Delay in follow-up after an abnormal mammogram is associated with advanced disease stage, poorer survival, and increased anxiety. Despite the implementation of many patient navigator programs across the country, there are few published, peer-reviewed studies documenting its effectiveness. We tested the effectiveness of a patient navigator in improving timeliness to diagnosis, decreasing anxiety, and increasing satisfaction in urban minority women after an abnormal mammogram. Women with suspicious mammograms were randomly assigned to usual care (N=50) or usual care plus intervention with a patient navigator (N=55). There were no demographic differences between the two groups. Women in the intervention group had shorter times to diagnostic resolution (mean 25.0 vs. 42.7 days; p=.001), with 22% of women in the control group without a final diagnosis at 60 days vs. 6% in the intervention group. The intervention group also had lower mean anxiety scores (decrease of 8.0 in intervention vs. increase of 5.8 in control; p<.001), and higher mean satisfaction scores (4.3 vs. 2.9; p<.001). Patient navigation is an effective strategy to improve timely diagnostic resolution, significantly decrease anxiety, and increase patient satisfaction among urban minority women with abnormal mammograms.
Our recent study indicated that overexpression of Sp1 enhances the proliferation of lung cancer cells, while represses metastasis. In this study, we found that the transcriptional activity of FOXO3 was increased, but its protein levels decreased following Sp1 expression. Sp1 increased expression of miR-182, which was then recruited to the 3'-untranslated region of FOXO3 mRNA to silence its translational activity. Knockdown of miR-182 inhibited lung cancer cells growth, but enhanced the invasive and migratory abilities of these cells through increased N-cadherin expression. Repression of FOXO3 expression in the miR-182 knockdown cells partially reversed this effect, suggesting that miR-182 promotes cancer cell growth and inhibits cancer metastatic activity by regulating the expression of FOXO3. The expression of several cancer metastasis-related genes such as ADAM9, CDH9 and CD44 was increased following miR-182 knockdown. In conclusion, in the early stages of lung cancer progression, Sp1 stimulates miR-182 expression, which in turn decreases FOXO3 expression. This stimulates proliferation and tumor growth. In the late stages, Sp1 and miR-182 decline, thus increasing FOXO3 expression, which leads to lung metastasis.
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