2014 Nobel predictions

26 September 2014

Posted by: Richard Scrase

Category: Communications & media

victor–ambros–male–portrait.pngThe Nobel Prize in Physiology or Medicine for 2014 will be announced at 11.30am on Monday 6 October. Until then, UAR is placing its bets on who is going to win. It’s pretty hard to guess who’s going to win in any one year but we’ll give it a go nonetheless, despite our failure last year!

The Nobel prizes are a rich source of information about the role of animals in research, just take the example of Frederick G. banting who at 32 was the youngest Medicine Laureate ever. He was awarded the 1923 Medicine Prize for the discovery of insulin, a discovery based on research with dogs.

Our first guess is based on the winner of the Laker prize announced a few days ago.

Kazutoshi Mori and Peter Walter
For discoveries concerning the unfolded protein response — an intracellular quality control system that detects harmful misfolded proteins in the endoplasmic reticulum and signals the nucleus to carry out corrective measures. 

Kazutoshi Mori and Peter Walter discoveries concerned the unfolded protein response, an intracellular quality-control system that detects harmful misfolded proteins in the endoplasmic reticulum and signals the nucleus to carry out corrective measures. Kazutoshi Mori (Kyoto University) and Peter Walter (University of California, San Francisco) identified core components of this process and unveiled unexpected aspects of its mechanism.

Our second prediction, borrowed from Science Watch,  is Michael H. Wigler, Charles Lee and Stephen W. Scherer  

For their discovery of large-scale copy number variation and its association with specific diseases.

When the human genome was first published it was assumed that the genome was 99% identical in all humans and differences such as eye colour were just down to 3 million single-nucleotide polymorphisms, or SNPs. In 2004 Lee and Scherer together and Wigler independently blew this assumption apart.

Both groups had found that there are large areas of the genome where long stretches, often encompassing several adjacent genes, are either duplicated or deleted. These differences between genomes are now called copy number variants (CNVs). Far from genomes being 99% identical, CNVs cover around 12–13% of the genome and about 2,900 genes, roughly one in ten of all known genes. CNVs tend to be stable and inherited from the parents, although they can also arise spontaneously, and identical twins may differ in copy number variants. Although most CNVs do not seem to be associated with disease, some are. Scherer and Wigler have both shown an association between CNVs and autism spectrum diseases, and CNVs have also been identified in schizophrenia, systemic lupus erythematosus, some cancers, and even reduced susceptibility to HIV infection. The severity of diseases such as lupus and muscular dystrophy has been linked to differences in the number of copies of the DNA sequences in question.

Jeremy Cherfas, Biology correspondent, ScienceWatch

Last year we predicted (wrongly) that Napoleone Ferrera would receive a prize, and we think he is still in with a chance this year.

For isolating vascular endocthelial growth factor (VEGF)

Napo Ferrera moved back into academia after spending 24 years working for the biotech company Genentech. While there, he spearheaded the development of an entirely new class of cancer drugs. He and his lab were the first to isolate vascular endothelial growth factor (VEGF), a protein that regulates the formation of new blood vessels. After creating an antibody to selectively target VEGF, Ferrara noticed that it prevented growth of human tumour cells transplanted into nude mice. Bevacizumab (better known as Avastin®) is a humanised version of the mouse antibody, and has been licensed for use in a wide range of cancers including breast, colorectal, glioblastoma, lung and kidney.


Last edited: 1 October 2014 11:03