Study: Certain Leukemias Related to Treatment

  (NIH) - 2/22/2013 0 - A new study describes the pattern of risk for one form of cancer, acute myeloid leukemia (AML), that has risen over the past three decades for adults who have previously been treated with chemotherapy for other forms of cancer, notably non-Hodgkin’s lymphoma.
   The findings, from researchers at the National Cancer Institute (NCI), part of NIH, and colleagues, appeared online in Blood on Feb.14, 2013. Although these findings were based on small numbers of patients, they are intriguing in light of recent changes in treatment practices for these cancer patients.
   The researchers noted that chemotherapy is often a very effective treatment for cancer, and the subsequent risk of leukemia is generally low for an individual patient. The authors indicated that the increased risk among NHL survivors could be due to prolonged survival in recent years for some lymphoma subtypes that are associated with multiple courses of chemotherapy.
   Over the study time period, the researchers observed declining risk among patients treated for ovarian cancer, myeloma, and possibly lung cancer. The decreased risk among patients with ovarian cancer is consistent with a shift from use of an alkylating agent called melphalan to platinum-based chemotherapy in the early 1980s.
   “It has long been known that some types of chemotherapy are associated with a high risk of developing subsequent leukemia, particularly when treatments include certain alkylating agents,” said lead author Lindsay Morton, Ph.D., in NCI’s Radiation Epidemiology Branch in the Division of Cancer Epidemiology and Genetics. “The goal of this study was to better understand how cancer patients’ risk of developing leukemia has changed over time.”
   The authors also found evidence that the risk of treatment-related AML has increased since 2000 among patients treated for esophageal, prostate, and cervical cancer and since the 1990s among patients treated for cancers of the bones and joints and of the endometrium.
   Morton and colleagues used data from NCI’s Surveillance Epidemiology and End Results (SEER) cancer registries to evaluate the risk of leukemia in more than 426,000 adults who had been diagnosed with cancer between 1975 and 2008 and who had received chemotherapy as part of their initial cancer treatment.
   Among these patients, the authors identified 801 people who subsequently developed AML. Because the data came from SEER cancer registries, information on specific drugs used to treat each individual patient was not available. A unique feature of the study was the ability to evaluate leukemia risks in a large number of patients treated with chemotherapy in the current treatment era (2001-2008).
   The researchers say it is important to identify patient groups that have the highest risks of treatment-related leukemia, particularly for patients with cancers that have favorable survival potential, so that efforts to prevent a return of the disease can be implemented where possible. Future studies are needed to gather information on the risks associated with specific chemotherapy agents, which could not be obtained from this study.
   “In addition, it will be interesting to evaluate the role of a patient’s genetic susceptibility to treatment-related leukemia,” added Morton. “If certain inherited traits predispose patients to a second malignancy as a result of treatment, clinicians could more accurately weigh the risk of leukemia against the established benefits of chemotherapy.”

Group says ethanol blend would be nightmare

   (EWG) 2/19/2013 - The Environmental Working Group recently welcomed the introduction of legislation to block the use of gasoline containing 15 percent corn ethanol by U.S. Sens. Roger Wicker (R-Miss.) and David Vitter (R-La.), calling it a good first step in addressing concerns about the broader use of higher ethanol blends.
   Currently most gasoline contains no more than 10 percent corn ethanol, but the Environmental Protection Agency decided last year to permit the use of the higher blend, known as E15, in cars and trucks made since 2001.
   “E15 is a consumer nightmare waiting to happen,” EWG Vice President of Government Affairs Scott Faber said. “If every major carmaker, AAA and the Coast Guard are all saying the same thing, it’s time for Congress to take notice.”
   E15 has been found to cause engine damage in tests conducted by the U.S. Department of Energy and manufacturers of boats and cars. Chrysler, Toyota and other auto makers have that said that their warranties will not cover E15-related claims, and others warn that E15 does not meet the fuel requirements detailed in their owners’ manuals.
   The American Automobile Association has called on EPA to suspend the sale of E15 due to the likelihood of confusion at the pump and costly vehicle damage. In July 2009, the U.S. Coast Guard told the EPA that it, too, opposed the introduction of E15, citing possible safety risks to recreational boaters.

Former co-founder of hedge fund sentenced

   NEW YORK - 2/14/2013 - Steven Fortuna, who co-founded the hedge fund S2 Capital LLC (S2), was sentenced today to two years of probation for his participation in an insider trading scheme in which he obtained and traded on material, nonpublic information about various publicly-traded companies from employees at other hedge funds, announced U.S. Attorney for the Southern District of New York Preet Bharara. Fortuna pleaded guilty in October 2009 to three counts of conspiracy to commit securities fraud and one count of securities fraud under a cooperation agreement with the government. He was sentenced on February 13 in federal court by U.S. District Judge Sidney H. Stein.
   According to court documents, statements made during Fortuna’s guilty plea proceeding and the government’s sentencing submission in his case suggest that from July 2008 through March 2009, while working as a portfolio manager at a hedge fund he co-founded, Fortuna obtained inside information concerning various technology companies from employees at other hedge funds for the purpose of trading on that information. The inside information was disclosed by company insiders in breach of their duties to their respective employers.
   For example, in July and August 2008, Fortuna obtained inside information concerning Akamai Inc. from Danielle Chiesi, a portfolio manager at New Castle Partners, a hedge fund. Chiesi told Fortuna that Akamai planned to report that its revenue guidance for the following quarter would miss expectations and that, internally, the company believed that its stock price would fall following the quarterly earnings announcement. Fortuna executed trades based on that Inside Information, and earned approximately $2.4 million in profits for S2.
   As part of the conditions of his probation, Fortuna, 50, of Westwood, Mass., was ordered to serve six months on home confinement with electronic monitoring, and 120 hours of community service during each of the years of his probation. He was also ordered to pay forfeiture in the amount of $200,000, and a $400 special assessment fee.
   Mr. Bharara praised the investigative work of the FBI. He also thanked the U.S. Securities and Exchange Commission.
   This case was brought in coordination with President Barack Obama’s Financial Fraud Enforcement Task Force, on which Mr. Bharara serves as a Co-Chair of the Securities and Commodities Fraud Working Group. The case is being handled by the Office’s Securities and Commodities Fraud Task Force. Assistant U.S. Attorney Antonia M. Apps is in charge of the prosecution.

Link identified between metabolism, breast cancer

   (NIH) - 2/6/2013 - A protein associated with conditions of metabolic imbalance, such as diabetes and obesity, may play a role in the development of aggressive forms of breast cancer, according to new findings by researchers at the National Cancer Institute (NCI), part of the National Institutes of Health, and their colleagues. Metabolic imbalance is often caused by elevated carbohydrate intake, which can lead to over-activating a molecule called C-terminal binding protein (CtBP). This over-activation, in turn, can increase the risk of breast cancer. Results of their work appeared in Nature Communications, Feb. 5, 2013.
   “Modifying diet and maintaining a healthy diet, combined with developing pharmacological ways of lessening CtBP activity, may one day lead to a way to break the link between cancer and obesity,” said Kevin Gardner, M.D., Ph.D., head of NCI’s Transcription Regulation Section, Genetics Branch.
   It has been known, primarily through population based studies, that there is a strong link between obesity and cancer. But the mechanism behind this link has been uncertain. A previous study conceived and carried out in Gardner’s laboratory found that CtBP repressed expression of a gene associated with breast cancer (BRCA1) at an early age by sensing when the cell was in a high metabolic state that, in turn, led to processing large amounts of carbohydrates in the body.
    This early study suggested that obesity and weight gain may contribute to breast cancer by decreasing the level of the BRCA1 tumor suppressor gene expression in response to high carbohydrate intake. This explains, in part, why women who have hereditary mutations of BRCA1 also experience an increased risk of breast cancer if they gain weight.
   Gardner’s new study expands upon his past work. He analyzed prior gene expression studies to determine if gene pathways, repressed by CtBP, were diminished in breast cancer patients who suffered from more aggressive clinical outcomes. Gardner’s team began first with the human breast cancer cells in the laboratory. They measured the association of CtBP and the genes it bound to in order to regulate expression. The researchers combined this approach with genome sequencing to confirm how, and where, CtBP bound to genes associated with breast cancer. Next, they integrated analyses with gene expression studies in cells in which they observed decreased the levels of CtBP by RNA interference (a process that inhibits gene expression), or by decreasing carbohydrate feeding of the cells.
   The scientists found that, under conditions where they decreased the levels of CtBP, DNA repair increased and the cells developed stability and growth control. They determined that gene pathways targeted by CtBP were also disrupted in more aggressive breast cancers. Moreover, patients with high levels of CtBP in their tumors had shortened survival. And they showed that a small molecular inhibitor previously shown to bind to CtBP was able to reverse the gene-repressive effects of CtBP in breast cancer cells even under conditions of high carbohydrate feeding.
   “Our new work suggests that targeting CtBP may provide a way of treating breast cancer and possibly preventing breast cancer,” Gardner said. “Research should continue to focus on the link between obesity, CtBP and breast cancer. This will require more population-based studies and multi-disciplinary teams of scientist to investigate these links.”
   This project was funded by NCI project number 1Z01BC010847-01.
   Source: National Institutes of Health

Decision On Tossing Ethanol Mandate Applauded

   (EWG) - Washington - 2/4/2013 - A U.S. Appeals Court decision to throw out the 2012 federal mandate requiring refiners to blend cellulosic ethanol into the domestic gasoline supply should be wake-up call to Congress that the nation’s biofuels policy is in sore need of reform, said Environmental Working Group Vice President for Government Affairs Scott Faber.
  The U.S. Court of Appeals in Washington, D.C. sided on Friday with gasoline refiners who argued that requirements for using cellulosic ethanol under the Renewable Fuel Standard were based on unrealistic production forecasts by the Environmental Protection Agency.
   “The ethanol mandate has been a disaster for most farmers, consumers, taxpayers and the environment. The court's decision to strike down large parts of the mandate creates a rare opportunity to reform the mandate to help consumers and the environment and to pave the way for truly sustainable biofuels. Now is the time to reform the ethanol mandate to reduce the amount of food and feed being diverted to fuel and to create a level playing field for promising new fuels that don't pit our energy needs against our food and environmental needs," Faber said.