"Malignant Mesothelioma Asbestos Oregon": 09/04/08

Thursday, September 4, 2008

Fwd: Residents Ordered Out Of Troubled Apartment Complex (WRTV Indianapolis)

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From: Yahoo! News Search Results for asbestos cancer <rssfwd@rssfwd.com>
Date: Thu, Sep 4, 2008 at 7:38 AM
Subject: Residents Ordered Out Of Troubled Apartment Complex (WRTV Indianapolis)
To: mesothelioma77@gmail.com

INDIANAPOLIS -- After court-ordered asbestos cleanup was halted when the owners of a troubled northeast-side apartment complex refused to pay, those still living in the Timber Ridge Apartments were told Wednesday they would have to leave.

Wed, 03 Sep 2008 21:50:48 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/asbestos+cancer/SIG=12chsvp7n/*http%3A//www.theindychannel.com/news/17383554/detail.html?rss=ind&psp=news
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Fwd: A fusion protein containing murine vascular endothelial growth factor and tissue factor induces thrombogenesis and suppression of tumor growth in a colon carcinoma model.

---------- Forwarded message ----------
From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Thu, Sep 4, 2008 at 7:39 AM
Subject: A fusion protein containing murine vascular endothelial growth factor and tissue factor induces thrombogenesis and suppression of tumor growth in a colon carcinoma model.
To: mesothelioma77@gmail.com

[1]J Zhejiang Univ Sci B. 2008 Aug.; 9(8): 602-609
Huang FY, Li YN, Wang H, Huang YH, Lin YY, Tan GH

Induction of tumor vasculature occlusion by targeting a thrombogen to newly formed blood vessels in tumor tissues represents an intriguing approach to the eradication of primary solid tumors. In the current study, we construct and express a fusion protein containing vascular endothelial growth factor (VEGF) and tissue factor (TF) to explore whether this fusion protein has the capability of inhibiting tumor growth in a colon carcinoma model. The murine cDNA of VEGF A and TF were amplified by reverse transcriptase polymerase chain reaction (RT-PCR), and then cloned into prokaryotic expression plasmid pQE30 with a linker. The expression product recombinant VEGF-TF (rVEGF-TF) was purified and proved to have comparable enzyme activity to a commercial TF and the capability of specific binding to tumor vessels. Significant decrease of tumor growth was found in the mice administered with rVEGF-TF on Day 6 after initiated rVEGF-TF treatment (P

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Source: http://www.hubmed.org/display.cgi?uids=18763309
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Fwd: Protein kinase C beta in malignant pleural mesothelioma.

---------- Forwarded message ----------
From: HubMed - mesothelioma cancer <rssfwd@rssfwd.com>
Date: Thu, Sep 4, 2008 at 7:39 AM
Subject: Protein kinase C beta in malignant pleural mesothelioma.
To: mesothelioma77@gmail.com

[1]Anticancer Drugs. 2008 Oct; 19(9): 841-8
Faoro L, Loganathan S, Westerhoff M, Modi R, Husain AN, Tretiakova M, Seiwert T, Kindler HL, Vokes EE, Salgia R

Malignant pleural mesothelioma (MPM) is a disease with few therapeutic options. Protein kinase C beta (PKCbeta) is involved in important cellular functions. Enzastaurin (LY317615.HCl) is a novel inhibitor of PKC in clinical development. MPM cell lines (7) and patient tumor tissues (24) were evaluated for expression of PKCbeta by immunoblotting and immunohistochemistry, respectively. In-vitro cell growth assays were performed with enzastaurin with or without cisplatin. Cell migration was evaluated with the wound healing assay. Downstream signaling (survival and focal adhesion pathways) was studied by immunoblotting for related molecules in the presence of phorbol ester with or without enzastaurin. Expression for PKCbeta1 was seen in all cases, with a mean integrated optical density of 152.5 (standard deviation=95.47, n=24), whereas PKCbeta2 expression was less intense, with a mean integrated optical density of 11.45 (standard deviation=16.27, n=21). There was a trend toward lower overall survival among patients expressing above-median PKCbeta1 (P=0.064), but not PKCbeta2. Robust expression of PKCbeta1 and low expression of PKCbeta2 were observed in MPM cell lines. Treatment of MPM cell lines with enzastaurin revealed an IC50 of 5 mumol/l, and strong synergism was observed when combined with cisplatin. Wound healing assay revealed that treatment of H2461 cells with enzastaurin reduced migration by 59.2%. Enzastaurin treatment led to disruption of F-actin architecture. Downstream signaling showed reduced phosphorylation of AKT, FAK (focal adhesion kinase), p130Cas, S6 ribosomal protein, and paxillin. PKCbeta1 was expressed in the majority of MPM samples. Enzastaurin has preclinical activity against MPM, and exhibited synergism with cisplatin. PKCbeta inhibition in MPM might be able to reduce the invasiveness of MPM by affecting cytoskeletal function.

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Source: http://www.hubmed.org/display.cgi?uids=18765998
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Fwd: Quality of life in long-term, disease-free survivors of breast cancer: a follow-up study.

---------- Forwarded message ----------
From: Connotea: Bookmarks matching tags breast and cancer <rssfwd@rssfwd.com>
Date: Thu, Sep 4, 2008 at 7:39 AM
Subject: Quality of life in long-term, disease-free survivors of breast cancer: a follow-up study.
To: mesothelioma77@gmail.com

[1]

[2]Quality of life in long-term, disease-free survivors of breast cancer: a follow-up study.

Patricia Ganz et al.

Journal of the National Cancer Institute 94 (1), 39-49 (02 Jan 2002)

info:pmid/11773281 | info:doi/10.1093/jnci/94.1.39

Importante studio di follow-up, QoL. Sottolinea ottima qualità di vita. Citare?

Posted by [3]marcobaciarello to [4]gabapain [5]morbidity [6]qol [7]breast [8]survival [9]Epidemiology [10]surgery [11]survey [12]cancer on [13]Sun Aug 24 2008 at 20:31 UTC | [14]info | related

marcobaciarello

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Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11773281
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