Quantum process tomography with coherent states

We develop an enhanced technique for characterizing quantum optical processes based on probing unknown quantum processes only with coherent states. Our method substantially improves the original proposal [M. Lobino et al., Science 322, 563 (2008)], which uses a filtered Glauber-Sudarshan decomposition to determine the effect of the process on an arbitrary state. We introduce a new relation between the action of a general quantum process on coherent state inputs and its action on an arbitrary quantum state. This relation eliminates the need to invoke the Glauber-Sudarshan representation for states; hence it dramatically simplifies the task of process identification and removes a potential source of error. The new relation also enables straightforward extensions of the method to multi-mode and non-trace-preserving processes. We illustrate our formalism with several examples, in which we derive analytic representations of several fundamental quantum optical processes in the Fock basis. In particular, we introduce photon-number cutoff as a reasonable physical resource limitation and address resource vs accuracy trade-off in practical applications. We show that the accuracy of process estimation scales inversely with the square root of photon-number cutoff.Comment: 18 pages, 2 figure

Periodic and discrete Zak bases

Weyl's displacement operators for position and momentum commute if the product of the elementary displacements equals Planck's constant. Then, their common eigenstates constitute the Zak basis, each state specified by two phase parameters. Upon enforcing a periodic dependence on the phases, one gets a one-to-one mapping of the Hilbert space on the line onto the Hilbert space on the torus. The Fourier coefficients of the periodic Zak bases make up the discrete Zak bases. The two bases are mutually unbiased. We study these bases in detail, including a brief discussion of their relation to Aharonov's modular operators, and mention how they can be used to associate with the single degree of freedom of the line a pair of genuine qubits.Comment: 15 pages, 3 figures; displayed abstract is shortened, see the paper for the complete abstrac

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