Conclusions: Intraobserver and interobserver reproducibility of all strain and torsion parameters was excellent. Inter-study reproducibility of CMR tagging by SPAMM varied between different parameters as described in the results Rabusertib order above and was superior for Ecc and LV torsion. The variation in LV Ecc measurement due to altered
slice orientation is negligible compared to the variation due to slice location.”
“Background: Since ovarian cancer is associated with high frequency of p53 mutation, the availability of p53 reactivation and induction of massive apoptosis (PRIMA-1) offers a possible new therapeutic strategy for overcoming this devastating disease. Although Akt activation is believed to be a determinant in chemoresistance in ovarian cancer, whether Akt plays a role in regulating the effectiveness of PRIMA-1 in sensitizing chemoresistant ovarian cancer cells with p53 mutation to cisplatin (CDDP), remains to be determined.
Methods: In the present studies, we examined the influence of Akt down-regulation following dominant-negative (DN-Akt) expression
selleck products on the ability of PRIMA-1 (0-10 mu M) to facilitate CDDP (0-10 mu M)-induced apoptosis in p53-mutated chemoresistant ovarian cancer cells (A2780cp).
Results: Apoptosis rate was significantly higher at the combined treatment of low PRIMA-1 concentrations (0.156 – 0.938 mu M) plus CDDP (10 mu M) in the DN-Akt groups than control (p<0.001). Apoptosis in cells treated with PRIMA-1
(0.156 mu M) and CDDP treatment (10 mu M) was significantly suppressed by p53-siRNA. PRIMA-1 increased phospho-p53 (Ser15) content in Akt down-regulated cells treated with CDDP.
Conclusions: These results demonstrate that PRIMA-1 can sensitize chemoresistant ovarian cancer cells with p53 mutation to CDDP when Akt is down-regulated, and the action of PRIMA-1 is associated with p53 activation. Our findings Pexidartinib solubility dmso raise the possibility that PRIMA-1 may be useful candidate for adjuvant therapy with CDDP in chemoresistant ovarian cancer with p53 mutation when Akt is down-regulated.”
About 10% of all gastric cancers (GCs) are Epstein-Barr virus (EBV)-associated. However, the oncogene of EBV in gastric carcinogenesis has not yet been established. In the present study, we investigated the virus-derived transcripts in the EBV-infected GC cell line to explore the viral oncogene of EBV-positive GCs.
Materials and Methods
We used the SNU719 cell line, a naturally derived EBV-infected GC cell line. The individual expressed sequence tags from the cDNA libraries of SNU719 were searched against the mRNA subset extracted from the GenBank data base. Sequence reaction was carried out for the EBV-associated clones. Reverse transcription-polymerase chain reaction was performed after cells were partitioned into nuclear and cytoplasmic fractions.