Sunday, February 24, 2008

Fw: Common Factor Between Mesothelioma And Money



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From: Search for mesothelioma diagnosis <rssfwd@rssfwd.com>
To: shell8377@yahoo.com
Sent: Wednesday, February 20, 2008 3:40:09 AM
Subject: Common Factor Between Mesothelioma And Money

Submitted by MakemoneyToday on February 19, 2008 - 9:36am. Cancer information mesothelioma survival surviving Survivor Apart from the common "m", is there anything else in common between Mesothelioma and money? ...

Tue, 19 Feb 2008 18:46:43 GMT

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Source: http://bloggerparty.com/common_factor_between_mesothelioma_and_money
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Never miss a thing. Make Yahoo your homepage.

Fwd: Community Notes (Greene County Daily World)



---------- Forwarded message ----------
From: Yahoo! News Search Results for asbestos cancer <rssfwd@rssfwd.com>
Date: Thu, Feb 14, 2008 at 11:06 PM
Subject: Community Notes (Greene County Daily World)
To: mesothelioma77@gmail.com


In accordance with Indiana Open Door Law, a meeting to determine Common Construction Wage Rates has been arranged for the Town of Worthington -- Williams House Hotel Asbestos Abatement project and other such business as may be brought before the committee on that date.

Fri, 15 Feb 2008 02:19:34 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/asbestos+cancer/SIG=11ekt5bpe/*http%3A//gcdailyworld.com/story/1311582.html
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Fwd: CAG members hear from expert (The Ambler Gazette)



---------- Forwarded message ----------
From: Yahoo! News Search Results for mesothelioma <rssfwd@rssfwd.com>
Date: Thu, Feb 14, 2008 at 10:49 PM
Subject: CAG members hear from expert (The Ambler Gazette)
To: mesothelioma77@gmail.com


At the BoRit asbestos site Community Advisory Group meeting Feb. 6 Co-chairman Fred Conner of Whitpain introduced Edward Emmett, University of Pennsylvania professor and director of community outreach and education at the university's Center of Excellence in Environmental Toxicology, whose expertise the group is considering for scientific assistance.

Wed, 13 Feb 2008 08:27:35 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/mesothelioma/SIG=12sc8sral/*http%3A//www.zwire.com/site/news.cfm?newsid=19289678&BRD=1306&PAG=461&dept_id=187829&rfi=6
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Fwd: International Lung Cancer Conference, Liverpool - 9-12 July 2008 (Medical News Today)



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From: Yahoo! News Search Results for mesothelioma <rssfwd@rssfwd.com>
Date: Thu, Feb 14, 2008 at 10:49 PM
Subject: International Lung Cancer Conference, Liverpool - 9-12 July 2008 (Medical News Today)
To: mesothelioma77@gmail.com


From 9th - 12th July 2008, the new Arena and Convention Centre, Liverpool shall see the arrival of some of the world's leading lung cancer experts and will offer an opportunity to develop future strategies for early lung cancer detection, molecular diagnostics and therapeutics.

Wed, 13 Feb 2008 11:15:50 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/mesothelioma/SIG=11mgu0n29/*http%3A//www.medicalnewstoday.com/articles/97120.php
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Fwd: HOME PAGE (The Hindu)



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From: Yahoo! News Search Results for mesothelioma <rssfwd@rssfwd.com>
Date: Thu, Feb 14, 2008 at 10:49 PM
Subject: HOME PAGE (The Hindu)
To: mesothelioma77@gmail.com


Market rebounds on positive overseas signals; Sensex gains 817 pts Mumbai, Feb. 14 Share prices staged a strong comeback on the Indian bourses on Thursday as domestic and foreign investors bought at lower levels. The market sentiment was boosted by positive signals from the overseas markets, but ...

Thu, 14 Feb 2008 18:25:28 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/mesothelioma/SIG=11sgffkel/*http%3A//www.thehindubusinessline.com/2008/02/15/index.htm
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Fwd: MicroRNA-21 targets tumor suppressor genes in invasion and metastasis.



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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Thu, Feb 14, 2008 at 11:07 PM
Subject: MicroRNA-21 targets tumor suppressor genes in invasion and metastasis.
To: mesothelioma77@gmail.com


[1]Cell Res. 2008 Feb 12;
Zhu S, Wu H, Wu F, Nie D, Sheng S, Mo YY

MicroRNAs (miRNAs) are a class of naturally occurring small non-coding RNAs that target protein-coding mRNAs at the post-transcriptional level. Our previous studies suggest that mir-21 functions as an oncogene and has a role in tumorigenesis, in part through regulation of the tumor suppressor gene tropomyosin 1 (TPM1). Given that TPM1 has been implicated in cell migration, in this study we further investigated the role of mir-21 in cell invasion and tumor metastasis. We found that suppression of mir-21 in metastatic breast cancer MDA-MB-231 cells significantly reduced invasion and lung metastasis. Consistent with this, ectopic expression of TPM1 remarkably reduced cell invasion. Furthermore, we identified two additional direct mir-21 targets, programmed cell death 4 (PDCD4) and maspin, both of which have been implicated in invasion and metastasis. Like TPM1, PDCD4 and maspin also reduced invasiveness of MDA-MB-231 cells. Finally, the expression of PDCD4 and maspin inversely correlated with mir-21 expression in human breast tumor specimens, indicating the potential regulation of PDCD4 and maspin by mir-21 in these tumors. Taken together, the results suggest that, as an oncogenic miRNA, mir-21 has a role not only in tumor growth but also in invasion and tumor metastasis by targeting multiple tumor/metastasis suppressor genes. Therefore, suppression of mir-21 may provide a novel approach for the treatment of advanced cancers.Cell Research advance online publication 12 February 2008; doi: 10.1038/cr.2008.24.



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Source: http://www.hubmed.org/display.cgi?uids=18270520
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Fwd: A high-affinity human monoclonal antibody specific to the alternatively spliced EDA domain of fibronectin efficiently targets tumor neo-vasculature in vivo.



---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Thu, Feb 14, 2008 at 11:06 PM
Subject: A high-affinity human monoclonal antibody specific to the alternatively spliced EDA domain of fibronectin efficiently targets tumor neo-vasculature in vivo.
To: mesothelioma77@gmail.com


[1]Int J Cancer. 2008 Feb 12;
Villa A, Trachsel E, Kaspar M, Schliemann C, Sommavilla R, Rybak JN, Rösli C, Borsi L, Neri D

The alternatively spliced extra-domain B of fibronectin is one of the best characterized markers of tumor angiogenesis. Similarly, the extra-domain A (EDA), which can also be inserted in the fibronectin transcript by a mechanism of alternative splicing, has been shown to preferentially accumulate around new blood vessels in certain tumors, but this antigen has not been investigated so far as a target for antibody-based biomolecular intervention. We here describe the generation of 3 human monoclonal antibodies (named F8, B7 and D5), which recognize the same epitope of EDA, but which differ in terms of their dissociation constant to the human antigen (K(D) = 3.1, 16 and 17 nM, measured for monomeric preparations of the F8, B7 and D5 antibodies, respectively, in recombinant scFv format). When the 3 antibody fragments were cloned and expressed with a 5 amino acid linker, the 3 resulting homodimeric antibody preparations displayed comparable tumor: organ ratios in quantitative biodistribution studies, performed in immunocompetent 129SvEv mice, bearing subcutaneous syngeneic F9 murine tumors. The percent injected dose per gram (%ID/g) values in tumors 24 hr after intravenous injection were 9.3, 10.2 and 13 for F8, B7 and D5, respectively. The F8 antibody may serve as useful building block for the development of antibody-based targeted anti-cancer therapeutics. Preclinical and clinical investigations are facilitated by the fact that F8 recognizes the human and mouse antigen with comparable affinity, and by the observation that EDA over-expression is detectable not only in solid tumors, but also in hematological malignancies. (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18271006
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Fwd: Targeted combinatorial therapy of non-small cell lung carcinoma using a GST-fusion protein of full-length or truncated MDA-7/IL-24 with Tarceva.



---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Thu, Feb 14, 2008 at 11:06 PM
Subject: Targeted combinatorial therapy of non-small cell lung carcinoma using a GST-fusion protein of full-length or truncated MDA-7/IL-24 with Tarceva.
To: mesothelioma77@gmail.com


[1]J Cell Physiol. 2008 Feb 12;
Gupta P, Emdad L, Lebedeva IV, Sarkar D, Dent P, Curiel DT, Settleman J, Fisher PB

Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24), a cytokine belonging to the IL-10 family, displays cancer-specific apoptosis-inducing properties when delivered by a replication-incompetent adenovirus (Ad.mda-7) or as a GST-tagged recombinant protein (GST-MDA-7). Previous studies demonstrated that an adenovirus expressing M4, a truncated version of MDA-7/IL-24 containing amino acid residues 104-206, also induced similar cancer-specific apoptosis. We generated recombinant GST-M4 proteins and examined the potency of GST-MDA-7 and GST-M4 on a panel of epidermal growth factor receptor (EGFR) wild type and mutant non-small cell lung carcinoma (NSCLC) cells either as a single agent or in combination with a reversible EGFR inhibitor, Tarceva. The combination of either GST-MDA-7 or GST-M4 ( approximately 0.1 microM) and Tarceva (10 microM), at sub-optimal apoptosis-inducing concentrations synergistically enhanced growth inhibition and apoptosis induction over that observed with either agent alone. The combination treatment also augmented inhibition of EGFR signaling, analyzed by phosphorylation of EGFR and its downstream effectors AKT and ERK1/2, over that with single-agent therapy. Tarceva enhanced GST-MDA-7 and GST-M4 toxicity in cells expressing mutated EGFR proteins that are resistant to the inhibitory effects of Tarceva. In total, these data suggest that combined treatment of NSCLC cells with an EGFR inhibitor can augment the efficacy of GST-MDA-7 and GST-M4 and that the EGFR inhibitor Tarceva may mediate this combinatorial effect by inhibiting multiple tyrosine kinases in addition to the EGFR. This approach highlights a potential new combinatorial strategy, which may prove beneficial for NSCLC patients with acquired resistance to EGFR inhibitors. J. Cell. Physiol. (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18270968
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