Abl expression in human fetal and adult tissues, tumours, and tumour microvessels

J Pathol. 1997 Nov;183(3):325-9. doi: 10.1002/(SICI)1096-9896(199711)183:3<325::AID-PATH941>3.0.CO;2-A.

Abstract

Abl kinases encoded by the abl oncogenes inhibit apoptosis without affecting cell proliferation. The aim of this study was to examine a wide range of normal fetal and adult human tissues and a variety of tumour types for Abl immunoreactivity. Sections from 193 paraffin blocks of normal fetal and adult tissues and 72 blocks from representative tumours were stained immunohistochemically using a polyclonal antibody to c-Abl/Bcr-Abl oncoprotein. Weak Abl immunoreactivity was observed in many adult tissues. Moderately intense or strong staining (cytoplasmic, nuclear or membranous) was consistently seen in hyaline cartilage, adipocytes, and ciliated epithelium. In fetal tissues, there was a broadly similar staining pattern, but Abl expression was also seen in muscle (all types) and occasionally in endothelial cells. The most intense staining was seen in sites of endochondral ossification and in the umbilical cord stroma. Negatively staining tissues included epidermis and squamous mucosa, lymph nodes, tonsil, spleen, hepatocytes, and adrenals. Most tumours showed focal or weak Abl immunoreactivity. The most intense staining was seen in chondrosarcoma, liposarcoma, and diffuse gastric (signet ring) adenocarcinoma. In the latter two tumour types, Abl expression was also observed in tumour microvessels. These results suggest that Abl not only functions as an apoptosis inhibitor, but also may have a role in connective tissue maturation and differentiation and in tumour growth and angiogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Chondrocytes / metabolism
  • Female
  • Fetus / metabolism*
  • Humans
  • Immunoenzyme Techniques
  • Neoplasm Proteins / metabolism
  • Neoplasms / blood supply
  • Neoplasms / metabolism*
  • Neovascularization, Pathologic / metabolism*
  • Proto-Oncogene Proteins c-abl / metabolism*
  • Tissue Distribution

Substances

  • Neoplasm Proteins
  • Proto-Oncogene Proteins c-abl