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Background The present study aimed to determine the prognostic value of the size of metastatic lymph node (LN) in non-surgical patients with esophageal squamous cell carcinoma (ESCC). Methods Three hundred seventy-six ESCC patients treated with definitive (chemo-) radiotherapy from January 2013 to March 2016 were reviewed. We analyzed potential associations of metastatic nodal size with responses, patterns of failure, and survival. Log-rank testing and Cox proportional hazards regression models were used to assess the impact of the clinical factors on survival. Results The 3-years over survival (OS) rates following a median follow-up of 28.2 months were 53.2, 46.2, 35.5, and 22.7% for the N0 group, the &gt;0.5 to ≤1 cm group, the &gt;1 to ≤2 cm group, and the &gt;2 cm group, respectively. The progression-free survival (PFS) rates for 2 years were 50.9, 44.2, 26.6, and 23.4% for the N0 group, the &gt;0.5 to ≤1 cm group, the &gt;1 to ≤2 cm group, and the &gt;2 cm group, respectively. The objective response rates (ORR) for the 280 patients with metastatic LNs were 43.1% for the LN &gt;0.5 to ≤1 cm group, 46.9% for the LN &gt;1 to ≤2 cm group, and 25.5% for the LN ≥2 cm group. The LN &gt;2 cm group had the worst ORR of the three groups with LNs. Gross tumor volume (GTV) failure was the most common failure pattern, followed by distant failure and out of GTV LN failure, with incidences of 47.9% (180 of 376), 42% (158 of 376), and 13.8% (52 of 376), respectively. Nodal size correlated statistically with GTV failure and distant failure but not with out-of-GTV nodal failure. After adjusting for age, sex, T category, Primary tumor location, and CRT, the size of metastatic LNs was an independent prognostic factor for OS and PFS in multivariate analyses. Conclusions Nodal size is one of prognostic factors for non-surgical patients with ESCC and correlated statistically with GTV failure and distant failure. Copyright © 2020 Zhao, Zhang, Wang, Wang, Geng, Zhu and Li.Desmoplastic small round cell tumor (DSRCT) is a devastating disease which most commonly affects adolescents, with a male predominance. Despite the best multimodality treatment efforts, most patients will ultimately not survive more than 3-5 years after diagnosis. Some research trials in soft-tissue sarcoma and Ewing sarcoma include DSRCT patients but few studies have been tailored to the specific clinical needs and underlying cytogenetic abnormalities characterizing this disease such as the typical EWSR1-WT1 gene fusion. Downstream activation of EWSR1-WT1 gene fusion includes signaling pathways of platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and insulin growth factor (IGF)-1. Other biological pathways that are activated and expressed in DSRCT cells include endothelial growth factor receptor (EGFR), androgen receptor pathway, c-KIT, MET, and transforming growth factor (TGF) beta. Investigation of somatic mutations, copy number alterations (CNA), and chromosomes in DSRCT samples suggests that deregulation of mesenchymal-epithelial reverse transition (MErT)/epithelial-mesenchymal transition (EMT) and DNA damage repair (DDR) may be important in DSRCT. This mini review looks at known druggable targets in DSRCT and existing clinical evidence for targeted treatments, particularly multityrosine kinase inhibitors such as pazopanib, imatinib, and sorafenib alone or in combination with other agents such as mTOR (mammalian target of rapamycin) inhibitors. The aim is to increase shared knowledge about current available treatments and identify gaps in research to further efforts toward clinical development of targeted agents. Copyright © 2020 Bexelius, Wasti and Chisholm.Sézary syndrome (SS) is a genetically and clinically distinct entity among cutaneous T-cell lymphomas (CTCL). SS is characterized by more aggressive disease compared to the most common indolent type of CTCL, mycosis fungoides. However, there are limited available genomic data regarding SS. To characterize and expand current mappings of the genomic landscape of CTCL, whole exome sequencing (WES) was performed on peripheral blood samples from seven patients with SS. We detected 21,784 variants, of which 21,140 were novel and 644 were previously described. Filtering revealed 551 nonsynonymous variants among 525 mutated genes-25 recurrent mutations and 1 recurrent variant. Several recurrently mutated genes crucial to pathogenesis pathways, including Janus kinase (JAK)/signal transducers and activators of transcription (STAT), peroxisome proliferator-activated receptors (PPAR), PI3K-serine/threonine protein kinases (AKT), and fibroblast growth factor receptors (FGFR), were identified. Furthermore, genetic mutations spanned both known and novel genes, supporting the idea of a long-tail distribution of mutations in lymphoma. Acknowledging these genetic variants and their affected pathways may inspire future targeted therapies. WES of a limited number of SS patients revealed both novel findings and corroborated complexities of the "long-tail" distribution of previously reported mutations. Copyright © 2020 Mirza, Horna, Teer, Song, Akabari, Hussaini and Sokol.Methylation of DNA, RNA or protein is a reversible modification. The proteins and genes that regulate this modification can be a candidate target for tumor therapy. However, the characteristics of methyltransferase related genes in glioma remain obscure. In this study, we systematically analyzed the relationship between methyltransferase-related genes expression profiles and outcomes in glioma patients based on The Cancer Genome Atlas and Chinese Glioma Genome Atlas RNA sequencing datasets. Consensus clustering identified two robust groups with significantly different pathological features and prognosis. Then a methyltransferase-related risk signature was built by a Cox proportional hazards model with elastic net penalty. [https://www.selleckchem.com/products/cc-115.html CC115] Moreover, the risk score is associated with patients' clinical and molecular features and can be used as an independent prognostic indicator for patients with glioma. Furthermore, genes associated with the high-risk group were involved in various aspects of the malignant progression of glioma via Gene Ontology analysis and Gene Set Enrichment Analysis.