Silvamcmillan5390

Neuroendocrine tumors (NETs) associated with carcinoid syndrome (CS) overproduce serotonin, mediated by tryptophan hydroxylase-1 (TPH1). The TPH inhibitor telotristat ethyl (TE) reduces peripheral serotonin and relieves CS symptoms. We conducted a real-world clinical practice study to explore the effects of TE on tumor growth in patients with NETs and CS.

Single-arm, pre/post chart review study of patients with advanced NETs who received TE for ≥6 months and had ≥2 radiological scans within 12 months before and ≥1 scan after TE initiation. Linear regression and longitudinal analyses assessed changes in tumor size controlling for background NET treatment.

Two hundred patients were enrolled, most (61%) had well-differentiated gastrointestinal NETs (61%) and received TE for an average of 12 months (SD, 7.3). Mean reduction in tumor size after TE initiation was 0.59 cm (p=0.006). Longitudinal analysis showed an 8.5% reduction in tumor size (p=0.045) from pre- to post-TE periods. Documented NET treatment prior to initiating TE and time between scans were not significant predictors of changes in tumor size. VX-11e Results were consistent in a subgroup of patients with the same documented NET treatment before and after initiating TE.

TE may have antitumor effects consistent with serotonin overproduction in tumor growth.

TE may have antitumor effects consistent with serotonin overproduction in tumor growth.

Dexamethasone combined with 5-hydroxytryptamine type 3 receptor antagonists (5-HT3 RA) dual regimen is the standard prophylaxis regimen for patients receiving moderately emetogenic chemotherapy (MEC). However, it has been found in real-world practice that chemotherapy-induced nausea and vomiting (CINV) remains poorly controlled among patients with gastrointestinal tumor, especially in those with high-risk factors for vomiting, such as female, young, and non-alcoholic individuals. Hence, we aimed to evaluate the efficacy of an olanzapine-containing triple regimen in this clinical setting.

We retrospectively reviewed the clinical records of gastrointestinal tumor patients who received mFOLFOX6, XELOX, or FOLFIRI chemotherapy at two institutions. All patients included were female and less than 55 years old, with no history of drinking. The patients were divided into two groups for olanzapine-containing triple therapy (olanzapine, tropisetron, and dexamethasone) and non-olanzapine dual therapy (tropisetron ananzapine-containing triple antiemetic regimen exhibit better efficacy and QoL as compared to non-olanzapine dual regimen. Further randomized studies are required to confirm these results.

This retrospective study indicates that in gastrointestinal tumor patients with high-risk factors for CINV who were receiving MEC, olanzapine-containing triple antiemetic regimen exhibit better efficacy and QoL as compared to non-olanzapine dual regimen. Further randomized studies are required to confirm these results.

Non-small cell lung carcinoma (NSCLC) is often fatal; advanced NSCLC has a 5-year survival rate less than 20%. Platinum-based chemotherapy, in particular,

-diamminedichloroplatinum (II) (cisplatin or DDP), is employed for the treatment of NSCLC; however, the drug resistance occurs frequently. Autophagy is defined as the process of intracellular degradation of cytoplasmic materials in the lysosome; however, the correlation between autophagy and drug resistance remains controversial. Herein, we investigated the correlation between autophagy and cisplatin resistance and also explored the underlying mechanisms.

We demonstrated that DDP-resistant NSCLC A549 (A549/DDP) cells had higher autophagy activity in comparison with its parental A549 cells; DDP treatment induced a time- and dose-dependent decrease of autophagy. Intriguingly, inhibition of autophagy with pharmacological drugs or knockdown of ATG5 or Beclin-1 aggravated cell death induced by DDP treatment, indicating that autophagy played protective rolefor the reversal of DDP chemoresistance for NSCLC treatment.

Our study provides novel insights into the association between MiTF and DDP chemoresistance in NSCLC cells, and suggests targeting MiTF and/or autophagy might be a potential strategy for the reversal of DDP chemoresistance for NSCLC treatment.

This study was designed to investigate the relationship between long-chain non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1)/miR-23a-23a and melanoma.

Fifty-two cases of corresponding non-tumor normal tissues and 109 cases (including 62 cases of primary melanoma and 47 cases of metastatic melanoma) were collected. Real-time fluorescent PCR quantified lncRNA MALAT1 and miR-23a, and counted the 3-year survival of high/low miR-23 and high/low lncRNA MALAT1 populations. We predicted the binding site according to the sequence information of lncRNA MALAT1 and miR-23a. lncRNA MALAT1 siRNA and miR-23a mimics vectors were constructed and transfected into melanoma cell lines respectively to observe their effects on cells.

Compared with corresponding non-tumor normal tissues, lncRNA MALAT1 in melanoma tissue increased while miR-23a decreased. Compared with primary melanoma, metastatic melanoma was higher and miR-23a was lower. Downregulation of lncRNA MALAT1 caused upregulation of miR-23a, and lncRNA MALAT1 could bind to miR-23a. Downregulating lncRNA MALAT1 or upregulating miR-23a inhibited cell proliferation, migration and invasion and promoted apoptosis. Rescue experiments revealed that downregulation of miR-23a could offset cell changes caused by downregulation of lncRNA MALAT1.

lncRNA MALAT1 promotes malignant proliferation of melanoma cells through miR-23a.

lncRNA MALAT1 promotes malignant proliferation of melanoma cells through miR-23a.

This study aimed to analyze the risk factors for esophageal squamous cell carcinoma (ESCC), especially extracapsular lymph node involving the esophagus (ECLNIE), occurring during or after radiotherapy (RT) in patients with esophageal perforation (EP).

In total, 306 patients with ESCC who received RT and/or chemotherapy between January 2016 and December 2017 in our hospital and who met the inclusion criteria of the study were recruited. The continuous variables were converted into classification variables using the receiver operating characteristic curve or common clinical parameters. Risk factors for EP were examined by univariable analysis using the chi-square test or Fisher's exact and by multivariable analysis using logistic regression model. Propensity score matching (PSM) was used to compensate for the differences in baseline characteristics, and the incidence of EP was compared after matching.

EP was observed in 26 patients (incidence rate, 8.5%). Univariable analysis revealed that age, BMI, T4 stage, tumor length, esophageal wall thickness, ECLNIE, necrotic areas, niche sign by esophagogram before RT, neutrophil-to-lymphocyte ratio, and prognostic nutritional index were significantly associated with EP among patients with ESCC who received radiotherapy.