I have a Business wire story on the the first test to diagnose fibromyalgia:
"First Test to Objectively Diagnose Fibromyalgia Now Available - New Peer-Reviewed Research Identifies Diagnostic Biomarkers for
Fibromyalgia SANTA MONICA, Calif.--( )--A recent peer-reviewed study, published in BMC Clinical Pathology,
reveals a medical breakthrough discovering multiple biomarkers based
upon highly sensitive and reproducible medical investigations. Conducted
by the University of Illinois College of Medicine at Chicago (UIC) and
EpicGenetics, a privately-held biomedical company, the research has led
to the development of The FM/a® Test (www.thefmtest.com),
the first test to objectively diagnose fibromyalgia."
- 'Drug holidays' beat cancer drug resistance in mice -
Introducing medication-free spells to some cancer treatments may keep patients alive for longer, studies in mice with skin cancer suggest.
The animals had melanoma, which can rapidly become resistant to treatments.
However, a study in the journal Nature showed tumours also became dependent on the drug to survive. Withdrawing treatment caused tumours to shrink.
I would be happy to have a drug holiday every once in a while. I mean am I building up a resistance to some of the medications I am on? Or do the days count when I just forget my pills (oops)? And then the article goes on with lots of big words!
- Skin cancer 'able to fight off body's immune system'
A deadly form of skin cancer is able to fend off the body's immune system, UK researchers have found.
Analysis of tumour and blood samples shows that melanoma knocks out the body's best immune defence.
Potential test could work out which patients are likely to respond to treatment, the Journal of Clinical Investigation reports.
Cancer Research UK said the body's response was a "complex puzzle".
- Key Enzyme Missing from Triple-negative breast cancer
Key Enzyme Missing from Aggressive Form of Breast Cancer, Groundbreaking Study Shows
Feb. 28, 2013 — A groundbreaking new study led by the University of Kentucky Markey Cancer Center's Dr. Peter Zhou found that triple-negative breast cancer cells are missing a key enzyme that other cancer cells contain -- providing insight into potential therapeutic targets to treat the aggressive cancer. Zhou's study is unique in that his lab is the only one in the country to specifically study the metabolic process of triple-negative breast cancer cells.
Normally, all cells -- including cancerous cells -- use glucose to initiate the process of making Adenosine-5'-triphosphate (ATP) for fuel to carry out essential functions. This process, called glycolysis, leads to other processes that use oxygen to make higher quantities of ATP -- but solid tumor cells, which have little access to oxygen, are forced to rely almost exclusively on aerobic glycolysis for survival.
- Zhou's study, published in Cancer Cell, showed that the powerful transcription factor complex Snail-G9a-Dnmt1 is over-expressed in triple-negative breast cancer, inhibiting the enzyme 1,6-bisphosphate (FBP1). The loss of this enzyme shuts down the glucose anabolic pathway and promotes the glucose catabolic pathway, leading to a large amount of glucose entering the tumor cells and thus "feeding" the aggressive cancer. This metabolic switch empowers the triple-negative breast cancer cells to suck more glucose from the body, increasing macromolecule biosynthesis in tumor cells and maintaining ATP production despite a dearth of nutrients and an oxygen-free environment.
- Early rheumatoid arthritis and resolving fibroblasts segregate according to Dickkopf related protein 1 expression
Dickkopf related protein 1 (DKK1) has been proposed as the master regulator of joint remodelling. This Wnt signalling pathway inhibitor is involved in osteoblast growth and differentiation. In rheumatoid arthritis, increased DKK1 plasma levels correlate with inflammation and bone erosions. Furthermore, patients with rheumatoid arthritis who carry genetic variants in the DKK1 gene have higher serum DKK1 levels and more progressive joint destruction, suggesting a fundamental role for DKK1 in rheumatoid arthritis. In the diseased joint, synovial fibroblasts are key mediators of bone and cartilage destruction via secretion of matrix metalloproteinases and regulation of monocyte to osteoclast differentiation. In this study we analysed whether DKK1 secretion might contribute to this effect. We hypothesised that synovial fibroblasts from patients with early rheumatoid arthritis would be characterised by high DKK1 expression compared with those from patients with resolving arthritis.