What does it take to be a leader – of cancer cells?
Adam Marcus and colleagues at Winship Cancer Institute are back, with an analysis of mutations that drive metastatic behavior among groups of lung cancer cells. The findings were published this week on the cover of Journal of Cell Science, and suggest pharmacological strategies to intervene against or prevent metastasis.
Marcus and former graduate student Jessica Konen previously developed a technique for selectively labeling “leader” Read more
Researchers have identified compounds that potently activate LRH-1, which regulates the metabolism of fat and sugar. These compounds have potential for treating diabetes, fatty liver disease and inflammatory bowel Read more
The placebo effect plays a big role in clinical trials for mood disorders such as depression. Emory psychiatrist Andy Miller hit upon something several years ago that could clear a path around the placebo effect.
A recent paper in Psychotherapy and Psychosomatics from Miller and psychiatry chair Mark Rapaport looks at clinical trials testing an anti-inflammatory drug against psoriasis, to see whether participants’ depressive symptoms improved. This sidesteps a situation where doctors’ main targets are the patients’ moods.
“These studies emphasize how difficult it is to interpret findings when these drugs are treating more than one problem,” Miller says. “Better to have a simpler study with just depression.”
Still, this line of research could clarify who could benefit from anti-inflammatory treatments and illuminate viable biomarkers and pathways. Two studies now underway at Emory specifically recruit patients with high levels of the inflammatory marker CRP, which Miller’s previous study showed was helpful in predicting response to infliximab.
The new paper results from a collaboration with Eli Lilly. Lilly’s ixekizumab (commercial name: Taltz) is an antibody against the cytokine IL-17A, used to treat moderate to severe psoriasis. Taltz was approved by the FDA in 2016, after clinical trials published in the New England Journal of Medicine. Read more
A recent WABE â€œCloser Lookâ€ interview with Mark Mulligan, executive director of the Emory Vaccine Centerâ€™s Hope Clinic, covers a lot of ground. It starts off with a segment — also aired on Marketplace — from reporter Michell Eloy, who visited the Hope Clinicâ€™s lab. We hear a machine processing blood samples from a study testing an experimental Ebola vaccine and a roundup of Ebola vaccine developments.
Then, reporters Rose Scott and Jim Burress discuss several different Ebola vaccines with Mulligan. One is based on chimpanzee adenovirus, was tested at the Hope Clinic and elsewhere in the USA and the UK, and then in Liberia. While this vaccine was safe and it appears to stimulate the immune system appropriately, the outbreak fizzled out (a good thing!) before it was possible to tell if the vaccine protected people from Ebola infection. Read more
Developing drugs that can change the progression of Alzheimer’s disease is a huge challenge. In the last few years, more than one pharmaceutical firm have abandoned clinical programs in Alzheimer’s that once looked promising. Still, Emory and Scripps scientists have found an approach that deserves a second look and more investigation.
One straightforward drug strategy against Alzheimerâ€™s is to turn down the brainâ€™s production of beta-amyloid, the key component of the diseaseâ€™s characteristic plaques. A toxic fragment of a protein found in healthy brains, beta-amyloid accumulates in the brains of people affected by the disease.
The enzyme that determines how much beta-amyloid brain cells generate is called BACE (beta-secretase or beta-site APP cleaving enzyme). Yet finding drugs that inhibit that elusive enzyme has been far from straightforward.
Now researchersÂ have identified a way to shut down production of beta-amyloid by diverting BACE to a different part of the cell and inhibiting its activity. The results were published this week in Journal of Neuroscience. Read more
For this monthâ€™s Current Concept feature, we would like to explain a term from cardiology that is likely to become more prominent:
â€œHeart failure with preserved ejection fractionâ€ (abbreviated as HFpEF and pronounced â€œheff-peffâ€).
Javed Butler, MD, an Emory expert on heart failure and deputy chief science officer for the American Heart Association, laid out in a recent seminar why this category of patients is so important. Look for more from him on this topic in the future.
The number of HFpEF patients is growing and they now make up the majority of patients with heart failure in the United States.
No treatments have been proven to benefit them, in terms of reducing mortality.* In clinical studies, medications such as ACE inhibitors, angiotensin receptor blockers and beta-blockers have not helped.
Once hospitalized, HFpEF patients have a high rate of readmission to the hospital within 30 days. The federal Medicare program is penalizing hospitals that have high rates of readmissions and heart failure is one of the largest contributors to readmissions.
The symptoms that drive people with HFpEF to the hospital are mainly fatigue and dyspnea, or shortness of breath, along with fluid in the lungs and swelling of the limbs. Along with heart failure, HFpEF patients often have conditions such as hypertension, anemia, diabetes, kidney disease or sleep apnea. Read more
A clinical trial testing a therapy for children with fragile X syndrome is closing down, after the sponsoring company announced that the drug, called arbaclofen, was not meeting its goals.
Readers of Emory Health magazine may remember Samuel McKinnon, an arbaclofen study participant who was featured in a 2012 article and video (below).
â€œWe were surprised,â€ Samuelâ€™s mother Wendy told us Monday. â€œBut we knew going in that there were no guarantees.â€
She reports that Samuel has made significant progress in the last couple of years. He likes playing and talking with the family’s new puppy, Biscuit. Samuel’s language skills have Ray Ban outlet blossomed and he will be headed to second grade this fall. But itâ€™s hard to say whether thatâ€™s mainly because of the experimental drug or because Samuel has been continuing to grow and work hard in school and in therapy, she says.
A sizable fraction of patients in the study appeared to benefit from the drug, just not the majority of them, says Emory genetics chair Steve Warren.