PubMed · 5317494
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Z Maratka, J Kudrmann. 1970. Segmental colitis. Concept and classification.. https://pubmed.ncbi.nlm.nih.gov/5317494/
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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.
BACKGROUND: Because of its role in cell motility and growth regulation, gelsolin, an actin-binding protein, has been considered a tumor suppressor and a potential prognostic marker in some neoplasias, such as breast and bladder cancer. Little is known about its immunoexpression in prostatic adenocarcinoma (PCA). METHODS: Formalin-fixed, paraffin-embedded tissues of 72 prostatectomy specimens with adenocarcinoma and 8 nonneoplastic prostates from autopsies were stained with a gelsolin monoclonal antibody using the Avidin-biotin-peroxidase complex (ABC) method after microwave antigen retrieval. Immunoreactivity was evaluated in PCA, prostatic intraepithelial neoplasia (PIN), benign prostatic hyperplasia (BPH), and nonproliferative glandular tissue and stroma. The results were statistically analyzed. RESULTS: Consistent gelsolin immunoreactivity was seen in prostatic stromal cells, smooth muscle, endothelia, and nerves. Variable gelsolin expression was seen in 20-100% (average (A) = 65.5%) of glandular cells in nonproliferative tissue (N = 75); 0-50% (A = 9.7%) in BPH (N = 59); 0-80% (A = 8.9%) in PIN (N = 61); and 0-90% (A = 9.3%) in PCA (N = 71). The level of gelsolin expression in nonproliferative prostatic tissue was similar between prostates with PCA (A = 63.4%) and nonneoplastic prostates (A = 67.5%). The level of gelsolin expression did not correlate with age, tumor size, Gleason score, or stage. CONCLUSIONS: Gelsolin is decreased in PCA, PIN, and BPH in comparison to nonproliferative tissue. The role of this downregulation in the development of PCA is not clear. The similar reduction seen in PIN and BPH suggests that this event takes place indiscriminately in hyperplasia and early tumorigenesis in the prostate, which might limit its prognostic significance in PCA.
PURPOSE: A phase II trial was designed to evaluate the toxicity and outcome of patients with locally advanced cervix cancer treated with accelerated hyperfractionated radiotherapy (AHFX). METHODS AND MATERIALS: In this prospective trial, AHFX doses of 1.25 Gy were administered twice daily at least 6 hours apart to a total pelvic dose of 57.5 Gy. A booster dose was then administered via either low-dose rate brachytherapy or external beam therapy to a smaller volume. All patients were accrued and treated at Peter MacCallum Cancer Institute (PMCI) between 1986 until April 1991. RESULTS: Sixty-one eligible patients were enrolled in this protocol; 2 (3.2%) had Stage IIB; 42 (68.9%) had Stage III; 8 (13.1%) had Stage IV and 9 (14.8%) had recurrent cervical cancer. Fifty-two patients (85%) completed the planned external beam without a treatment break. Thirty patients had acute toxicity that required regular medication. One patient died of acute treatment related toxicity. Fifty-five patients received booster therapy: 45 with intrauterine brachytherapy, 6 with interstitial brachtherapy, and 4 with external beam. The median follow-up of surviving patients was 6 years. Overall 5-year survival is 27% and 5-year relapse free survival is 36%. Nineteen patients died with pelvic disease and the actuarial local control rate was 66%. There were 8 severe late complications observed in 7 patients. Seven required surgical intervention (an actuarial rate of 27%). Five patients also required total hip replacement. CONCLUSIONS: The local control rate was favorable compared with other series that have used standard fractionation, although overall survival remained similar. The severe late complication rate was high for this protocol and higher than similar protocols reported in the literature.