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Objective: This study aimed to investigate the value of artificial intelligence (AI) for distinguishing pathological subtypes of invasive pulmonary adenocarcinomas in patients with subsolid nodules (SSNs). Materials and methods: This retrospective study included 110 consecutive patients with 120 SSNs. The qualitative and quantitative imaging characteristics of SSNs were extracted automatically using an artificially intelligent assessment system. Then, radiologists had to verify these characteristics again. We split all cases into two groups: non-IA including 11 Atypical adenomatous hyperplasia (AAH) and 25 adenocarcinoma in situ (AIS) or IA including 7 minimally invasive adenocarcinoma (MIA) and 77 invasive adenocarcinoma (IAC). Variables that exhibited statistically significant differences between the non-IA and IA in the univariate analysis were included in the multivariate logistic regression analysis. Receiver operating characteristic (ROC) analyses were conducted to determine the cut-off values and their diagnostic performances. Results: Multivariate logistic regression analysis showed that the major diameter (odds ratio [OR] = 1.38; 95 % confidence interval [CI], 1.02-1.87; P = 0.036) and entropy of three-dimensional(3D) CT value (OR = 3.73, 95 % CI, 1.13-2.33, P = 0.031) were independent risk factors for adenocarcinomas. The cut-off values of the major diameter and the entropy of 3D CT value for the diagnosis of invasive adenocarcinoma were 15.5 mm and 5.17, respectively. To improve the classification performance, we fused the major diameter and the entropy of 3D CT value as a combined model, and the (AUC） of the model was 0.868 (sensitivity = 0.845, specificity = 0.806). Conclusion: The major diameter and entropy of 3D CT value can distinguish non-IA from IA. AI can improve performance in distinguishing pathological subtypes of invasive pulmonary adenocarcinomas in patients with SSNs.

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Peroxiredoxins (Prxs) are a ubiquitously expressed family of antioxidant enzymes that either facilitate or inhibit tumorigenesis, depending on the cancer type and Prx isoform. Prx2 is a typical Prx that has a dual role in tumorigenesis and tumor progression. However, the expression of Prx2 and its precise role in cervical cancer remains to be elucidated. Therefore, the present study aimed to investigate the expression of Prx2 and its association with the progression and prognosis of cervical squamous cell cancer (CSCC). In the present study, the clinicopathological data of 105 patients diagnosed with CSCC were collected from the medical record system at Jingzhou Central Hospital, Tongji Medical College of Huazhong University of Science and Technology (Jingzhou, China). Prx2 protein was also detected in 105 CSCC tissues and 40 adjacent peri-tumoral tissues by immunohistochemical staining. The relationships between Prx2 expression and clinicopathological features, vascular endothelial growth factor A (VEGF-A) expression and micro-vessel density (MVD) in CSCC were then analyzed. Progression-free survival (PFS) was also assessed using both univariate and multivariate analyses. The results of the present study demonstrated that the expression of Prx2 was upregulated in CSCC tissues compared with the adjacent peri-tumoral tissues (P<0.001). In addition, higher Prx2 expression was associated with greater depth of stromal invasion (P=0.023) and positive lymph vascular space invasion (P=0.044), while the Prx2 expression level was not associated with age, tumor size, histological grade, lymph node (LN) metastasis or International Federation of Gynecology and Obstetrics (FIGO) stage (all P>0.05). Furthermore, increased Prx2 expression was associated with high MVD (P=0.016), while expression of VEGF-A was not associated with Prx2 expression (P>0.05). Kaplan-Meier analysis showed that patients with high Prx2 expression (log-rank test, P=0.039), high MVD (log-rank test, P=0.015), a higher FIGO stage (log-rank test, P=0.021) and LN metastasis (log-rank test, P=0.022) had a shorter PFS time than patients with low Prx2 expression, low MVD, a lower FIGO stage and without LN metastasis, respectively. Cox proportional hazard regression analysis revealed that expression of Prx2 [hazard ratio (HR), 2.551; 95% confidence interval (CI), 1.056-6.162; P=0.037], MVD (HR, 2.436; CI, 1.034-5.735; P=0.042) and FIGO stage (HR, 1.543; CI, 1.027-2.319; P=0.037) were independent factors for PFS time. In conclusion, the results of the present study suggested that Prx2 could act as a potential biomarker for predicting CSCC progression and prognosis and could be a novel target for antiangiogenic therapy of CSCC.

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BACKGROUND: Neoadjuvant chemotherapy (NACT) before radical hysterectomy has been widely used for locally advanced cervical cancer (LACC); However, its efficacy is yet to be determined. METHODS: Effective and predictive biomarkers, which may aid in predicting the chemotherapy responses, were explored in this study. Initially, the expression of HIF-1α, VEGF-A, and Ki67 was detected in 42 paired (pre-NACT and post-NACT) LACC tissues, as well as 40 nonneoplastic cervical epithelial tissues by immunohistochemistry. Then, the correlation of the expression of HIF-1α, VEGF-A, Ki67 with the efficacy of NACT, as well as factors that affect the efficacy of NACT was analyzed. RESULTS: A clinical response occurred in 66.7% (28/42) of the patients, including 57.1% (16/28) with a complete response and 42.9% (12/28) with a partial response; While 33.33% (14/42) were non-responders, including 42.9% (6/14) with stable disease and 57.1% (8/14) with progressive disease. HIF-1α, VEGF-A, and Ki67 were overexpressed in LACC tissues compared to nonneoplastic tissues (P < .01, respectively); While the expression of HIF-1α, VEGF-A, and Ki67 was significantly decreased after NACT (P < .01, respectively). What's more, in the response group, HIF-1α, VEGF-A, and Ki67 expression were significantly decreased after chemotherapy in the post-chemotherapy cervical cancer tissues compared with the pre-chemotherapy cervical cancer tissues (all P < .05). Additionally, patients with lower histological grade and lower expression of HIF-1α, VEGF-A, and Ki67 were more responsive to NACT (P < .05, respectively); Moreover, the histological grade [P = .025, HR (95% CI): 0.133 (0.023-0.777)], HIF-1α [P = .019, HR (95% CI): 0.599 (0.390-0.918)], and Ki67 [P = .036, HR (95% CI): 0.946 (0898-0.996)] were independent risk factors affecting the efficacy of NACT in LACC. CONCLUSION: Expression of HIF-1α, VEGF-A, and Ki67 were significantly decreased after NACT, and decreasing expression of HIF-1α, VEGF-A, and Ki67 were related to good response to NACT, suggesting HIF-1α, VEGF-A, and Ki67 may be implicated in evaluating the efficacy of NACT in LACC.

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Liver kinase B1 (LKB1) is a newly discovered tumor suppressor gene that plays a role in tumorigenesis and cancer progression. However, LKB1 expression and its precise impact on gastric cancer (GC) have not yet been elucidated. The aim of this study was to explore the significance of LKB1 expression, as well as its correlation with epithelial-mesenchymal transition (EMT) in GC. In the present study, LKB1 protein was detected in 107 GC tissue samples and adjacent paracancerous tissues by immunohistochemical staining. The relationship of LKB1 expression with clinicopathological features and its correlation with 3 EMT-related markers (E-cadherin, ß-catenin, and vimentin) in GC were analyzed. Results revealed that the expression of LKB1 was decreased in GC tissues compared with that in adjacent paracancerous tissues (P = .005). GC patients with greater invasion depth (P = .007), higher pathological TNM stage (P = .014), and lymph node metastasis (P = .026) showed lower LKB1 expression; furthermore, E-cadherin and ß-catenin expression decreased, whereas vimentin expression increased (all P < .05). Kaplan-Meier analysis indicated that the expression of LKB1, E-cadherin, ß-catenin, and vimentin, as well as differentiation, invasion, pathological TNM, and lymph node metastasis, was associated with disease-free survival (DFS) (all P < .05). Multivariate analysis also showed that LKB1 expression (hazard ratio, 0.578 [0.351-0.950]; P = .031) may be an independent factor for DFS. In conclusion, LKB1 expression was decreased in GC, and this positively correlated with EMT and a shorter DFS, suggesting that LKB1 could act as an independent factor in predicting GC progression.

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OBJECTIVE: To investigate the clinico-pathologic features, treatment and prognosis of Castleman disease. METHODS: The clinico-pathologic data of 16 patients diagnosed as Castleman disease from January 2002 to December 2014 were analyzed retrospectively. RESULTS: The median age was 28.5 (7-73)years old. There were 14 unicentric cases, 92.8% (13/14) of which was diagnosed as hyaline-vascular type. Two multicentric cases was diagnosed as plasmatcyic type. All the patients were treated by surgical resection and their median follow-up was 55.5 (2-150)months. As a result, 13 unicentric cases achieved sustained remission, 1 unicentric case with plasmatocytic type relapsed at 60th month after surgical resection. CONCLUSION: Clinical subtype and histopathogenic type are the dominating progonostic factors in Castleman patients. The clinical presentation of unicentric disease has been found to be benigns and the surgical resection can be used as first-line treatment method in clinic. The clinical presentation of multicentric disease may be stable or advanced, and the prognosis of advanced cases is poor as there are no effective treatments.

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