A Bayesian network meta-analysis of the primary definitive therapies for locoregionally advanced nasopharyngeal carcinoma: IC+CCRT, CCRT+AC, and CCRT alone.

BACKGROUND: The major aim of this Bayesian network analysis was to determine the optimal treatment strategy for locoregionally advanced nasopharyngeal carcinoma (LANPC). METHOD: We systematically searched databases and extracted data from randomized clinical trials involving LANPC patients randomly assigned to receive induction chemotherapy followed by concurrent chemoradiotherapy (IC+CCRT), CCRT followed by adjuvant chemotherapy (CCRT+AC), or CCRT. RESULTS: In the network analysis, IC+CCRT was significantly better than CCRT alone for 5-year FFS (odds ratio [OR]: 1.63, 95% credible interval [CrI] 1.16-2.29), DMFS (OR: 1.56, 95% CrI 1.08-2.22), and LFRS (OR: 1.62, 95% CrI 1.02-2.59), but not OS (OR: 1.35, 95% CrI 0.92-2.00). Rank probabilities showed that IC+CCRT was ranked the best followed by CCRT+AC and CCRT for all 5-year outcomes. Although compared to IC+CCRT and CCRT, CCRT+AC did not significantly improve survival but had the highest 5-year survival rates. CONCLUSIONS: IC+CCRT could be recommended as a front-preferred primary definitive therapy for patients with LANPC.

[Rule of acupoint selection for cancer pain based on association rule and entropy clustering].

OBJECTIVE: To analyze the rule of acupoint selection for cancer pain based on data mining. METHODS: The published literature regarding acupuncture for cancer pain in the recent 10 years was searched in PubMed, CNKI, VIP and Wanfang database. The acupoint selection was summarized and analyzed by TCMISS V2.5. RESULTS: Totally 68 literature was collected and 73 acupoint prescriptions were included, involving 117 acupoints. These acupoints were mainly in bladder meridian, stomach meridian, liver meridian and spleen meridian. Among them, 40 acupoints used more than 4 times were identified, and the top three acupoints were Zusanli (ST 36, 65 times), Neiguan (PC 6, 55 times) and Taichong (LR 3, 50 times). A total of 68 acupoint combinations used more than 19 times were identified, and the top three acupoint combinations were Zusanli (ST 36)-Neiguan (PC 6), Taichong (LR 3)-Zusanli (ST 36) and Zusanli (ST 36)-Sanyinjiao (SP 6). There were 103 acupoint combinations with strong association; based on the entropy clustering algorithm, 20 new acupoint combinations and 10 new acupoint prescriptions were obtained. CONCLUSION: The main meridians for cancer pain are bladder meridian, stomach meridian, liver meridian and spleen meridian, with Zusanli (ST 36), Neiguan (PC 6), Taichong (LR 3), Hegu (LI 4), Sanyinjiao (SP 6) and ashi points as core acupoints, and regulating spleen-stomach and treating qi-blood are the main principles.

Marked response to nab-paclitaxel in EGFR mutated lung neuroendocrine carcinoma: A case report.

RATIONALE: Lung cancer is the leading cause of cancer-related death in the world. Tyrosine kinase inhibitors (TKIs), which target mutated epidermal growth factor receptor (EGFR), have been the first-line treatment of late-stage lung adenocarcinoma harboring EGFR mutation. EGFR mutations are mostly identified in lung adenocarcinoma. However, it is rarely seen in lung neuroendocrine carcinoma, and treatment strategies remain under reported. PATIENT CONCERNS: Here, we describe a 54-year-old Chinese man diagnosed with lung adenocarcinoma (cT4N3M1b, stage IV) with neuroendocrine differentiation and L858R mutation on exon 21. He developed progressive disease in liver 4 months later, and the biopsy of liver metastases showed neuroendocrine carcinoma maintained the same EGFR mutation. DIAGNOSES: Lung adenocarcinoma and neuroendocrine carcinoma were identified by biopsy. INTERVENTIONS: After a combined treatment with nab-paclitaxel and erlotinib, the patient achieved partial remission. OUTCOMES: The patient's overall survival was 27 months. LESSONS: This case highlights that EGFR mutated lung neuroendocrine carcinoma is not responsive to single-agent EGFR-TKI. However, combined application with nab-paclitaxel can improve its efficacy and prolong the patient's survival.

[Effect of Jiangtang Xiaozhi Tablet on Insulin Resistance KK-AY Transgenic Mice Model of Diabetes Mellitus].

Objective To observe effects of Jiangtang Xiaozhi Tablet (JTXZT) on homeostasis model of assessment for insulin resistance index (HOMA-IR) , insulin sensitivity index ( ISI) , expres- sions of insulin (INS) and insulin receptor (InsR) in pancreas tissues of KK-A(y) transgenic mice model of diabetes mellitus (DM). Methods KK-A(y) transgenic mice were fed with high fat forage to induce hyper- glycemic obese DM model. The C,7ice at same age were used as a normal control group (fed with e- qual volume of sterile water, n =11). Successful modeled 55 mice with DM obesity were divided into 5 groups by random digit table (11 in each group) , including the model group (fed with equal volume of ster- ile water, with no treatment) , the Pioglitazone Hydrochloride Tablet treatment group (8 mg/kg; as a posi- tive control group) , and JTXZT groups [high (10. 0 g crude drugs/kg) , middle (5. 0 g crude drugs/kg) and low dose (2. 5 g crude drugs/kg) ]. All medications were fed by gastrogavage, once per day for 8 succes- sive weeks. All mice were weighed and levels of random blood glucose (RBG) determined after 8 weeks of treatment. Blood was collected from ophthalmic vein. Levels of insulin (INS) , serum total cholesterol (TC) and triglyceride (TG) were detected. HOMA-IR and ISI were calculated. The morphological changes of pancreas tissues were extracted for performed pathological examinations. The expressions of INS and insulin receptor (InsR ) were measured by immunohistochemistry ( IHC ). Expressions of insulin receptorp ßInsRP) and insulin receptor substrate-1 (IRS-1) in pancreas tissues were detected using Western blot. Results Compared with the normal control group, obesity, obviously increased blood glu- cose and blood lipids occurred in each group after modeling (P <0. 01). After 8 weeks of medication mice in the model group had put up body weight (P <0. 01) , blood glucose and blood lipids were kept on quite higher levels. Compared with the model group, body weight, serum levels of TG, INS, and HOMA-IR obvi- ously decreased in each JTXZT group (P <0. 05, P <0. 01). Besides, RBG decreased obviously lower in the high dose JTXZT group (P <0. 01). ISI obviously increased in low and high dose JTXZT groups (P < 0. 05, P <0. 01). Pathological results of HE staining in pancreas showed that atrophied islets with obvious- ly reduced numbers in the model group. They were sparsely distributed with reduced islet density.-Islet cells were compensatively hypertrophy, with degenerated vacuoles. Apoptosis of islet cells could also be seen in the model group, manifested as swollen cytoplasm and paryopyknosis. Islet number was obvious- ly increased in high and middle dose JTXZT groups, with reduced apoptosis and degenerated cells. Re- sults of IHC assay showed, as compared with the normal control group, the grey values of INS and InsR were significantly decreased in the model group (P <0. 01). Compared with the model group, IOD values of INS and InsR (IOD) were significantly increased in each JTXZT group (P <0. 05, P <0. 01). Results from Western blot showed that protein expressions of InsRP ßnd IRS-1 were obviously decreased in the model group, as compared with the normal control group (P <0. 01). Compared with the model group, protein expressions of InsRP ßnd IRS-1 were obviously increased in each JTXZT group (P <0. 01) , but with no statistical difference as compared with the Pioglitazone Hydrochloride Tablet treatment group (P > 0. 05). Conclusions JTXZT had obvious roles in decreasing levels of blood glucose, serum lipids, and improving insulin resistance in KK-Ayt(r) ansgenic mice model with diabetic obesity. Its mechanism might involve in increasing expressions of lnsRp and IRS-1 in pancreas cells, promoting the integration of INS to its receptors, and thereby improving glucose metabolism , lipid metabolism , and IR state.

Lung adenocarcinoma harboring concomitant SPTBN1-ALK fusion, c-Met overexpression, and HER-2 amplification with inherent resistance to crizotinib, chemotherapy, and radiotherapy.

Crizotinib is a multi-targeted tyrosine kinase inhibitor (TKI) with activity against mesenchymal-epithelial transition factor (MET) and anaplastic lymphoma kinase (ALK). However, the concomitant oncogenic drivers may affect the sensitivity of crizotinib. Herein, we present a 69-year-old never-smoker Chinese male with advanced lung adenocarcinoma harboring concomitant spectrin beta non-erythrocytic 1 (SPTBN1)-ALK fusion, c-Met overexpression, and human epidermal growth factor receptor-2 (HER-2) amplification with inherent resistance to crizotinib, chemotherapy, and radiotherapy. Although the patient received timely and comprehensive treatment, the overall survival was only 8 months. Therefore, c-Met overexpression, HER-2 gene amplification, and SPTBN1-ALK gene fusion can coexist in lung adenocarcinoma and may become a potential biomarker of cancer refractory to crizotinib, chemotherapy, and radiotherapy as well as of a relatively poor prognosis. In addition, the novel SPTBN1-ALK fusion gene may become a potential target for anti-tumor therapy.