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HIV Transmission In Europe Occurs Primarily In Vacation Destinations, Study Finds
HIV in Europe is transmitted primarily in vacation destinations, according to a study published recently in the journal Retrovirology, the PA/Google.com reports. For the study, researchers led by Dimitrios Paraskevis of the University of Athens analyzed samples of HIV-1 subtype B virus, the most prevalent form of HIV in Europe, from 16 European countries and Israel (PA/Google.com, 5/20). The researchers created a family tree of the virus and examined its genetic characteristics to determine how it has evolved.The study found that tourists are more likely to contract HIV in Greece, Portugal, Serbia and Spain, which are popular vacation destinations. Meanwhile, HIV-positive people in Austria, Belgium, Denmark and Luxembourg are more likely to have contracted the virus outside of these countries. The study also found that HIV-positive people in Israel, Norway, the Netherlands, Sweden, Switzerland and the United Kingdom contract the virus both within these countries and in other countries. In addition, the study found that in Poland the virus spread mainly among residents through injection drug use. "Viruses move around with travelers -- thus health programs within countries should not only target the national populations, prevention efforts must also be aimed at migrants, travelers and tourists -- who are both major s and targets of HIV," Paraskevis said (BBC News, 5/20). Lisa Power, head of policy at the Terrence Higgins Trust, said that the findings are not a "surprise," adding, "We"ve known for some time with high levels of mobility in the world these days that it"s very easy for viruses to move around. What it tells us is that you can"t limit HIV prevention and support just to permanent residents" (PA/Google.com, 5/20).
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A Novel Marker Of Colorectal Carcinoma
Colorectal cancer is thought to result from a combination of environmental factors: diet, lifestyle, chronic inflammation and accumulation of specific genetic alterations. The pathogenesis and development of colorectal cancer involves multi-genes and multi-steps. TSPAN1 (GenBank Accession No. AF065388) is a new member of TM4SF located at chromosome 1 p34.1. It encodes a 241 amino acid protein. TSPAN1 was reported as a tumor-related gene recently.
News of the day
UC Davis Grant Zeroes In On Novel Asthma Diagnosis, Treatment
An entomology professor at the University of California, Davis who discovered a novel therapeutic target for treating inflammation, has received a three-year $750,000 grant from the American Asthma Foundation to investigate whether his discovery will work on asthma, a chronic disease affecting 300 million people worldwide, including 23 million Americans.
Endocrinology

Gene Signature Helps Predict Breast Cancer Prognosis

Vanderbilt-Ingram Cancer Center researchers have uncovered a gene signature that may help predict clinical outcomes in certain types of breast cancer. In the Journal of Clinical Investigation, Harold (Hal) Moses, M.D., and colleagues report that this gene signature - which is associated with the transforming growth factor-beta (TGF-í²) signaling pathway - correlates with reduced relapse-free survival in patients with breast cancer, especially in those with estrogen receptor (ER) positive tumors. The results suggest that assessing TGF-í² signaling may be a useful aid in determining breast cancer prognosis and in guiding treatment. The work also sheds light on how TGF-í² affects tumor growth and progression. TGF-í² is a well-known regulator of tumor growth and metastasis. In the early stages of cancer, TGF-í² signaling inhibits tumor growth. But for unclear reasons, most tumors eventually lose their sensitivity to TGF-í², and the once-beneficial protein begins promoting tumor growth and metastasis during later cancer stages. Loss of TGF-í² signaling has been linked to tumor progression in human breast cancer. To identify mechanisms by which TGF-í² regulates tumor progression and metastasis, Brian Bierie, Ph.D., a former graduate student in the Moses lab, developed mammary cancer cell lines from mice lacking the TGF-í² type II receptor (Tí²RII), an important component of the TGF-í² signaling pathway. Bierie examined gene expression in these cell lines and found that TGF-í² signaling regulates the expression of chemokines, inflammation-associated chemical signals that direct the migration of cells - particularly, the expression of chemokines CXCL1 and CXCL5. To determine the clinical relevance of this gene expression profile, Moses and Bierie collaborated with Christine Chung, M.D., and biostatistician Yu Shyr, Ph.D., to probe human breast cancer gene expression profiles available in public databases. They found that the gene signature representing a complete elimination of TGF-í² signaling correlated with significantly reduced relapse-free survival in all patients. This association was even stronger in patients with estrogen receptor (ER) positive tumors, a subtype of breast cancer that responds well to anti-estrogen therapies like tamoxifen. The results suggest that testing for this gene signature could aid in the prognosis and treatment of breast cancer, especially in ER positive tumors. The signature also points to chemokines as important mediators of TGF-í²"s effects on tumor growth. "I think one of the most significant aspects of this is that it is the first real demonstration that a major function of TGF-í² signaling is to suppress chemokine expression," said Moses, the Hortense B. Ingram Professor of Molecular Oncology, professor of Cancer Biology, and director of the Frances Williams Preston Laboratories. The results also point to several potential therapeutic approaches, including the inhibition of chemokines or their receptors, Moses said. Moses and colleagues previously found that inhibiting certain chemokines in a mouse model of breast cancer significantly decreased the number of lung metastases by decreasing the migration of myeloid cells - a type of immune cell involved in tumor progression - into the tumor. Targeting these myeloid cells would be a new kind of approach because it focuses on targeting normal cells outside of the tumor, or in the "stroma." "We"ve had decades of treatment targeted to the cancer cell, but very little in treatment of the stromal component," Moses said. Previous genetic signatures have been used to segregate patients that might benefit from chemotherapy from those that would derive little or no benefit - a step toward personalized cancer therapy. Moses suspects the TGF-í² associated signature could provide additional guidance in individualizing cancer treatment. "Gene profiling and biomarkers are the current directions of research to select treatments likely to benefit a given patient," Moses noted. "That"s the way the field is moving. That"s what we have to do." Other Vanderbilt co-authors include: Daniel Stover, M.D., Nikki Cheng, Ph.D., Anna Chytil and Mary Aakre. The research was supported by grants from the National Institutes of Health, the T. J. Martell Foundation, and the Robert J. and Helen C. Kleberg Foundation. Melissa Marino Vanderbilt University Medical Center


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