Background and purpose:Currently, subjective questionaire is the most frequently used methods to evaluate swallowing dysfunctions after radiotherapy in nasopharyngeal carcinoma patients, while lacking of effective objective examinations. This study aimed to explore effective methods to evaluate swallowing dysfunctions after radiotherapy in nasopharyngeal carcinoma patients, and gain knowledge of the incidence and severity of swallowing dysfunctions. Methods: From Oct. 2013 to Dec. 2013, 128 consecutive outpatients with previously treated nasopharyngeal carcinoma received esophageal barium lfuoroscopy examination at there regularly follow-ups to evaluate swallowing function. Among these patients, 89 were primary treated with intensity modulated radiation therapy (IMRT) and 39 with conventional radiotherapy (CRT). In this study, each patient received esophageal barium lfuoroscopy examination for 3 times with thin, thick and pasty barium and were dynamically observed using X-ray fluoroscopy from front and lateral direction. Swallowing dysfunctions were defined as follows:①The bolus could not be swallowed and blocked in the mouth;②The dilute barium diverted to the glottis or trachea;③Residual barium delayed in the pyriform sinus and vallecula;④The movement of the hyoid bone or epiglottis were restricted;⑤Bolus prolong through the pharynx;⑥Barium slowed down when went though the esophageal entrance. Results:Of the 128 patients, incidence of dysphagia was 60.2%for the entire cohort, 52.8%for IMRT group and 76.9%for CRT group. Incidence of dysphagia for IMRT group was signiifcantly lower than CRT group (P=0.018). Dysphagia incidence within 1 year, 1 to 2 years and more than 2 years after RT were 63.1%, 33.3%and 69.0%, respectively (P=0.019). Conclusion:There was a high incidence of swallowing dysfunction for the nasopharyngeal carcinoma patients treated with radiotherapy and dysphagia incidence decreased when treated with IMRT. Esophageal barium lfuoroscopy examination is objective method to evaluate the incidence and severity of the swallowing dysfunction.

BACKGROUNDSerine threonine kinase 15 (STK15) is a kind of mitotic kinase. The overexpression of STK15 is significantly associated with carcinogenesis in many tumors, however, its expression and significance in human lung cancer are still unclear. The aim of this study is to investigate the expression of STK15 in squamous cell carcinoma and adenocarcinoma of the lung and to analyze the correlation between STK15 expression and clinicopathological factors.

METHODSThe pattern of STK15 protein expression was detected in 44 squamous cell carcinomas, 36 adenocarcinomas and 20 paracancerous lung tissue samples by immunohistochemistry method using anti-STK15 antibody. The relative quantity of STK15 protein expression was detected by Western blot, and STK15 mRNA expression was detected by RT-PCR in 40 fresh lung cancer samples and corresponding paracancerous lung tissues.

RESULTSPositive expression rate of STK15 protein was 68.75% (55/80) in lung cancer tissues and 0% in paracancerous controls (P < 0.001). STK15 expression was significantly related to differentiation grade of lung cancer (P=0.011), but not to histological classification, TNM stages or lymphatic metastasis (P > 0.05). The relative expression levels of STK15 protein (P < 0.001 ) and STK15 mRNA (P < 0.001) in lung cancer tissues were both significantly higher than those of corresponding paracancerous lung tissues.

CONCLUSIONSThe expression of STK15 protein and STK15 mRNA is significantly higher in lung cancer tissues than that in paracancerous lung tissues. The expression of STK15 correlates with differentiation of lung cancer.

Objective:To determine lysophosphatidic acid receptor 6 (LPAR6) expression in patients with mycosis fungoides (MF) , a variant of cutaneous T-cell lymphoma (CTCL) , and to investigate its role and mechanism of action in the development and prognosis of CTCL.Methods:A total of 110 patients with confirmed MF were collected from Department of Dermatology, Peking University First Hospital from 2011 to 2020, including 24 with large-cell transformation (LCT) and 25 with non-large cell transformation (NLCT) in the discovery cohort, and 24 with LCT and 37 with NLCT in the validation cohort. RNA sequencing and RT-PCR were conducted to determine the LPAR6 expression in patients in the discovery cohort and validation cohort respectively. LPAR6 expression was compared between patients with LCT and those with NLCT, and its effect on the prognosis of patients was evaluated. Two LPAR6-overexpressing CTCL cell lines MyLa and Sz4 were constructed to evaluate the effect of LPAR6 overexpression on proliferative activity of MyLa and Sz4 cells, with the cells normally expressing LPAR6 as the control group; after the treatment with LPAR6-related ligand lysophosphatidic acid (LPA) , 2S-OMPT, adenosine triphosphate (ATP) or adenosine (ADO) , the effects of LPAR6 activation on the proliferative activity and apoptosis of LPAR6-overexpressing MyLa and Sz4 cells were evaluated by the MTS method and flow cytometry respectively. Log-rank test was used for prognostic analysis, and t test or Mann-Whitney U test was used for comparisons between two groups. Results:As RNA sequencing showed, LPAR6 was one of the significantly underexpressed genes in the LCT group in the discovery cohort; in the validation cohort, LPAR6 expression (median[ Q1, Q3]) was significantly lower in the LCT group (204.90[81.90, 512.70]) than in the NLCT group (809.40[417.50, 1 829.20], U= 242.00, P= 0.002) ; in the two cohorts, the underexpression of LPAR6 was significantly associated with increased risk of poor prognosis (both P < 0.01) . Cell proliferation assay showed no significant difference in the proliferative activity of MyLa or Sz4 cells between the LPAR6 overexpression group and control group at 0, 24, 48 and 72 hours during the experiment (all P > 0.05) ; 48 hours after activation of LPAR6 by LPA, 2S-OMPT, ATP and ADO in MyLa cells, the LPAR6 overexpression group showed significantly decreased cellular proliferative activity (1.38 ± 0.01, 1.04 ± 0.01, 1.09 ± 0.03, 1.23 ± 0.01, respectively) compared the control group (1.73 ± 0.04, 1.23 ± 0.01, 1.24 ± 0.01, 1.42 ± 0.03, t= 30.33, 18.38, 4.78, 5.75, respectively, all P < 0.05) , but significantly increased cell apoptosis rate (17.93% ± 0.88%, 17.75% ± 0.35%, 23.97% ± 0.57%, 31.44% ± 0.34%, respectively) compared the control group (3.98% ± 0.03%, 7.81% ± 0.59%, 11.95% ± 0.85%, 12.02% ± 0.48%, t= 15.93, 14.49, 11.74, 33.01, respectively, all P < 0.05) ; 48 hours after activation of LPAR6 by 2S-OMPT and ADO in Sz4 cells, compared with the control group, the LPAR6 overexpression group also showed significantly decreased cellular proliferative activity (2S-OMPT: 1.29 ± 0.04 vs. 1.48 ± 0.01; ADO: 1.27 ± 0.01 vs. 1.51 ± 0.02; both P < 0.05) , but significantly increased cell apoptosis rate (2S-OMPT: 41.70% ± 0.70% vs. 29.35% ± 0.55%; ADO: 37.05% ± 0.15% vs. 24.60% ± 1.00%; both P < 0.05) . Conclusions:LPAR6 was underexpressed in the patients with LCT, and its underexpression was significantly associated with increased risk of poor prognosis. In vitro activation of LPAR6 could inhibit the proliferation of CTCL cells and promote their apoptosis, suggesting that the decrease of LPAR6 expression may be one of the important mechanisms underlying disease progression in patients with LCT.