2 research outputs found
Immunohistochemical detection of somatostatin receptor subtypes sst1 and sst2A in human somatostatin receptor positive tumors
Although in situ hybridization has been used to examine the distribution
of messenger RNA for somatostatin receptor subtypes (sst) in human tumors,
the cellular localization of sst1 and sst2A receptors has not been
reported. In this study, we describe the cellular localization of human
sst1 and sst2A receptor proteins in both cryostat- and paraffin-embedded
sections of 25 human tumor tissues using two recently developed polyclonal
antibodies. Six somatostatin (SS) receptor (SSR) positive tumors (two
gastrinomas, three carcinoids, one pheochromocytoma) and one SSR negative
tumor (renal cell carcinoma), selected by positive and negative SSR
autoradiography, respectively, were studied by both immunohistochemistry
and Western blot analysis. The six SSR positive tumors expressed sst2A,
while 4 of 5 expressed sst1 as well. The SSR negative tumor did not
express either sst1 or sst2A. Western blot analysis of wheat germ
agglutinin purified membrane proteins confirmed the presence of the sst1
and sst2A glycosylated receptors. The paraffin-embedded sections gave best
information with respect to the subcellular localization. Sst1
immunoreactivity was observed both on the membrane and in the cytoplasm,
while sst2A showed predominantly membrane-associated immunoreactivity.
This subcellular distribution of sst1 or sst2A receptors was confirmed in
paraffin-embedded sections of 8 additional intestinal carcinoids, 5
gastrinomas and 5 pheochromocytomas. Sst1 receptors were detected in 7 out
of 8 carcinoids, in all gastrinomas, and in 4 out of 5 pheochromocytomas,
while 6 out of 8 carcinoids, all gastrinomas, and 3 out of 5
pheochromocytomas expressed sst2A receptors. In conclusion, sst1 and sst2A
receptors show a differential subcellular localization in human SSR
positive tumors. The use of SSR subtype selective antibodies to detect the
subcellular distribution of SSR subtypes in individual tumor cells is an
important step forward to understand more about the pathophysiological
role of the different SSR subtypes in human tumors
Gain of chromosome 8q is a frequent finding in pleuropulmonary blastoma.
Contains fulltext :
53430.pdf (publisher's version ) (Closed access)Pleuropulmonary blastomas are rare malignant intrathoracic tumors of early childhood. They appear as a pulmonary- and/or pleural-based mass and their pathogenesis and relationship to other pediatric solid tumors is not well understood. In this study, paraffin-embedded material of five cases of pleuropulmonary blastoma was analyzed for genetic alterations by comparative genomic hybridization and five genetic loci by fluorescence in situ hybridization. Comparative genomic hybridization identified aberrations in all pleuropulmonary blastomas, including four amplifications in three tumors at chromosomes 5q33-34, 11q22.2-ter, 15q25-ter, and 19q11-13.2. The most frequent DNA gains involved 8q11-22.2 (four cases) and 20q (two cases), whereas the most common losses included 9p21-24 (two cases) and 11p14 (three cases). Chromosome 8 gains were confirmed by fluorescent in situ hybridization, resulting in the detection of up to five copies of chromosome 8 centromeres per nucleus. In the two surviving patients, chromosome 8 gains were the only genetic abnormality, suggesting that this might be an early event in pleuropulmonary blastoma carcinogenesis. The identification of new genetic alterations as well as the confirmation of previously reported ones (especially 8q gains) in pleuropulmonary blastoma should help to improve our understanding of both the molecular mechanisms underlying the tumorigenesis of pleuropulmonary blastoma and the relationship of pleuropulmonary blastoma with other pediatric tumors