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Skin Cancer, mesothelioma, Mesothelioma Cancer, Mesothelioma Lwayer
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Wednesday, May 21, 2008

Fwd: Expression of short-form oncostatin M receptor as a decoy receptor in lung adenocarcinomas.



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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Wed, May 21, 2008 at 8:29 AM
Subject: Expression of short-form oncostatin M receptor as a decoy receptor in lung adenocarcinomas.
To: mesothelioma77@gmail.com


[1]J Pathol. 2008 Apr 14;
Chen D, Chu CY, Chen CY, Yang HC, Chiang YY, Lin TY, Chiang IP, Chuang DY, Yu CC, Chow KC

Oncostatin M (OSM) is a member of the interleukin-6 (IL-6) family of cytokines, and binds to the OSM receptor (OSMR) to inhibit cancer growth. Four forms of OSMR have been identified: leukemia inhibitory factor receptor (LIFR), OSMRbeta, short-form OSMR (OSMRs) and soluble OSMR (sOSMR). In this study, we examined the type and expression of OSMR in lung adenocarcinomas (LADCs). Expression of OSMR was determined by reverse transcription-polymerase chain reaction (RT-PCR), immunoblotting, immunohistochemistry and confocal immunofluorescent microscopy (CIM). Our results showed that, among the four forms of OSMR, OSMRs was mainly expressed in LADC, and expression level of OSMRs correlated with patient survival. CIM revealed that OSMRs was localized on the cell membrane of LADC cell lines in vitro. OSMRs acts as a decoy receptor by reducing the inhibitory effect of OSM on cell growth. Decrease in OSMRs expression by siRNA increased cell sensitivity to OSM, and ectopic expression of OSMRs reduced cell sensitivity to OSM. These results suggest that expression of OSMRs, which operates as a decoy receptor for OSM, is correlated with disease progression and adverse prognosis in patients with LADC. Copyright (c) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.



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Source: http://www.hubmed.org/display.cgi?uids=18491353
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Fwd: Inhibitory effects of nordihydroguaiaretic acid (NDGA) on the IGF-1 receptor and androgen dependent growth of LAPC-4 prostate cancer cells.



---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Wed, May 21, 2008 at 8:29 AM
Subject: Inhibitory effects of nordihydroguaiaretic acid (NDGA) on the IGF-1 receptor and androgen dependent growth of LAPC-4 prostate cancer cells.
To: mesothelioma77@gmail.com


[1]Prostate. 2008 May 19;
Ryan CJ, Zavodovskaya M, Youngren JF, Campbell M, Diamond M, Jones J, Shiry L, Allan G, Maddux BA, Goldfine ID

BACKGROUND: Nordihydroguaiaretic acid (NDGA) is an inhibitor of the IGF-1 receptor (IGF-1R) in breast and other cancers, and concomitantly inhibits tumor growth both in cultured cells and animals. The current study evaluates the effect of NDGA on the androgen-stimulated growth of human prostate cancer cells. METHODS: LAPC-4 prostate cancer cells in tissue culture were androgen starved for 3 days, 1 nM dihydrotestosterone (DHT) and other androgens were then added for up to 7 days, and cell proliferation measured. IGF-1R protein expression was measured by Western blot, and IGF-1R mRNA expression by quantitative PCR. IGF-1R receptor kinase activation was measured by ELISA. RESULTS: After 7 days, LAPC-4 growth was doubled by 1 nM DHT. NDGA had a rapid effect to inhibit IGF-1R autophosphorylation induced by IGF-1. DHT increased the expression of IGF-1R protein and mRNA levels. Maximal IGF-1R protein levels were observed 3 days after the addition of androgen. In addition, NDGA, at 10 microM or less, inhibited DHT-induced proliferation in both cells grown in plates and cells grown in soft agar. Androgen receptor (AR) studies by FRET revealed that NDGA had no conformational effects on the AR in response to ligand. CONCLUSIONS: NDGA blocks the DHT-induced growth of LAPC-4 prostate cancer cells by several mechanisms including rapid inhibition of the IGF-1R kinase, and a dose-dependent inhibition of androgen stimulation of IGF-1R expression. Clinical studies of this agent will determine its efficacy in the setting of androgen-dependent prostate cancer. Prostate 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18491370
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Fwd: Cumulative effect of five genetic variants on prostate cancer risk in multiple study populations.



---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Wed, May 21, 2008 at 8:29 AM
Subject: Cumulative effect of five genetic variants on prostate cancer risk in multiple study populations.
To: mesothelioma77@gmail.com


[1]Prostate. 2008 May 19;
Sun J, Chang BL, Isaacs SD, Wiley KE, Wiklund F, Stattin P, Duggan D, Carpten JD, Trock BJ, Partin AW, Walsh PC, Grönberg H, Xu J, Isaacs WB, Zheng SL

BACKGROUND: A strong cumulative effect of five genetic variants and family history on prostate cancer risk was recently reported in a Swedish population (CAPS). We carried out this study to confirm the finding in two U.S. study populations and perform a combined analysis to obtain a more stable estimate of the odds ratio (OR) for prostate cancer. METHODS: We evaluated three SNPs at 8q24 and one SNP each at 17q12 and 17q24.3 in two study populations in the U.S. The first was a hospital-based case-control study population at Johns Hopkins Hospital (JHH), including 1,563 prostate cancer patients and 576 control subjects. The second was the National Cancer Institute Cancer Genetic Markers of Susceptibility (CGEMS) Initiative, including 1,172 prostate cancer patients and 1,157 control subjects. RESULTS: We confirmed a cumulative effect of five risk variants on prostate cancer risk. Based on a total of 5,628 cases and 3,514 controls from JHH, CGEMS, and CAPS, men who carry any combination of 1, 2, 3, and 4 or more of these five risk variants have an estimated OR (95% CI) of 1.41 (1.20-1.67), 1.88 (1.59-2.22), 2.36 (1.95-2.85), and 3.80 (2.77-5.22) for prostate cancer, respectively, compared to men who do not have any of these five risk variants. When family history was included, the cumulative effect was stronger. DISCUSSION: These results provide an important confirmation for the cumulative effect of five genetic risk variants on prostate cancer risk. The more stable OR estimates of the cumulative effect of these six risk factors are a major step toward individual risk characterization for this disease. Prostate (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18491292
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Fwd: Nanotubes pose cancer risk (The Charlotte Observer)



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From: Yahoo! News Search Results for asbestos cancer <rssfwd@rssfwd.com>
Date: Wed, May 21, 2008 at 8:30 AM
Subject: Nanotubes pose cancer risk (The Charlotte Observer)
To: mesothelioma77@gmail.com


Certain types of carbon nanotubes -- microscopic graphite cylinders used in a small but growing number of Space Age applications -- could pose a similar cancer risk as asbestos if inhaled, scientists reported Tuesday. Researchers found that mice injected with nanotubes quickly developed the same biological damage associated with early exposure to asbestos fibers, a known carcinogen. The study ...

Wed, 21 May 2008 10:10:49 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/asbestos+cancer/SIG=11qaqic5l/*http%3A//www.charlotteobserver.com/162/story/633230.html
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