Cancer cells compress intratumour vessels

Padera, Timothy P.; Stoll, Brian R.; Tooredman, Jessica B.; Capen, Diane E.; Tomaso, Emmanuelle di; Jain, Rakesh K.

doi:10.1038/427695a

Cited by 757 publications

(585 citation statements)

References 8 publications

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“…These results are supported by well-known clinical observations (e.g., [148]). As the tumor grows and engulfs vessels in its vicinity, the tumor may compress the vessels [155] and disrupt flow of nutrients, leading to further necrosis and even temporary mass and vascular regression [211,99]. A growing tumor contends with increasing mechanical resistance from normal brain tissue, which has physical properties resembling a gel [153,68].…”

Section: Resultsmentioning

confidence: 99%

Nonlinear Modeling and Simulation of Tumor Growth

Cristini

Frieboes

et al. 2008

Selected Topics in Cancer Modeling

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Section: Resultsmentioning

confidence: 99%

Nonlinear Modeling and Simulation of Tumor Growth

Cristini

Frieboes

et al. 2008

Selected Topics in Cancer Modeling

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“…In addition, reduced PVC coverage, EC dissociation, and an excess of vesiculo-vaculor organelles (VVOs) results in marked tumor vessel permeability, with excess extravasation of fluid and protein into the extracellular compartment (Jain 2005b). This leakiness, together with a relative absence of functional intratumoral lymphatic vessels (Padera et al 2004;Hagendoorn et al 2006), leads to a marked increase in the tumor interstitial fluid pressure (IFP) to a level that equilibrates with intravascular pressure, which results in reduced transvascular flow (Boucher et al 1990Roh et al 1991;Less et al 1992;Leunig et al 1992;Stohrer et al 2000;Tong et al 2004;Willett et al 2004). Furthermore, the compressive forces applied by the proliferating mass of cancer cells can cause vascular compression and collapse (Padera et al 2004).…”

Section: Vascular Abnormalities In Solid Tumorsmentioning

confidence: 99%

Vascular Normalization as a Therapeutic Strategy for Malignant and Nonmalignant Disease

Goel

Wong

Jain

2011

Cold Spring Harbor Perspectives in Medicine

300

267

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Pathological angiogenesis-driven by an imbalance of pro-and antiangiogenic signaling-is a hallmark of many diseases, both malignant and benign. Unlike in the healthy adult in which angiogenesis is tightly regulated, such diseases are characterized by uncontrolled new vessel formation, resulting in a microvascular network characterized by vessel immaturity, with profound structural and functional abnormalities. The consequence of these abnormalities is further modification of the microenvironment, often serving to fuel disease progression and attenuate response to conventional therapies. In this article, we present the "vascular normalization" hypothesis, which states that antiangiogenic therapy, by restoring the balance between pro-and antiangiogenic signaling, can induce a more structurally and functionally normal vasculature in a variety of diseases. We present the preclinical and clinical evidence supporting this concept and discuss how it has contributed to successful treatment of both solid tumors and several benign conditions.

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“…For example, an endothelial cell within a tumor microenvironment will experience hypoxia that alone can change the expression of up to 2000 genes (Dachs and Chaplin, 1998). Tumors also show nutrient (for example, glucose) deprivation, acidic extracellular pH, high interstitial pressure (Helmlinger et al, 1997), excess of pro-angiogenic activity (for example, vascular endothelial (VE) growth factor) and increased mechanical compression (Padera et al, 2004). Each of these factors may influence the transcriptome.…”

Section: Introductionmentioning

confidence: 99%