We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 4

1.
Figure 2

Figure 2. Subgroup analysis of ALDH1A1, CD44 and CD133 based on setting of recurrent tumor collection. From: Stem cell pathways contribute to clinical chemoresistance in ovarian cancer.

Expression of ALDH1A1, CD44 and CD133 was broken down into subcategories based on the setting in which the recurrent tumor was retrieved. A) ALDH1A1, CD44 and CD133 expression was higher in samples collected immediately after the completion of primary therapy (persistent tumor; n=12). B) Samples collected at first recurrence before initiating secondary therapy (untreated recurrence; n=20) were composed of similar percentages of each marker. C) In tumors collected from recurrent, platinum-resistant patients (treated recurrence; n=13), only CD133 was increased in expression. Error bars represent SEM. *P<0.05, **P<0.01.

Adam D. Steg, et al. Clin Cancer Res. ;18(3):869-881.
2.

Figure 1. Change in expression of ALDH1A1, CD44 and CD133 from primary to recurrent ovarian cancer. From: Stem cell pathways contribute to clinical chemoresistance in ovarian cancer.

A) ALDH1A1, CD44 and CD133 expression in 45 high grade ovarian adenocarcinomas was examined using immunohistochemistry. The estimated percentage of positive cells for each sample, with mean (black bars) and median, are shown. B) For all three proteins examined, staining was heterogeneous, rather than diffusely positive. Examples of high and low frequency expression for each are shown (black bar = 100 μm). C) A higher magnification of CD44 and CD133 expression in primary ovarian cancer specimens, demonstrating cell surface expression. D) The average number of positive cells for ALDH1A1, CD44 and CD133 among the 45 primary samples was compared to the average among matched recurrent samples. Only CD133 was significantly higher in recurrent samples. Error bars represent SEM. *P<0.001. E) In order to evaluate the change in each subpopulation for each patient, in addition to the mean of the entire group, the change for each tumor is shown in individual graphs.

Adam D. Steg, et al. Clin Cancer Res. ;18(3):869-881.
3.

Figure 4. Downregulation of Gli1/2 leads to decreased cell viability and downregulation of Gli2, but not Gli1, sensitizes ovarian cancer cells to cisplatin in vitro. From: Stem cell pathways contribute to clinical chemoresistance in ovarian cancer.

A) mRNA expression of GLI1 and GLI2 was quantified in 8 different ovarian cancer cell lines using quantitative PCR. Gene expression is shown as log2 transformed ΔC T values. B) Downregulation of Gli1/2 in A2780cp20 and ES2 cells using 2 different siRNA constructs was determined by quantitative PCR. Each siRNA construct demonstrated selectivity for the GLI gene to which it was designed against. ND = not detectable; *P<0.01. C) Knockdown of Gli1 or Gli2 alone diminished A2780cp20 cell viability, whereas only knockdown of Gli2 diminished ES2 cell viability as determined by MTT assay. Increased sensitivity to cisplatin (CDDP) was noted in A2780cp20 and ES2 cells transfected with GLI2 siRNAs, but not GLI1 siRNAs. D) Cell cycle analysis (PI staining) of A2780cp20 cells exposed to control siRNA, GLI1 siRNA or GLI2 siRNA for a total of 72 hours. Downregulation of Gli2, and to a lesser extent Gli1, led to an accumulation of cells in the sub-G0 or apoptotic fraction. Data are representative of 3 independent experiments.

Adam D. Steg, et al. Clin Cancer Res. ;18(3):869-881.
4.

Figure 3. Endoglin is expressed in persistent ovarian tumor and ovarian cancer cell lines and its downregulation leads to decreased cell viability.<. From: Stem cell pathways contribute to clinical chemoresistance in ovarian cancer.

A) Matched primary/persistent ovarian tumor pairs (n = 12) were subjected to immunohistochemical analysis of endoglin to evaluate changes in expression. Persistent tumors were found to have a higher density of endoglin staining compared to primary specimens. Representative histologic sections are shown for a matched pair (black bar = 100 μm). B) mRNA expression of endoglin was quantified in 8 different ovarian cancer cell lines using quantitative PCR. Gene expression is shown as log2 transformed ΔCT values (difference between the CT value of the gene of interest (endoglin) and that of the housekeeping gene (RPLP0)). C) Downregulation of endoglin in ES2 and HeyA8MDR cells using 2 different siRNA constructs was determined by Western blot analysis. βactin was used as a loading control. D) ES2 and HeyA8MDR cells transiently transfected with anti-endoglin siRNAs had decreased viability as determined by MTT assay. E) Cell cycle analysis (PI staining) revealed that downregulation of endoglin led to an accumulation of both ES2 and HeyA8MDR cells in the sub-G0 or apoptotic fraction. Data are representative of 3 independent experiments. *P<0.001.

Adam D. Steg, et al. Clin Cancer Res. ;18(3):869-881.

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk