According to the scientists at Lawson Health Research Institute in London, Ontario, LKB1, a molecule that regulates the metabolism of many adult cells, is an important molecule in the cancer’s promotion and survival.

Ovarian cancer continues to be one of the most serious women’s cancers with a lack in reliable early detection tests and few treatment options. In order to find out how and why ovarian cancer cells grow and take on such lethal characteristics, Lawson’s Dr. Trevor Shepherd and his team grow the cancer cells in 3D structures, called “spheroids”. Spheroids are sticky and can attach themselves to different organs, where they can sit dormant and unnoticed for months or years before growing and becoming resistant to chemotherapy.

Recently, Dr. Shepherds’ lab discovered that the spheroids activate a ‘stress signal’, and the major molecule controlling this signal is called LKB1.

“Previous studies stated that LKB1 was a tumour suppressor in ovarian cancer, meaning that tumour cells need to get rid of LKB1 to cause cancer,” says Dr. Shepherd, “but our work is in direct conflict with these studies, because we definitively show that ovarian cancer cells still have LKB1 and that this molecule allows ovarian cancer spheroids to change their metabolism, promote tumour cell survival and make them more resistant to chemotherapy.”

According to Dr. Shepherd, currently, there are no therapies or medication that target LKB1.

“Based on these findings our lab is exploring several different strategies to understand and target LKB1 and its related molecules in ovarian cancer spheroids, and developing the essential pre-clinical models to see if this can be translated to ovarian cancer patients.”

The groundbreaking Alzheimer’s Disease Neuroimaging Initiative (ADNI) has studied the brain’s progression from cognitive impairment to Alzheimer’s disease, imaging the brain, collecting clinical measurements and biological specimens and generating an unprecedented volume of data for more than 1,700 participants. The initiative has demonstrated that while amyloid brain deposits are a leading factor in dementia, there is considerable heterogeneity in cognitive decline in aging.

Key to this discovery from ADNI has been its Biostatistics Core, one of eight ADNI cores, led by Laurel Beckett, chief of the Division of Biostatistics in the UC Davis Department of Public Health Sciences. Beckett and her colleagues described their work in “The Alzheimer’s Disease Neuroimaging Initiative phase 2: Increasing the length, breadth, and depth of our understanding,” published online on July 16^th in a special issue of Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. The Core has developed and applied new methods to characterize the entire spectrum of disease progression, illustrating both the classic progression of Alzheimer’s through the buildup of amyloid plaques and alternative pathways to cognitive decline.

ADNI aggregates sensitive and specific markers of very early Alzheimer’s progression, including magnetic resonance imaging (MRI), positron emission tomography (PET), and clinical and neuropsychological assessments, for impaired and control participants from age 50 to 90 at 57 sites across the United States and Canada, including UC Davis.

“ADNI highlights the complexities and the richness of the data that inform our current knowledge of the progression of cognitive impairment to Alzheimer’s disease,” Beckett said.

“New imaging measures clearly show that amyloid pathology in the brain is an ominous prodromal sign for progression, whether defined as conversion to mild cognitive impairment (MCI), or deteriorating cognitive and functional measurements,” the study states. Other data show that certain other participants have “many characteristics consistent with vascular pathology, rather than amyloid-based abnormalities.”

Other study authors include Danielle J. Harvey and Naomi Saito of UC Davis and Michael C. Donohue and Paul Aisen of UC San Diego.