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[“Organic Hair Growth Inhibitor

Second, intensity of neovascularization cannot be determined by gross inspection of a tumor.A white neurof ibrosarcoma of one or more cubic centimeters may have a microvessel density by microscopy that is similar to the microvessel density of a reddish hepatic carcinoma of similar size, except in the whitish tumor, the vessels are more compressed.Third, the lower the vascularity of a tumor, the more susceptible it appears to be to antiangiogenic therapy.Highly vascularized tumors may require higher doses of an angiogenesis inhibitor or combinations of angiogenesis inhibitors to achieve a tumor response.In the past years, microvessel density quantif ication has become a reproducible prognostic factor for risk of metastasis.The most plausible explanation for this correlation is that most human tumors contain angiogenic and nonangiogenic cells, both of which enter the circulation, but only the angiogenic cells can form detectable metastases.Although there are a few reports in which microvessel density did not correlate with risk of metastasis or mortality, this could be due to technical or http://inhibit09.online/archives/57 biologic causes.For example, if a primary tumor that was the source of a biopsy for quantif ication of microvessel density, generated a high level of circulating angiogenesis inhibitor, which suppressedhttp://inhibit09.online/archives/51 growth of distant metastases, the prognostic value of this test could be negated.In tumors, however, degree of vascularization and tumor growth are loosely coupled, or even uncoupled.This may be because in tumor cells, expression of angiogenic factors, such as VEGF, are no longer regulated by oxygen concentration.During tumor reg ression under antiangiogenic therapy, microvessel density may decrease if capillary dropout exceeds tumor cell dropout, increase if tumor cell dropout exceeds capillary dropout, or, remain the same if disappearance of capillaries and tumor cells parallel each other. Figure shows osteosarcomas taken from mice treated with endostatin until there was more than a inhibition of growth.Despite the fact that this drug inhibitedgrowth of both treated tumors depicted, the intensity of vascularization after treatment differed signif icantly between the tumors.Microvascular density was quantif ied over the entire histological section rather than over vascular hotspots, in order to avoid the effects of heterogeneity of vascularization in the tissue sample.Microvascular density dropped sharply in one treated tumor but rose slightly in the second, yet both tumors were equivalently reduced in size by the treatment relative to control.Thus, detection of a decrease in microvessel density during treatment with an angiogenesis inhibitor, suggests that the agent is active.However, the absence of a decrease in microvessel density does not indicate that the agent is ineffective.Human osteosarcoma xenografts were treated with the angiogenic inhibitor endostatin.Shown are tumor size, vascularization as detected by an antibody to CD, and vascular density quantif ied by digitized imaging for a control and two endostatintreated tumors.Endostatin signif icantly inhibited tumor growth in treated tumors.Despite the fact that endostatin inhibited both treated tumors, the posttreatment level of vascularization of the two tumors varies considerably.Entire tumor sections were scored for microvascular density rather than just vascular hotspots, thereby avoiding effects of heterogeneity in vascularization over the sample.Sections were scored by imaging as many microscopefields at X as it took to cover the entire sections.

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