Most primary intestinal natural killer (NK)-cell and T-cell lymphomas (PINKTL) in the Northern Europe are enteropathy-associated T-cell lymphomas, a complication of celiac disease, which is rare in the East. Primary intestinal NK-cell lymphoma is extremely rare and is poorly characterized. We investigated 30 cases of PINKTL from Taiwan with male: female at 2:1, median age at 55.5, 80% with jejunal/ileal involvement, 77% with perforation, 27% with multicentric tumors, and 67% at stage IE. All 7 cases tested for serum IgA anti-tissue transglutaminase were negative. Only 3 (10%) tumors showed enteropathy. Six (20%) were NK-cell lymphoma and 24 (80%) were T-cell lymphoma. The tumor cells in 21/30 (70%) cases were small to medium sized, which correlated with the coexpression of both CD8 and CD56. All tumors expressed at least 1 cytotoxic marker. All 6 NK-cell lymphomas were negative for betaF1, diffusely positive for Epstein-Barr virus-encoded mRNA (EBER), and polyclonal for T-cell receptor gene rearrangement. Five (22%) of the 24 T-cell tumors expressed betaF1, 8 (35%) of the 23 tumors were positive for EBER, and 20 (95%) of the 21 tumors were clonal for T-cell receptor. The overall 1-year survival was 36%. Univariate regression analysis showed that NK-cell lineage, multicentricity, and perforation were associated with poor prognosis. NK-cell lineage (P=0.037) was a poor prognostic factor by multivariate Cox proportional hazard regression analysis. PINKTL in Taiwan is predominantly not enteropathic with a high frequency of perforation, small to medium tumor cell size and cytotoxic phenotype. Primary intestinal NK-cell lymphoma carries a very poor prognosis, and is probably a distinct entity.

Background Patients with end-stage renal disease (ESRD) are at a higher risk for chronic hepatitis, liver cirrhosis (LC) and mortality than the general population. Optimal modalities of renal replacement therapy for ESRD patients with concomitant end-stage liver disease remain controversial. We investigated the long-term outcome for chronic liver disease among dialysis patients in an endemic area. Methods Using Taiwan’s National Health Insurance claim data (NHRI-NHIRD-99182), We performed a longitudinal cohort study to investigate the impact of comorbidities on mortality in dialysis patients. We followed up 11293 incident hemodialysis (HD) and 761 peritoneal dialysis (PD) patients from the start of dialysis until the date of death or the end of database period (December 31, 2008). A Cox proportional hazards model was used to identify the risk factors for all-cause mortality. Results Patients receiving PD tended to be younger and less likely to have comorbidities than those receiving HD. At the beginning of dialysis, a high prevalence rate (6.16 %) of LC was found. Other than well-known risk factors, LC (hazard ratio [HR] 1.473, 95 % CI: 1.329-1.634) and dementia (HR 1.376, 95 % CI: 1.083-1.750) were also independent predictors of mortality. Hypertension and mortality were inversely associated. Dialysis modality and three individual comorbidities (diabetes mellitus, chronic lung disease, and dementia) interacted significantly on mortality risk. Conclusions LC is an important predictor of mortality; however, the effect on mortality was not different between HD and PD patients.

Background: Numerous transmembrane receptor tyrosine kinase pathways have been found to play an important role in tumor progression in some cancers. This study was aimed to evaluate the clinical impact of Eph receptor A4 (EphA4) in patients with rectal cancer treated with neoadjuvant concurrent chemoradiotherapy (CCRT) combined with mesorectal excision, with special emphasis on tumor regression.Methods: Analysis of the publicly available expression profiling dataset of rectal cancer disclosed that EphA4 was the top-ranking, significantly upregulated, transmembrane receptor tyrosine kinase pathway-associated gene in the non-responders to CCRT, compared with the responders. Immunohistochemical study was conducted to assess the EphA4 expression in pre-treatment biopsy specimens from 172 rectal cancer patients without distant metastasis. The relationships between EphA4 expression and various clinicopathological factors or survival were statistically analyzed.Results: EphA4 expression was significantly associated with vascular invasion (P=0.015), post-treatment depth of tumor invasion (P=0.006), pre-treatment and post-treatment lymph node metastasis (P=0.004 and P=0.011, respectively). More importantly, high EphA4 expression was significantly predictive for lesser degree of tumor regression after CCRT (P=0.031). At univariate analysis, high EphA4 expression was a negative prognosticator for disease-specific survival (P=0.0009) and metastasis-free survival (P=0.0001). At multivariate analysis, high expression of EphA4 still served as an independent adverse prognostic factor for disease-specific survival (HR, 2.528; 95% CI, 1.131-5.651; P=0.024) and metastasis-free survival (HR, 3.908; 95% CI, 1.590-9.601; P=0.003).Conclusion: High expression of EphA4 predicted lesser degree of tumor regression after CCRT and served as an independent negative prognostic factor in patients with rectal cancer.

MicroRNAs are small noncoding RNAs acting as novel biomarkers of various diseases and potential regulators of protein expression and functions. Syndecan-1 is the heparan sulfate proteoglycan associated with malignancy of various cancers, including breast cancer. In this study, we proposed a experimental workflow to investigate potential microRNAs that regulate SDC1 expression and affect breast cancer cell mobility.MicroRNA candidates were selected from available Gene Expression Omnibus datasets on breast malignancy. Further in silico duplex hybridization and multiplex PCR approach were used to screen potential microRNAs. Analysis showed increased syndecan-1 expression but decreased miR-122-5p level upon breast malignancy. Western blot and in vitro luciferase assay confirmed the targeting of 3′-untranslated region of syndecan-1 and suppression of syndecan-1 expression by miR-122-5p. The suppression of syndecan-1 expression by miR-122-5p or shRNAs against syndecan-1 increased breast cancer cell mobility; while overexpression of syndecan-1 inhibited cell mobility. In further, miR-122-5p was enriched in liver cell-derived exosomes that was able to suppress syndecan-1 expression and increase cell mobility in breast cancer cells.In conclusion, our results suggested the downregulation of SDC1 by miR-122-5p or liver-cell-derived exosomes would enhance breast cancer cell mobility. Metastasis or mobility of breast cancer cells might be affected by circulating miR-122-5p and not directly correlated with progression of breast cancer.