The morphological diversity of cyanobacteria poses an intriguing question in the biology and evolution of cell differentiation.
The analogy between evolution of organisms and evolution of cell populations is compelling (Table 3): in both cases what drives change is mutation, but it is Darwinian selection that enables clones that have a growth advantage to expand, thus providing a larger target size for the next mutation to hit [ 15, 17, 18].
The analogy between evolution of organisms and evolution of cell populations is compelling: in both cases what drives change is mutation, but it is Darwinian selection that enables clones that have a growth advantage to expand, thus providing a larger target size for the next mutation to hit[ 14, 16, 17].
The analogy between evolution of organisms and evolution of cell populations is compelling: in both cases what drives change is mutation, but it is Darwinian selection that enables clones that have a growth advantage to expand, thus providing a larger target size for the next mutation to hit.
Our results raise a new paradigm beyond the clonal expansion and evolution of cancer cells, where a population of metastasis-initiating PCa cells recruits and activates bystander cells, including 'dormant' cancer cells, through RANK-mediated signal amplification.
In return, the immune cells in the microenvironment influence the growth and evolution of cancerous cells (e.g. immune-editing [ 66]).
Conversely, immune cells in the microenvironment can affect the growth and evolution of cancer cells.
In turn, the immune cells in the microenvironment can affect the growth and evolution of tumoural cells.
Using antibodies to basal cell markers, we analyzed biopsies with MGH to profile the distribution and evolution of reserve cells and their relationship to these epithelial components.
This raises several questions regarding the biology and evolution of prokaryotic cells.
