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Article ; Online: Immune Signatures Dominate Molecular Subtyping to Predict Response to Neoadjuvant Immunotherapy.

Meeks, Joshua J / Robertson, A Gordon

2020 Volume 77, Issue 6, Page(s) 711–712

MeSH term(s)	Antibodies, Monoclonal, Humanized ; Humans ; Immunotherapy ; Neoadjuvant Therapy ; Urinary Bladder Neoplasms
Chemical Substances	Antibodies, Monoclonal, Humanized ; pembrolizumab (DPT0O3T46P)
Language	English
Publishing date	2020-04-17
Publishing country	Switzerland
Document type	Editorial ; Comment
ZDB-ID	193790-x
ISSN	1873-7560 ; 1421-993X ; 0302-2838
ISSN (online)	1873-7560 ; 1421-993X
ISSN	0302-2838
DOI	10.1016/j.eururo.2020.03.021
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Zs.A 1247: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Reply to Fredrik Liedberg, Pontus Eriksson, and Gottfrid Sjödahl's Letter to the Editor re: A. Gordon Robertson, Clarice S. Groeneveld, Brian Jordan, et al. Identification of Differential Tumor Subtypes of T1 Bladder Cancer. Eur Urol;2020:533-7.

Meeks, Joshua J / Dyrsjkøt, Lars / Robertson, A Gordon

European urology

2020 Volume 78, Issue 6, Page(s) e230–e231

MeSH term(s)	Humans ; Rare Diseases ; Urinary Bladder Neoplasms
Language	English
Publishing date	2020-09-29
Publishing country	Switzerland
Document type	Letter ; Comment
ZDB-ID	193790-x
ISSN	1873-7560 ; 1421-993X ; 0302-2838
ISSN (online)	1873-7560 ; 1421-993X
ISSN	0302-2838
DOI	10.1016/j.eururo.2020.09.030
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Zs.A 1247: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: spongEffects: ceRNA modules offer patient-specific insights into the miRNA regulatory landscape.

Boniolo, Fabio / Hoffmann, Markus / Roggendorf, Norman / Tercan, Bahar / Baumbach, Jan / Castro, Mauro A A / Robertson, A Gordon / Saur, Dieter / List, Markus

Bioinformatics (Oxford, England)

2023 Volume 39, Issue 5

Abstract: Motivation: Cancer is one of the leading causes of death worldwide. Despite significant improvements in prevention and treatment, mortality remains high for many cancer types. Hence, innovative methods that use molecular data to stratify patients and ... ...

Abstract	Motivation: Cancer is one of the leading causes of death worldwide. Despite significant improvements in prevention and treatment, mortality remains high for many cancer types. Hence, innovative methods that use molecular data to stratify patients and identify biomarkers are needed. Promising biomarkers can also be inferred from competing endogenous RNA (ceRNA) networks that capture the gene-miRNA gene regulatory landscape. Thus far, the role of these biomarkers could only be studied globally but not in a sample-specific manner. To mitigate this, we introduce spongEffects, a novel method that infers subnetworks (or modules) from ceRNA networks and calculates patient- or sample-specific scores related to their regulatory activity. Results: We show how spongEffects can be used for downstream interpretation and machine learning tasks such as tumor classification and for identifying subtype-specific regulatory interactions. In a concrete example of breast cancer subtype classification, we prioritize modules impacting the biology of the different subtypes. In summary, spongEffects prioritizes ceRNA modules as biomarkers and offers insights into the miRNA regulatory landscape. Notably, these module scores can be inferred from gene expression data alone and can thus be applied to cohorts where miRNA expression information is lacking. Availability and implementation: https://bioconductor.org/packages/devel/bioc/html/SPONGE.html.
MeSH term(s)	Humans ; Female ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Gene Regulatory Networks ; Breast Neoplasms/genetics ; Machine Learning ; Gene Expression Regulation, Neoplastic ; RNA, Long Noncoding/genetics
Chemical Substances	MicroRNAs ; RNA, Long Noncoding
Language	English
Publishing date	2023-04-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btad276
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Article ; Online: Molecular Subtypes of Non-muscle Invasive Bladder Cancer.

Lerner, Seth P / Robertson, A Gordon

Cancer cell

2016 Volume 30, Issue 1, Page(s) 1–3

Abstract: In this issue of Cancer Cell, Hedegaard et al. report a comprehensive multi-center transcriptional analysis of non-muscle invasive urothelial bladder cancer. They describe three molecular subtypes similar to those seen in other cohorts, as well as a ... ...

Abstract	In this issue of Cancer Cell, Hedegaard et al. report a comprehensive multi-center transcriptional analysis of non-muscle invasive urothelial bladder cancer. They describe three molecular subtypes similar to those seen in other cohorts, as well as a unique CIS signature associated with risk of progression to muscle invasive cancer.
MeSH term(s)	Disease Progression ; Humans ; Neoplasm Invasiveness ; Urinary Bladder Neoplasms
Language	English
Publishing date	2016--11
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2016.06.012
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 104: Show issues

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Article ; Online: Tumor-derived GCSF Alters Tumor and Systemic Immune System Cell Subset Composition and Signaling.

Matos, Israel / Barvalia, Maunish / Chehal, Manreet K / Robertson, A Gordon / Kulic, Iva / Silva, Jessica A F D / Ranganathan, Abhinandan / Short, Amy / Huang, Yu-Hsuan / Long, Erin / Priatel, John J / Dhanji, Salim / Nelson, Brad H / Krebs, Danielle L / Harder, Kenneth W

Cancer research communications

2023 Volume 3, Issue 3, Page(s) 404–419

Abstract: While immunotherapies such as immune checkpoint blockade and adoptive T-cell therapy improve survival for a subset of human malignancies, many patients fail to respond. Phagocytes including dendritic cells (DC), monocytes, and macrophages (MF) ... ...

Abstract	While immunotherapies such as immune checkpoint blockade and adoptive T-cell therapy improve survival for a subset of human malignancies, many patients fail to respond. Phagocytes including dendritic cells (DC), monocytes, and macrophages (MF) orchestrate innate and adaptive immune responses against tumors. However, tumor-derived factors may limit immunotherapy effectiveness by altering phagocyte signal transduction, development, and activity. Using Cytometry by Time-of-Flight, we found that tumor-derived GCSF altered myeloid cell distribution both locally and systemically. We distinguished a large number of GCSF-induced immune cell subset and signal transduction pathway perturbations in tumor-bearing mice, including a prominent increase in immature neutrophil/myeloid-derived suppressor cell (Neut/MDSC) subsets and tumor-resident PD-L1 Significance: Tumor-derived GCSF leads to systemic immune population changes. GCSF blockade restores immune populations, improves immunotherapy, and reduces tumor size, paralleling human colorectal cancer data. GCSF inhibition may synergize with current immunotherapies to treat GCSF-secreting tumors.
MeSH term(s)	Humans ; Mice ; Animals ; Myeloid Cells ; Myeloid-Derived Suppressor Cells ; Signal Transduction ; Lymphocytes, Tumor-Infiltrating ; Colonic Neoplasms/metabolism
Language	English
Publishing date	2023-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-22-0278
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Article ; Online: A transcriptional network of cell cycle dysregulation in noninvasive papillary urothelial carcinoma.

Warrick, Joshua I / Knowles, Margaret A / Hurst, Carolyn D / Shuman, Lauren / Raman, Jay D / Walter, Vonn / Putt, Jeffrey / Dyrskjøt, Lars / Groeneveld, Clarice / Castro, Mauro A A / Robertson, A Gordon / DeGraff, David J

Scientific reports

2022 Volume 12, Issue 1, Page(s) 16538

Abstract: Human cancers display a restricted set of expression profiles, despite diverse mutational drivers. This has led to the hypothesis that select sets of transcription factors act on similar target genes as an integrated network, buffering a tumor's ... ...

Abstract	Human cancers display a restricted set of expression profiles, despite diverse mutational drivers. This has led to the hypothesis that select sets of transcription factors act on similar target genes as an integrated network, buffering a tumor's transcriptional state. Noninvasive papillary urothelial carcinoma (NIPUC) with higher cell cycle activity has higher risk of recurrence and progression. In this paper, we describe a transcriptional network of cell cycle dysregulation in NIPUC, which was delineated using the ARACNe algorithm applied to expression data from a new cohort (n = 81, RNA sequencing), and two previously published cohorts. The transcriptional network comprised 121 transcription factors, including the pluripotency factors SOX2 and SALL4, the sex hormone binding receptors ESR1 and PGR, and multiple homeobox factors. Of these 121 transcription factors, 65 and 56 were more active in tumors with greater and less cell cycle activity, respectively. When clustered by activity of these transcription factors, tumors divided into High Cell Cycle versus Low Cell Cycle groups. Tumors in the High Cell Cycle group demonstrated greater mutational burden and copy number instability. A putative mutational driver of cell cycle dysregulation, such as homozygous loss of CDKN2A, was found in only 50% of High Cell Cycle NIPUC, suggesting a prominent role of transcription factor activity in driving cell cycle dysregulation. Activity of the 121 transcription factors strongly associated with expression of EZH2 and other members of the PRC2 complex, suggesting regulation by this complex influences expression of the transcription factors in this network. Activity of transcription factors in this network also associated with signatures of pluripotency and epithelial-to-mesenchymal transition (EMT), suggesting they play a role in driving evolution to invasive carcinoma. Consistent with this, these transcription factors differed in activity between NIPUC and invasive urothelial carcinoma.
MeSH term(s)	Carcinoma in Situ ; Carcinoma, Papillary/pathology ; Carcinoma, Transitional Cell/genetics ; Carcinoma, Transitional Cell/pathology ; Cell Cycle/genetics ; Gene Regulatory Networks ; Humans ; Transcription Factors/genetics ; Urinary Bladder Neoplasms/genetics ; Urinary Bladder Neoplasms/pathology
Chemical Substances	Transcription Factors
Language	English
Publishing date	2022-10-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-20927-9
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Article ; Online: Integrative modeling identifies genetic ancestry-associated molecular correlates in human cancer.

Robertson, A Gordon / Yau, Christina / Carrot-Zhang, Jian / Damrauer, Jeffrey S / Knijnenburg, Theo A / Chambwe, Nyasha / Hoadley, Katherine A / Kemal, Anab / Zenklusen, Jean C / Cherniack, Andrew D / Beroukhim, Rameen / Zhou, Wanding

STAR protocols

2021 Volume 2, Issue 2, Page(s) 100483

Abstract: Cellular and molecular aberrations contribute to the disparity of human cancer incidence and etiology between ancestry groups. Multiomics profiling in The Cancer Genome Atlas (TCGA) allows for querying of the molecular underpinnings of ancestry-specific ... ...

Abstract	Cellular and molecular aberrations contribute to the disparity of human cancer incidence and etiology between ancestry groups. Multiomics profiling in The Cancer Genome Atlas (TCGA) allows for querying of the molecular underpinnings of ancestry-specific discrepancies in human cancer. Here, we provide a protocol for integrative associative analysis of ancestry with molecular correlates, including somatic mutations, DNA methylation, mRNA transcription, miRNA transcription, and pathway activity, using TCGA data. This protocol can be generalized to analyze other cancer cohorts and human diseases. For complete details on the use and execution of this protocol, please refer to Carrot-Zhang et al. (2020).
MeSH term(s)	DNA Methylation/genetics ; Databases, Genetic ; Female ; Genomics/methods ; Humans ; Male ; MicroRNAs/genetics ; Models, Genetic ; Neoplasms/genetics ; Transcription, Genetic/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2021-04-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2021.100483
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Article ; Online: RTNsurvival: an R/Bioconductor package for regulatory network survival analysis.

Groeneveld, Clarice S / Chagas, Vinicius S / Jones, Steven J M / Robertson, A Gordon / Ponder, Bruce A J / Meyer, Kerstin B / Castro, Mauro A A

Bioinformatics (Oxford, England)

2019 Volume 35, Issue 21, Page(s) 4488–4489

Abstract: Motivation: Transcriptional networks are models that allow the biological state of cells or tumours to be described. Such networks consist of connected regulatory units known as regulons, each comprised of a regulator and its targets. Inferring a ... ...

Abstract	Motivation: Transcriptional networks are models that allow the biological state of cells or tumours to be described. Such networks consist of connected regulatory units known as regulons, each comprised of a regulator and its targets. Inferring a transcriptional network can be a helpful initial step in characterizing the different phenotypes within a cohort. While the network itself provides no information on molecular differences between samples, the per-sample state of each regulon, i.e. the regulon activity, can be used for describing subtypes in a cohort. Integrating regulon activities with clinical data and outcomes would extend this characterization of differences between subtypes. Results: We describe RTNsurvival, an R/Bioconductor package that calculates regulon activity profiles using transcriptional networks reconstructed by the RTN package, gene expression data, and a two-tailed Gene Set Enrichment Analysis. Given regulon activity profiles across a cohort, RTNsurvival can perform Kaplan-Meier analyses and Cox Proportional Hazards regressions, while also considering confounding variables. The Supplementary Information provides two case studies that use data from breast and liver cancer cohorts and features uni- and multivariate regulon survival analysis. Availability and implementation: RTNsurvival is written in the R language, and is available from the Bioconductor project at http://bioconductor.org/packages/RTNsurvival/. Supplementary information: Supplementary data are available at Bioinformatics online.
MeSH term(s)	Gene Expression ; Gene Regulatory Networks ; Probability ; Software ; Survival Analysis
Language	English
Publishing date	2019-03-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btz229
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Article ; Online: Immune activation is essential for the antitumor activity of EZH2 inhibition in urothelial carcinoma.

Piunti, Andrea / Meghani, Khyati / Yu, Yanni / Robertson, A Gordon / Podojil, Joseph R / McLaughlin, Kimberly A / You, Zonghao / Fantini, Damiano / Chiang, MingYi / Luo, Yi / Wang, Lu / Heyen, Nathan / Qian, Jun / Miller, Stephen D / Shilatifard, Ali / Meeks, Joshua J

Science advances

2022 Volume 8, Issue 40, Page(s) eabo8043

Abstract: The long-term survival of patients with advanced urothelial carcinoma (UCa) is limited because of innate resistance to treatment. We identified elevated expression of the histone methyltransferase EZH2 as a hallmark of aggressive UCa and hypothesized ... ...

Abstract	The long-term survival of patients with advanced urothelial carcinoma (UCa) is limited because of innate resistance to treatment. We identified elevated expression of the histone methyltransferase EZH2 as a hallmark of aggressive UCa and hypothesized that EZH2 inhibition, via a small-molecule catalytic inhibitor, might have antitumor effects in UCa. Here, in a carcinogen-induced mouse bladder cancer model, a reduction in tumor progression and an increase in immune infiltration upon EZH2 inhibition were observed. Treatment of mice with EZH2i causes an increase in MHC class II expression in the urothelium and can activate infiltrating T cells. Unexpectedly, we found that the lack of an intact adaptive immune system completely abolishes the antitumor effects induced by EZH2 catalytic inhibition. These findings show that immune evasion is the only important determinant for the efficacy of EZH2 catalytic inhibition treatment in a UCa model.
MeSH term(s)	Animals ; Carcinogens ; Carcinoma, Transitional Cell ; Cell Line, Tumor ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Histone Methyltransferases ; Mice ; Urinary Bladder Neoplasms/metabolism
Chemical Substances	Carcinogens ; Histone Methyltransferases (EC 2.1.1.-) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; Ezh2 protein, mouse (EC 2.1.1.43)
Language	English
Publishing date	2022-10-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abo8043
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Article ; Online: Expression-based subtypes define pathologic response to neoadjuvant immune-checkpoint inhibitors in muscle-invasive bladder cancer.

Robertson, A Gordon / Meghani, Khyati / Cooley, Lauren Folgosa / McLaughlin, Kimberly A / Fall, Leigh Ann / Yu, Yanni / Castro, Mauro A A / Groeneveld, Clarice S / de Reyniès, Aurélien / Nazarov, Vadim I / Tsvetkov, Vasily O / Choy, Bonnie / Raggi, Daniele / Marandino, Laura / Montorsi, Francesco / Powles, Thomas / Necchi, Andrea / Meeks, Joshua J

Nature communications

2023 Volume 14, Issue 1, Page(s) 2126

Abstract: Checkpoint immunotherapy (CPI) has increased survival for some patients with advanced-stage bladder cancer (BCa). However, most patients do not respond. Here, we characterized the tumor and immune microenvironment in pre- and post-treatment tumors from ... ...

Abstract	Checkpoint immunotherapy (CPI) has increased survival for some patients with advanced-stage bladder cancer (BCa). However, most patients do not respond. Here, we characterized the tumor and immune microenvironment in pre- and post-treatment tumors from the PURE01 neoadjuvant pembrolizumab immunotherapy trial, using a consolidative approach that combined transcriptional and genetic profiling with digital spatial profiling. We identify five distinctive genetic and transcriptomic programs and validate these in an independent neoadjuvant CPI trial to identify the features of response or resistance to CPI. By modeling the regulatory network, we identify the histone demethylase KDM5B as a repressor of tumor immune signaling pathways in one resistant subtype (S1, Luminal-excluded) and demonstrate that inhibition of KDM5B enhances immunogenicity in FGFR3-mutated BCa cells. Our study identifies signatures associated with response to CPI that can be used to molecularly stratify patients and suggests therapeutic alternatives for subtypes with poor response to neoadjuvant immunotherapy.
MeSH term(s)	Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Neoadjuvant Therapy ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/genetics ; Gene Expression Profiling ; Muscles/pathology ; Tumor Microenvironment/genetics
Chemical Substances	Immune Checkpoint Inhibitors
Language	English
Publishing date	2023-04-27
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-37568-9
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