Objective To establish a prognostic index (PI) for patients with stage III-IV nasopharyngeal carcinoma (NPC) patients to personalize recommendations for induction chemotherapy (IC) before intensity-modulated radiotherapy (IMRT). Patients and Methods Patients received concurrent chemoradiotherapy (CCRT) with or without IC. Factors used to construct the PI were selected by a multivariate analysis of progression-free survival (PFS), which was the primary endpoint (P 0.8), the addition of IC significantly improved PFS, OS, and DMFS, but not LRFS. In multivariate analyses, IC was a protective factor for PFS, OS, and DMFS in the high-risk subgroup, while it had no significant benefit in the low-risk subgroup. Conclusion The proposed prognostic model effectively stratifies patients with stage III-IV NPC. High-risk patients are candidates for IC before CCRT, while low-risk patients are unlikely to benefit from it. Copyright © 2020 Sun, Xiao, Lu, Liu, Chen, Yuan, Tang and Mai.Background Serous cystadenoma (SCA), mucinous cystadenoma (MCN), and intraductal papillary mucinous neoplasm (IPMN) are three subtypes of pancreatic cystic neoplasm (PCN). Due to the potential of malignant-transforming, patients with MCN and IPMN require radical surgery while patients with SCA need periodic surveillance. However, accurate pre-surgery diagnosis between SCA, MCN, and IPMN remains challenging in the clinic. Methods This study enrolled 164 patients including 76 with SCA, 40 with MCN and 48 with IPMN. Patients were randomly split into a training cohort (n = 115) and validation cohort (n = 41). We performed statistical analysis and Boruta method to screen significantly distinct clinical factors and radiomics features extracted on pre-surgery contrast-enhanced computed tomography (CECT) images among three subtypes. Three reliable machine-learning algorithms, support vector machine (SVM), random forest (RF) and artificial neural network (ANN), were utilized to construct classifiers based on importantty and translational value of CECT-based radiomics classifiers for differentiation among SCA, MCN, and IPMN. Copyright © 2020 Shen, Yang, Yang, Yang, Xu, Zhuo, Wang, Lu, Liu, Zheng, Niu and Xu.Thanks to the development of modern chemotherapeutic regimens, survival after surgery for pancreatic ductal adenocarcinoma (PDAC) has improved and pancreatologists worldwide agree that the treatment of PDAC demands a multidisciplinary approach. Neoadjuvant treatment (NAT) plays a major role in the treatment of PDAC since only about 20% of patients are considered resectable at the time of diagnosis. Moreover, increasing data demonstrating the benefits of NAT for borderline resectable/locally advanced PDAC are driving a shift from up-front surgery to NAT in the multidisciplinary treatment of even resectable PDAC. Our understanding of the role of NAT in PDAC has evolved from tumor shrinkage to controlling potential micrometastases and selecting patients who may benefit from radical resection. The present review gives an overview on the current literature of NAT concepts for BR/LA PDAC and resectable PDAC. Copyright © 2020 Oba, Ho, Bao, Al-Musawi, Schulick and Chiaro.Resistance to radiation and chemotherapy in colorectal cancer (CRC) patients contribute significantly to refractory disease and disease progression. Herein, we provide mechanistic rationale for acquired or inherent chemotherapeutic resistance to the anti-tumor effects of 5-fluorouracil (5-FU) that is linked to oncogenic GLI1 transcription activity and NBS1 overexpression. Patients with high levels of GLI1 also expressed high levels of NBS1. Non-canonical activation of GLI1 is driven through oncogenic pathways in CRC, like the BRAFV600E mutation. GLI1 was identified as a novel regulator of NBS1 and discovered that by knocking down GLI1 levels in vitro, diminished NBS1 expression, increased DNA damage/apoptosis, and re-sensitization of 5-FU resistant cancer to treatment was observed. Furthermore, a novel GLI1 inhibitor, SRI-38832, which exhibited pharmacokinetic properties suitable for in vivo testing, was identified. GLI1 inhibition in a murine BRAFV600E variant xenograft model of CRC resulted in the same down-regulation of NBS1 observed in vitro as well as significant reduction of tumor growth/burden. GLI1 inhibition could therefore be a therapeutic option for 5-FU resistant and BRAFV600E variant CRC patients. Copyright © 2020 Zhang, Ma, Avery, Sambandam, Nguyen, Xu, Suto and Boohaker.The EGFR/HER2 signaling network is an effective therapeutic target for HER2-positive cancers, which are known for their aggressive biological course. Evidence indicates that the EGFR/HER2 network plays a role in the aggressive basal-like subtype as well. Here, we studied the potential role of miR-125a-3p as a modulator of the EGFR/HER2 pathway in basal-like breast cancer. Over-expression of miR-125a-3p reduced the migratory capability of MDA-MB-231 cells and led to an increase in the expression of ErbB2 transcript and protein. The induced ErbB2 responded to trastuzumab and underwent internalization and subsequent intra-lysosomal degradation. Trastuzumab treatment further reduced the migratory capability and induced the apoptosis of the cells. An in-vivo mouse model, which supported the in-vitro findings, showed a synergistic effect for miR-125a-3p and trastuzumab. Trastuzumab-treated miR-125a-3p-induced tumors were significantly smaller than control induced tumors.  https://www.selleckchem.com/products/pd-1-pd-l1-inhibitor-3.html  Our findings indicate that, in the basal-like subtype of breast cancer, miR-125a-3p may act as a tumor suppressor. miR-125a-3p induces an increase in the expression of ErbB2 that may render the cells suitable for treatment with anti-HER2 therapies. Copyright © 2020 Ninio-Many, Hikri, Burg-Golani, Stemmer, Shalgi and Ben-Aharon.Background Primary liver cancer is a leading cause of cancer deaths worldwide. Global burden varies, reflecting geographical distribution of viral hepatitis. Our objective was to perform a systematic review and meta-analysis of published current trends in incidence of adult liver cancers and histological types worldwide. Methods This study used systematic searches of PubMed, Embase, CINAHL, and Web of Science databases for English-language peer-reviewed articles published from 1 January 2008 to 01 September 2019. Inclusion criteria were population-based studies of adult liver cancer patients with quantitative estimates of temporal trends in incidence for liver cancers and/or histological types. For multiple studies from the same geographical area, only the publication that reported the most recent trends for the same cancer type and population subgroup was included. Review was conducted per PRISMA guidelines. Two authors independently extracted data and critically assessed studies. Proposed contributors to observed trends were extracted from included articles.