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Is translational research compatible with preclinical publication strategies?

DOI: 10.1186/1748-717x-1-4

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Abstract:

In a survey of clinical trials of potential anticancer drugs performed by Nygren and Larsson in 2003 [1], it was concluded that "in earlier phase (trials) no or modest anticancer activity was reported" and it was speculated that "the expanding knowledge in tumour biology might not easily translate into new substantially better anticancer drugs". This statement leads to questions of whether the process of translational research is slower than anticipated, and – if so – why this might be. One obvious factor is the complexity of biology; we do not yet quite understand all details with regard to how cancer cells work. How can we then expect to cure cancer? However, we here argue that translational cancer research might suffer from shortcomings, in academic laboratories in particular. We discuss a number of factors which we believe contribute. Our article is meant to be provocative.The French Nobel laureate Jacques Monod remarked in 1965 that "What is true for E. coli is true for an elephant, only more so." One of the main outcomes of the genomic sequencing projects is the recognition that many genes, including those associated with various diseases in humans, are evolutionary conserved from yeast to man. Genomic sequence comparisons have revealed that 61% of Drosophila melanogaster and up to 97% mouse genes are similar to human genes. Many of the mechanisms developed by prokaryotic and eukaryotic cells to use energy, regulate gene expression and respond to environmental challenges utilize similar basic biochemical processes.However, and significantly, there are important differences between mouse and human cells. Biological mechanisms that control life span (replicative senescence) and apoptosis are not perfectly conserved. It is well known that mouse cells easily become immortalized in culture, whereas human cells do not. More recent studies have shown that p53, p16(INK4a), and telomere regulatory functions appear to be differentially regulated during replicative senes

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