Our study examined the association between molecular features and clinical results of pancreatic ductal adenocarcinoma (PDAC) patients, aiming to explore the genomic determinants of the recurrence and prognosis of PDAC after surgical removal.

Brain metastases are one of the most common intracranial neoplasms. Increasing evidence have indicated that systemic immunotherapy may provide long-term benefits for brain metastases. Herein, we presented the results of an immune oncology panel RNA sequencing platform for patients with brain metastases from different primary sites.

Nuclear receptor coactivator 1 (NCOA1) plays crucial roles in the regulation of gene expression mediated by a wide spectrum of steroid receptors such as androgen receptor (AR), estrogen receptor α (ER α), and estrogen receptor β (ER β). Therefore, dysregulations of NCOA1 have been found in a variety of cancer types. However, the clinical relevance and the functional roles of NCOA1 in human esophageal squamous cell carcinoma (ESCC) are less known. We found in this study that elevated levels of NCOA1 protein and/or mRNA as well as amplification of the NCOA1 gene occur in human ESCC. Elevated levels of NCOA1 due to these dysregulations were not only associated with more aggressive clinic-pathologic parameters but also poorer survival. Results from multiple cohorts of ESCC patients strongly suggest that the levels of NCOA1 could serve as an independent predictor of overall survival. In addition, silencing NCOA1 in ESCC cells remarkably decreased proliferation, migration, and invasion. These findings not only indicate that NCOA1 plays important roles in human ESCC but the levels of NCOA1 also could serve as a potential prognostic biomarker of ESCC and targeting NCOA1 could be an efficacious strategy in ESCC treatment.

The prognostic value of tumor size in neuroblastoma (NB) patients has not been fully evaluated. Our purpose is to elucidate the prognostic significance of tumor size in surgery performed on neuroblastoma patients.

Recent studies have demonstrated that various long non-coding RNAs (lncRNAs) participate in the gastric cancer (GC) development and metastasis. Some lncRNAs exert their regulatory function by interacting with microRNAs. Here we identified a novel lncRNA RP11-81H3.2 that was highly expressed in the GC tissue and cell lines. RP11-81H3.2 knockdown significantly inhibited the proliferation, migration, and invasion of GC cells. Mechanistically, we demonstrated that RP11-81H3.2 directly interacted with miR-339 while miR-339 regulated the HNRNPA1 expression by targeting HRRNPA1 3'-UTR. RP11-81H3.2-miR-339-HNRNPA1 interaction network regulated the GC cell proliferation, migration, and invasion. Moreover, our results confirmed that RP11-81H3.2 knockdown suppressed the tumor growth of GC in a xenograft model in vivo. In summary, the results suggest that RP11-81H3.2 functions as an oncogene in GC and could be utilized as a promising diagnosis and therapeutic marker for GC treatment.

Quantitative methods of Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) interpretation, including the percent change in FDG uptake from baseline (ΔSUV), are under investigation in lymphoma to overcome challenges associated with visual scoring systems (VSS) such as the Deauville 5-point scale (5-PS).

Breast cancer (BRCA) is the second leading cause of cancer-related death among female worldwide. Recent studies have revealed that LACTB was frequently repressed and functioned as a bona fide new tumor suppressor in a series of cancers, including BRCA. However, the molecular mechanisms underlying LACTB dysregulation in BRCA have not been reported. In the present study, we find that LACTB is repressed in BRCA and associated with poor prognosis by BRCA tissue microarray (TMA) analysis. Moreover, we confirm that LACTB is a direct target of miR-374a, which is significantly overexpressed and associated with malignancies in BRCA. Mechanistically, applying loss-of-function and gain-of-function approaches in a series of in vitro and in vivo experiments show that miR-374a knockdown suppresses the cell proliferative and colony formation activity, as well as migration and invasion capacity, but LACTB silencing in these cells reverses this change. Furthermore, we find that miR-374a silencing markedly reduces the tumor growth in xenograft mouse models. In summary, our findings suggest the miR-374a/LACTB axis plays a critical role in the tumorigenicity and progression of BRCA. miR-374a/LACTB axis may be a potential target in the development of therapeutic strategies for BRCA patients.

Cancer is mostly a disease of aging, and older patients with cancer are generally frailer. This study aimed to describe the characteristics and in-hospital outcomes and explore factors associated with duration, cost, and mortality during first hospitalization, in older patients with cancer admitted to a top-ranked hospital in China.

Protein Kinase D (PKD) family contains PKD1, PKD2, and PKD3 in human. Compared to consistent tumor-suppressive functions of PKD1 in breast cancer, how PKD2/3 functions in breast cancer are not fully understood. In the current study, we found that PKD2 and PKD3 but not PKD1 were preferentially overexpressed in breast cancer and involved in regulating cell proliferation and metastasis. Integrated phosphoproteome, transcriptome, and interactome showed that PKD2 was associated with multiple cancer-related pathways, including adherent junction, regulation of actin cytoskeleton, and cell cycle-related pathways. ELAVL1 was identified as a common hub-node in networks of PKD2/3-regulated phosphoproteins and genes. Silencing ELAVL1 inhibited breast cancer growth in vitro and in vivo. Direct interaction between ELAVL1 and PKD2 or PKD3 was demonstrated. Suppression of PKD2 led to ELAVL1 translocation from the cytoplasm to the nucleus without significant affecting ELAVL1 expression. Taken together, we characterized the oncogenic functions of PKD2/3 in breast cancer and their association with cancer-related pathways, which shed lights on the oncogenic roles and mechanisms of PKDs in breast cancer.

This study was designed to investigate the prognostic value of the number and sites of extracranial metastasis (ECM) in NSCLC patients with BM. NSCLC patients with BM from the Surveillance, Epidemiology, and End Results (SEER) database from 2010 to 2015 were enrolled in analysis. Patients from 2010 to 2013 were included in the training set and those from 2014 to 2015 in the validation set. ECM sites among different subtypes of NSCLC were compared by Chi-square tests. Kaplan-Meier methods and Cox regression models were performed to analyze survival data. Competing-risks analysis was used to predict cumulative incidence rates for CSS and non-CSS cause. We included 5974 patients in the training cohort and 3561 patients in the validation cohort. Most (nearly 80%) NSCLC patients with BM showed 0-1 involved extracranial organ, with the most and least common ECM organ being bone and distant lymph nodes (DLNs) among all subtypes of NSCLC, respectively. The number of involved extracranial organs was an independent prognostic factor for patients with BM from NSCLC (p < 0.001). Patients with 0-1 ECM had better survival than those with larger number of involved extracranial organs (p < 0.001). Cumulative incidence rates for CSS were increased with the number of ECM raising (p < 0.001). All involved extracranial organs were associated with worse survival (p < 0.05). In patients with single-organ ECM, we observed a better prognosis in lung and bone metastasis, while liver metastasis showed worst survival. But the difference in survival in these patient groups was relatively small. Patients with liver metastasis had higher cumulative incidence rates for CSS than that in patients with lung and bone metastasis (p < 0.05). More extracranial metastases were associated with poor prognosis in NSCLC patients with BM and ECM sites showed limited effect on survival. Tailored treatments would be reasonable for BM patients from NSCLC with different metastasis patterns.

Lung large cell neuroendocrine carcinoma (L-LCNEC) is a rare, aggressive tumor, for which the optimal treatment strategies for LCNEC have not yet been established. In order to explore how to improve the outcome of prognosis for patients with LCNEC, this study investigated the effect of different treatments based on the data obtained from the Surveillance, Epidemiology, and End Results (SEER) database.

We compared the efficacy, safety, and costs of hypofractionated radiotherapy (HFRT) and conventional fractionated radiotherapy (CFRT) for the neoadjuvant treatment of esophageal cancer.

In this study, we aimed to investigate the viability of utilizing CytoSorter® system to detect circulating tumor cells (CTCs) and to evaluate the diagnostic value of CTCs in breast cancer (BC).

The goal of this study was to establish and validate two nomograms for predicting the long-term overall survival (OS) and cancer-specific survival (CSS) in lip squamous cell carcinoma (LSCC).

Long noncoding RNAs (lncRNAs) act as essential regulators in cancer tumorigenesis. Our study aimed to explore the underlying mechanism of lncRNA human leukocyte antigen complex group 11 (HCG11) in cervical cancer (CC) progression. Long noncoding RNA HCG11 was downregulated in CC. Functional assays demonstrated that lncRNA HCG11 inhibited CC cell proliferation and invasion. Then, we confirmed that lncRNA HCG11 could directly bind to miR-942-5p. Moreover, inhibition of miR-942-5p suppressed the growth and invasion of CC cells, and growth factor-independent transcription repressor 1 (GFI1) gene was the target gene of miR-942-5p. Long noncoding RNA HCG11 increased the expression of GFI1 and suppressed cell proliferation and invasion by acting as a miR-942-5p sponge. Finally, the overexpression of lncRNA HCG11 suppressed the proliferation and metastasis of CC cells in vivo.

Multidrug resistance (MDR) is a primary limitation of breast cancer chemotherapy. The common mechanism of MDR is various anticancer drugs can be effluxed by the cell membrane protein P-glycoprotein (P-gp). Here, we found that ectopic overexpression of Shc3 was detected specifically in drug-resistant breast cancer cells, consequently reducing sensitivity to chemotherapy and promoting cell migration by mediating P-gp expression. However, the molecular mechanism underlying the interplay between P-gp and Shc3 in breast cancer is unknown. We reported an additional resistance mechanism involving an increase in the active form of P-gp after Shc3 upregulation. MCF-7/ADR and SK-BR-3 cells can be sensitive to doxorubicin after knockdown of Shc3. Our results indicated that the interaction between ErbB2 and EphA2 is indirect and regulated by Shc3, and also, this complex is essential for activation of the MAPK and AKT pathways. Meanwhile, Shc3 promotes ErbB2 nuclear translocation, followed by a subsequent increase of the COX2 expression through ErbB2 binding to the COX2 promoter. We further demonstrated that COX2 expression was positively correlated with P-gp expression and the Shc3/ErbB2/COX2 axis upregulates P-gp activity in vivo. Our results show the crucial roles of Shc3 and ErbB2 in modulating P-gp efficacy in breast cancer cells and suggest that Shc3 inhibition may enhance the sensitivity to chemotherapeutic drugs that target oncogene addiction pathways.