Crude and adjusted analysis of association between change in HRQOL score assessed by FACT-Hep at 1 and 2 month and survival time from CCA diagnosis to death.

<p>Crude and adjusted analysis of association between change in HRQOL score assessed by FACT-Hep at 1 and 2 month and survival time from CCA diagnosis to death.</p

Health-Related Quality of Life and Survival of Cholangiocarcinoma Patients in Northeastern Region of Thailand

<div><p>In northeast Thailand, cholangiocarcinoma (CCA) is a major cause of mortality. Patients with CCA have a poor prognosis and short-term survival. The purpose of this study was to investigate the association between health-related quality of life (HRQOL) and survival time, and to explore whether change in HRQOL score is related to survival among CCA patients. The study was performed between February 2011 and January 2012, and included 171 patients with newly diagnosed CCA from 5 tertiary hospitals in four provinces of northeast Thailand. The HRQOL was measured at baseline, 1 month, and 2 months after diagnosis by the FACT-Hep questionnaire (Thai version 4). The outcome was survival time from diagnosis. Cox’s proportional hazard model was used to evaluate the association between HRQOL and survival time. A higher overall score on HRQOL was associated with a significantly better survival (HR per 5 units increase in HRQOL was 0.92, 95% CI: 0.88–0.96). Two of the separate domains contributing to the overall HRQOL—functional well-being and hepatobiliary cancer subscale—were found to have independent effects on survival, even after adjustment for potential confounding variables, and the other domains of HRQOL. CCA patient whose HRQOL scores had improved (≥9 units) at the 1st month of follow up had a reduced probability of dying from the disease (HR: 0.56, 0.32–0.95) after adjustment for the same confounding factors. A positive association between HRQOL at diagnosis and survival time was found. An improvement in HRQOL score in the first months after diagnosis further increases survival.</p></div

Kaplan-Meier survival estimate of time from diagnosis to time of death by HRQOL score in the CCA patients assessed by FACT-Hep.

<p>Kaplan-Meier survival estimate of time from diagnosis to time of death by HRQOL score in the CCA patients assessed by FACT-Hep.</p

Base line HRQOL score of CCA patients assessed by FACT-Hep.

<p>Base line HRQOL score of CCA patients assessed by FACT-Hep.</p

Crude and adjusted analysis of association between scores on the component domains of the HRQOL scale assessed by FACT-Hep and mortality of CCA patients.

<p>Crude and adjusted analysis of association between scores on the component domains of the HRQOL scale assessed by FACT-Hep and mortality of CCA patients.</p

CKD stage progression from the first observation to the last observation.

<p><b>(1,630 patients).</b> Shaded bars represent stable patients whereas those below the shaded bars represent improved CKD stage, and those above the bars represent patients whose CKD stage progressed.</p

Association between process of care and progression of CKD.

<p>Association between process of care and progression of CKD.</p

Study flow.

<p>Study flow.</p

Association between clinical targets of care and progression of CKD.

<p>Association between clinical targets of care and progression of CKD.</p

Effects of arecoline on proliferation of oral squamous cell carcinoma cells by dysregulating c-Myc and miR-22, directly targeting oncostatin M

<div><p>Arecoline, the major alkaloid of areca nut, is known to induce oral carcinogenesis, however, its mechanism is still needed to elucidate. This study investigated the effects of arecoline on cell viability and cell-cycle progression of oral squamous cell carcinoma (OSCC) cells as well as a relevant cellular gene expression. The results showed that a low concentration of arecoline (0.025 μg/ml) increased OSCC cell viability, proportion of cells in G2/M phase and cell proliferation. Simultaneously, it induced IL-6, STAT3 and c-Myc expression. Interestingly, c-<i>myc</i> promoter activity was also induced by arecoline. MiR-22 expression in arecoline-treated OSCC cells was suppressed and comparable to an upregulated c-Myc expression. In arecoline-treated OSCC cells, oncostatin M (OSM) expression was significantly upregulated and inversely correlated with miR-22 expression. Likewise, OSM expression and its post-transcriptional activity were significantly decreased in miR-22-transfected OSCC and 293FT cells. This result demonstrated that miR-22 directly targeted OSM. Interestingly, miR-22 played an important role as a tumor suppresser on suppressing cell proliferation, migration and cell-cycle progression of OSCC cells. This result suggested the effect of arecoline to promote cell proliferation and cell-cycle progression of OSCC cells might be involved in induction of c-Myc expression and reduction of miR-22 resulting in OSM upregulation.</p></div