Multifocal PTMC with TTD > 1 cm has a similar risk of LNM as a clinical papillary cancer. Routine central neck dissection is recommended in this subgroup of patients.
IONM system implemented in transoral thyroid surgery was feasible and serviceable in preventing RLN injury. The method of TOETVA shows promise for thyroidectomy with CND due its ideal cosmetic results.
According to the present SET data, level II dissection by SET was a feasible and safe procedure. With reasonable costs and satisfactory cosmetic results, oncoplastic SET via breast approach might gain wider acceptance in the near future.
Background
Remote access and endoscopic thyroid surgery has been gaining popularity because it allows patients to avoid a visible scar in the neck. There is limited data on transoral endoscopic thyroidectomy when it relates to patients with papillary thyroid carcinoma. We aim to evaluate the safety of ipsilateral central compartment dissection for patients who undergo transoral thyroidectomy (thyroidectomy vestibular approach–compartment lymph node dissection).
Patients and Methods
A total of 80 patients who underwent thyroidectomy vestibular approach–compartment lymph node dissection for papillary thyroid carcinoma from June 2015 to September 2016 were identified. Over the same period, a matched cohort of 80 patients who underwent open thyroidectomy with routine ipsilateral central compartment dissection was also identified (Open-compartment lymph node dissection). The two groups were analyzed in terms of patient characteristics, perioperative clinical results and post-operative outcomes.
Results
All patients were female with a mean age of 32-year. There was no difference in mean maximum tumor size and number of lymph nodes dissected. Moreover, there was no difference in average positive lymph nodes between thyroidectomy vestibular approach–compartment lymph node dissection and Open-compartment lymph node dissection (1.48 vs 1.08, P = 0.647). Operative time was longer in the thyroidectomy vestibular approach–compartment lymph node dissection group (193 vs 102 min, P < 0.001). Thyroidectomy specific complications were similar with rates of temporary recurrent laryngeal nerve palsy of 6.3 vs 8.8% and temporary hypocalcemia rates of 2.5 vs 5% in the thyroidectomy vestibular approach–compartment lymph node dissection and Open-compartment lymph node dissection groups, respectively.
Conclusions
Thyroidectomy vestibular approach–compartment lymph node dissection is a feasible and safe option for select patients with papillary thyroid carcinoma who require central node dissection compared with Open-compartment lymph node dissection, and can be a viable alternative for patients wishing to avoid a visible scar.
The tumor suppressor gene TP53 and its negative regulator murine double minute 2 are involved in multiple cellular pathways. Two potentially functional single nucleotide polymorphisms (SNPs) MDM2 SNP309 and TP53 R72P have been extensively investigated to be associated with breast cancer risk. However, the original studies as well as the subsequent meta-analysis, have yielded contradictory results for the individual effect of the two SNPs on breast cancer risk, plus that conflicting results also existed for the combined effects of MDM2 SNP309 and TP53 R72P on breast cancer risk. This meta-analysis aimed to clarify the individual and combined effects of these two genes on breast cancer risk. We performed a meta-analysis of publications with a total 9,563 cases and 9,468 controls concerning MDM2 SNP309 polymorphism and 19,748 cases and 19,962 controls concerning TP53 R72P. Odds ratios (ORs) with 95 % confidence intervals (CIs) were used to assess the strength of the association. In overall meta-analysis, individuals with the MDM2 SNP309TG genotype were associated with a borderline higher breast cancer risk than those with TT genotype (OR = 1.11, 95 % CI: 1.00-1.24, P (heterogeneity) = 0.007), whereas the TP53 R72P CC or GC genotype had no effects on breast cancer risk. In the stratified analyses, a significant association between MDM2 SNP309 and breast cancer risk were observed in Asian, but null significant association between TP53 R72P and breast cancer risk were found even in various subgroups. Moreover, no significant combined effects of MDM2 SNP309 and TP53 R72P were observed on breast cancer risk. The borderline association between MDM2 SNP309 and breast cancer risk in overall analysis should be treated with caution, and no significant combined effects for the two SNPs on breast cancer risk suggested functional investigations warranted to explore the molecular mechanism of the TP53-MDM2 circuit genes.
Recent studies have indicated that long non-coding RNAs play crucial roles in numerous cancers, including thyroid cancer, while their function in the mechanism of thyroid cancer 131I resistance has not been elucidated to date. The present study identified a functional long non-coding RNA, SLC6A9-5:2, which was involved in the radioactive therapy resistance of thyroid cancer. We demonstrated that SLC6A9-5:2 was remarkably downregulated in 131I-resistant thyroid cancer cell lines and 131I-insensitive patients and was positively correlated with Poly (ADP-ribose) polymerase 1 (PARP-1) expression and its activation. After downregulating SLC6A9 or blocking PARP-1 artificially, the sensitive thyroid cancer cells mostly displayed a tolerant phenotype under 131I exposure. Furthermore, SLC6A9-5:2 overexpression was positively correlated with PARP-1 mRNA and protein levels, which restored the sensitivity of resistant thyroid cancer cells. The present study further revealed that cancer cell death was primarily caused by ATP exhaustion in excessive DNA repair with high PARP-1 activity. In patients with thyroid cancer, a positive correlation between SLC6A9-5:2 and PARP-1 was identified, and low SLC6A9-5:2 expression was associated with a worse prognosis of papillary thyroid carcinoma. Hence, our data provide a new lncRNA-mediated regulatory mechanism implying that SLC6A9-5:2 can be used as a novel therapeutic target for 131I-resistant thyroid cancer.
Abstract:We have investigated comprehensively the effects of thyroid function on gallstone formation in a mouse model. Gonadectomized gallstone-susceptible male C57BL/6 mice were randomly distributed into three groups each of which received an intervention to induce hyperthyroidism, hypothyroidism, or euthyroidism. After 5 weeks of feeding a lithogenic diet of 15% (w/w) butter fat, 1% (w/w) cholesterol, and 0.5% (w/w) cholic acid, mice were killed for further experiments. The incidence of cholesterol monohydrate crystal formation was 100% in mice with hyperthyroidism, 83% in hypothyroidism, and 33% in euthyroidism, the differences being statistically significant. Among the hepatic lithogenic genes, Trβ was found to be up-regulated and Rxr down-regulated in the mice with hypothyroidism. In contrast, Lxrα, Rxr, and Cyp7α1 were up-regulated and Fxr down-regulated in the mice with hyperthyroidism. In conclusion, thyroid dysfunction, either hyperthyroidism or hypothyroidism, promotes the formation of cholesterol gallstones in C57BL/6 mice. Gene expression differences suggest that thyroid hormone disturbance leads to gallstone formation in different ways. Hyperthyroidism induces cholesterol gallstone formation by regulating expression of the hepatic nuclear receptor genes such as Lxrα and Rxr, which are significant in cholesterol metabolism pathways. However, hypothyroidism induces cholesterol gallstone formation by promoting cholesterol biosynthesis.
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