Vascular endothelial growth factor (VEGF) and its receptors have been implicated in promoting solid tumor growth and metastasis via stimulating tumor-associated angiogenesis.
Prolactin has been implicated in promoting paternal care behaviors but little evidence of causality has been found to date except for birds and fish.
Although frustration has long been implicated in promoting aggression, the potential for poor frustration tolerance to function as a risk factor for physical child abuse risk has received minimal attention.
Certainly, SCC genes have been implicated in promoting HR [13], [16].
The PI3-K/Akt pathway has been implicated in promoting neuronal survival, proliferation and differentiation, synaptogenesis as well as translocation of VGCCs to the plasma membrane.
Bmi1 has previously been implicated in promoting tumor cell survival and cell cycle progression in a tissue culture model system [25], [26].
Moreover, a growing number of miRNAs have been implicated in promoting or suppressing tumorigenesis in a variety of tissues [8] [10], suggesting that they may play a role as a novel class of oncogenes or tumour suppressor genes.
Although both canonical and non-canonical Wnt signaling have been implicated in promoting melanocyte proliferation, migration and differentiation at other body sites [40], the lack of Conductin-lacZ reporter expression within the mammary melanocytic hyperplasia strongly favors non-canonical signaling.
Transforming growth factor-β (TGFβ), a Th2 cytokine that can increase the expression of connective tissue proteins [60] [65], has been implicated in promoting fibrosis in mdx and DMD muscle.
Pheromones have also been implicated in promoting male acceleration of female puberty, the Vandenbergh effect [9], which is characterized by the development of reproductive organs, a hallmark of which is uterine growth, and an increase in hormone signaling [5].
However, Casp9DN did not significantly accelerate T-cell lymphoma alone, or in combination with Lck-Bax38/1, or with Beclin 1+/− mice, two tumor-prone strains in which altered mitochondrial function has been implicated in promoting tumor development.
