Fwd: Natural killer cell neoplasms.

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From: HubMed - cancer <rssfwd@rssfwd.com>
Date: Fri, Feb 22, 2008 at 10:18 AM
Subject: Natural killer cell neoplasms.
To: mesothelioma77@gmail.com


[1]Cancer. 2008 Feb 19;
Liang X, Graham DK

Natural killer (NK) cell tumors are an uncommon and heterogeneous group of disorders. The World Health Organization (WHO) classified mature NK cell neoplasms into 2 types: 1) extranodal NK cell lymphoma, nasal type and 2) aggressive NK cell leukemia. The mature NK cell tumors are prevalent in Asia and Central and South America. These tumors show polymorphic neoplastic infiltrate with angioinvasion and/or angiodestruction, cytoplasmic azurophilic granules, CD2-positive (CD2(+))/CD3-negative (CD3(-))/cCD3epsilon(+)/CD56(+) phenotype, and strong association with Epstein-Barr virus (EBV). Loss of chromosomes 6q, 11q, 13q, and 17p are recurrent aberrations. Although blastic NK cell lymphoma, currently referred to as CD4(+)/CD56(+) hematodermic neoplasm, also was included in the NK cell lymphoma category in the WHO classification scheme, existing evidence indicates a plasmacytoid dendritic cell derivation as opposed to an NK cell origin. Recently, rare cases of CD56(+) immature lymphoid tumors have been reported in the literature. These tumors are characterized by blastic appearance, CD3(-)/CD4(-)/CD56(+)/CD13(-)/CD33(-) phenotype, T-cell receptor and immunoglobulin genes in germline configuration, and no evidence of EBV, suggesting a true immature NK cell derivation. For this article, the authors reviewed the recent concepts and progress in clinicopathologic features, pathogenesis, genetic characteristics, diagnosis, differential diagnosis, treatment approaches, and outcomes of all subtypes of NK cell neoplasms. Cancer 2008. (c) 2008 American Cancer Society.



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Source: http://www.hubmed.org/display.cgi?uids=18286525
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Fwd: XPC polymorphisms play a role in tissue-specific carcinogenesis: a meta-analysis.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Fri, Feb 22, 2008 at 10:18 AM
Subject: XPC polymorphisms play a role in tissue-specific carcinogenesis: a meta-analysis.
To: mesothelioma77@gmail.com


[1]Eur J Hum Genet. 2008 Feb 20;
Francisco G, Menezes PR, Eluf-Neto J, Chammas R

XPC participates in the initial recognition of DNA damage during the DNA nucleotide excision repair process in global genomic repair. Polymorphisms in XPC gene have been analyzed in case-control studies to assess the cancer risk attributed to these variants, but results are conflicting. To clarify the impact of XPC polymorphisms in cancer risk, we performed a meta-analysis that included 33 published case-control studies. Polymorphisms analyzed were Lys939Gln and Ala499Val. The overall summary odds ratio (OR) for the associations of the 939Gln/Gln genotype with risk of cancer was 1.01 (95% confidence interval (95% CI): 0.94-1.09), but there were statistically significant associations for lung cancer, observed for the recessive genetic model (Lys/Lys+Lys/Gln vs Gln/Gln), (OR 1.30; 95% CI: 1.113-1.53), whereas for breast cancer a reduced but nonsignificant risk was observed for the same model (OR 0.87; 95% CI: 0.74-1.01). The results for Ala499Val showed a significant overall increase in cancer risk (OR 1.15; 95% CI: 1.02-1.31), and for bladder cancer in both the simple genetic model (Ala/Ala vs Val/Val) (OR 1.30; 95% CI: 1.04-1.61) and the recessive genetic model (Ala/Ala+Ala/Val vs Val/Val) (OR 1.32; 95% CI: 1.06-1.63). Our meta-analysis supports that polymorphisms in XPC may represent low-penetrance susceptibility gene variants for breast, bladder, head and neck, and lung cancer. XPC is a good candidate for large-scale epidemiological case-control studies that may lead to improvement in the management of highly prevalent cancers.European Journal of Human Genetics advance online publication, 20 February 2008; doi:10.1038/ejhg.2008.6.



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Source: http://www.hubmed.org/display.cgi?uids=18285822
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Fwd: Additional MDA-MB-231 breast cancer cell matrix metalloproteinases promote invasiveness.

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Fri, Feb 22, 2008 at 10:17 AM
Subject: Additional MDA-MB-231 breast cancer cell matrix metalloproteinases promote invasiveness.
To: mesothelioma77@gmail.com


[1]J Cell Physiol. 2008 Feb 19;
Hegedüs L, Cho H, Xie X, Eliceiri GL

We are interested in two aspects of a given type of metastatic breast cancer: which potentially cancer-relevant genes are expressed and which factors determine invasiveness. Using reverse transcription real-time PCR, we detected gene expression of 26 matrix metalloproteinases (MMPs) in MDA-MB-231 breast cancer cells, including those of MMP-12, MMP-16 variant 2, MMP-19, MMP-20, MMP-21, MMP-23, MMP-24, MMP-25, MMP-25 variant 2, MMP-L1, MMP-26, MMP-27, and MMP-28, in contrast to the 13 MMPs detected until now in these cells. We found that MMP genes are expressed at widely different levels in these cells, over five orders of magnitude. After individual siRNA-induced depletions, we found that six additional species of cancer cell MMPs promote invasiveness in MDA-MB-231 cells: MMP-3, MMP-11, MMP-12, MMP-17, MMP-19, and MMP-23, thus raising the total to 12 endogenous MMPs which do so in these cells. The data support the conclusion that some cancer cell MMPs, although expressed at low levels, are needed for cancer trait in MDA-MB-231 cells, and that several endogenous MMPs play non-redundant roles in this process. The mRNA level of MMP-11, but not of other MMPs, rose substantially following individual siRNA-targeted depletion of cancer cell MMP-17 mRNA, while no MMP mRNA increased appreciably after degradation of other MMP mRNAs. This supports the conclusion that MMP-17 may be a member of an intracellular signaling pathway which downregulates MMP-11 mRNA. J. Cell. Physiol. (c) 2008 Wiley-Liss, Inc.



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Source: http://www.hubmed.org/display.cgi?uids=18286480
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Fw: ASBESTOS killer on the increase

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From: Search for mesothelioma diagnosis <rssfwd@rssfwd.com>
To: shell8377@yahoo.com
Sent: Wednesday, February 27, 2008 7:16:11 PM
Subject: ASBESTOS killer on the increase

A SILENT killer will cause devastation in more Suffolk families than ever before this year, it has been warned today.

Wed, 27 Feb 2008 16:10:18 GMT

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Source: http://www.eveningstar.co.uk/content/eveningstar/news/story.aspx?brand=ESTOnline&category=News&tBrand=ESTOnline&tCategory=News&itemid=IPED26%20Feb%202008%2011%3A57%3A29%3A510
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Fwd: [Future directions of anticancer drug development in Japan.]

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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Wed, Feb 20, 2008 at 4:02 AM
Subject: [Future directions of anticancer drug development in Japan.]
To: mesothelioma77@gmail.com


[1]Gan To Kagaku Ryoho. 2008 Feb; 35(2): 351-60
Akaza H, Kawai K, Tsuruo T, Tsukagoshi S, Aiba K, Shimada Y, Kakeji Y, Ishikawa H, Ikeda T, Nakamura S, Tamura T, Yamamoto N, Isonishi S, Hinotsu S, Hirose M, Katsura J

At the 13th Oncology Forum, future directions of anticancer drug development in Japan were discussed. Development of anticancer drugs in the 1990s was based on the concept of total cell kill, but now development of molecular targeted drugs becomes the mainstream. Unfortunately, molecular targeted drugs and antibody agents are mostly foreign products and translational research in Japan is poor as it stands now. As future directions of anticancer drug development, international collaborative development is considered essential, but there are various obstacles to the conduct of international collaborative studies. Companies, medical institutions and regulatory agencies must make collaborative efforts to overcome these obstacles. As future development of anticancer agents in individual cancer regions in Japan is considered, gastric cancer therapy is progressing considerably with the advent of S-1 and in the future, development of multi-agent combination therapy including molecular targeted agents is expected. Much progress in colon cancer therapy has been made owing to accumulation of evidence in recent years. Multi-agent chemotherapy combined with antibody agent, which is advancing overseas, is introduced to Japan. Clinical development of combination therapy with a high therapeutic index, including compounds discovered in Japan, is expected in the future. Although conventionally hormone therapy has been considered as first-line treatment of breast cancer and used in combination with chemotherapy, with the advent of antibody agents in recent years, HER2 sensitivity has greatly affected the algorithm of treatment. Future development of molecular targeted drugs and individualised diagnosis using cDNA array, etc. are likely to advance individualisation of treatment. On the other hand, large-scale clinical trials are required to prove a small difference in adjuvant therapy, etc. and accordingly international studies are becoming indispensable. For urological cancers, molecular targeted drugs have been proved effective in renal cancer and future development of molecular targeted drugs for prostate cancer and testicular tumors is desirable. At that time, elucidation of the mechanism of action of molecular targeted drug and strategic drug development designed to increase its efficacy are expected. As a future direction of anticancer drug development, there are many cancers in whose international collaborative studies Japan can participate. Studies of prostate cancer and renal cell carcinoma can be internationalised while internationalisation of studies in ovarian and pancreatic cancers is essential. Phase III should be performed as international collaborative studies and depending on the type of cancer and drug, collaborative studies in an Asian region are effective. When participating in an international collaborative study, Japan needs to recruit subjects at a speed similar to the rest of the world, but differences in medical environment including clinical trials pose a problem. To solve this problem, it is considered effective not only to pursue the Western environment but also to improve staff such as nurses and CRC. The number of Japanese patients necessary for Phase III studies is individual developmental strategy and needs to be examined by both companies and regulatory agencies.



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Source: http://www.hubmed.org/display.cgi?uids=18281781
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Fwd: Speak Out ... Auburn's run of success vs. Alabama is ending

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From: Search for lung cancer <rssfwd@rssfwd.com>
Date: Wed, Feb 20, 2008 at 4:02 AM
Subject: Speak Out ... Auburn's run of success vs. Alabama is ending
To: mesothelioma77@gmail.com

For six long, painful years, the graceless Tommy Tuberville and his merry band at Auburn have feasted on a decimated Alabama Crimson Tide football program.

Wed, 20 Feb 2008 08:21:10 GMT

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Source: http://www.annistonstar.com/opinion/2008/as-letters-0220-speakout-8b19u2531.htm
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Fwd: Wild Card -- Weekend

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From: Live Search News: asbestos cancer <rssfwd@rssfwd.com>
Date: Tue, Feb 19, 2008 at 7:36 AM
Subject: Wild Card -- Weekend
To: mesothelioma77@gmail.com


Spokane Spokesman-Review - ... Christmas season continues to give us a look under the hood re: what it's like to work in a mid-major newsroom, including insight into what interns discuss here and the heartache a young journalist feels when he spends the day with a 2-year-old cancer ...

Fri, 15 Feb 2008 23:53:00 GMT

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Source: http://www.spokesmanreview.com/blogs/hbo/archive.asp?mon=Dec2005
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