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Pitt Study: Esophageal Cancer Risk Higher in Medically Treated GERD Patients with Fewest Symptoms
University of Pittsburgh researchers have found that patients with lower levels of GERD symptoms have an increased likelihood of developing esophageal cancer. Patients with mild symptoms of GERD are less likely to be screened for Barrett's esophagus - a common precursor to cancer - than those with more severe symptoms. Read a complete analysis of the research here.
Scientists use stem cell-cancer cell hybrids to decrease tumor progression
In a study recently published in the International Journal of Oncology, scientists at the Chinese Academy of Sciences in Beijing showed that fusing human umbilical stem cells (human mesenchymal stem cells, or hMSC) with esophageal cancer cells (ECC), reduces the tumor-forming potential of the hybrids when compared to esophageal cancer cells alone. The researchers, led by Yong Wang in the lab of Shixin Lu, studied the tumorigenicity of these hybrids in cell culture and in mice. A hallmark of cancer cells is their increased rate of growth and division, as well as their resistance to apoptosis - the process of programmed, intentional cell death.
Apoptosis is a critical process by which old, defective or mutated cells self-destruct in order to allow turnover of normal tissues (in the case of old cells) or to prevent propagation of defects (in the case of genetic mutations). Remarkably, fusion of the hMSCs with ECCs led to increased apoptosis. In mice, tumors containing hybrid cells were significantly smaller, and had a longer latency period.
Furthermore, Wang and colleagues showed that a protein called DUSP6, shown in the past to be expressed at lower levels in ECCs, significantly increased apoptosis and inhibited growth when added back to those cells in culture. Researchers have a long way to go before developing methods such as the hybridization described by Wang et al into therapies, but work such as this helps scientists understand the processes and signals that could lead to improved treatments and outcomes for esophageal cancer.
Common mutation in skin and lung squamous cell carcinomas identified
Protein receptors that take signals from outside of a cell and activate cellular responses (e.g. telling the cell to grow, divide, or produce anti-inflammatory molecules) are critical to normal development of tissue, as well as maintaining homeostasis in fully developed tissues. The Notch receptors are proteins embedded in cell membranes that receive signals from nearby cells. Notch signaling is important in helping cells to decide how to develop as they grow from early-stage "progenitors" into more functionally specific daughter cells. In squamous cell carcinomas (SCC), this differentiation process is defective, leading to abnormal daughter cells that ultimately form tumors. SCCs can affect the esophagus, lungs, skin, and cervix.
In a recently published study in the Proceedings of the National Academy of Science, an interdisciplinary group of scientists led by Nicholas Wang and Zachary Sanborn of Lawrence Berkeley National Laboratory, and Raymond Cho of the University of California, San Francisco, identified several previously unknown mutations in the Notch family of receptors in skin and lung tumors which lead to defective Notch signaling. Their results indicate "that [non-functional] Notch plays a prominent role in multiple variants of SCC." Previous work from other studies showed that mutations causing hyperactive Notch play a role in cancers such as leukemia. As a result, cancer researchers have looked into the possibility of inhibiting Notch activity as a way of treating leukemia. However, this work by Wang et al, along with previous research showing reductions in Notch activity in skin cancers, is important for indicating that the context/location of Notch activity is critical for understanding its effects on cancer formation. Furthermore, these studies confirm that cancer therapies designed to inhibit Notch signaling have to take into account the potential side effects (some of which have been observed) of blocking this pathway.
National Cancer Institute awards multi-site, $8 million grant to study Barrett's Esophagus.
The grant will fund research to help develop models of Barrett's esophagus and its progression to esophageal adenocarcinoma, and includes researchers from Penn State, Columbia University, and the Mayo Clinic. Additionally, the group funded by this grant will coordinate efforts with researchers at the University of Michigan and Vanderbilt University.
For more, see the Penn State press release.
Analysis of 500,000 adults reveals no association between fat intake and esophageal cancer.
Healthy diet and lifestyle are keys to reducing the risk of cancer. However, a statistical analysis of nearly 500,000 adults recently published in the International Journal of Cancer indicates that increased dietary fat intake is not associated with increased risk for esophageal cancer, as has been previously suggested by some (but not all) studies.
In the report, researchers looked at approximately half a million adults ages 50-71 who, in 1995-96 filled out health surveys provided by the AARP. These surveys included questions on diet and health activities. Using state cancer registry databases, the researchers were able to determine who in the original group had been diagnosed with various forms of esophageal and gastric cancers. Statistical analysis controlling for other variables including but not limited to age, gender, smoking habits, and ethnicity, showed that although survey respondents who reported higher fat intake were more likely to contract diabetes, the same was not true for esophageal cancer.
Breaking down the results by fat type and source of the fat (i.e. red meat vs. margarine), the researchers still saw no significant correlation between fat intake and esophageal cancer. This study was one of the few to look at the potential association between fat intake and esophageal cancer, and among those was the largest, leading to much stronger statistical confidence in the results.
As with any study, the authors note limitations to their methodology, and, these results do not nullify the need for healthy diet and lifestyle in disease prevention. However, the work done in this analysis provides a valuable clarification of previously inconsistent results.
