Fwd: Diagnostic significance of 'atypia' in instrumented versus voided urine specimens.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Fri, Jun 13, 2008 at 11:19 PM
Subject: Diagnostic significance of 'atypia' in instrumented versus voided urine specimens.
To: mesothelioma77@gmail.com


[1]Cancer. 2008 Jun 11;
Kapur U, Venkataraman G, Wojcik EM

BACKGROUND.: Urine cytology plays an important role in monitoring patients with a history of urothelial carcinoma. Because it is difficult to reliably discriminate artifacts induced by instrumentation, inflammation, or therapy those of from malignant cells, many of these specimens are categorized as atypical. The objective of the current study was to study the prevalence and significance of atypical urine cytology with regard to the effect of instrumentation and prior biopsy. METHODS.: All urine cytology cases seen during a 4-year period (2001-2004) with a diagnosis of atypical urothelial cells (AU) were obtained from the cytopathology computer database. In all cases with available surgical follow-up, the following data were extracted: total number and type of urine specimen, the primary histologic diagnosis, and follow-up histologic diagnosis. RESULTS.: In all, 1653 voided and 3502 instrumented urine specimens were examined. A diagnosis of AU was rendered in 115 (6.9%) of the voided urine specimens and in 277 (7.9%) of the instrumented specimens. Follow-up histology was available in 70 cases, including 55 instrumented and 15 voided urine specimens. A nonbenign follow-up diagnosis was observed in 18 of 55 (32.7%) cases in the instrumented group and in 7 of 15 (46.6%) cases in the voided group. Voided urine was marginally associated with a worse subsequent biopsy diagnosis (Pexact Monte Carlo = .09) CONCLUSIONS.: An AU diagnosis is more predictive of a subsequent adverse biopsy diagnosis in voided urine specimens compared with instrumented urines. In the absence of a benchmark for the atypia rate, it is prudent to keep the atypia rate low to keep it more meaningful. This important category should be used by the pathologist to convey concern and recognize the difficulty in interpretation of specimens that may require close follow-up. Cancer (Cancer Cytopathol) 2008. (c) 2008 American Cancer Society.



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Source: http://www.hubmed.org/display.cgi?uids=18548527
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Fwd: Effects of antisense RNA targeting of ODC and AdoMetDC on the synthesis of polyamine synthesis and cell growth in prostate cancer cells using a prostatic androgen-dependent promoter in adenovirus.

---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Fri, Jun 13, 2008 at 11:19 PM
Subject: Effects of antisense RNA targeting of ODC and AdoMetDC on the synthesis of polyamine synthesis and cell growth in prostate cancer cells using a prostatic androgen-dependent promoter in adenovirus.
To: mesothelioma77@gmail.com


[1]Prostate. 2008 Jun 11;
Li W, Liu X, Wang W, Sun H, Hu Y, Lei H, Liu G, Gao Y

PURPOSE: This study was designed to investigate the use of a prostatic androgen-dependent promoter to mediate antisense targeting of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (AdoMetDC) and its effects on the synthesis of polyamine. We also examined the potential of this construct for prostate cancer therapy. METHODS: pADxsi-PSES-AdoMetDC-ODC-PolyA AV was constructed and used to infect various cancer cell lines, including LNCaP, HT-29, H1299, HepG2. The effects of pADxsi-PSES-AdoMetDC-ODC-PolyA AV on the expression of ODC and AdoMetDC, in addition to the cell cycle, apoptosis and p21 levels, were analyzed through Western blotting and cytometry. A Matrigel invasion assay was used to analyze the effects of the recombinant virus on tumor cell invasion. The effect on polyamine content was also determined, and the relationship between inhibition of cellular ODC and AdoMetDC and decreases in polyamine were also investigated using a polyamine recovery assay. RESULTS: Treatment with pADxsi-PSES-AdoMetDC-ODC-PolyA at an MOI of 90 significantly inhibited the proliferation of LNCaP cells, which could not be recovered through the addition of exogenous putrescine. The expression of ODC and AdoMetDC was also reduced, as was the polyamine content. The G1 phase of LNCaP cells was delayed, but no increase in apoptosis was detected. The down-regulation of ODC and AdoMetDC led to increased p21 expression. CONCLUSIONS: The pADxsi-PSES-AdoMetDC-ODC-PolyA AV specifically inhibited the expression of ODC and AdoMetDC and the synthesis of polyamine, while it induced p21 expression, resulting in cell growth arrest in the G1 phase in prostate cancer cells but not in other cells. Prostate (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18548481
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