Fwd: Elusive Target In Cancer Cells Targeted By Magnolia Compound (Medical News Today)

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From: Yahoo! News Search Results for lung cancer <rssfwd@rssfwd.com>
Date: Mon, Jul 14, 2008 at 4:55 AM
Subject: Elusive Target In Cancer Cells Targeted By Magnolia Compound (Medical News Today)
To: mesothelioma77@gmail.com


A natural compound from magnolia cones blocks a pathway for cancer growth that was previously considered "undruggable," researchers have found. A laboratory led by Jack Arbiser, MD, PhD, at Emory University School of Medicine, has been studying the compound honokiol, found in Japanese and Chinese herbal medicines, since discovering its ability to inhibit tumor growth in mice in 2003.

Mon, 14 Jul 2008 08:17:40 GMT

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Source: http://us.rd.yahoo.com/dailynews/rss/search/lung+cancer/SIG=11nivncqb/*http%3A//www.medicalnewstoday.com/articles/114841.php
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Fwd: Genetic polymorphisms in oestrogen metabolic pathway and breast cancer: a positive association with combined CYP/GST genotypes.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Mon, Jul 14, 2008 at 4:55 AM
Subject: Genetic polymorphisms in oestrogen metabolic pathway and breast cancer: a positive association with combined CYP/GST genotypes.
To: mesothelioma77@gmail.com


[1]Clin Exp Med. 2008 Jun; 8(2): 65-71
Torresan C, Oliveira MM, Torrezan GT, de Oliveira SF, Abuázar CS, Losi-Guembarovski R, Lima RS, Urban CA, Cavalli IJ, Ribeiro EM

The cytochrome P450 family (CYPs) and the glutathione S-transferase (GSTs) enzymes play an important role in the metabolism of environmental carcinogens and of oestrogen and can affect breast cancer risk. In this study we examine the role of the genes CYP1A1, CYP17, CYP2D6, GSTM1, GSTP1 and GSTT1 in breast cancer risk in Brazilian women. The study population consisted of 102 incident breast cancer cases and 102 healthy controls. Genotyping analyses were performed by PCR-based methods. A significant finding was observed between GSTP1 Ile-Val polymorphism and breast cancer risk (OR = 1.81; CI 95% = 1.04-3.16). A significant association was observed between women with 0-2 risk genotypes and those with 4 or more risk genotypes (OR = 2.42; CI 95% = 1.13-5.18) when the potential combined effects of the risk genotypes were examined. No significant differences between cases and controls were found correlating the genotypes and the clinical-histopathological parameters. In conclusion, in our population only GSTP1 was associated with breast cancer risk. However, when the genes were tested in combination, a significant association in the breast cancer risk was observed.



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Source: http://www.hubmed.org/display.cgi?uids=18618215
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Fwd: East Alton law firm gives $10.2 million for cancer research facility (The Telegraph)

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From: Yahoo! News Search Results for asbestos cancer <rssfwd@rssfwd.com>
Date: Mon, Jul 14, 2008 at 4:55 AM
Subject: East Alton law firm gives $10.2 million for cancer research facility (The Telegraph)
To: mesothelioma77@gmail.com


SPRINGFIELD - The founder of a successful East Alton law firm said Thursday the firm's gift of $10.2 million for cancer research demonstrates its commitment to doing good.

Sat, 12 Jul 2008 03:56:46 GMT

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Fwd: Rad51 overexpression rescues radiation resistance in BRCA2-defective cancer cells.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Mon, Jul 14, 2008 at 4:55 AM
Subject: Rad51 overexpression rescues radiation resistance in BRCA2-defective cancer cells.
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[1]Mol Carcinog. 2008 Jul 10;
Brown ET, Holt JT

Breast cancers with BRCA2 mutations exhibit DNA repair defects and are particularly sensitive to radiation. BRCA2 interacts with Rad51 in a complex manner involving internal BRC and C-terminal TR2 domains which play a key role in homologous recombination. BRCA2 expression also modulates Rad51 protein levels such that Rad51 protein is relatively decreased in BRCA2-defective cancer cells. This is mediated in part through BRCA2's capacity to protect Rad51 from caspase-3 proteolytic degradation. In order to distinguish between functional and expression related roles for BRCA2 we studied the results of Rad51 overexpression in mouse and human cells with inactivating BRCA2 mutations. The results show that overexpression of wild-type Rad51 partially rescues BRCA2 deficiency but that overexpression of a caspase-3 resistant Rad51 completely complements the BRCA2 defect in radiation responsiveness. These results indicate that Rad51 can compensate for some aspects of a BRCA2 gene defect and suggest that Rad51 expression levels may be an important modifier of the BRCA2 defective genotype. (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18618591
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Fwd: Expression of TNF-alpha leader sequence renders MCF-7 tumor cells resistant to the cytotoxicity of soluble TNF-alpha.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Mon, Jul 14, 2008 at 4:55 AM
Subject: Expression of TNF-alpha leader sequence renders MCF-7 tumor cells resistant to the cytotoxicity of soluble TNF-alpha.
To: mesothelioma77@gmail.com


[1]Breast Cancer Res Treat. 2008 Jul 10;
Yan D, Qin N, Zhang H, Liu T, Yu M, Jiang X, Feng W, Wang J, Yin B, Zhang T, Zhou M, Li Z

Transmembrane TNF-alpha (tmTNF-alpha) contains a leader sequence (LS) that can be phosphorylated and cleaved at its cytoplasmic portion, inducing IL-12 production. We observed that the breast cancer cell line MDA-MB-231 expressing transmembrane TNF-alpha (tmTNF-alpha) at high level was resistant to soluble TNF-alpha (sTNF-alpha)-induced cytotoxicity, accompanied by constitutive NF-kappaB activation. In contrast, MCF-7 cells expressing tmTNF-alpha at very low level were sensitive to sTNF-alpha-induced cell death and had no detectable NF-kappaB activation. Consistently, siRNA-mediated tmTNF-alpha knockdown blocked NF-kappaB activation and rendered MDA-MB-231 sensitive. To test our hypothesis that TNF-LS may play an important role in determining the sensitivity of tumor cells to sTNF-alpha, we stably transfected MCF-7 cells with TNF-LS. We found that transfection of TNF-LS or wild-type TNF-alpha containing LS constitutively activated NF-kappaB and conferred the cytotoxic resistance of MCF-7 cells, while transfection of a mutant tmTNF-alpha lacking the cytoplasmic segment of LS neither activated NF-kappaB nor affected the sensitivity. However, NF-kappaB inhibitor PDTC suppressed NF-kappaB activation and reconstituted sensitivity of TNF-LS/MCF-7 cells. To check whether TNF-LS is required to be cleaved or internalized for NF-kappaB activation to occur, we used signal peptide peptidase inhibitor (Z-LL)(2)-ketone and receptor internalization inhibitor MDC to treat cells. Interestingly, both inhibitors increased TNF-LS expression on the cell surface and enhanced NF-kappaB activation. These results indicate that membrane-anchored TNF-LS contributes to constitutive activation of NF-kappaB and resistance to sTNF-alpha-induced cell death. Therefore, TNF-LS appears to be responsible for tmTNF-alpha-induced resistance in the breast cancer cells.



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Source: http://www.hubmed.org/display.cgi?uids=18618239
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Fwd: Breast cancer survivors at work.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Mon, Jul 14, 2008 at 4:55 AM
Subject: Breast cancer survivors at work.
To: mesothelioma77@gmail.com


[1]J Occup Environ Med. 2008 Jul; 50(7): 777-84
Hansen JA, Feuerstein M, Calvio LC, Olsen CH

INTRODUCTION:: Residual symptoms such as fatigue, cognitive limitations, and emotional distress can be experienced by cancer survivors. These symptoms may impact their abilities at work. It is unclear to what degree these symptoms are associated with work in occupationally active breast cancer survivors, the most prevalent cancer survivor group. METHODS:: A sample of 100 women working part- or full-time with a history of breast cancer and a noncancer comparison group (n = 103) completed questionnaires related to physical fatigue, depression, anxiety, and cognitive limitations. Demographic variables, job stress, type of job, stage at diagnosis, treatment exposure, and health behaviors were also measured as potential confounders. RESULTS:: Four years postdiagnosis breast cancer survivors reported higher levels of age-adjusted work limitations (F = 32.708, P

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Source: http://www.hubmed.org/display.cgi?uids=18617833
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Fwd: Yes-associated protein (YAP) functions as a tumor suppressor in breast.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Mon, Jul 14, 2008 at 4:55 AM
Subject: Yes-associated protein (YAP) functions as a tumor suppressor in breast.
To: mesothelioma77@gmail.com


[1]Cell Death Differ. 2008 Jul 11;
Yuan M, Tomlinson V, Lara R, Holliday D, Chelala C, Harada T, Gangeswaran R, Manson-Bishop C, Smith P, Danovi SA, Pardo O, Crook T, Mein CA, Lemoine NR, Jones LJ, Basu S

Yes-associated protein (YAP) has been shown to positively regulate p53 family members and to be negatively regulated by the AKT proto-oncogene product in promoting apoptosis. On the basis of this function and its location at 11q22.2, a site of frequent loss of heterozygosity (LOH) in breast cancer, we investigated whether YAP is a tumor suppressor in breast. Examination of tumors by immunohistochemistry demonstrated significant loss of YAP protein. LOH analysis revealed that protein loss correlates with specific deletion of the YAP gene locus. Functionally, short hairpin RNA knockdown of YAP in breast cell lines suppressed anoikis, increased migration and invasiveness, inhibited the response to taxol and enhanced tumor growth in nude mice. This is the first report indicating YAP as a tumor suppressor, revealing its decreased expression in breast cancer as well as demonstrating the functional implications of YAP loss in several aspects of cancer signaling.Cell Death and Differentiation advance online publication, 11 July 2008; doi:10.1038/cdd.2008.108.



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Source: http://www.hubmed.org/display.cgi?uids=18617895
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