Nominations are open now for the 2018 Omenn Prize, to be awarded at the 2019 ISEMPH Meeting in Zurich. The submission deadline is March 31, 2019
The International Society for Evolution, Medicine & Public Health invites nominations for the Omenn Prize of $5000 for the best article published in 2016 in any scientific journal on a topic related to evolution in the context of medicine and public health. It will be awarded in August 2019 at the ISEMPH Meeting in Zurich.
The prize, provided by the generosity of Gilbert S. Omenn, will be awarded to the first author of the winning article. One of the authors will be invited to present a talk at the meeting. Authors are encouraged to nominate their own articles, but nominations of articles by others are also welcome.
Nominations close March 31, 2019
Any relevant peer-reviewed article with a publication date of 2018 for the final version of the article is eligible, but the prize is intended for work that uses evolutionary principles to advance understanding of a disease or disease process. The prize committee will give priority to articles with implications for human health, but many basic science or theoretical articles have such implications.
The Prize Committee for this year is chaired by Andrew Read (Penn State, infectious disease) and includes Mel Greaves (FRS, Cancer, London); Steve Simpson (FRS, Sydney, nutrition); Thom McDade (Northwestern, anthro); Nina Wale (U Mich, last year’s winner); and Isabel Gordo (Portugal, pop gen). Papers by committee members, their students and lab group members are not eligible, and articles by their co-authors or close associates are subject to special conditions. The winner will be invited to present a talk at the meeting of the International Society for Evolution and Medicine.
Back on June 4th I published a post on the Evmedreview which I titled “A new role for an old villain”. In it I documented the recent research by Rob Moir of Harvard University which has shown that beta-amyloid – long accused of causing Alzheimer’s disease – is a potent anti-microbial protein. The inevitable conclusion of such research, if backed up by other investigators, is that, whatever neurotoxic effects can or cannot be attributed to beta-amyloid, it has been primarily been adopted in the brain as a crude but effective part of the armamentarium of the innate immune system, evolved to fight pathogens. In fact, Rob Moir’s recent research, which built on joint research at Harvard with Stephanie Soscia, reported in PLoS 1 (see the link above for all further links) is bolstered by at least 4 further papers on the antimicrobial role of beta-amyloid and a paper published last week in Nature: Scientific Reports, by Philipp Spitzer et al of Friedrich-Alexander-University, Erlangen, Germany, titled “Amyloidogenic amyloid-β-peptide variants induce microbial agglutination and exert antimicrobial activity”, adds considerable heft to the idea because it defines the anti-microbial role of beta-amyloid in great detail, pinning the strongest anti-microbial properties to the longer-chain forms of beta-amyloid, Aß-42, which are singled out by supporters of the amyloid hypothesis as being much more toxic to the brain than Aß-40, and that the way that Aß-42 agglutinates into clumps – again identified as a major feature of Alzheimer’s pathology – is actually an important property of its anti-microbial action.
A research group drawn from the University of Chicago and University of Nottingham, UK, has just published a paper on Peto’s Paradox with direct reference to the evolution of large body size in elephants. This link takes you to the abstract where there is a download of the entire PDF. Of particular interest is the proposed role of several TP53 retrogenes in making elephant cells more sensitive to DNA damage and apoptosis. Here’s the abstract:
“A major constraint on the evolution of large body sizes in animals is an increased risk of developing cancer. There is no correlation, however, between body size and cancer risk. This lack of correlation is often referred to as ‘Peto’s Paradox’. Here we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Proboscidean) lineage. Furthermore we show that several of the TP53 retrogenes (TP53RTGs) are transcribed and likely translated. While TP53RTGs do not appear to directly function as transcription factors, they do contribute to the enhanced sensitivity of elephant cells to DNA damage and the induction of apoptosis by regulating activity of the TP53 signaling pathway. These results suggest that an increase in the copy number of TP53 may have played a direct role in the evolution of very large body sizes and the resolution of Peto’s paradox in Proboscideans.”
A new paper published last week in Nature Medicine shows that the gut microbes present in some one-month old infants predict a three-fold higher risk of developing allergies by age 2 and asthma by age 4, says a press release issued by the University of California in San Francisco. The study’s senior author, Susan Lynch of UCSF believes that a particular signature of a depleted or dysbiotic microbiome at this very early age could identify neonates at risk and allow physicians in the near future to treat with probiotics or fecal transplants to re-engineer a healthy microbiome in a truly preventative approach.
Carlo Maley has recently tweeted the arrival of a new paper on measurement of clonal diversity in oesophageal cancer, and the use of such diversity markers in predicting which patients with non-dysplastic Barrett’s Oesophagus will progress to cancer and which will not. Carlo has previously collaborated with two of the great exponents of this “clonal diversity” approach to cancer prognosis – Brian Reid, of the Fred Hutchinson Cancer research Center in Seattle, and Trevor Graham of the Barts Cancer Institute in London. Graham and Maley are among the authors of this paper.
Barrett’s is a pre-cancerous lesion of the lower oesophagus, usually caused by long-term acid reflux from the stomach, and is notorious for the failure of current screening techniques to identify pathological changes in oesophageal cells that can reliably tell you the risk of progression to cancer. As Brian Reid has said, oncologists end up in a position where their screening technique – usually once-in-a-lifetime screening of Barrett’s patients at the age of 50 – selectively detects those dysplasias that are going to remain stable for life – the patient will die with them, not of them – and selectively misses those fast-moving changes that will transition to cancer. The over-diagnosis of benign cases is running at 95% and the under-diagnosis of lethal cancer is also running at 95% – an abysmal track record. And since that over-diagnosis often impels oncologists to wade in with very difficult surgery to remove the entire oesophagus, causing many patients to die on the operating table – or soon after – or consigning them to a very poor quality of life thereafter, it is essential that a more reliable method of distinguishing oesophageal sheep from goats is found as soon as possible. Has this research team found the answer?