Syndicate content

Archive - Jul 29, 2014

Date
  • All
  • 1
  • 2
  • 3
  • 4
  • 5
  • 6
  • 7
  • 8
  • 9
  • 10
  • 11
  • 12
  • 13
  • 14
  • 15
  • 16
  • 17
  • 18
  • 19
  • 20
  • 21
  • 22
  • 23
  • 24
  • 25
  • 26
  • 27
  • 28
  • 29
  • 30
  • 31

Wound-Healing Abilities of p53-Isoform May Be Hijacked by Cancers

Researchers at Cold Spring Harbor Laboratory (CSHL) have discovered a new function of the body's most important tumor-suppressing protein. Called p53 (image), this protein has been called "the guardian of the genome." It normally comes to the fore when healthy cells sense damage to their DNA caused by stress, such as exposure to toxic chemicals or intense exposure to the sun's UV rays. If the damage is severe, p53 can cause a cell to commit preprogrammed cell-suicide, or apoptosis. Mutant versions of p53 that no longer perform this vital function, on the other hand, are enablers of many different cancers. Cancer researcher Dr. Raffaella Sordella, Ph.D., a CSHL Associate Professor, together with colleagues, report today (July 29, 2014) online in PNAS the discovery of a p53 cousin they call p53-psi. It is a previously unknown variant of the p53 protein, generated by the same gene, called TP53 in humans, that gives rise to other forms of p53. Dr. Sordella and colleagues observed that p53-psi, when expressed, reduces the expression of a molecular glue called E-cadherin, which normally keeps cells in contact within epithelial tissue, the tissue that forms the lining of the lung and many other body organs. This is accompanied by expression of key cellular markers associated with tumor invasiveness and metastatic potential. (These are markers of EMT, or epithelial-to-mesenchymal transition.) Consistently, Dr. Sordella and her team found levels of p53-psi to be elevated in early-stage lung tumors with poor prognosis. Careful investigation revealed that p53-psi generates pro-growth effects by interacting with a protein called cyclophillin D (CypD), at the membrane of the cell's energy factories, the mitochondria, and by spurring the generation of oxidizing molecules called reactive oxygen species (ROS).

Gene Mutations Linked to Salivary Gland Tumors

Research conducted at the Florida campus of The Scripps Research Institute (TSRI) has discovered links between a set of genes known to promote tumor growth and mucoepidermoid carcinoma, an oral cancer that affects the salivary glands. The discovery could help physicians develop new treatments that target the cancer’s underlying genetic causes. Baseball Hall of Famer Tony Gwynn (image) recently died from complication of salivary gland cancer at the age of 54, bringing this disease into national prominence and, in his case, was widely attributed to the lengthy use of chewing tobacco. The new research, recently published online ahead of print on July 28, 2014 by PNAS, shows that a pair of proteins joined together by a genetic mutation—known as CRTC1/MAML2 (C1/M2)—work with MYC, a protein commonly associated with other cancers, to promote the oral cancer’s growth and spread. “This research provides new insights into the molecular mechanisms of these malignancies and points to a new direction for potential therapies,” says TSRI biologist Michael Conkright, Ph.D., who led the study. The C1/M2 protein is created when the genes encoding CRTC1 and MAML2 mutate into a single gene through a process known as chromosomal translocation. Such mutant “chimera” genes are linked to the formation of several forms of cancer. The team discovered that the C1/M2 protein further activates genetic pathways regulated by MYC, in addition to CREB, to begin a series of cellular changes leading to the development of mucoepidermoid carcinoma. “The identification of unique interactions between C1/M2 and MYC suggests that drugs capable of disrupting these interactions may have therapeutic potential in the treatment of mucoepidermoid carcinomas, ” said Antonio L.

Scientists ID Irreversible Inhibitor for KRAS Gene Mutation Involved in Lung, Colon, and Pancreatic Cancers

University of Texas (UT) Southwestern Medical Center cancer researchers have found a molecule that selectively and irreversibly interferes with the activity of a mutated cancer gene common in 30 percent of tumors. The molecule, SML-8-73-1 (SML), interferes with the KRAS gene, or Kirsten rat sarcoma viral oncogene homolog. The gene produces proteins called K-Ras (image) that influence when cells divide. Mutations in K-Ras can result in normal cells dividing uncontrollably and turning cancerous. These mutations are found particularly in cancers of the lung, pancreas, and colon. In addition, people who have the mutated gene are less responsive to therapy. Researchers have unsuccessfully tried to develop a drug to inhibit K-Ras for some 30 years. “RAS proteins including KRAS have not been ‘druggable’ for many decades despite a lot of effort from academia and industry,” said senior author Kenneth Westover, M.D., Ph.D, Assistant Professor of Radiation Oncology and Biochemistry, and a member of UT Southwestern’s Harold C. Simmons Cancer Center. “We are exploring irreversible inhibitors as a solution, which we believe may pave the way for the development of KRAS-targeted compounds with therapeutic potential and perhaps compounds that target other RAS family proteins involved in cancer,” Dr. Westover said. Dr. Westover works as both a clinician as a member of the Lung Radiation Oncology Team at the Simmons Cancer Center, and as a researcher. The Westover laboratory investigates the molecular basis of cancer with an eye toward developing compounds that perturb cancer biology, and therefore have potential to become therapies. Dr. Westover’s lab has been particularly targeting KRAS because this gene is the most commonly mutated oncogene in cancer. Building on previous work, Dr.

BioQuick Wins Fifth Consecutive Publishing Excellence Award

BioQuick Online News(TM)(http://www.bioquicknews.com) has recently been awarded an APEX 2014 Award for Publishing Excellence in the category of electronic publications. BioQuick also won prestigious APEX Publishing Excellence Awards in 2013, 2012, 2011, and 2010. BioQuick presently features over 1,500 available online articles on major life science advances in the last five years and articles of interest are readily accessible by means of a powerful search engine. BioQuick has readers in over 160 countries and includes a Japanese language edition (http://biomarket.jp/m/bioquicknews/index.php), directed by Yoshimitsu Obata, M.S., in Tokyo. To find out more information about BioQuick and to pursue advertising and sponsorship possibilities in this high-quality, far-reaching life science publication, please contact editor & publisher Mike O’Neill (M.A. in Immunology & Microbiology from Duke University and 15 years writing experience at Applied Biosystems) at logophile2000@yahoo.com. To learn more about the highly competitive international APEX Publishing Awards, please visit the awards web site at http://www.apexawards.com. One indicator of the overall quality of the competition is the high-quality organizations numbering among the winners. This year, these winners include the LA Times, the Washington Post, the Ford Motor Company, AARP, National Institute on Aging (NIH), Medscape from WebMD, Vanguard, American Medical Association, American Airlines, Lockheed Martin, Neurology Today, Walt Disney Company, CBS Corporation, Purdue University, American Society of Clinical Oncology, Sandia National Laboratories, Toyota Motor Sales, American Society of Plastic Surgeons, National MS Society, Consortium of Multiple Sclerosis Centers, Emergency Medicine News, Thermo Fisher Scientific, JAMA Network, U.