BackgroundThyroid cancer is the most common malignant disease of the endocrine system. Previous studies indicate a rapid increase in the incidence of thyroid cancer in recent decades, and this increase has aroused the great public concern. The aim of this study was to analyze the trends in incidence, mortality and clinical-pathological patterns of thyroid cancer in Zhejiang province.MethodsPopulation-based incidence and mortality rates of thyroid cancer were collected from eight cancer registries in Zhejiang from 2000 to 2012. The incidence and mortality rates were age-standardized to Segi’s world population. A Joinpoint model was used to examine secular trends in age-adjusted thyroid cancer rates with the Joinpoint Regression Program Version 4.0.0. Thyroid cancer patients were recruited from Zhejiang Cancer Hospital from 1972 to 2014. Patient demographics, tumor histology and tumor size were compared among the different periods of 1972–1985, 1986–1999 and 2000–2014.ResultsThe age-standardized incidence rate of thyroid cancer in Zhejiang cancer registries was 2.75/105 in 2000, and increased to 19.42/105 in 2012. Additionally, we observed significantly increasing incidence rates with the Annual Percent Change (APC) of 22.86% (95%CI, 19.2%–26.7%). The age-standardized mortality of thyroid cancer in Zhejiang cancer registries was 0.23/105 in 2000 and 0.25/105 in 2012. No significant change in mortality rate was found. We observed a rapid increase in the proportions of papillary thyroid carcinoma (PTC) in 12,508 patients with thyroid carcinoma identified in the Zhejiang Cancer Hospital from 1972 to 2014 while the proportions of poorly differentiated thyroid cancer (PDTC), medullary thyroid carcinoma (MTC) and follicular thyroid carcinoma (FTC) decreased over the decades. In the PTC cases, the proportion of patients with maximum tumor diameter (MTD) < 1 cm dramatically and significantly increased from 0 in 1972–1985 to 32.1% in 2000–2014.ConclusionsA rapid increase in incidence and a stable trend in mortality of thyroid cancer were found in the distribution of thyroid cancer. Most of the increased incidence was PTC, especially the papillary thyroid microcarcinoma (PTMC) with MTD < 1 cm. This increase in incidence might be due to increased diagnosis with advanced technology.

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Background Disease caused by SARS-CoV-2 broke out in Wuhan in December 2019. We utilized confirmed cases outside Hubei Province to analyze epidemiologic characteristics and evaluate the effect of traffic restrictions implemented in Hubei beginning on 23 January 2020. Methods Information on 7015 confirmed cases from 19 January to 8 February 2020 in all provinces outside Hubei was collected from the national and local health commissions in China. Incubation period and interval times were calculated using dates of the following events: contact with an infected person, onset, first visit, and diagnosis. We evaluated changes in incubation period and interval times. Results The average age of all cases was 44.24 years. The median incubation period was 5 days and extended from 2 days on 23 January to 15 days on 8 February. The proportion of imported cases decreased from 85.71% to 33.19% after 23 January. In addition, lengths of intervals between onset and diagnosis, onset and first visit, and first visit and diagnosis decreased over time. Conclusions Rapidly transmitting COVID-19 has a short incubation period. The onset mainly occurred among young to middle-aged adults. Traffic restrictions played an important role in the decreased number of imported cases outside Hubei.

Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. However, we know little of mutational spectrum in the Chinese population. Thus, here we report the identification of somatic mutations for Chinese PTC using 402 tumor-normal pairs (Discovery: 91 pairs via exome sequencing; validation: 311 pairs via Sanger sequencing). We observed three distinct mutational signatures, evidently different from the two mutational signatures among Caucasian PTCs. Ten significantly mutated genes were identified, most previously uncharacterized. Notably, we found that long non-coding RNA (lncRNA) GAS8-AS1 is the secondary most frequently altered gene and acts as a novel tumor suppressor in PTC. As a mutation hotspot, the c.713A>G/714T>C dinucleotide substitution was found among 89.1% patients with GAS8-AS1 mutations and associated with advanced PTC disease (P = 0.009). Interestingly, the wild-type lncRNA GAS8-AS1 (A713T714) showed consistently higher capability to inhibit cancer cell growth compared to the mutated lncRNA (G713C714). Further studies also elucidated the oncogene nature of the G protein-coupled receptor LPAR4 and its c.872T>G (p.Ile291Ser) mutation in PTC malignant transformation. The BRAF c.1799T>A (p.Val600Glu) substitution was present in 59.0% Chinese PTCs, more frequently observed in patients with lymph node metastasis (P = 1.6 × 10(-4)). Together our study defines a exome mutational spectrum of PTC in the Chinese population and highlights lncRNA GAS8-AS1 and LPAR4 as potential diagnostics and therapeutic targets.

BackgroundMalignant parotid tumors are rare metastases originating from nasopharyngeal carcinoma (NPC). This study aimed to investigate the clinicopathological features and outcome of patients with metastasis of NPC to parotid lymph nodes after surgical therapy.MethodsWe enrolled 14 NPC patients who had metastatic disease to parotid lymph nodes after IMRT. They received surgical treatment by total parotidectomy with neck dissection, superficial parotidectomy with neck dissection, partial parotidectomy with neck dissection, total parotidectomy, or superficial parotidectomy. Their age, gender, histopathology, clinical findings, and treatment outcome were analyzed.ResultsAfter radiotherapy, parotid metastasis represented as uncontrolled disease in three cases and as recurrent disease in 11 cases. All the 14 patients received salvaged surgery successfully. Pathologic findings showed grade 3 in most patients. The follow-up ranged from 11 to 120 months and the overall three- and five-year survival was 49.5% and 37.1%, respectively.ConclusionsMetastasis to parotid lymph nodes should be examined in NPC patients after IMRT. Resection of the inferior parotid lymph nodes is recommended for patients with cervical metastasis, and superficial or total parotidectomy and adjuvant therapy are recommended for intraparotid lymph node metastasis.

BackgroundCD133 and Nestin, as the markers of cancer stem cells, have recently been reported frequently in the pathogenesis and development of human gliomas. However, the prognostic role of CD133 and Nestin in gliomas still remains controversial. In this study, we aimed to evaluate the association between the expression of CD133 and Nestin and the outcome of glioma patients by conducting a systematic review and meta-analysis.MethodsWe performed systematically electronic and manual searches through the database of Pubmed and embase (until to December 25, 2014) for titles and abstracts which investigated the relationships between CD133 and Nestin expression and outcome of glioma patients. A systematic review and meta-analysis was executed to generate Pooled hazard ratios (HRs) with 95 % confidence intervals (CIs) for overall survival (OS) and progression-free survival (PFS).ResultsA total of 1,490 patients from 32 studies (13 articles) were included in the analysis. 19 studies and 13 studies investigated correlation between CD133 expression or Nestin and survival in gliomas, respectively. Our results showed that high CD133 expression in patients with glioma was associated with poor prognosis in terms of OS (HR 1.69; 95 % CI, 1.16–2.47; P =0.0060) and PFS (HR, 1.64; 95 % CI, 1.12–2.39; P = 0.010). In addition, high Nestin expression were associated with worse OS (HR 1.751; 95 % CI, 1.19–2.58, p = 0.004) but has no significant association with PFS (HR 1.55; 95 % CI, 0.96–2.51, p = 0.074). Even more important, the results of the subgroup meta-analyses show that that high CD133 expression was associated with worse prognosis in terms of OS and PFS in patients with WHO IV glioma but not WHO II-III. On the other hand, Nestin high expression was associated with worse prognosis in terms of OS and PFS in patients with WHO II-III glioma but not WHO IV.ConclusionHigh level of CD133 expression trends to correlate with a worse OS and PFS in glioma patients, especially WHO IV gliomas and Nestin high expression trends to correlate with a worse OS in glioma patients especially WHO II–III, revealing both the markers of cancer stem cells may as the potential pathological prognostic markers for glioma patients.

BackgroundCervical lymph node metastases are very common in papillary thyroid cancer (PTC), and typically spread in a predictable stepwise fashion in clinical practice. However, lateral lymph node metastasis (LLNM) without central lymph node metastasis (CLNM) as skip metastasis is not rare in PTC. The aim of this study was to investigate the incidence, risk factors and pattern of skip metastasis in PTC.MethodsA total of 271 patients with PTC and suspicious LLN diagnosed by pre-operation examinations who underwent total thyroidectomy and central lymph node dissection plus lateral lymph node dissection between January 2008 and December 2011 were enrolled in this study. Clinicopathological features were collected, and the pattern of cervical lymph node metastasis and skip metastasis were analyzed.ResultsThe LLNM rate was 74.9% (203/271, diagnosed by postoperative pathology examination) and significantly associated with extrathyroid extension (ETE), primary tumor located at the upper pole, and CLNM (p < 0.05). The skip metastasis rate was 14.8% (30/203) and was more frequently found in microcarcinoma patients, especially when the primary tumor size was ≤0.5 cm (p = 0.001 OR = 12.9). However, skip metastasis was unrelated to the remaining factors examined.ConclusionSmall cancers with a pre-operation diagnosis of LLNM are more likely to have skip metastases, especially when the primary tumor size is less than 0.5 cm in diameter; however, this type of metastasis appears to develop in a random fashion. Thus, additional research is needed to identify potential predictive factors, such as a primary tumor located at the upper pole.

Abstract. CDH1, a cell adhesion molecule, which plays a key role in maintaining the epithelial phenotype, is regarded as an invasion-suppressor gene in light of accumulating evidence from in vitro experiments and clinical observations. In an attempt to clarify the mechanism responsible for inactivation of this gene in carcinomas, we investigated the methylation status of the CDH1 gene 5'-cpG islands and its regulatory mechanism in the progression of esophageal squamous cell carcinoma. Real-time methylation-specific polymerase chain reaction (qMSP) and treatment with the demethylating agent 5-aza-2'-deoxycytidine (5-Aza-cdR) were conducted to analyze the methylation status at the CDH1 promoter region in the human esophageal carcinoma cell lines, Ec1 and Ec9706. A total of 235 invasive esophageal squamous cell carcinomas (EScc) at stages I-IV and their corresponding normal tissue samples, were included in an immunohistochemistry study and methylation analysis of CDH1. The results demonstrate that in Ec1 and Ec9706 cells, the CDH1 promoter is methylated and treatment with 5-Aza-cdR restored CDH1 expression. Enhanced CDH1 expression decreased cell migration, invasion ability and increased adhesion ability. decreased CDH1 expression was detected in 59.6% of EScc tissues, compared with their adjacent non-neoplastic epithelia, which had a close correlation with the primary tumor status, lymph node status, distant metatasis and clinicopathologic stage. Hypermethylation at the CDH1 promoter was detected in 97.9% of 140 cases of EScc with low CDH1 expression. The methylation of CDH1 promoters (P=0.929) was closely correlated with the lack of expression of their corresponding proteins. The cox regression model for survival analysis showed that increases in CDH1 methylation had a greater impact on the prognosis than tumor clinical stage. These findings suggest that CDH1 gene silencing by promoter hypermethylation and the resultant reduction of CDH1 expression may play an important role in the progression of EScc. CDH1 methylation was a significant predictor of survival in EScc patients after surgery.