No abstract

Purpose:To investigate the change of breast density with quantitative magnetic resonance (MR) imaging in the contralateral normal breast of patients receiving neoadjuvant chemotherapy. Materials and Methods:This study was approved by the institutional review board and was HIPAA compliant. Informed consent was obtained. Fifty-four patients with breast cancer (mean age, 47 years; age range, 30-74 years) treated with NAC protocol and enrolled in a breast MR imaging research study were studied. The density in the contralateral normal breast was analyzed by using an MR imaging-based segmentation method. The effect of chemotherapy on the change of density following the doxorubicin and cyclophosphamide (AC) and the AC and taxane regimen was evaluated. The dependence on age was investigated by using a multivariate regression model. Results:In patients who underwent both AC and taxane follow-up, the mean percentage of change from the individual's baseline density was 2 10% (95% confi dence interval: 2 12.8%, 2 7.2%) after AC and 2 12.7% (95% confi dence interval: 2 16%, 2 9.4%) after AC and taxane. In patients who underwent both follow-up studies after one to two and four cycles of AC, the mean percentage of change was 2 9.4% (95% confi dence interval: 2 13.5 %, 2 5.3%) after one to two cycles of AC and 2 14.7% (95% confi dence interval: 2 20.6%, 2 8.7%) after four cycles of AC. The percentage reduction of density was signifi cantly dependent on age. Patients younger than 40 years had a greater reduction after chemotherapy than patients older than 55 years ( P = .01). Conclusion:By using three-dimensional MR imaging, patients receiving chemotherapy showed reduction of breast density, and the effects were signifi cant after initial treatment with one to two cycles of the AC regimen.q RSNA, 2010

Metastasis is the most dangerous risk faced by patients with hereditary non-polyposis colon cancer (HNPCC). The expression of matrix metalloproteinases (MMPs) has been observed in several types of human cancers and regulates the efficacy of many therapies. Here, we show that treatment with various concentrations of prostaglandin E2 (PGE2; 0, 1, 5 or 10 μM) promotes the migration ability of the human LoVo colon cancer cell line. As demonstrated by mRNA and protein expression analyses, EP2 and EP4 are the major PGE2 receptors expressed on the LoVo cell membrane. The Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt cell survival pathway was upregulated by EP2 and EP4 activation. Following the activation of the PI3K/Akt pathway, β-catenin translocated into the nucleus and triggered COX2 transcription via LEF-1 and TCF-4 and its subsequent translation. COX2 expression correlated with the elevation in the migration ability of LoVo cells. The experimental evidence shows a possible mechanism by which PGE2 induces cancer cell migration and further suggests PGE2 to be a potential therapeutic target in colon cancer metastasis. On inhibition of PGE2, in order to determine the downstream pathway, the levels of PI3K/Akt pathway were suppressed and the β-catenin expression was also modulated. Inhibition of EP2 and EP4 shows that PGE2 induces protein expression of COX-2 through EP2 and EP4 receptors in LoVo colon cancer cells.