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Archive - Nov 2012

Date

November 3rd

New Means to Kill Malaria Parasiste

Malaria causes up to 3 million deaths each year, predominantly afflicting vulnerable people such as children under five and pregnant women, in tropical regions of Africa, Asia, and Latin America. Treatments are available for this disease, but the Plasmodium parasite is fast becoming resistant to the most common drugs, and health authorities say they desperately need new strategies to tackle the disease. This new potential treatment uses molecules that interfere with an important stage of the parasite's growth cycle and harnesses this effect to kill them. The impact is so acute it kills ninety per cent of the parasites in just three hours and all those tested in laboratory samples of infected human blood cells, within twelve hours. The research was carried out by chemists at Imperial College London and biological scientists from the research institutions Institut Pasteur and CNRS in France. Their work was published in the the October 9, 2012 issue of PNAS. Lead researcher Dr. Matthew Fuchter, from Imperial College London, said: "Plasmodium falciparum causes 90 per cent of malaria deaths, and its ability to resist current therapies is spreading dramatically. Whilst many new drugs are in development, a significant proportion are minor alterations, working in the same way as current ones and therefore may only be effective in the short term. We believe we may have identified the parasite’s 'Achilles' Heel, using a molecule that disrupts many vital processes for its survival and development." The research has identified two chemical compounds that affect Plasmodium falciparum's ability to carry out transcription, the key process that translates genetic code into proteins. These compounds are able to kill the parasite during the long period of its complex life cycle while it inhabits the blood-stream.

Whitehead Scientists Identify Major Flaw in Standard Approach to Global Gene Expression Analysis

Whitehead Institute researchers report that common assumptions employed in the generation and interpretation of data from global gene expression analyses can lead to seriously flawed conclusions about gene activity and cell behavior in a wide range of current biological research. "Expression analysis is one of the most commonly used methods in modern biology," says Whitehead Member Dr. Richard Young. "So we are concerned that flawed assumptions may affect the interpretation of many biological studies." Much of today's interpretation of gene expression data relies on the assumption that all cells being analyzed have similar total amounts of messenger RNA (mRNA), the roughly 10% of a cell's RNA that acts as a blueprint for protein synthesis. However, some cells, including aggressive cancer cells, produce several times more mRNA than other cells. Traditional global gene expression analyses have typically ignored such differences. "We've highlighted this common assumption in gene expression analysis that potentially affects many researchers," says Dr. Tony Lee, a scientist in Dr. Young's lab and a corresponding author of the article published in the October 26, 2012 issue of Cell. "We provided a concrete example of the problem and a solution that can be implemented by investigators." Members of the Dr. Young lab recently uncovered the flaw while investigating genes expressed in cancer cells expressing high levels of c-Myc, a gene regulator known to be highly expressed in aggressive cancer cells. When comparing cells with high and low c-Myc levels, they were surprised to find very different results using different approaches to gene expression analysis.

November 3rd

New Clues for Overcoming Tamoxifen-Resistant Breast Cancer

A University of Cincinnati (UC) cancer biology team reports breakthrough findings about specific cellular mechanisms that may help overcome endocrine (hormone) therapy-resistance in patients with estrogen-positive breast cancers, combating a widespread problem in effective medical management of the disease. Xiaoting Zhang, Ph.D., and his colleagues have identified a specific estrogen receptor co-activator—known as MED1—as playing a central role in mediating tamoxifen resistance in human breast cancer. The team reported its findings online in the Nov. 1, 2012, issue of Cancer Research, a scientific journal of the American Association for Cancer Research. According to the National Cancer Institute, nearly 227,000 women are diagnosed with breast cancer annually in the United States. About 75 percent have estrogen-positive tumors and require adjuvant hormone therapy such as tamoxifen, a drug that works by interfering with estrogen’s ability to stimulate breast cancer cell growth. Despite advances in hormone therapy drugs, cancer surveillance research has shown that 50 percent of patients will develop resistance to the drug and experience a cancer relapse. The hormones estrogen and progesterone can stimulate the growth of some breast cancers. Hormone therapy is used to stop or slow the growth of these tumors. Hormone-sensitive (i.e., positive) breast cancer cells contain specific proteins known as hormone receptors that become activated once hormones bind to them, leading to cancer growth. Based on new findings, UC Cancer Institute scientists believe that tamoxifen resistance may be driven by a novel molecular "crosstalk” point between the estrogen and HER2 (human epidermal growth factor receptor 2) signaling pathways.

Multicenter Team Identifies Promising Treatment for Polycystic Kidney Disease

A drug therapy shows promise for treating an inherited form of kidney disease called autosomal dominant polycystic kidney disease (ADPKD), Mayo Clinic researchers say. The medication, tolvaptan, slowed the pace of kidney cyst growth over the three years of the study. The phase three clinical trial results were being presented on November 3, 2012 at the American Society of Nephrology annual meeting and published online in the New England Journal of Medicine. The multicenter study found tolvaptan demonstrated a nearly 50 percent reduction in the rate of increase in total kidney volume (a measurement of kidney cyst growth) in ADPKD patients over the study period, compared to placebo. "ADPKD is the most common inherited and the fourth most common overall cause of kidney failure worldwide," says lead author Vicente Torres, M.D., Ph.D., Mayo Clinic nephrologist. "In most patients with this disease, relentless cyst growth within the kidneys destroys the tissue, causes hypertension and painful complications, and negatively impacts the quality of life," Dr. Torres says. "The results of this study reveal a potential treatment that blunts kidney growth, lessens associated symptoms, and slows kidney function decline when given over three years." While the trial findings are encouraging, tolvaptan has not yet been approved for this indication, Dr. Torres notes. [Press release] [New England Journal of Medicine]