Cancers have been interpreted either as somatic evolution of cheater cells that escape replication regulation or alternatively as non-healing wounds. Both the interpretations have substantial support as well as glaring anomalies but the two have not been put together to make a coherent synthesis. We argue here that mechanisms and pathways to escape the normal regulation of cell proliferation do not need to evolve de novo. Mechanisms to override the normal regulation have already evolved for wound healing and tissue regeneration. Almost all of the hallmarks of cancer are also seen in the wound healing process. This suggests that cancer develops not by any de novo gain of function but by exaptation of pre-evolved wound healing functions. Somatic evolution that makes the wound healing triggers constitutive is not mutation limited but selection limited and the selective forces are dependent on the tissue microenvironment. Some mechanisms for such selection have been suggested. Many more need to be investigated. A series of mechanisms have evolved to minimize the risk of cancers which may fail in an altered lifestyle context. We support our synthesis with multiple lines of evidence and also make differential testable predictions. This evolutionary perspective suggests novel lines of research and also has translatable implications for cancer prevention.

Studying the dynamics of urban form means questioning the processes of evolution of the form in general. The discussion on the architecture of buildings and urban spaces has drawn the concept of adaptation from the theories of natural evolution. These notes propose a reflection on the opposite concept of exaptation proposed by the biologist and paleontologist Stephen Jay Gould in 1982. Through some examples (some different transformations of the Roman amphitheaters of the imperial age and the metamorphoses that occurred to the Chinese urban fabrics, originally made by courtyard houses, in the contemporary city), it is possible to extend to urban form the idea of casual co-optation for new uses of organs and anatomical parts developed for other reasons. This kind of reflections opens up innovative considerations on the potential of transitional urban analysis and its repercussions on evolutive urban transformation processes.

The chapter presents the current state of research concerning the development of the BE + past participle constructions from Latin to Spanish. Starting from the description in Rosemeyer (2014) and the theoretical background collated in Kailuweit & Rosemeyer (2015), it will be shown that the functional change does not follow traditional grammaticalisation paths. Several concepts that deal with cases contradicting traditional grammaticalisation theory will be discussed. ‘Exaption’ (Lass 1990, 1997) focussing on total defunctionalisation does not account for the fact that the resultative value of the BE + past participle construction, marginal in Latin, becomes central in Mediaeval Spanish. ‘Refunctionalisation’ Smith (2008) captures this aspect in a more appropriate way. However, the development of the construction could be also conceived as the opposite of what Pountain (2000) describes as ‘capitalisation’: a process of ‘decapitalisation’ by which a feature is exploited not for wider, but for more restricted purposes.

This article challenges the notion of the randomness of mutations in eukaryotic cells by unveiling stress-induced human non-random genome editing mechanisms. To account for the existence of such mechanisms, I have developed molecular concepts of the cell environment and cell environmental stressors and, making use of a large quantity of published data, hypothesized the origin of some crucial biological leaps along the evolutionary path of life on Earth under the pressure of natural selection, in particular, 1) virus-cell mating as a primordial form of sexual recombination and symbiosis; 2) Lamarckian CRISPR-Cas systems; 3) eukaryotic gene development; 4) antiviral activity of retrotransposon-guided mutagenic enzymes and finally; 5) the exaptation of antiviral mutagenic mechanisms to stress-induced genome editing mechanisms directed at “hypertranscribed” endogenous genes. Genes transcribed at their maximum rate (hypertranscribed), yet still unable to meet new chronic environmental demands generated by “pollution”, are inadequate and generate more and more intronic retrotransposon transcripts. In this scenario, RNA-guided mutagenic enzymes (e.g. AID/APOBECs), which have been shown to bind to retrotransposon RNA-repetitive sequences, would be surgically targeted by intronic retrotransposons on opened chromatin regions of the same “hypertranscribed” genes. RNA-guided mutagenic enzymes may therefore “Lamarkianly” generate single nucleotide polymorphisms (SNP) and copy number variations (CNV), as well as transposon transposition and chromosomal translocations in the restricted areas of hyperfunctional and inadequate genes, leaving intact the rest of the genome. CNV and SNP of hypertranscribed genes may allow cells to surgically explore a new fitness scenario, which increases their adaptability to stressful environmental conditions. Like the mechanisms of immunoglobulin somatic hypermutation, non-random genome editing mechanisms may generate several cell mutants, and those codifying for the most environmentally-adequate proteins would have a survival advantage and would therefore be Darwinianly selected. Non-random genome editing mechanisms represent a link between environmental changes and biological novelty and plasticity, and provide a molecular basis to reconcile gene-centered and “ecological” views of evolution.