Abstract Objectives To investigate prognostic factors in patients with head and neck Mucoepidermoid Carcinoma (MEC), especially the impact of treatment modalities on survival. Methods Patients with primary head and neck MEC between 2000 and 2015 were obtained from the Surveillance, Epidemiology, and End Results (SEER) database. Prognostic factors related to Overall Survival (OS) and Cancer-Specific Survival (CSS), as well as the impact of treatments, were evaluated by multivariable Cox regression analysis. Results We identified 2692 patients diagnosed with head and neck MEC, of whom 1397 (51.89%) had a parotid gland primary, 569 (22.14%) died, and 341 (12.67%) died of MEC. Older age (≥53 years), males, unmarried, lower income, tumor site in other head and neck areas, higher tumor grade, larger tumor size, and higher stage were related to poorer OS and CSS. Patients who did not undergo surgery (HR = 3.20, 95% CI 2.45‒4.18) had worse OS, while no significant difference was detected between partial and total organ excision on patients’ OS (p = 0.729). For combination therapy, patients who received radiotherapy only (HR = 3.21, 95% CI 2.27-4.53) or no surgery and no radiotherapy (HR = 2.59, 95% CI 1.83-3.67) were correlated with worse OS (vs. surgery only), but no significant difference was detected between surgery only and surgery combined with radiotherapy on patients’ OS (p = 0.218). For CSS, the corresponding results were consistent with OS. Conclusion Surgical resection only may be a better survival option for head and neck MEC. , (MEC) 200 201 Surveillance Epidemiology SEER (SEER database (OS CancerSpecific Cancer Specific CSS (CSS) treatments analysis 269 139 51.89% 5189 51 89 (51.89% 56 22.14% 2214 22 14 (22.14% 34 12.67% 1267 12 67 (12.67% ≥53 53 (≥5 years, years years) males unmarried income areas grade size HR 320 3 20 3.20 95 2.45‒4.18 245418 2 45 4 18 p 0.729. 0729 0.729 . 0 729 0.729) therapy 321 21 3.21 2.274.53 227453 2.27 4.53 27 2.27-4.53 259 59 2.59 1.833.67 183367 1.83 3.67 1 83 1.83-3.67 vs. vs (vs only, only) 0.218. 0218 0.218 218 0.218) (MEC (CSS 26 13 51.89 518 5 8 (51.89 22.14 221 (22.14 12.67 126 6 (12.67 ≥5 (≥ 32 3.2 9 2.45‒4.1 24541 072 0.72 72 274 2.274.5 22745 227 2.2 453 4.5 2.27-4.5 25 2.5 833 1.833.6 18336 183 1.8 367 3.6 1.83-3.6 021 0.21 51.8 (51.8 22.1 (22.1 12.6 (12.6 ≥ ( 3. 2.45‒4. 2454 07 0.7 7 2.274. 2274 2. 4. 2.27-4. 1.833. 1833 1. 36 1.83-3. 02 0.2 51. (51. 22. (22. 12. (12. 2.45‒4 245 0. 2.274 2.27-4 1.833 1.83-3 (51 (22 (12 2.45‒ 24 2.27- 1.83- (5 (2 (1 2.45 2.4

Pancreatic cancer is well known to be the most deadly malignancy with the worst survival rate of all cancers. High temperature requirement factor A1 (HtrA1) plays an important role in cancer cell proliferation, migration, apoptosis, and differentiation. This study aimed to explore the function of HtrA1 in pancreatic cancer cell growth and its underlying mechanism. We found that the expression of HtrA1 was lower in pancreatic cancer tissue compared to the adjacent normal tissue. Consistently, HtrA1 levels were also decreased in two human pancreatic cancer cell lines, PANC-1 and BXPC-3. Moreover, enforced expression of HtrA1 inhibited cell viability and colony formation of PANC-1 and BXPC-3 cells. Overexpression of HtrA1 promoted apoptosis and suppressed migratory ability of tumor cells. On the contrary, siRNA-mediated knockdown of HtrA1 promoted the growth potential of pancreatic cancer cells. In addition, we found that up-regulation of HtrA1 reduced the expression of Notch-1 in pancreatic cancer cells. On the contrary, knockdown of HtrA1 increased the expression levels of Notch-1. Furthermore, overexpression of Notch-1 abolished the anti-proliferative effect of HtrA1 on pancreatic cancer cells. Taken together, our findings demonstrated that HtrA1 could inhibit pancreatic cancer cell growth via regulating Notch-1 expression, which implied that HtrA1 might be developed as a novel molecular target for pancreatic cancer therapy.

Abstract BACKGROUND: Recent mutation analysis identified several missense mutations in CARD14 in psoriasis. OBJECTIVES: We performed the genomic sequence analysis on CARD14 in southern Chinese Han Cantonese with Psoriasis Vulgaris (PsV) to reveal more causative missense mutations. METHODS: A total of 131 patients with PsV and 207 matched controls were included. We conducted sequence analysis of all the exon and exon-intron boundaries of CARD14 in the group of PsV patients and subsequent case control analysis of potential sequence variants of significance. RESULTS: We found five rare mutations and four of them are annotated or reported. Only the variant (c.1291C>G) has not been reported and annotated, but the variant was also found in controls. No significant difference was detected among all rare variant allele frequencies of patients and controls. CONCLUSION: None of the new definite variants were pathogenic. The other pathogenic mutations for PsV are still elusive in our cohort.