[Clinicopathological observation of 10 cases of salivary secretory carcinoma].

Objective: To investigate the clinical and pathological features of salivary secretory carcinoma (SSC). Methods: Ten cases of SSC confirmed in the Department of Pathology,Capital Medical University School of Stomatology from January 2014 to December 2021 were retrospectively included, including 5 males and 5 females, with a median age of 46.5 years. The microscopic morphology, immunophenotype, special staining and clinical follow-up of 10 cases of salivary secretory carcinoma were observed. Ten patients were tested with S-100, vimentin, mammaglobin, Dog-1, p63 and Ki-67, 9 cases with cytokeratin (CK) 8/18, 8 with CK7, 6 with calponin, 5 with smooth muscle actin (SMA) and GCDFP15, 4 with CK5/6 and 1 with SOX10. The ETV6-NTRK3 fusion gene was detected by fluorescence in situ hybridization. Results: Seven of the 10 SSC were located in the parotid gland and 3 were located in the cheeks. Histomorphology showed solid, papillary-cystic, follicular, microcystic, and macrocystic types. In 7 cases, tumor cells were dominated by single arrangement type, while certain mixed arrangements existed in some areas. The cytoplasm of the tumor cells was rich in eosinophilic, fine granular or vacuolar shapes, and clear cytoplasm was seen in 2 cases. The nuclei were mostly oval-shaped vesicular nuclei, with nucleoli in the center. Immunohistochemistry showed CK7 (8/8) positive, CK8/18 (9/9) positive, S-100 (10/10) positive, vimentin (5/10) positive, (4/10) partially positive and (1/10) less partially positive, mammaglobin (7/10) positive, (1/10) partially positive and (2/10) some individual cells positive, Dog-1 (10/10) negative, CK5/6 (4/4) negative, p63 (7/10) negative and (3/10) partially positive, SMA (5/5) negative, calponin (6/6) negative, and Ki-67 index was 5%-20%. Secretions of 5 cases showed periodic acid-Schiff (PAS) and PAS with diastase (PAS-D) staining positive. All 10 cases showed ETV6-NTRK3 fusion positive. Six cases were successfully followed up for 32-91 months, of which 2 cases recurred after 28 and 74 months and underwent surgical resection again. All cases followed up are alive and disease-free. Conclusions: The salivary secretory carcinoma is a rare low-grade malignant tumor. In certain cases, morphology is atypical and mammaglobin is immunohistochemically positive in only individual tumor cells. Therefore, the diagnosis should be supported with morphology, immunohistochemical staining, and molecular feature preferably.

[Analysis of clinical characteristics and prognosis of 235 pancreatic neuroendocrine tumors underwent Sunitinib treatment].

Objective: To investigate the clinical characteristics, treatment, and prognostic factors of pancreatic neuroendocrine tumors (pNETs) patients treated with Sunitinib. Methods: The clinical data of pNETs patients from Pfizer Drug Assistance Program of Cancer Foundation of China from April 2013 to November 2017 were retrospectively analyzed. Follow-up and statistical analysis were performed. Results: A total of 235 patients were enrolled, the patients' overall survival time was between 4 and 252 months, the 3-years and 5-years survival rates were 73.8% and 60.8%, respectively. Univariate analysis showed that factors such as age, Ki-67 index and surgery were associated with the 3-years survival rates of pNETs patients (P<0.05). Multivariate analysis demonstrated that the age, Ki-67 index and surgery were independent prognostic factors for pNETs patients (P<0.05). For patients with liver metastases, univariate analysis revealed that surgery was associated with prognosis (P<0.05). The 5-years survival rate of 124 patients with extending usage of Sunitinib was 53.3%. Conclusion: PNETs are rare tumors with atypical clinical symptoms and the patients often have metastasis at the initiate diagnosis. The age, Ki-67 index and surgery are associated with the prognosis of pNETs patients.

Knockdown of lncRNA XIST inhibits hypoxia-induced glycolysis, migration and invasion through regulating miR-381-3p/NEK5 axis in nasopharyngeal carcinoma.

OBJECTIVE: Hypoxia is an important feature of nasopharyngeal carcinoma (NPC). Growing evidence demonstrated that long non-coding RNAs (lncRNAs) could participate in cancer progression and hypoxia regulation. However, the exact roles and underlying mechanism of lncRNA X-inactive specific transcript (XIST) in NPC under hypoxia are still unclear. MATERIALS AND METHODS: The expressions of XIST, microRNA-381-3p (miR-381-3p) and NIMA related kinase 5 (NEK5) were detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The glucose consumption and lactate production were measured using the glucose assay kit and lactate assay kit, respectively. Western blot assay was used to determine the protein levels of hexokinase II (HK2) and NEK5. Transwell assay was employed to evaluate cell migration and invasion. The interaction between miR-381-3p and XIST or NEK5 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. The mice xenograft model was established to investigate the roles of XIST in NPC progression in vivo. RESULTS: XIST and NEK5 were highly expressed while miR-381-3p was lowly expressed in NPC (tissues and cells) and hypoxia-induced NPC cells. Deficiency of XIST or NEK5 suppressed hypoxia-induced glycolysis and metastasis in NPC cells. Moreover, miR-381-3p could directly bind to XIST and its inhibition reversed the inhibitory effects of XIST knockdown on glycolysis and metastasis under hypoxia. NEK5 was a direct target of miR-381-3p and its interference attenuated the promotive effects of miR-381-3p downregulation on glycolysis and metastasis under hypoxic conditions. Besides, interference of XIST decreased tumor growth by upregulating miR-381-3p and downregulating NEK5. CONCLUSIONS: XIST knockdown inhibited glycolysis and metastasis in hypoxia-induced NPC cells through regulating miR-381-3p/NEK5 axis, providing new insights into the pathogenesis of NPC.

Patients with brain metastases derived from gastrointestinal cancer: clinical characteristics and prognostic factors.

PURPOSE: This study seeks to evaluate the natural history, outcome, and possible prognostic factors in patients with brain metastases derived from gastrointestinal cancers. METHODS: The clinical features, prognostic factors, and the effects of different treatment modalities on survival were retrospectively investigated in 103 patients with brain metastases derived from gastrointestinal cancers. RESULTS: The median time from diagnosis of primary tumor to brain metastasis was 22.00 months. The interval between diagnosis of primary tumor relapse and brain metastasis was 8.00 months. The median follow-up time was 7.80 months. The median survival time after diagnosis of brain metastases was 4.10 months for all patients and 1.17 months for patients who received only steroids (36.9 %), 3.97 months for patients who only received whole-brain radiation therapy (WBRT 31.1 %), 11.07 months for patients who received gamma-knife surgery alone or/and WBRT (20.4 %), and 13.70 months for patients who underwent surgery and radiotherapy (12 patients, 11.6 %) (P < 0.001). Multivariate analysis revealed that recursive partitioning analysis (RPA) class, extracranial metastasis, and chemotherapy were independent prognostic factors. Brain metastasis derived from gastrointestinal tract cancer is rare, and overall patient survival is poor. CONCLUSION: RPA class, chemotherapy after brain metastases, and treatment regimens were independent prognostic factors for the survival of patients with brain metastases derived from gastrointestinal cancers.

Analysis of lactate dehydrogenase activities and isoenzyme patterns in colorectal cancer tissues.

AIM: To investigate the relationship between lactate dehydrogenase (LDH) activity or LDH isoenzyme patterns and the pathogenesis of colorectal cancer. METHODS: Activities of tissue LDH and LDH isoenzyme patterns in 16 patients with colorectal cancer were assayed using spectrophotometric procedures and agarose gel electrophoresis, respectively. RESULTS: The total and specific activities of LDH were significantly higher in colorectal cancer tissues than those in adjacent noncancerous tissues (P < 0.001). The LDH isoenzyme pattern was also different from that in the control. The percentage of LDH5 doubled and the ratio of LDH4 + LDH5/LDH1 + LDH2 was 3.6 ± 1.4 in cancer tissue, significantly greater than in the control. CONCLUSIONS: The increased LDH activity in colorectal cancer tissues resulted mainly from the increased LDH5, suggesting that the alteration of LDH activity and isoenzyme patterns were related to the pathogenesis of colorectal cancer.