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A global metagenomic map of urban microbiomes and antimicrobial resistance

Danko, David ; Bezdan, Daniela ; Afshin, Evan E. ; [et al.]

Elsevier BV ; 2021

In: Cell Vol. 184, No. 13 ( 2021-06), p. 3376-3393.e17

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In: Cell, Elsevier BV, Vol. 184, No. 13 ( 2021-06), p. 3376-3393.e17

Type of Medium: Online Resource

ISSN: 0092-8674

URL: Article

DOI: 10.1016/j.cell.2021.05.002

RVK:

XA 36269

RVK:

WA 15000

Language: English

Publisher: Elsevier BV

Publication Date: 2021

detail.hit.zdb_id: 187009-9

detail.hit.zdb_id: 2001951-8

SSG: 12

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Pleiotropy-guided transcriptome imputation from normal and tumor tissues identifies candidate susceptibility genes for breast and ovarian cancer

Kar, Siddhartha P. ; Considine, Daniel P.C. ; Tyrer, Jonathan P. ; [et al.]

Elsevier BV ; 2021

In: Human Genetics and Genomics Advances Vol. 2, No. 3 ( 2021-07), p. 100042-

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In: Human Genetics and Genomics Advances, Elsevier BV, Vol. 2, No. 3 ( 2021-07), p. 100042-

Type of Medium: Online Resource

ISSN: 2666-2477

URL: Article

DOI: 10.1016/j.xhgg.2021.100042

Language: English

Publisher: Elsevier BV

Publication Date: 2021

detail.hit.zdb_id: 3058157-6

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Abstract A30: Super-enhancer-associated long noncoding RNA UCA1 interacts directly with AMOT to inhibit Hippo signaling pathway in epithelial ovarian cancer

Lin, Xianzhi ; Spindler, Tassja J. ; de Souza Fonseca, Marcos A ; [et al.]

American Association for Cancer Research (AACR) ; 2020

In: Molecular Cancer Research Vol. 18, No. 8_Supplement ( 2020-08-01), p. A30-A30

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In: Molecular Cancer Research, American Association for Cancer Research (AACR), Vol. 18, No. 8_Supplement ( 2020-08-01), p. A30-A30

Abstract: Long noncoding RNAs (lncRNAs) have emerged as critical regulators of tumorigenesis and yet their mechanistic role remains challenging to characterize. Here, we present LncRNA Interpreter, a strategy integrating functional proteomics with interacting proteins to characterize lncRNAs. Its robustness is exemplified by lncRNA Urothelial Cancer Associated 1 (UCA1), a driver of ovarian cancer development. Reverse phase protein array (RPPA) analysis indicates that UCA1 inhibits Hippo signaling pathway and in vivo RNA antisense purification (iRAP) of UCA1 interacting proteins identified angiomotin (AMOT), a known YAP regulator, as direct binding partner. Loss-of-function experiments show that AMOT mediates Hippo signaling pathway inhibition by UCA1. UCA1 enhances the AMOT-YAP interaction to prevent YAP phosphorylation and facilitate its nuclear translocation. Together, our LncRNA Interpreter pipeline identified UCA1 as an lncRNA regulator of the Hippo signaling pathway and highlighted the UCA1-AMOT-YAP signaling axis in ovarian cancer development. LncRNA Interpreter can readily be applied to other lncRNAs implicated in complex diseases. Citation Format: Xianzhi Lin, Tassja J. Spindler, Marcos A de Souza Fonseca, Rosario I. Corona, Ji-Heui Seo, Felipe S Dezem, Lewyn Li, Janet M. Lee, Henry W. Long, Thomas A. Sellers, Beth Y. Karlan, Houtan Noushmehr, Matthew L. Freedman, Simon A. Gayther, Kate Lawrenson. Super-enhancer-associated long noncoding RNA UCA1 interacts directly with AMOT to inhibit Hippo signaling pathway in epithelial ovarian cancer [abstract]. In: Proceedings of the AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; 2019 May 8-11; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(8_Suppl):Abstract nr A30.

Type of Medium: Online Resource

ISSN: 1541-7786 , 1557-3125

URL: Article

DOI: 10.1158/1557-3125.HIPPO19-A30

Language: English

Publisher: American Association for Cancer Research (AACR)

Publication Date: 2020

detail.hit.zdb_id: 2097884-4

SSG: 12

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Copy Number Variants Are Ovarian Cancer Risk Alleles at Known and Novel Risk Loci

DeVries, Amber A ; Dennis, Joe ; Tyrer, Jonathan P ; [et al.]

Oxford University Press (OUP) ; 2022

In: JNCI: Journal of the National Cancer Institute Vol. 114, No. 11 ( 2022-11-14), p. 1533-1544

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In: JNCI: Journal of the National Cancer Institute, Oxford University Press (OUP), Vol. 114, No. 11 ( 2022-11-14), p. 1533-1544

Abstract: Known risk alleles for epithelial ovarian cancer (EOC) account for approximately 40% of the heritability for EOC. Copy number variants (CNVs) have not been investigated as EOC risk alleles in a large population cohort. Methods Single nucleotide polymorphism array data from 13 071 EOC cases and 17 306 controls of White European ancestry were used to identify CNVs associated with EOC risk using a rare admixture maximum likelihood test for gene burden and a by-probe ratio test. We performed enrichment analysis of CNVs at known EOC risk loci and functional biofeatures in ovarian cancer–related cell types. Results We identified statistically significant risk associations with CNVs at known EOC risk genes; BRCA1 (PEOC = 1.60E-21; OREOC = 8.24), RAD51C (Phigh-grade serous ovarian cancer [HGSOC] = 5.5E-4; odds ratio [OR] HGSOC = 5.74 del), and BRCA2 (PHGSOC = 7.0E-4; ORHGSOC = 3.31 deletion). Four suggestive associations (P & lt; .001) were identified for rare CNVs. Risk-associated CNVs were enriched (P & lt; .05) at known EOC risk loci identified by genome-wide association study. Noncoding CNVs were enriched in active promoters and insulators in EOC-related cell types. Conclusions CNVs in BRCA1 have been previously reported in smaller studies, but their observed frequency in this large population-based cohort, along with the CNVs observed at BRCA2 and RAD51C gene loci in EOC cases, suggests that these CNVs are potentially pathogenic and may contribute to the spectrum of disease-causing mutations in these genes. CNVs are likely to occur in a wider set of susceptibility regions, with potential implications for clinical genetic testing and disease prevention.

Type of Medium: Online Resource

ISSN: 0027-8874 , 1460-2105

URL: Article

DOI: 10.1093/jnci/djac160

RVK:

XA 10000

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2022

detail.hit.zdb_id: 2992-0

detail.hit.zdb_id: 1465951-7

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DNA methylation-based signatures classify sporadic pituitary tumors according to clinicopathological features

Mosella, Maritza S ; Sabedot, Thais S ; Silva, Tiago C ; [et al.]

Oxford University Press (OUP) ; 2021

In: Neuro-Oncology Vol. 23, No. 8 ( 2021-08-02), p. 1292-1303

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In: Neuro-Oncology, Oxford University Press (OUP), Vol. 23, No. 8 ( 2021-08-02), p. 1292-1303

Abstract: Distinct genome-wide methylation patterns cluster pituitary neuroendocrine tumors (PitNETs) into molecular groups associated with specific clinicopathological features. Here we aim to identify, characterize, and validate methylation signatures that objectively classify PitNET into clinicopathological groups. Methods Combining in-house and publicly available data, we conducted an analysis of the methylome profile of a comprehensive cohort of 177 tumors (Panpit cohort) and 20 nontumor specimens from the pituitary gland. We also retrieved methylome data from an independent PitNET cohort (N = 86) to validate our findings. Results We identified three methylation clusters associated with adenohypophyseal cell lineages and functional status using an unsupervised approach. Differentially methylated probes (DMP) significantly distinguished the Panpit clusters and accurately assigned the samples of the validation cohort to their corresponding lineage and functional subtypes memberships. The DMPs were annotated in regulatory regions enriched with enhancer elements, associated with pathways and genes involved in pituitary cell identity, function, tumorigenesis, and invasiveness. Some DMPs correlated with genes with prognostic and therapeutic values in other intra- or extracranial tumors. Conclusions We identified and validated methylation signatures, mainly annotated in enhancer regions that distinguished PitNETs by distinct adenohypophyseal cell lineages and functional status. These signatures provide the groundwork to develop an unbiased approach to classifying PitNETs according to the most recent classification recommended by the 2017 WHO and to explore their biological and clinical relevance in these tumors.

Type of Medium: Online Resource

ISSN: 1522-8517 , 1523-5866

URL: Article

DOI: 10.1093/neuonc/noab044

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2021

detail.hit.zdb_id: 2094060-9

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Integrative multi-omics analyses to identify the genetic and functional mechanisms underlying ovarian cancer risk regions

Dareng, Eileen O. ; Coetzee, Simon G. ; Tyrer, Jonathan P. ; [et al.]

Elsevier BV ; 2024

In: The American Journal of Human Genetics ( 2024-5)

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In: The American Journal of Human Genetics, Elsevier BV, ( 2024-5)

Type of Medium: Online Resource

ISSN: 0002-9297

URL: Article

DOI: 10.1016/j.ajhg.2024.04.011

RVK:

XA 10000

Language: English

Publisher: Elsevier BV

Publication Date: 2024

detail.hit.zdb_id: 1473813-2

SSG: 12

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Predicting master transcription factors from pan-cancer expression data

Reddy, Jessica ; Fonseca, Marcos A. S. ; Corona, Rosario I. ; [et al.]

American Association for the Advancement of Science (AAAS) ; 2021

In: Science Advances Vol. 7, No. 48 ( 2021-11-26)

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In: Science Advances, American Association for the Advancement of Science (AAAS), Vol. 7, No. 48 ( 2021-11-26)

Abstract: Critical developmental “master transcription factors” (MTFs) can be subverted during tumorigenesis to control oncogenic transcriptional programs. Current approaches to identifying MTFs rely on ChIP-seq data, which is unavailable for many cancers. We developed the CaCTS (Cancer Core Transcription factor Specificity) algorithm to prioritize candidate MTFs using pan-cancer RNA sequencing data. CaCTS identified candidate MTFs across 34 tumor types and 140 subtypes including predictions for cancer types/subtypes for which MTFs are unknown, including e.g. PAX8, SOX17, and MECOM as candidates in ovarian cancer (OvCa). In OvCa cells, consistent with known MTF properties, these factors are required for viability, lie proximal to superenhancers, co-occupy regulatory elements globally, co-bind loci encoding OvCa biomarkers, and are sensitive to pharmacologic inhibition of transcription. Our predictions of MTFs, especially for tumor types with limited understanding of transcriptional drivers, pave the way to therapeutic targeting of MTFs in a broad spectrum of cancers.

Type of Medium: Online Resource

ISSN: 2375-2548

URL: Article

DOI: 10.1126/sciadv.abf6123

Language: English

Publisher: American Association for the Advancement of Science (AAAS)

Publication Date: 2021

detail.hit.zdb_id: 2810933-8

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US Severe Acute Respiratory Syndrome Coronavirus 2 Epsilon Variant: Highly Transmissible but With an Adjusted Muted Host T-Cell Response

Plummer, Jasmine T ; Contreras, Deisy ; Zhang, Wenjuan ; [et al.]

Oxford University Press (OUP) ; 2022

In: Clinical Infectious Diseases Vol. 75, No. 11 ( 2022-11-30), p. 1940-1949

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In: Clinical Infectious Diseases, Oxford University Press (OUP), Vol. 75, No. 11 ( 2022-11-30), p. 1940-1949

Abstract: The multiple mutations comprising the epsilon variant demonstrate the independent convergent evolution of severe acute respiratory syndrome coronavirus (SARS-CoV-2), with its spike protein mutation L452R present in the delta (L452R), kappa (L452R), and lambda (L452Q) variants. Methods Coronavirus disease 2019 (COVID-19) variants were detected in 1017 patients using whole-genome sequencing and were assessed for outcome and severity. The mechanistic effects of the epsilon versus non-epsilon variants were investigated using a multiomic approach including cellular response assays and paired cell and host transcriptomic and proteomic profiling. Results We found that patients carrying the epsilon variant had increased mortality risk but not increased hospitalizations (P & lt; .02). Cells infected with live epsilon compared with non-epsilon virus displayed increased sensitivity to neutralization antibodies in all patients but a slightly protective response in vaccinated individuals (P & lt; .001). That the epsilon SARS-CoV-2 variant is more infectious but less virulent is supported mechanistically in the down-regulation of viral processing pathways seen by multiomic analyses. Importantly, this paired transcriptomics and proteomic profiling of host cellular response to live virus revealed an altered leukocyte response and metabolic messenger RNA processing with the epsilon variant. To ascertain host response to SARS-CoV-2 infection, primary COVID-19–positive nasopharyngeal samples were transcriptomically profiled and revealed a differential innate immune response (P & lt; .001) and an adjusted T-cell response in patients carrying the epsilon variant (P & lt; .002). In fact, patients infected with SARS-CoV-2 and those vaccinated with the BNT162b2 vaccine have comparable CD4+/CD8+ T-cell immune responses to the epsilon variant (P & lt; .05). Conclusions While the epsilon variant is more infectious, by altering viral processing, we showed that patients with COVID-19 have adapted their innate immune response to this fitter variant. A protective T-cell response molecular signature is generated by this more transmissible variant in both vaccinated and unvaccinated patients.

Type of Medium: Online Resource

ISSN: 1058-4838 , 1537-6591

URL: Article

DOI: 10.1093/cid/ciac295

RVK:

XA 10000

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2022

detail.hit.zdb_id: 2002229-3

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