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Recent Publications by Members

2017 Publications

Title
AuthorsReferencePMID
Contributions of individual domains to function of the HIV-1 Rev response element.O'Carroll IPThappeta YFan LRamirez-Valdez EASmith SWang YXRein A.J Virol. 2017 Aug 16. pii: JVI.00746-17. doi: 10.1128/JVI.00746-17. [Epub ahead of print]28814520

Dissection of specific binding of HIV-1 Gag to the 'packaging signal' in viral RNA.

Comas-Garcia MDatta SABaker LVarma RGudla PRRein A.Elife. 2017 Jul 20;6. pii: e27055. doi: 10.7554/eLife.27055.28726630

Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer.

Li XLSubramanian MJones MFChaudhary RSingh DKZong XGryder BSindri SMo MSchetter AWen XParvathaneni SKazandjian DJenkins LMTang WElloumi FMartindale JLHuarte MZhu YRobles AIFrier SMRigo FCam MAmbs SSharma SHarris CCDasso MPrasanth KVLal A.Cell Rep. 2017 Sep5;20(10):2408-2423. doi: 10.1016/j.celrep.2017.08.041.28877474

Prosurvival long noncoding RNA PINCR regulates a subset of p53 targets in human colorectal cancer cells by binding to Matrin 3.

Chaudhary RGryder BWoods WSSubramanian MJones MFLi XLJenkins LMShabalina SAMo MDasso MYang YWakefield LMZhu YFrier SMMoriarity BSPrasanth KVPerez-Pinera PLal A.Elife. 2017 Jun 5;6. pii: e23244. doi: 10.7554/eLife.23244.28580901

Oncogenic Activation of the RNA Binding Protein NELFE and MYC Signaling in Hepatocellular Carcinoma.

Dang HTakai AForgues MPomyen YMou HXue WRay DHa KCHMorris QDHughes TRWang XW.Cancer Cell. 2017Jul10;32(1):101-114.e8. doi: 10.1016/j.ccell.2017.06.002.28697339

The Functional Cycle of Rnt1p: Five Consecutive Steps of Double-Stranded RNA Processing by a Eukaryotic RNase III.

Song HFang XJin LShaw GXWang YXJi X.Structure. 2017 Feb 7;25(2):353-363. doi: 10.1016/j.str.2016.12.013. Epub 2017 Jan 19.28111020
Virus-Mediated Alterations in miRNA Factors and Degradation of Viral miRNAs by MCPIP1.  Happel CRamalingam DZiegelbauer JM.PLoS Biol. 2016 Nov 28;14(11):e2000998. doi: 10.1371/journal.pbio.2000998. eCollection 2016 Nov.27893764

Viral MicroRNAs Repress the Cholesterol Pathway, and 25-Hydroxycholesterol Inhibits Infection.

Serquiña AKPKambach DMSarker OZiegelbauer JM.MBio. 2017 Jul 11;8(4). pii: e00576-17. doi: 10.1128/mBio.00576-17.28698273
    
    

 

 

Other publications

pubmed: (caplen n[au] or fel...
NCBI: db=pubmed; Term=(Caplen N[AU] OR Felber B[AU] OR Franchini V[AU] OR Freed E[AU] OR Gottesman S[AU] OR Grewal S[AU] OR Harris C[AU] OR Hu W[AU] OR Huang J[AU] OR Hughes S[AU] OR Jessup J[AU] OR Ji X[AU] OR Johnson P[AU] OR Kashlev M[AU] OR KewalRamani V[AU] OR Khan J[AU] OR Kwong K[AU] OR Lal A[AU] OR Larson D[AU] OR LeGrice S[AU] OR Luo J[AU] OR Meltzer P[AU] OR Merlino G[AU] OR Mili V[AU] OR Misteli T[AU] OR Oberdoerffer S[AU] OR Pathak V[AU] OR Pavlakis G[AU] OR Rein A[AU] OR Ried T[AU] OR Shapiro B[AU] OR Singer D[AU] OR Staudt L[AU] OR Strathern J[AU] OR Wang Y[AU] OR Wang X[AU] OR Weissman A[AU] OR Young H[AU] OR Zhang Y[AU] OR Zheng ZM[AU] OR Zhurkin V[AU] OR Ziegelbauer J[AU]) AND (Bethesda OR Frederick)
Randomized Phase III Trial of Ibrutinib and Rituximab Plus Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone in Non-Germinal Center B-Cell Diffuse Large B-Cell Lymphoma.
Related Articles

Randomized Phase III Trial of Ibrutinib and Rituximab Plus Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone in Non-Germinal Center B-Cell Diffuse Large B-Cell Lymphoma.

J Clin Oncol. 2019 Mar 22;:JCO1802403

Authors: Younes A, Sehn LH, Johnson P, Zinzani PL, Hong X, Zhu J, Patti C, Belada D, Samoilova O, Suh C, Leppä S, Rai S, Turgut M, Jurczak W, Cheung MC, Gurion R, Yeh SP, Lopez-Hernandez A, Dührsen U, Thieblemont C, Chiattone CS, Balasubramanian S, Carey J, Liu G, Shreeve SM, Sun S, Zhuang SH, Vermeulen J, Staudt LM, Wilson W, PHOENIX investigators

Abstract
PURPOSE: Ibrutinib has shown activity in non-germinal center B-cell diffuse large B-cell lymphoma (DLBCL). This double-blind phase III study evaluated ibrutinib and rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in untreated non-germinal center B-cell DLBCL.
PATIENTS AND METHODS: Patients were randomly assigned at a one-to-one ratio to ibrutinib (560 mg per day orally) plus R-CHOP or placebo plus R-CHOP. The primary end point was event-free survival (EFS) in the intent-to-treat (ITT) population and the activated B-cell (ABC) DLBCL subgroup. Secondary end points included progression-free survival (PFS), overall survival (OS), and safety.
RESULTS: A total of 838 patients were randomly assigned to ibrutinib plus R-CHOP (n = 419) or placebo plus R-CHOP (n = 419). Median age was 62.0 years; 75.9% of evaluable patients had ABC subtype disease, and baseline characteristics were balanced. Ibrutinib plus R-CHOP did not improve EFS in the ITT (hazard ratio [HR], 0.934) or ABC (HR, 0.949) population. A preplanned analysis showed a significant interaction between treatment and age. In patients age younger than 60 years, ibrutinib plus R-CHOP improved EFS (HR, 0.579), PFS (HR, 0.556), and OS (HR, 0.330) and slightly increased serious adverse events (35.7% v 28.6%), but the proportion of patients receiving at least six cycles of R-CHOP was similar between treatment arms (92.9% v 93.0%). In patients age 60 years or older, ibrutinib plus R-CHOP worsened EFS, PFS, and OS, increased serious adverse events (63.4% v 38.2%), and decreased the proportion of patients receiving at least six cycles of R-CHOP (73.7% v 88.8%).
CONCLUSION: The study did not meet its primary end point in the ITT or ABC population. However, in patients age younger than 60 years, ibrutinib plus R-CHOP improved EFS, PFS, and OS with manageable safety. In patients age 60 years or older, ibrutinib plus R-CHOP was associated with increased toxicity, leading to compromised R-CHOP administration and worse outcomes. Further investigation is warranted.

PMID: 30901302 [PubMed - as supplied by publisher]

----An Ultra-Dense Haploid Genetic Map for Evaluating the Highly Fragmented Genome Assembly of Norway Spruce (Picea abies).
Related Articles

----An Ultra-Dense Haploid Genetic Map for Evaluating the Highly Fragmented Genome Assembly of Norway Spruce (Picea abies).

G3 (Bethesda). 2019 Mar 21;:

Authors: Bernhardsson C, Vidalis A, Wang X, Scofield DG, Schiffthaler B, Baison J, Street NR, García-Gil MR, Ingvarsson PK

Abstract
Norway spruce (Picea abies (L.) Karst.) is a conifer species of substanital economic and ecological importance. In common with most conifers, the P. abies genome is very large (∼20 Gbp) and contains a high fraction of repetitive DNA. The current P. abies genome assembly (v1.0) covers approximately 60% of the total genome size but is highly fragmented, consisting of >10 million scaffolds. The genome annotation contains 66,632 gene models that are at least partially validated (www.congenie.org), however, the fragmented nature of the assembly means that there is currently little information available on how these genes are physically distributed over the 12 P. abies chromosomes. By creating an ultra-dense genetic linkage map, we anchored and ordered scaffolds into linkage groups, which complements the fine-scale information available in assembly contigs. Our ultra-dense haploid consensus genetic map consists of 21,056 markers derived from 14,336 scaffolds that contain 17,079 gene models (25.6% of the validated gene models) that we have anchored to the 12 linkage groups. We used data from three independent component maps, as well as comparisons with previously published Picea maps to evaluate the accuracy and marker ordering of the linkage groups. We demonstrate that approximately 3.8% of the anchored scaffolds and 1.6% of the gene models covered by the consensus map have likely assembly errors as they contain genetic markers that map to different regions within or between linkage groups. We further evaluate the utility of the genetic map for the conifer research community by using an independent data set of unrelated individuals to assess genome-wide variation in genetic diversity using the genomic regions anchored to linkage groups. The results show that our map is sufficiently dense to enable detailed evolutionary analyses across the P. abies genome.

PMID: 30898899 [PubMed - as supplied by publisher]

Taxonomy of the order Mononegavirales: second update 2018.
Related Articles

Taxonomy of the order Mononegavirales: second update 2018.

Arch Virol. 2019 Apr;164(4):1233-1244

Authors: Maes P, Amarasinghe GK, Ayllón MA, Basler CF, Bavari S, Blasdell KR, Briese T, Brown PA, Bukreyev A, Balkema-Buschmann A, Buchholz UJ, Chandran K, Crozier I, de Swart RL, Dietzgen RG, Dolnik O, Domier LL, Drexler JF, Dürrwald R, Dundon WG, Duprex WP, Dye JM, Easton AJ, Fooks AR, Formenty PBH, Fouchier RAM, Freitas-Astúa J, Ghedin E, Griffiths A, Hewson R, Horie M, Hurwitz JL, Hyndman TH, Jiāng D, Kobinger GP, Kondō H, Kurath G, Kuzmin IV, Lamb RA, Lee B, Leroy EM, Lǐ J, Marzano SL, Mühlberger E, Netesov SV, Nowotny N, Palacios G, Pályi B, Pawęska JT, Payne SL, Rima BK, Rota P, Rubbenstroth D, Simmonds P, Smither SJ, Song Q, Song T, Spann K, Stenglein MD, Stone DM, Takada A, Tesh RB, Tomonaga K, Tordo N, Towner JS, van den Hoogen B, Vasilakis N, Wahl V, Walker PJ, Wang D, Wang LF, Whitfield AE, Williams JV, Yè G, Zerbini FM, Zhang YZ, Kuhn JH

Abstract
In October 2018, the order Mononegavirales was amended by the establishment of three new families and three new genera, abolishment of two genera, and creation of 28 novel species. This article presents the updated taxonomy of the order Mononegavirales as now accepted by the International Committee on Taxonomy of Viruses (ICTV).

PMID: 30663023 [PubMed - indexed for MEDLINE]

Corticotropin releasing hormone can selectively stimulate glucose uptake in corticotropinoma via glucose transporter 1.
Related Articles

Corticotropin releasing hormone can selectively stimulate glucose uptake in corticotropinoma via glucose transporter 1.

Mol Cell Endocrinol. 2018 07 15;470:105-114

Authors: Lu J, Montgomery BK, Chatain GP, Bugarini A, Zhang Q, Wang X, Edwards NA, Ray-Chaudhury A, Merrill MJ, Lonser RR, Chittiboina P

Abstract
BACKGROUND: Pre-operative detection of corticotropin (ACTH) secreting microadenomas causing Cushing's disease (CD) improves surgical outcomes. Current best magnetic resonance imaging fails to detect up to 40% of these microadenomas. 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) is specific, but not sensitive in detecting corticotropinomas. Theoretically, secretagogue stimulation with corticotropin releasing hormone (CRH) could improve detection of adenomas with 18F-FDG PET. Previous attempts with simultaneous CRH stimulation have failed to demonstrate increased 18F-FDG uptake in corticotropinomas. We hypothesized that CRH stimulation leads to a delayed elevation in glucose uptake in corticotropinomas.
METHODS: Clinical data was analyzed for efficacy of CRH in improving 18FDG-PET detection of corticotropinomas in CD. Glucose transporter 1 (GLUT1) immunoreactivity was performed on surgical specimens. Ex-vivo, viable cells from these tumors were tested for secretagogue effects (colorimetric glucose uptake), and for fate of intracellular glucose (glycolysis stress analysis). Validation of ex-vivo findings was performed with AtT-20 cells.
RESULTS: CRH increased glucose uptake in human-derived corticotroph tumor cells and AtT-20, but not in normal murine or human corticotrophs (p < 0.0001). Continuous and intermittent (1 h) CRH exposure increased glucose uptake in AtT-20 with maximal effect at 4 h (p = 0.001). Similarly, CRH and 8-Br-cAMP led to robust GLUT1 upregulation and increased membrane translocation at 2 h, while fasentin suppressed baseline (p < 0.0001) and CRH-mediated glucose uptake. Expectedly, intra-operatively collected corticotropinomas demonstrated GLUT1 overexpression. Lastly, human derived corticotroph tumor cells demonstrated increased glycolysis and low glucose oxidation.
CONCLUSION: Increased and delayed CRH-mediated glucose uptake differentially occurs in adenomatous corticotrophs. Delayed secretagogue-stimulated 18F-FDG PET could improve microadenoma detection.

PMID: 28986303 [PubMed - indexed for MEDLINE]

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Last updated by Fox, Susan (NIH/NCI) [E] on Mar 21, 2019