Figure 4
Wnt gene profiling demonstrates elevated expression of Wnt5a in ATL patient samples. (A-C) PCR amplification of typical canonical Wnts (A), noncanonical Wnts (B), and their coreceptors (C) from cDNA derived from ATL patient samples. R.PBMCs were used as controls. GAPDH amplification in nonsaturating conditions served as a control for the quality and quantity of the samples. Open boxes highlight genes differentially expressed between R.PBMCs and ATL patients. (D-F) Real-time PCR analysis of Wnt5a, PTHLH, and RANKL expression from cDNA derived from ATL patients. Samples were normalized to GAPDH expression and the fold change was calculated by comparing values to R.PBMCs normalized gene expression.

Wnt gene profiling demonstrates elevated expression of Wnt5a in ATL patient samples. (A-C) PCR amplification of typical canonical Wnts (A), noncanonical Wnts (B), and their coreceptors (C) from cDNA derived from ATL patient samples. R.PBMCs were used as controls. GAPDH amplification in nonsaturating conditions served as a control for the quality and quantity of the samples. Open boxes highlight genes differentially expressed between R.PBMCs and ATL patients. (D-F) Real-time PCR analysis of Wnt5a, PTHLH, and RANKL expression from cDNA derived from ATL patients. Samples were normalized to GAPDH expression and the fold change was calculated by comparing values to R.PBMCs normalized gene expression.

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