The morphological effects of the anti–tumor agents flavone acetic acid and 5,6–dimethyl xanthenone acetic acid on the colon 38 mouse tumor

Flavone acetic acid and 5,6-dimethyl xanthenone acetic acid have a broad spectrum of anti-tumor activity in mice, and act by stimulating immune cells and inhibiting tumor blood flow, resulting in hemorrhagic necrosis within 24 hrs. To study the evolution of hemorrhagic necrosis, subcutaneous Colon 3...

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Veröffentlicht in:Pathology 1994, Vol.26 (2), p.161-169
Hauptverfasser: Jonathan Zwi, L., Baguley, Bruce C., Gavin, John B., Wilson, William R.
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container_title Pathology
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creator Jonathan Zwi, L.
Baguley, Bruce C.
Gavin, John B.
Wilson, William R.
description Flavone acetic acid and 5,6-dimethyl xanthenone acetic acid have a broad spectrum of anti-tumor activity in mice, and act by stimulating immune cells and inhibiting tumor blood flow, resulting in hemorrhagic necrosis within 24 hrs. To study the evolution of hemorrhagic necrosis, subcutaneous Colon 38 tumors were examined by light and electron microscopy from 30 min to 24 hrs after treatment with these agents, and measurements of tumor energy metabolites made. The results show that both agents cause apoptosis beginning at 30 min, and that by 4 hrs necrosis supervenes, accompanied by rupture of tumor blood vessels. The absence of early endothelial cell damage or thrombosis suggests that vessel rupture, and consequent loss of blood flow and energy metabolite depletion, is caused by loss of extravascular mechanical support by the tumor parenchyma.
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To study the evolution of hemorrhagic necrosis, subcutaneous Colon 38 tumors were examined by light and electron microscopy from 30 min to 24 hrs after treatment with these agents, and measurements of tumor energy metabolites made. The results show that both agents cause apoptosis beginning at 30 min, and that by 4 hrs necrosis supervenes, accompanied by rupture of tumor blood vessels. The absence of early endothelial cell damage or thrombosis suggests that vessel rupture, and consequent loss of blood flow and energy metabolite depletion, is caused by loss of extravascular mechanical support by the tumor parenchyma.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>8090588</pmid><doi>10.1080/00313029400169411</doi><tpages>9</tpages></addata></record>
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source Taylor & Francis; MEDLINE; Alma/SFX Local Collection
subjects Adenocarcinoma - blood supply
Adenocarcinoma - metabolism
Adenocarcinoma - pathology
adenosine triphosphate
Adenosine Triphosphate - metabolism
Animals
Apoptosis - drug effects
blood vessels
Colonic Neoplasms - blood supply
Colonic Neoplasms - metabolism
Colonic Neoplasms - pathology
flavone acetic acid
Flavones
Flavonoids - pharmacology
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Inbred DBA
Microscopy, Electron
Necrosis
neoplasms
Phosphocreatine - metabolism
Xanthenes - pharmacology
xanthenone acetic acid
Xanthones
title The morphological effects of the anti–tumor agents flavone acetic acid and 5,6–dimethyl xanthenone acetic acid on the colon 38 mouse tumor
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