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Health Care Overhaul Could Include Changes To Doctor Payments
The Wall Street Journal reports that "Democratic centrists said they won a tentative commitment from the White House to back a proposal to curb the growth of Medicare costs. ... One proposal pushed both by President Barack Obama and some centrists is to give the executive branch the authority to implement cuts to Medicare spending that would be recommended by independent experts. Congress could stop the cuts, but only if it acted swiftly. Fiscal conservatives say that under the current system, which gives Congress more power, lawmakers shy away from politically tough votes to restrain Medicare costs."

Health Industry Officials Offer $2 Trillion Savings Plan To The White House
"Health industry officials delivered a plan to the White House Monday documenting how they"ll attempt to save $2 trillion over a decade through measures like reducing hospitalizations and cutting down on paperwork," the Associated Press reports. "Health insurers, doctors, hospitals, drug-makers and others were under pressure to make good on a pledge they made last month to curb their own costs to help President Barack Obama achieve his health care overhaul goals." Their three big areas of savings: $150 billion to $180 billion would come from more efficient use of health care services, $350 billion to $850 billion from better management of chronic diseases, and $500 billion to $700 billion through administrative improvements such as standardizing claim forms (Werner, 6/1).
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ZIOPHARM Presents Positive Darinaparsin Clinical Data At ASCO's Prestigious Clinical Science Symposium
ZIOPHARM Oncology, Inc. (Nasdaq: ZIOP) announced today that it presented positive data from both Phase II intravenous (IV) and Phase I oral studies of darinaparsin (ZinaparTM or ZIO-101), the novel organic arsenic molecule, as part of the prestigious Clinical Cancer Symposia at the 45th Annual American Society of Clinical Oncology (ASCO) meeting held in Orlando, FL, May 29th to June 2nd.
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Deadly Leukemia Stem Cells Found And Eliminated By New Targeted Therapy

New research describes a molecular tool that shows great promise as a therapeutic for human acute myeloid leukemia (AML), a notoriously treatment-resistant blood cancer. The study, published by Cell Press in the July 2nd issue of the journal Cell Stem Cell, describes exciting preclinical studies in which a new therapeutic approach selectively attacks human cancer cells grown in the lab and in animal models of leukemia. AML is a cancer of the white blood cells that has an extremely poor prognosis and does not respond well to conventional chemotherapy. "The cellular and molecular basis for this dismal picture is unclear," offers senior study author Associate Professor Richard Lock from the Children"s Cancer Institute Australia and the University of New South Wales. "However, previous research has suggested that leukemia stem cells (LSCs) may lie at the heart of post-treatment relapse and chemoresistance." LSCs are cells that can initiate AML and are critical for its long-term growth. Associate Professor Lock and colleagues exploited the fact that the molecule CD123 is expressed at very high levels on LSCs but not on normal blood cells. CD123 is part of the interleukin-3 receptor, a protein that interacts with a growth factor (called a cytokine) that influences cell survival and proliferation. The researchers created a therapeutic antibody that recognized and bound to CD123 with the hope that this antibody would selectively interfere with AML-LSC survival. When AML-LSCs from human patients were transplanted into mice treated with the antibody, called 7G3, cytokine signaling in the tumor cells was blocked. Further, 7G3 impaired migration of the AML-LSCs to bone marrow and activated the innate immune system of the host mouse to destroy the AML-LSCs. Overall, treatment with 7G3 substantially improved mouse survival when compared with control groups. The researchers go on to report that a CD123-targeting antibody is currently being used in phase 1 clinical trials of advanced AML and that there are no signs of treatment-related toxicity. These results hold substantial promise for future cancer therapeutics. "The recent characterization of defined populations of cancer stem cells in a range of human malignancies, as well as their relative resistance to conventional chemotherapy and radiotherapy, supports the broad applicability of our approach and provides rationale for the progression of AML-LSC-targeted therapeutics from preclinical evaluation to clinical trials," concludes Associate Professor Lock. The researchers include Liqing Jin, University Health Network, Toronto, Canada; Erwin M. Lee, University of New South Wales, Sydney, Australia; Hayley S. Ramshaw, Centre for Cancer Biology, Adelaide, Australia; Samantha J. Busfield, CSL Limited, Melbourne, Australia; Armando G. Peoppl, University Health Network, Toronto, Canada; Lucy Wilkinson, Queensland Institute of Medical Research, Brisbane, Australia; Mark A. Guthridge, Centre for Cancer Biology, Adelaide, Australia; Daniel Thomas, Centre for Cancer Biology, Adelaide, Australia; Emma F. Barry, Centre for Cancer Biology, Adelaide, Australia; Andrew Boyd, Queensland Institute of Medical Research, Brisbane, Australia; David P. Gearing, CSL Limited, Melbourne, Australia; Gino Vairo, CSL Limited, Melbourne, Australia; Angel F. Lopez, Centre for Cancer Biology, Adelaide, Australia; John E. Dick, University Health Network, Toronto, Canada; and Richard B. Lock, University of New South Wales, Sydney, Australia. Cathleen Genova Cell Press


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