The many malignant-like phenotypes observed upon loss of a single polarity regulator must be driven by altered gene expression.
This transition is driven by altering social needs and the wish for a more patient-centred care [ 18, 21, 27].
As suggested by organ weight analysis, differences in body weights were driven by altered body composition and in particular by drastically reduced fat in M/Mt-CK−/− mice.
These findings suggest that the majority of differences between preM and postM breast tumors are driven by altered hormone levels, and thus areonly observed in ER+ disease.
Potentially, increased expression of these genes may be driven by the altered cytokine environment within psoriasis lesions [ 5, 6, 16].
In the uninfected fetuses and newborns, the disruption of the TLR9 signaling pathway, engaged in the induction of type I IFNs, might also be driven by the altered TLR4 molecule.
We hypothesize that clinically observed differences in cytoreduction between conventional vs. liposomal doxorubicin may be driven by differences in tumor properties that alter the deposition of drug into tumor cells.
We tentatively argue that the observed pattern could be driven by intrinsic features of the predator, namely, altered prey preferences with increasing age coupled with a general preference for large-bodied prey, or changing nutritional needs at different developmental stages.
Second, neuroblastoma cells dedifferentiate in hypoxia (Bhaskara et al., 2012; Jögi et al., 2002, 2004), suggesting that altered differentiation could be driven by 5-hmC changes because the TET enzymes regulate transitions between pluripotent and differentiated states (Ito et al., 2010; Koh et al., 2011; Madzo et al., 2014).
Therefore, any differences between HFD-fed Ins1−/−: Ins2+/− and Ins1−/−: Ins2+/+ female mice would likely be driven by attenuated hyperinsulinaemia in young Ins1−/−: Ins2+/− mice, rather than altered glucose homeostasis.
