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We review several recent mathematical approaches used to describe and analyze cell proliferation data.
We found no regulation in proliferation data from dedifferentiated or embryonic cells, and we observed a dual control in proliferation data from normal mouse bone marrow cells, and from normal human fibroblasts (however, the latter was a short series).
As expected from the proliferation data, tumor volumes increased most rapidly in papillary tumors of compound mice (Figure 2F).
Data are also supported by the immunohistochemical investigations of keratinocyte pathway and kinetics of inflammatory cells proliferation (data not shown).
Addition of ACK2, a Kit neutralizing antibody, also did not influence GS cell proliferation (data not shown).
Importantly, Notch pathway inhibition with GSI did not affect BM-PC survival or proliferation (data not shown).
Perivascular PDGFRβ expression in the surrounding non-malignant tissue was also positively correlated with epithelial cell proliferation (data not shown).
The proliferation data was corroborated by examining phosphorylated histone H3 (p-H3), an indicator of G2/M phase.
Cultures were performed in triplicate for each experiment, and the average proliferation data was used for analysis.
Also, combined P21 silencing and SB431542 treatment did not prevent radiation-induced inhibition of proliferation (data not shown).
Statistical evaluations of cell frequency measurements and proliferation data were performed using the unpaired Student's t-test.
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