Sentence examples for evolution and clonal from inspiring English sources

While Ploidy-Seq can provide a powerful approach for study genome evolution and clonal diversity in human tumors, there are also several notable limitations.

Advances in cancer genomics have revealed the spectrum of somatic mutations that give rise to human AML and drawn our attention to its molecular evolution and clonal architecture.

Furthermore, studies have begun to unveil the effect of population dynamics on the outcomes of evolution, providing direct evidence of parallel evolution and clonal interference and support for historical contingencies [ 4- 7].

On one hand, aneuploidy impairs cell growth and transformation [21]– [23]; however, aneuploidy, with aid from oncogenic mutations, may also enable the transformed cells to undergo changes and adaptation, evolution, and clonal selection to promote tumor progression [12], [15], [24].

Here we have described a whole-genome analysis of such a cancer, and our studies have provided insights into the genetic identity of the individual that founded the DFTD clone, as well as patterns of ongoing DFTD somatic evolution and clonal dynamics.

It is probable that other cancer types and even individual cancers have their own idiosyncrasies with regards to their evolution and clonal diversity; however, many of the principles outlined here are likely to apply and the body of knowledge amassed for AML can inform efforts to understand and most importantly to treat many other malignancies.

Acquisition of somatic mutations and chromosomal aberrations is a hallmark of cancer development and clonal evolution of cancer cells [24].

These results suggest that even after the acquisition of key driver mutations in the nascent cancer cells, these cells must still undergo continuous evolution and likely clonal selection before developing into clinically apparent tumors.

Our model predicts response patterns highlighting the interference of epitope and linked non-epitope loci with each other's evolution and function: Clonal interference limits functionality and speed of adaptation, because beneficial mutations are continuously lost in the competition between strains (Gerrish and Lenski 1998).

The application of the WES approach allowed determining the clonality and clonal evolution patterns during the CML progression.

Although both the hierarchical and the stochastic stem cell model are compatible with clonal evolution, the high frequency of phenotypically diverse leukaemia-propagating cells as described here (stochastic model) will more easily facilitate clonal evolution and the generation of clonal complexity.