The slightly higher breast density with PR expression suggests a stronger estrogenic response in mammographically dense breasts possibly leading to stronger cell proliferation, an idea supported by associations of breast density with hyperplasia and other benign breast pathology [ 8, 10, 45, 46].
Surprisingly, strong T cell proliferation also was observed by day 6 in response to MDDC that had been stimulated with virus prior to co-culture in the presence of SEB (86.3%, 90%, and 80.3% for rHRSV, UV-rHRSV, and IAV, respectively).
However, RNAi silencing of α-spec or β-spec does produce a strong stem cell proliferation response, similar to overexpression of Yki (Fig 7D G).
IGF1 is the major mediator of growth hormone effects; it thus has a strong influence on cell proliferation and differentiation and is a potent inhibitor of apoptosis (Furstenberger and Senn 2002).
Pharmacological inhibition of IMPDH induced a moderate reduction of cell viability and a strong decrease of cell proliferation, but no increase in chemosensitivity.
Strong deregulation of cell proliferation by AP2C3 overexpression is also indicated by the presence of multiple nuclei in stomata cells of AP2C3oe plants.
As shown in Figure 4A, cDCs induced strong CD4 T cell proliferation ex vivo following influenza infection (48% recruited into cell division), whereas IKDCs only induced the proliferation in 3% and B220−NK cells in 5% of co-cultured CD4 T cells.
This high overlap with ER regulation probably reflects an strong association with cell proliferation beyond cancer hormone-dependencies. Overall, all except two of the signatures examined here showed significant over-representation of one or more of the molecular evidences associated with the regulation of cell proliferation and death.
A strong inhibition of cell proliferation and survival was observed in cells treated with these inhibitors.
Induced apoptosis exerted a strong impact on cell proliferation, as monitored by real-time cell analysis.
