Scientists at Cincinnati Children’s Hospital Medical Center report Oct. 29 in Nature they used human pluripotent stem cells — which can become any cell type in the body — to grow a miniature version of the stomach…
Oncologists use erlotinib to treat lung cancers that have a mutation in a gene called epidermal growth factor receptor (EGFR). The gene mutation causes EGFR to run like it has a stuck accelerator, and erlotinib blocks the overactive molecule. The study shows that while erlotinib effectively causes tumors to shrink — suggesting that the drug is helping — this drug also increases the aggressiveness of the tumor so that growth is accelerated when therapy ends. This study finds that this is due to a secondary and previously unknown effect of inhibiting EGFR…
The multi-institutional group, led by scientists at Cancer and Blood Diseases Institute (CBDI) at Cincinnati Children’s Hospital Medical Center, publish their results in the journal’s online edition on Aug. 24. The researchers suggest their laboratory findings in mouse models of the disease could lead to a more targeted and effective molecular therapy that would also reduce the harmful side effects of current treatments, which include chemotherapy, radiation or surgery. “Although current treatments improve survival rates, patients suffer severe side effects and relapse tumors carry mutations that resist treatment,” said lead investigator Q. …
However, a new Cincinnati Cancer Center (CCC) study, published in the advance online edition of the journal Oncotarget, provides hope that previously studied SapC-DOPS could be used for treatment of brain cancer that has spread. Xiaoyang Qi, PhD, member of the CCC, associate director and associate professor in the division of hematology oncology at the University of Cincinnati (UC) College of Medicine and a member of the UC Cancer and Neuroscience Institutes and the Brain Tumor Center, says this critical data shows promise for finding treatment for one of the deadliest cancers. A lysosomal protein saposin C (SapC), and a phospholipid, known as dioleoylphosphatidylserine (DOPS), can be combined and assembled into tiny cavities, or nanovesicles, to target and kill many forms of cancer cells…
source : http://www.sciencedaily.com/releases/2014/05/140516203220.htm
source : http://www.sciencedaily.com/releases/2014/05/140514153231.htm
source : http://www.sciencedaily.com/releases/2014/04/140422100103.htm
source : http://www.sciencedaily.com/releases/2014/03/140311184702.htm
source : http://www.sciencedaily.com/releases/2014/03/140303211409.htm
But new research appearing the week of Jan. 13 in Proceedings of the National Academy of Sciences (PNAS) suggests that activation of AMPK may actually fuel cancer growth. Researchers from Cincinnati Children’s Hospital Medical Center who led the study also recommend that clinicians testing metformin for cancer treatment consider a careful re-evaluation of their clinical data. The researchers report on extensive laboratory tests that conclude metformin does stop cancer, although not by activating AMPK…