a specialized niche for these stem-like cells. In addition, microglial cells, which can contribute up to 30% of a brain tumor mass, play a role in glioblastoma cell invasion. Moreover, non-neoplastic astrocytes can be converted into a reactive phenotype by the glioma microenvironment and can then secrete a number of factors which influences tumor biology. The young brain may have the capacity to inhibit gliomagenesis by the endogenous neural precursor cells, which secrete tumor suppressive factors. The factors, pathways, and interactions described in this review provide a new prospective on the cell biology of primary brain tumors, which may ultimately generate new treatment modalities. However, our picture of the multiple interactions between parenchymal and tumor cells is still incomplete. V

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“…Angiogenesis, the process of formation of new blood vessels from existing blood capillaries, is one major contributor to glioblastoma multiforme carcinogenesis and helps the tumor cells to flourish (Tate & Aghi, 2009). To maintain the demand of food, nutrients, and oxygen, tumor cells recruit new blood vessels from those already present (Folkman, 1971;Tate & Aghi, 2009).…”

Section: Angiogenesismentioning

confidence: 99%

“…To maintain the demand of food, nutrients, and oxygen, tumor cells recruit new blood vessels from those already present (Folkman, 1971;Tate & Aghi, 2009). Likewise, malignant gliomas are highly vascularised and have an angiogenic phenotype (Jain et al, 2007).…”

Section: Angiogenesismentioning

confidence: 99%