[Show abstract][Hide abstract] ABSTRACT: The exchange of opinions motivated by Dr. Baker's article "Paradoxes in carcinogenesis should spur new avenues of research: An historical perspective" illustrates the reasons why the field of cancer research is stuck in a dead end. This paralysis presents a rich opportunity for philosophers, historians and sociologists of science to decipher the whys of this impasse. On the strictly biological front, we suggest to reinstate in cancer research the time proven practice so productive in the physical sciences of discarding wrong hypotheses and theories. We share the suggestion by Dr. Baker to stop trying to unify the two main theories of carcinogenesis, i.e., the Somatic Mutation Theory (SMT) and the Tissue Organization Field Theory (TOFT) because they are incompatible. Dr. Baker suggests breaching the impasse by investing in paradox-driven research. We discuss the barriers to the implementation of this novel strategy, and the significant impact that this strategy will have on knowledge at large and its application for the prevention and cure of cancer.
Disruptive science and technology. 05/2013; 1(3):154-156.
[Show abstract][Hide abstract] ABSTRACT: Despite intense research efforts that have provided enormous insight, cancer continues to be a poorly understood disease. There has been much debate over whether the cancerous state can be said to originate in a single cell or whether it is a reflection of aberrant behaviour on the part of a 'society of cells'. This article presents, in the form of a debate conducted among the authors, three views of how the problem might be addressed. We do not claim that the views exhaust all possibilities. These views are (a) the tissue organization field theory (TOFT) that is based on a breakdown of tissue organization involving many cells from different embryological layers, (b) the cancer stem cell (CSC) hypothesis that focuses on genetic and epigenetic changes that take place within single cells, and (c) the proposition that rewiring of the cell's protein interaction networks mediated by intrinsically disordered proteins (IDPs) drives the tumorigenic process. The views are based on different philosophical approaches. In detail, they differ on some points and agree on others. It is left to the reader to decide whether one approach to understanding cancer appears more promising than the other.
Journal of Biosciences 04/2014; 39(2):281-302. · 1.76 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Raw gene expression data and amino acid metabolic pathway of Saccharomyces cerevisiae were excavated by SMD (Stanford Microarray Database) and KEGG (Kyoto Encyclopedia of Genes and Genomes), respectively. The methionine and cysteine nutritional metabolic modules were selected and analyzed, expecting to establish the relationship between the modules, and find out the important genes, which made predominant contribution for the up-regulation and down-regulation of modules, to identify the differences and synergies in expression levels. The results show that four common genes exist between these two modules, comprising YAL012W (126.96.36.199), YFR055W (188.8.131.52), YJR130C (184.108.40.206) and YLR303W (220.127.116.11). For methionine modules, the five important genes were YAL012W (18.104.22.168), YDR502C (22.214.171.124), YER043C (126.96.36.199), YGR155W (188.8.131.52) and YLR303W (184.108.40.206), playing a decisive role in the gross of gene expression, while for cysteine modules, those are YAL012W (220.127.116.11), YLR303W (18.104.22.168), YNL247W (22.214.171.124) and YCL064C (126.96.36.199). Maybe the cooperative up-regulation relations exist between these two modules, while because of different gene numbers in modules, the synergies between gene expression gross values were not distinct. But certain crucial metabolite can be accumulated by controlling the important genes in the metabolic process.
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