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AIM:To observe the clinical effect of comprehensive operation for neovascular glaucoma(NVC).METHODS:Thirty-nine cases(39 eyes)with late neovascular glaucoma in our hospital from October 2010 to October 2013 were treated with cyclocryotherapy, retina condensation combined with trabeculectomy and anterior vitrectomy. The clinical data were retrospectively analyzed. RESULTS:All the patients were followed up for 6～12mo. The mean postoperative intraocular pressure(IOP)of 39 cases(39 eyes)was 12.94±2.33mmHg(1mmHg=0.133kPa)at 1wk, compared with preoperative IOP(57.31±6.72mmHg), which was decreased obviously. The pain was alleviated. During follow-up period, IOP of 35 eyes was normal(17.25±2.24mmHg)without using IOP-lowing drugs and the postoperative IOP was decreased to the normal range after using 1～2 kinds of drugs in 4 cases. The iris neovascularization of all patients eliminated at different extent. Conjunctival filtering blebs of 34 cases were dispersion and those of 5 cases were flat. No shallow anterior chamber or eyeball atrophy occurred during follow-up period. CONCLUSION:The therapy of cyclocryotherapy, retina condensation combined with trabeculectomy and anterior vitrectomy is safe and effective to reduce IOP and relieve suffering in patients with NVG.

Acinic cell carcinoma (AciCC) of the breast is a rare malignant epithelial neoplasm, with approximately 60 cases reported in the literature. It predominantly affects women and exhibits significant histological heterogeneity. The diagnosis of breast AciCC is primarily based on the presence of eosinophilic and/or basophilic granular cytoplasm and markers of serous acinar differentiation. Despite being considered a low-grade variant of conventional triple-negative breast cancer (TNBC), over 25% of patients with breast AciCC have adverse clinical outcomes. Additionally, in early research, microglandular adenosis (MGA) and atypical MGA were considered potential precursors for various breast cancers, including intraductal carcinoma, invasive ductal carcinoma, adenoid cystic carcinoma, metaplastic carcinoma, and AciCC. Similarly, some studies have proposed that breast AciCC should be considered a type of carcinoma developing in MGA with acinic cell differentiation rather than a distinct entity. Therefore, the pathogenesis of breast AciCC has not yet been clarified. Moreover, to the best of our knowledge, the literature has not summarized the latest prognosis and treatment of breast AciCC. In this review, we synthesized the current literature and the latest developments, aiming at exploring the clinicopathology, histological origin, molecular features, prognosis, and treatment of breast AciCC from a novel perspective., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Ge, Wei, Liu, Sun and Gao.)

Foci of spindle cell proliferation of the thyroid gland have been documented in adenoma and carcinoma, but not much in multinodular goiter. We report a case of spindle cell proliferation detected in multinodular goiter in a 61-year-old female. Histological examination revealed foci of solid area around the normal thyroid follicles. There were two components in this solid area; the first one was composed of epithelial cells with small bland ovoid nuclei and the second one with spindle cells with short spindle-shaped nuclei. Immunohistochemical analysis revealed that the spindle cells were positive for thyroid transcription factor (TTF)-1, Vimentin, CK (AE1/AE3), and negative for p63, etc. The cells with ovoid nuclei had more abundant CK (AE1/AE3) immunoreactivity than those with short spindle-shaped nuclei. In addition, the transition between these two cell types was clearly identified. We hypothesized that this area represented embryonic remnant of developing thyroid gland and therefore evaluated histological features of developing fetal thyroid but this lesion by no means simulated histological features of any developing stages of fetal thyroid gland. The spindle cell foci of thyroid gland could possibly arise from epithelial-mesenchymal transformation of thyroid follicular epithelium in this thyroid gland but it awaits further investigations for clarification., Competing Interests: None., (IJCEP Copyright © 2018.)

Background: Sodium-potassium-chloride cotransporter isoform 1 (NKCC1) is an active ions cotransporter and modulates cellular volume and migration. NKCC1 blockers can inhibit cancer cell growth., Aim: We aimed to elucidate the expression and prognostic significance of NKCC1 in non-small cell lung cancer (NSCLC)., Methods: We retrospectively analyzed 788 NSCLC patients with either adenocarcinoma (n = 503) or squamous cell carcinoma (n = 285) by immunohistochemistry to correlate NKCC1 expression with clinicopathologic and survival outcomes., Results: In adenocarcinoma, high NKCC1 expression was associated with larger tumor size (P = 0.013), vascular invasion (P < 0.001), lymphatic invasion (P < 0.001), perineural invasion (P = 0.019) and advanced pathologic stage (P < 0.001), but there are no significant correlations between NKCC1 expression and clinicopathological parameters in squamous cell carcinoma. Patients with high NKCC1 expression had significantly shorter disease-free survival (DFS;P < 0.001) and shorter overall survival (OS;P < 0.001) than those with low NKCC1 expression in adenocarcinoma. In squamous cell carcinoma, NKCC1 expression was not associated with prognosis. Multivariate analysis revealed that high NKCC1 expression was an independent prognostic factor for DFS in lung adenocarcinomas (HR, 1.709; 95% CI 1.029-2.130;P = 0.033) and for OS inEGFR-mutated adenocarcinoma patients (HR, 3.165; 95% CI 1.424-7.035;P = 0.005)., Conclusion: NKCC1 high expression predicted a bad clinical outcome for lung adenocarcinoma patients andEGFR-mutated subgroup. Therefore, NKCC1 may play a role in lung adenocarcinoma and novel therapeutic tactics could be developed by targeting NKCC1 protein., (© The Author 2015. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

The protein β-catenin exhibits a dual function in cells, by acting as a major structural component of cell-cell adherens junctions and as a central signaling molecule in the Wnt signaling pathway. However, how the regulation of β-catenin expression during tumor metastasis in non-small cell lung cancer (NSCLC) varies according to histological type remains unclear. To investigate the regulatory mechanism of β-catenin on tumor metastasis, the present study compared the expression of Wnt1, β-catenin and E-cadherin in 41 primary NSCLC tumors and their corresponding metastatic lesions by immunohistochemistry. Altered expression of β-catenin was more frequent in the metastatic tumors (34/41, 82.9%) than in the corresponding primary tumors (24/41, 58.5%; P<0.05). There were 12 cases [nine of adenocarcinoma (ADC) and three of squamous cell carcinoma (SqCC)] that revealed discordant β-catenin expression between the primary tumors and the corresponding metastatic lesions. Of these, 11 cases (11/12, 91.7%; nine ADCs and two SqCCs) demonstrated acquired β-catenin alterations in the metastatic lesions. Subgroup analysis of these nine ADCs revealed that six cases (6/9, 66.7%) were accompanied by E-cadherin loss but no Wnt1 overexpression. Subgroup analysis of the three SqCCs revealed discordant β-catenin expression. Two cases (2/3, 66.7%) demonstrated acquired β-catenin expression during metastatic progression with Wnt1 overexpression but no change in E-cadherin expression. One case of SqCC revealed normal β-catenin expression in the metastasis although the expression was aberrant in the primary tumor. The results of the present study revealed that the changes in β-catenin expression occurred during tumor metastasis by different mechanisms, depending on histological type. The alterations in β-catenin expression may be regulated by a cadherin-catenin system in ADCs with reduced membranous expression of E-cadherin, but mediated by Wnt1 overexpression in SqCCs with cytoplasmic or nuclear transition types.