Open AccessMicrovascular Changes in the Stroma of Human Colorectal Carcinomas: Ultrastructural Histochemical Study
Author(s) -
Ohtani Haruo,
Sasano Nobuaki
Publication year - 1989
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1989.tb02320.x
Subject(s) - stroma , pathology , ultrastructure , biology , angiogenesis , ulex europaeus , endothelial stem cell , epithelium , stromal cell , endothelium , lumen (anatomy) , monoclonal antibody , lectin , immunohistochemistry , antibody , agglutinin , microbiology and biotechnology , cancer research , immunology , medicine , in vitro , biochemistry , endocrinology
Ultrastructural histochemical studies were performed using Ulex europaeus agglutinin‐I lectin (UEA‐I) and anti‐endothelial monoclonal antibody BMA 120 in order to morphologically characterize the microvasculature of human colorectal carcinomas. In the normal mucosa, UEA‐I and BMA 120 were bound to luminal plasma membrane of endothelial cells, usually continuously. Capillaries in the stroma of invasive adenocarcinomas showed remarkable structural changes such as swelling of endothelial cells with well‐developed cell organelles and narrowing of the lumen. Reaction products for UEA‐I and BMA 120 were both observed along the luminal plasma membrane of endothelial cells, usually discontinuously, partially retaining the features of normal capillaries. Furthermore, we have confirmed an occurrence of solid capillary buds composed of a strand of large endothelial cells with a trace of lumen. They showed almost no reactivity to UEA‐I and BMA 120. Conventional electron microscopy revealed that they were present frequently in invasive carcinomas, but infrequently in intramucosal carcinomas and inflammatory lesions. Our results suggest that the stroma of invasive colorectal carcinomas abounds in immature capillaries and their precursors, which may indicate active tumor‐induced angiogenesis.