PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 7404917

Rectal ejaculation and prostatic carcinoma.

C C Carson·O E Akwari
View original source ↗Export metadata ↓

Abstract

A case of carcinoma of the prostate causing fistulous communication between the rectum and the prostatic ducts is presented. The patient's initial symptoms included gradual onset of inability to ejaculate and the complaint of ejaculation per rectum. Appropriate urologic studies demonstrated a fistulous connection between the area of the ejaculatory duct and the rectum. Microscopic studies of rectal discharge confirmed that semen was exiting through his rectum. All genitourinary symptoms in patients with carcinoma of the prostate warrant thorough investigation.

Explore related subjects

AdenocarcinomaAgedCastrationEjaculationFistulaHumansMaleProstatic DiseasesProstatic NeoplasmsRectal FistulaRectumCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C C Carson, O E Akwari. 1980. Rectal ejaculation and prostatic carcinoma.. https://doi.org/10.1016/0090-4295(80)90081-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Interaction of Galpha 12 and Galpha 13 with the cytoplasmic domain of cadherin provides a mechanism for beta -catenin release.

The G12 subfamily of heterotrimeric G proteins, comprised of the alpha-subunits Galpha12 and Galpha13, has been implicated as a signaling component in cellular processes ranging from cytoskeletal changes to cell growth and oncogenesis. In an attempt to elucidate specific roles of this subfamily in cell regulation, we sought to identify molecular targets of Galpha12. Here we show a specific interaction between the G12 subfamily and the cytoplasmic tails of several members of the cadherin family of cell-surface adhesion proteins. Galpha12 or Galpha13 binding causes dissociation of the transcriptional activator beta-catenin from cadherins. Furthermore, in cells lacking the adenomatous polyposis coli protein required for beta-catenin degradation, expression of mutationally activated Galpha12 or Galpha13 causes an increase in beta-catenin-mediated transcriptional activation. These findings provide a potential molecular mechanism for the previously reported cellular transforming ability of the G12 subfamily and reveal a link between heterotrimeric G proteins and cellular processes controlling growth and differentiation.

Adenocarcinoma↗