“Top artists announced to perform in tribute show - Indiana Gazette” plus 4 more |
- Top artists announced to perform in tribute show - Indiana Gazette
- Malignant Signature Identifies Possible Response To Therapy - Medical News Today
- Overexpressed protein converts noninvasive breast cancer into invasive ... - EurekAlert
- BMW Championship: Tracking Tiger, and Phil - Chicago Tribune
- Bras With Flair on the Square Seeks Bedazzled Bras and a Soon to be ... - PR Inside
| Top artists announced to perform in tribute show - Indiana Gazette Posted: 08 Sep 2009 07:59 AM PDT |
| Malignant Signature Identifies Possible Response To Therapy - Medical News Today Posted: 07 Sep 2009 03:57 AM PDT Main Category: Cancer / Oncology Also Included In: Pancreatic Cancer; Breast Cancer; Melanoma / Skin Cancer Article Date: 07 Sep 2009 - 4:00 PDT
A molecular signature that helps account for the aggressive behavior of a variety of cancers such as pancreatic, breast and melanoma may also predict the likelihood of successful treatment with a particular anti-cancer drug. The finding, which could lead to a personalized approach to treatment for a variety of solid tumors that are currently resistant to therapies, will be published September 6 in the advance online edition of Nature Medicine. Researchers at the Moores Cancer Center at the University of California, San Diego have discovered that a receptor sitting on the surface of certain aggressive tumor cells can activate a key enzyme, src-kinase, which helps tumor cells become more aggressive in the body. This enzyme is the target of the anticancer drug dasatinib, which blocks its activity and is currently approved for treating chronic myelogenous leukemia (CML). The scientists say that the presence of the receptor - a protein called integrin alpha-v beta-3 - on some of the more common solid tumors such as breast, colon, lung and pancreas could help identify individuals with many other types of cancer that are also likely to respond to the drug. "These results could enable us to identify the subpopulation of cancer patients who are likely to respond to treatment with dasatinib," said David Cheresh, PhD, professor and vice chair of pathology at the UC San Diego School of Medicine and the Moores UCSD Cancer Center, who led the work. "Rather than treat all patients with a given tumor type the same way, by identifying a specific molecular signature consisting of the receptor and its activated enzyme, we can customize the treatment in such a way that we impact the patients most likely to be sensitive to a drug." The researchers compared the growth properties of pancreatic and breast cancer cells that expressed the alpha-v beta-3 receptor versus those that did not, which led to the discovery of a molecular pathway that accounted for the increased malignancy. "Once we identified the pathway, we immediately realized that the drug dasatinib, which targets this pathway, would be a logical choice to use against these cancers," Cheresh said. The group's studies in a preclinical model of pancreatic cancer confirmed that those tumor cells with the receptor responded to the drug, while those not expressing receptors did not. Cheresh pointed to pancreatic cancer tumors, approximately 60 percent of which carry the marker on the tumor cell surface. "We would argue that pancreatic cancer patients with alpha-v beta-3 would respond to dasatinib," he said. Tumors lacking the marker appear to be resistant to the drug. "We discovered an unexpected pathway that accounts for increased malignancy in a population of some of the most dangerous cancers," Cheresh said, noting that the marker could be identified by a biopsy. "There are features of the findings that allow us to implicate dasatinib not just for a single tumor type, but for all tumors with the malignant signature." The findings have led to discussions about the potential design of a clinical trial. "These observations suggest a strategy for testing the effectiveness of dasatinib in breast cancer patients who are positive for the alpha-v beta-3 receptor," said Barbara Parker, MD, medical director of oncology services at the Moores UCSD Cancer Center. Co-authors include: Jay Desgrosellier, PhD, Leo Barnes, David Shields, PhD, Miller Huang, Steven Lau, Nicolas Prevost, David Tarin, MD, and Sanford Shattil, MD. Source  This posting includes an audio/video/photo media file: Download Now |
| Overexpressed protein converts noninvasive breast cancer into invasive ... - EurekAlert Posted: 08 Sep 2009 11:27 AM PDT ![[ Back to EurekAlert! ]](http://www.eurekalert.org/images/back2e.gif){kind=small} Public release date: 8-Sep-2009[ | E-mail |  Share ] Contact: Scott Merville Protein allows cells altered by the oncoprotein ErbB2/HER2 to escape their bondsHOUSTON ― Active, but non-invasive breast cancer is set free to roam as invasive breast cancer when an overexpressed protein converts it to a different cell type, scientists at The University of Texas M. D. Anderson Cancer Center report in the Sept. 9 issue of the journal Cancer Cell. "We have discovered a key molecular mechanism for the deadly transition of non-invasive breast cancer into invasive disease," said senior author Dihua Yu, M.D., Ph.D., professor in M. D. Anderson's Department of Molecular and Cellular Oncology. Overexpression of the protein 14-3-3ζ (zeta) launches a molecular cascade that removes bonds that tie the premalignant cells together and hold them in place, converting them from stationary epithelial cells to highly mobile mesenchymal-like cells, Yu and colleagues report. This epithelial-to-mesenchymal transition (EMT) is recognized as a crucial step in metastasis, the spread of cancer to distant organs that causes 90 percent of all cancer deaths. The researchers show that 14-3-3ζ teams with the oncoprotein ErbB2, also known as HER2, in a two-hit process to convert normal mammary cells to invasive cancer cells. In addition to identifying this key step in EMT, Yu notes the findings also provide:
Yu and colleagues previously showed that 14-3-3ζ is overexpressed in many other cancer types, like lung, liver, uterine, stomach cancers. "Our findings might have broader implications relating to the mechanism of invasion and metastasis in other types of cancer," Yu said. Unzipping cancer cells The team set out to address a longstanding puzzle, Yu said. ErbB2, an oncoprotein that promotes metastasis, is overexpressed in 50 to 60 percent of the noninvasive breast cancer known as ductal carcinoma in situ (DCIS). However, that same protein is overexpressed in only about 25 percent of invasive breast cancers, which seemed counterintuitive. In a series of lab experiments, Yu and colleagues showed that overexpression of ErbB2 accompanied by overexpression of 14-3-3ζ can change DCIS into invasive breast cancer. This only occurs in about half of ErbB2-overexpressing DCIS, the team found, explaining the numerical puzzle. Overexpression of ErbB2 converts normal breast duct cells into abnormal cells that reproduce quickly, are capable of moving, and resist programmed cell death that usually kills aberrant cells. What prevents these DCIS cells from becoming invasive, Yu said, is that they are locked together in zipper-like fashion by the cell surface protein E-cadherin, a trait known as cell-cell adhesion. "Overexpression of 14-3-3ζ is the catalyst for a molecular pathway that strips E-cadherin from the cells, setting the cells loose from each other," Yu said. These cells also change in appearance from blunt normal breast duct cells to a narrow spindle shape characteristic of a mesenchymal-like cell. Double overexpression reduces survival time Epithelial cells line an organ or its cavities and are generally immobile. Mesenchymal cells are mobile and can differentiate into many different cell types, for example, to repair injury. Epithelial-mesenchymal transition is known to repress E-cadherin, decrease cell-cell adhesion and increase a cell's capacity to move. An estimated 80 percent of all solid tumors are carcinomas, cancers of the epithelial tissue. Mice injected with a breast cancer cell line with both proteins overexpressed had three times the metastasis as mice with a control cancer cell line. The researchers examined 107 invasive breast cancer cases and found that 23 of the cancers overexpressed both proteins. Those patients also had significantly shorter survival times due to metastasis-related deaths than those whose tumors expressed one or neither of the proteins. Overexpressed 14-3-3ζ, the team showed, interacts with and stabilizes the receptor protein TβR1, which activates smad2/3 and moves them into the cell nucleus, where they in turn increase expression of ZFHX1B, which then represses expression of the adhesion protein E-cadherin. Yu said that it will be very challenging to target 14-3-3ζ by drugs because it also regulates other important proteins in normal cellular processes. The downstream components such as TβR1 can be targeted with drugs that are under clinical trials. Research was funded by grants from the National Cancer Institute, the U.S. Department of Defense Center of Excellence Grant and a synergistic Award, a Susan G. Komen Breast Cancer Foundation Promise Grant and the Royal Golden Jubilee Program of the Thailand Research Fund. Co-authors with Yu are first author Jing Lu, Ph.D., Hua Guo, M.D., Warapen Treekitkammongkol, Ph.D., Ping Li, Jian Zhang, Ph.D., Bin Shi, Ph.D., Xiaoyan Zhou, M.D., Ph.D., Tongzhen Chen, M.D., and Mien-Chie Hung, Ph.D., all of the Department of Molecular and Cellular Oncology; Hung also is associated with China Medical University and Hospital in Taiwan; Paul Chiao, Ph.D., of M. D. Anderson's Department of Surgical Oncology; Ayesegui Sahin, M.D., of M. D. Anderson's Department of Pathology; Chen Ling of the Molecular Oncology Group, McGill University Health Center in Montreal; Xinhua Feng, Ph.D., of the Department of Molecular and Cellular Biology, Baylor College of Medicine; and Victoria Seewaldt, M.D., of the Duke University Department of Medicine. About M. D. Anderson The University of Texas M. D. Anderson Cancer Center in Houston ranks as one of the world's most respected centers focused on cancer patient care, research, education and prevention. M. D. Anderson is one of only 40 comprehensive cancer centers designated by the National Cancer Institute. For six of the past eight years, including 2009, M. D. Anderson has ranked No. 1 in cancer care in "America's Best Hospitals," a survey published annually in U.S. News & World Report. [ | E-mail | Share ]
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| BMW Championship: Tracking Tiger, and Phil - Chicago Tribune Posted: 08 Sep 2009 11:13 AM PDT Team Fan ShopBears, Bulls, Cubs, Hawks, Sox: $4.99 3-day shipping on any order.  This posting includes an audio/video/photo media file: Download Now |
| Bras With Flair on the Square Seeks Bedazzled Bras and a Soon to be ... - PR Inside Posted: 08 Sep 2009 11:05 AM PDT 2009-09-08 19:56:24 - Cincy Chic to Host Third Annual Breast Cancer Awareness Event to Benefit Susan G. Komen for the Cure
Cincinnati, OH — September 8, 2009 — Cincy Chic, the leading online publication for women in Greater Cincinnati, is hosting its third annual Bras With Flair event on Fountain Square September 30, 2009. Cincy Chic is asking for donated and decorated bras from organizations and individuals in the Greater Cincinnati area and silent auction items for the after party at the Hilton Netherland Plaza.All bras will be displayed on Fountain Square during the event and proceeds from the silent auction items will go directly to the Susan G. Komen for the Cure. Those wishing to donate items to the silent auction or donate a decorated bra can drop off items at any LA Fitness location in the Tri-State area before September 25, 2009. "What better way to show support for the Susan G. Komen for the Cure than decorating a support garment of your own?" Cincy Chic Publisher Amy Storer-Scalia said. "The bras will be displayed at various times throughout the day on Fountain Square and during the grand finale fashion show at 6:30 p.m. Visitors can vote for their favorite design and the top ten bras that receive the most votes will be auctioned off at the after party." Cincy Chic, Elements Event and Conference Center and the Wedding Mafia will be giving away a wedding package valued around $25,000 to an engaged Cincinnati woman who is a Breast Cancer Survivor. The Elements and Conference Center and Wedding Mafia bridal package will be awarded to one engaged Breast Cancer survivor and 150 word nominations can be sent to info@cincychic.com. Cincinnati.com and Cincy Chic will also be donating a Breast Cancer Survivor Makeover valued at more than $5,000. Nominations for the Cincinnati.com makeover package can be submitted online at vovici.com/wsb.dll/s/5953g3f9f2. The deadline for each contest entry is September 15, 2009 and ten finalists will be chosen for a Cincy Chic reader vote from September 21 to September 25, 2009. For more information about the Cincy Chic event Bras With Flair on the Square, rules and contest information for the Wedding Giveaway or Breast Cancer Survivor Makeover visit www.cincychic.com/braswithflair or contact Cincy Chic at info@cincychic.com. To see "What's Chic this Week" in the city visit Cincy Chic's latest blog on the Cincinnati Enquirer site, cincinnati.com/blogs/cincychic/.
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