Skin Cancer Charts Graphs: 09/09/08

Tuesday, September 9, 2008

Fwd: Barbara S. Harris, 80; co-founder of an urban redevelopment training program at USC (Los Angeles Times)

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From: Yahoo! News Search Results for asbestos cancer <rssfwd@rssfwd.com>
Date: Sun, Sep 7, 2008 at 3:45 AM
Subject: Barbara S. Harris, 80; co-founder of an urban redevelopment training program at USC (Los Angeles Times)
To: mesothelioma77@gmail.com

After the L.A. riots in 1992, she and others worked with the university to launch a course on revitalizing minority communities. Barbara S. Harris, a property manager who co-founded the Ross Minority Program in Real Estate at USC, which trains students in the redevelopment of minority communities, has died. She was 80.

Sun, 07 Sep 2008 07:09:09 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/asbestos+cancer/SIG=12stv5u3p/*http%3A//www.latimes.com/news/obituaries/la-me-harris7-2008sep07,0,7781662.story?track=rss
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Fwd: A linear index for predicting joint health-states utilities from single health-states utilities.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Sep 7, 2008 at 3:45 AM
Subject: A linear index for predicting joint health-states utilities from single health-states utilities.
To: mesothelioma77@gmail.com

[1]Health Econ. 2008 Sep 4;
Basu A, Dale W, Elstein A, Meltzer D

Direct elicitation of utilities for joint health (JS) states may pose substantial interview burden, while traditional models to predict these utilities from utilities of component single states (SS) are inconsistent with the data. Using individual-level data on utilities for health states associated with prostate cancer, we report the performance of a new model that encompasses three traditional models - additive, multiplicative, and minimum - previously used for predicting utilities for joint health states. Describing utilities in terms of utility losses l(.) relative to prefect health, our final estimated linear index for predicting joint health-state utilities is El(JS)=0.05+0.72.max l(SS1),l(SS2)+0.33.min l(SS1),l(SS2)-0.18.l(SS1).l(SS2). Based on out-of-sample predictions, this model produces up to 50% reduction in mean-square error compared with traditional models and consistent prediction across different ranges of joint-state utilities, which the traditional models do not. Parameter estimates of the new model proposed here provide direct evidence on the inconsistencies of the traditional models, are grounded in psychological theory by emphasizing the more severe component of a joint health state, and provide a simple linear index to generate consistent predictions of utilities for joint health states. Further validation of this function for joint health states in other clinical scenarios is warranted. Copyright (c) 2008 John Wiley & Sons, Ltd.

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Source: http://www.hubmed.org/display.cgi?uids=18773392
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Fwd: Effects of Iejimalide B, a marine macrolide, on growth and apoptosis in prostate cancer cell lines.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Sep 7, 2008 at 3:45 AM
Subject: Effects of Iejimalide B, a marine macrolide, on growth and apoptosis in prostate cancer cell lines.
To: mesothelioma77@gmail.com

[1]J Cell Biochem. 2008 Sep 4;
Wang WL, McHenry P, Jeffrey R, Schweitzer D, Helquist P, Tenniswood M

Iejimalide B, a marine macrolide, causes growth inhibition in a variety of cancer cell lines at nanomolar concentrations. We have investigated the effects of Iejimalide B on cell cycle kinetics and apoptosis in the p53(+)/AR(+) LNCaP and p53(-)/AR(-) PC-3 prostate cancer cell lines. Iejimalide B, has a dose and time dependent effect on cell number (as measured by crystal violet assay) in both cell lines. In LNCaP cells Iejimalide B induces a dose dependent G(0)/G(1) arrest and apoptosis at 48 h (as measured by Apo-BrdU staining). In contrast, Iejimalide B initially induces G(0)/G(1) arrest followed by S phase arrest but does not induce apoptosis in PC-3 cells. qPCR and Western analysis suggests that Iejimalide B modulates the steady state level of many gene products associated with cell cycle (including cyclins D, E, and B and p21(waf1/cip1)) and cell death (including survivin, p21B and BNIP3L) in LNCaP cells. In PC-3 cells Iejimalide B induces the expression of p21(waf1/cip1), down regulates the expression of cyclin A, and does not modulate the expression of the genes associated with cell death. Comparison of the effects of Iejimalide B on the two cell lines suggests that Iejimalide B induces cell cycle arrest by two different mechanisms and that the induction of apoptosis in LNCaP cells is p53-dependent. J. Cell. Biochem. (c) 2008 Wiley-Liss, Inc.

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Source: http://www.hubmed.org/display.cgi?uids=18773415
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Fwd: Crosstalk between c-Myc and ribosome in ribosomal biogenesis and cancer.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Sep 7, 2008 at 3:45 AM
Subject: Crosstalk between c-Myc and ribosome in ribosomal biogenesis and cancer.
To: mesothelioma77@gmail.com

[1]J Cell Biochem. 2008 Sep 4;
Dai MS, Lu H

Protein production is driven by protein translation and relies on ribosomal biogenesis, globally essential for cell growth, proliferation, and animal development. Deregulation of these sophisticated cellular processes leads to abnormal homeostasis and carcinogenesis. Thus, their tight regulation is vitally important for a cell to warrant normal growth and proliferation. One newly identified key regulator for ribosomal biogenesis and translation is the oncoprotein c-Myc, whose aberrantly excessive level and activity are highly associated with human cancers, too. Recently, we have shown that ribosomal protein L11 functions as a feedback regulator of c-Myc. Hence, in this review, we will provide some prospects on the interplay between c-Myc and ribosomal proteins during ribosomal biogenesis and discuss its implications in cancer. J. Cell. Biochem. (c) 2008 Wiley-Liss, Inc.

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Source: http://www.hubmed.org/display.cgi?uids=18773413
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Fwd: Characterization of TRIM31, upregulated in gastric adenocarcinoma, as a novel RBCC protein.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Sun, Sep 7, 2008 at 3:45 AM
Subject: Characterization of TRIM31, upregulated in gastric adenocarcinoma, as a novel RBCC protein.
To: mesothelioma77@gmail.com

[1]J Cell Biochem. 2008 Sep 4;
Sugiura T, Miyamoto K

To explore the molecules associated with gastric adenocarcinoma, we used the gene expression profile database of various human tissues and identified TRIM31 upregulated in both patients with chronic gastritis and stomach cancer. TRIM31 is a new member of RBCC proteins composed of RING finger, B-box and coiled-coil domains. We characterized TRIM31 biochemically and found it possess properties in common with other RBCC proteins, such as occurrence of alternative splicing transcripts, in vitro autoubiquitylating activity and a tendency to homo-oligomerize. The primary localization site of TRIM31 is the cytoplasm but some fraction is potentially associated with the mitochondria. TRIM31 overexpression suppresses colony formation of HCT116 cells while knockdown of its expression with short interfering RNAs (siRNAs) consistently tends to enhance growth of AsPC-1 cells slightly. Thus, TRIM31 is a characteristic RBCC protein with the ability to regulate cell proliferation negatively and may be a potential biomarker of gastric cancer as it is overexpressed from the early stage of gastric carcinogenesis. J. Cell. Biochem. (c) 2008 Wiley-Liss, Inc.

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Source: http://www.hubmed.org/display.cgi?uids=18773414
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