(3-Hydroxy-2-{[1-(2-oxidophenyl)ethyl­idene]amino-κ2 O,N}propanoato-κO 1)diphenyltin(IV)

In the title compound, [Sn(C6H5)2(C11H11NO4)], the tin(IV) atom is penta-coordinated in a distorted trigonal-bipyramidal SnC2NO2 geometry. In the crystal structure, inter­molecular O—H⋯O hydrogen bonds link the mol­ecules into centrosymmetric dimers. Weak C—H⋯O inter­actions further link the dimers into chains extending in [010]

1,5-Bis(1-phenyl­ethyl­idene)carbonohydrazide

In the title mol­ecule, C17H18N4O, the two phenyl rings form a dihedral angle of 18.15 (17)°. In the crystal, pairs of inter­molecular N—H⋯O hydrogen bonds link the mol­ecules into centrosymmetric dimers. Weak inter­molecular C—H⋯O inter­actions further link the dimers into chains running along [010]

2-Amino-4-[4-(dimethyl­amino)­phen­yl]-5-oxo-5,6,7,8-tetra­hydro-4H-chromene-3-carbonitrile

In the title mol­ecule, C18H19N3O2, the fused cyclo­hexenone and pyran rings adopt sofa conformations. Inter­molecular N—H⋯N and N—H⋯O hydrogen bonds link mol­ecules into corrugated layers parallel to the bc plane

N′-Cyclo­hexyl­idenebenzohydrazide

In the title compound, C13H16N2O, the cyclo­hexane ring adopts a chair conformation. In the crystal structure, inter­molecular N—H⋯O and C—H⋯O hydrogen bonds link the mol­ecules into chains propagating in [001]

1-(1-Phenyl­ethyl­idene)carbonohydrazide

The title compound, C9H12N4O, crystallizes with two independent mol­ecules in the asymmetric unit. In the crystal, inter­molecular N—H⋯O and N—H⋯N hydrogen bonds link the mol­ecules into paired ribbons propagated in [100]. The crystal studied was a twin (twin law 00/00/001) with a minor component of 25%

(E)-N′-[(2-Hydroxy-1-naphthyl)methyl­ene]benzohydrazide monohydrate

In the title compound, C18H14N2O2·H2O, the dihedral angle between the benzene ring and the naphthalene system is 5.18 (10)°. Intra­molecular N—H⋯O hydrogen bonds influence the molecular conformation. In the crystal, inter­molecular N—H⋯O and O—H⋯O hydrogen bonds are observed as well as π–π inter­actions between the phenyl ring and the substituted ring of the naphthalene [centroid–centroid distance = 3.676 (11) Å]

2-Amino-4-(4-meth­oxy­phen­yl)-5-oxo-5,6,7,8-tetra­hydro-4H-chromene-3-carbonitrile

The title compound, C17H16N2O3, crystallizes with two independent mol­ecules in the asymmetric unit. In both mol­ecules, the fused cyclo­hexenone ring adopts a sofa conformation. In the crystal, N—H⋯N and N—H⋯O hydrogen bonds link the mol­ecules into corrugated layers parallel to the (101) plane

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin