As the breast cancer cells used in this study differed in their capacity to form focal adhesions, we explored the possibility that part of the heterogeneity of breast cancer was due to variations in adhesion-induced signaling through MAPK and Src pathways by different breast cancers.
The variation in adhesion classifications, mode of application of agents, lack of uniformity in surgical approaches and variations in the interpretation of results all make the assessment of the efficacy of the many agents difficult and almost impossible to compare.
The maximum range of variation in adhesion over sixty minutes correlates strongly with NRG1α-induced migration (r2 = 0.61).
Here we investigate the role of variation in adhesion properties and cumulative antibody repertoires in selecting for the observed patterns in expression [25], [26].
The observed variation in adhesion blocking antibodies between laboratories may be the result of DBLs generated in different protein expression systems, which may produce slightly different DBL conformations.
This normalization procedure was adopted because raw baseline adhesion states tended to show some drift over time, albeit much less than the pronounced variation in adhesion after NRG1 stimulation (Figure S1).
The maximum range of this variation in adhesion over time (hereafter abbreviated as MRVA) correlates highly with the effectiveness of NRG1α-induced cell migration, indicating that the MRVA measure has biological relevance, at least to these cells.
The variation in adhesion genes and the presence of T3SSs indicates that host cell adhesion is likely an important aspect of Providencia virulence.
In addition, the possibility of geographic variation in adhesion phenotypes causing severe malaria, linked to differences in malaria transmission levels and host immunity, has been neglected.
Indeed, wide variations exist in adhesion classification and surgical approaches, making comparison between the published evidence difficult.
