PubMed · 122855
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J D Eisen. 1975. NEBRASKA,s prenatal diagnostic program.. https://pubmed.ncbi.nlm.nih.gov/122855/
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The increase in the incidence of prostate cancer observed over the past 2 decades is suggested to be largely due to increased detection of insignificant tumors. To explore this assumption, we investigated trends in survival of prostate cancer patients in southeastern Netherlands, an area with almost 1 million inhabitants, where the age-adjusted incidence of prostate cancer increased by 53% between 1971 and 1989, i.e., before the introduction of prostate-specific antigen testing. Survival was calculated for all patients registered in the Eindhoven Cancer Registry between 1971 and 1989 (n = 2,562). In spite of earlier diagnosis, survival barely changed during this time period. Five-year relative survival improved slightly from 53% [95% confidence interval (CI) 47%, 59%] in 1975-1979 to 56% (CI 51%, 61%) in 1985-1989. Stratified analyses suggested an improvement since 1980 for patients below 75 years with localized tumors but, despite possible stage migration, decreased survival for those with metastasized and/or poorly differentiated tumors. Patients below 75 years whose tumors were diagnosed unexpectedly during transurethral resection of the prostate (TURP) exhibited a relative survival of 85% 5 years and 68% 10 years after diagnosis. Less extensive application of TURP in The Netherlands might explain why our findings do not agree with those in Sweden and the United States. Inference from country-specific trends in survival appears not to be necessarily generalizable to other countries with a similar increase in the incidence of prostate cancer. We conclude from our results that earlier diagnosis of prostate cancer between 1971 and 1989 may be accompanied by an increased incidence of an aggressive variant.
When we attempted to characterize the immunological state in G-CSF transgenic mice, a large number of not only granulocytes but also lymphoid cells expanded in various immune organs. Such lymphoid cells were present at unusual sites of these organs, e.g., the parenchymal space in the liver. We then determined the phenotype of these lymphoid cells by immunofluorescence tests. It was demonstrated that CD3intIL-2Rbeta+ cells (i.e., extrathymic T cells), including the NK1.1+ subset of CD3int cells (i.e., NKT cells), increased in the liver and all other tested organs. These T cells as well as NK cells mediated NK and NK-like cytotoxicity, especially at youth. However, they were not able to mediate such cytotoxicity in the presence of granulocytes. This result might be associated with deficiency in the hybrid resistance previously ascribed to these mice. In other words, G-CSF transgenic mice had a large number of extrathymic T cells (including NKT cells) and NK cells that mediate hybrid resistance, but their function was suppressed by activated granulocytes. Indeed, these granulocytes showed an elevated level of Ca2+ influx upon stimulation. The present results suggest that, in parallel with overactivation of granulocytes, extrathymic T cells and NK cells are concomitantly activated in number but that their function is suppressed in G-CSF transgenic mice.
We propose the name nucleotide pyrophosphatases/phosphodiesterases (NPP) for the enzymes that release nucleoside-5'-monophosphates from various pyrophosphate and phosphodiester bonds. Three structurally related mammalian NPPs are known, i.e. NPPalpha (autotaxin), NPPbeta (B10/gp130RB13-6) and NPPgamma (PC-1). We report here that these isozymes have a distinct tissue distribution in the rat but that they are all three expressed in hepatocytes. In FAO rat hepatoma cells only the level of NPPgamma was stimulated by TGF-beta1. In rat liver, the concentration of the transcripts of all three isozymes was found to increase manyfold during the first weeks after birth, but the increased expression of the NPPalpha mRNA was transient. The level of the NPP transcripts transiently decreased after hepatectomy, but NPPalpha mRNA was also lost after sham operation, which suggests that it may belong to the negative acute-phase proteins. The loss of the beta- and gamma-transcripts after hepatectomy was not due to a decreased NPP gene transcription or an increased turnover of the mature transcripts. However, hepatectomy also caused a similar loss of the nuclear pool of the NPPbeta and NPPgamma mRNAs. We conclude that a deficient processing and/or an increased turnover of the NPP pre-mRNAs underlies the hepatectomy-induced decrease of the beta- and gamma-transcripts. A similar loss of nuclear NPPgamma mRNA was also noted after treatment with cycloheximide, indicating that protein(s) with a high turnover control the stability and/or processing of the immature NPPgamma transcript.