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Sample FITC PE APC PI #1 Unstained none none none yes #2 Isotype Control IgG1 (5μl) IgG1 (5μl) IgG1 (10μl) yes #3 FITC Compensation CD34 (20μl) IgG1 (5μl) IgG1 (10μl) yes #4 PE Compensation IgG1 (5μl) CD38 (10μl) IgG1 (10μl) yes #5 APC Compensation IgG1 (5μl) IgG1 (5μl) CD34 (10μl) yes #6 The Sort Lin panel CD38 CD34 yes Cells are sorted as shown in Fig. 1.

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Cell loss was assayed after TE-1, TE-8, KY-5, KY-10, YES-1, and YES-2 cells were exposed to 20 80 μM curcumin for 30 hrs.

It is difficult to compare the molecular expression levels between YES-2 and T.Tn cells, as YES-2 cells were susceptible to IFN- λ more than T.Tn cells and Ad/IFN- λ2 produced more potent activities than Ad/IFN- λ1.

PCR analysis for DNA damage demonstrated that YES-2/AS-12 cells were more resistant to nuclear and mitochondrial DNA damage by cisplatin than were YES-2/Neo cells.

YES-2 cells were infected with replication-competent AdF35 and with Ad5/p53 or Ad5/LacZ, and then cell numbers were counted.

Nude mice injected with YES-2 cells were treated with intratumoral administrations of Ad5F35/MK and/or Ad5/p53.

YES-2 cells were infected with AdF35/MK or AF35/Sur and Ad5/p53, and the cell lysate was tested for the viral amounts produced (Fig.  5c).

The tumour growth was also retarded when YES-2 cells were mixed with Ad/IFN- λ2-infected P6X cells in comparison with the other cases.

AdF35/MK achieved cytotoxic effects relatively greater than Ad5/MK in TE-1, YES-2, YES-5 and T.Tn cells, whereas the cytotoxicity between the 2 kinds of Ad was similar in other cells and YES-6 cells were resistant to the Ad-mediated cytotoxicity.

The tumour development was delayed when YES-2 cells were mixed with Ad/IFN- λ2-infected P6X cells compared with the cases of uninfected or Ad/LacZ-infected P6X cells (P<0.01).

Interestingly, expression levels of pRb and phosphorylated pRb were down-regulated in T.Tn cells infected with AdF35/MK or AdF35/Sur, whereas those of phosphorylated pRb in the AdF35/MK- or AdF35/Sur-infected YES-2 cells were rather up-regulated.

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