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18 results on '"Wert-Lamas, Leon"'

1. A MIR17HG-derived long noncoding RNA provides an essential chromatin scaffold for protein interaction and myeloma growth

Author

Morelli, Eugenio, Fulciniti, Mariateresa, Samur, Mehmet K., Ribeiro, Caroline F., Wert-Lamas, Leon, Henninger, Jon E., Gullà, Annamaria, Aktas-Samur, Anil, Todoerti, Katia, Talluri, Srikanth, Park, Woojun D., Federico, Cinzia, Scionti, Francesca, Amodio, Nicola, Bianchi, Giada, Johnstone, Megan, Liu, Na, Gramegna, Doriana, Maisano, Domenico, Russo, Nicola A., Lin, Charles, Tai, Yu-Tzu, Neri, Antonino, Chauhan, Dharminder, Hideshima, Teru, Shammas, Masood A., Tassone, Pierfrancesco, Gryaznov, Sergei, Young, Richard A., Anderson, Kenneth C., Novina, Carl D., Loda, Massimo, and Munshi, Nikhil C.

Published
2023
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3. P-194 Non-coding RNA LINC01410 interacts with the minichromosome maintenance (MCM) complex and is a dependency in multiple myeloma

Author

Gramegna, Doriana, primary, Liu, Na, additional, Maisano, Domenico, additional, Ng, Jessica Fong, additional, Schavgoulidze, Anais, additional, Favasuli, Vanessa, additional, Gao, Claire, additional, Aktas-Samur, Anil, additional, Novina, Carl, additional, Gulla, Annamaria, additional, Anderson, Kenneth, additional, Wert-Lamas, Leon, additional, Samur, Mehmet, additional, Morelli, Eugenio, additional, Fulciniti, Mariateresa, additional, and Munshi, Nikhil, additional

Published
2023
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4. Bioprocessing of MIR17HG Results in Long and Short Noncoding RNAs with Targetable Tumor-Promoting Activity in Multiple Myeloma

Author

Morelli, Eugenio, primary, Gulla, Annamaria, additional, Liu, Na, additional, Maisano, Domenico, additional, Aktas-Samur, Anil, additional, Amodio, Nicola, additional, Ribeiro, Caroline, additional, Wert-Lamas, Leon, additional, Henninger, Jonathan, additional, Talluri, Srikanth, additional, Johnstone, Megan, additional, Gramegna, Doriana, additional, Vinaixa, Delaney, additional, Neri, Antonino, additional, Chauhan, Dharminder, additional, Hideshima, Teru, additional, Shammas, Masood A., additional, Tassone, Pierfrancesco, additional, Gryaznov, Sergei, additional, Young, Richard A., additional, Anderson, Kenneth C., additional, Novina, Carl D., additional, Loda, Massimo, additional, Fulciniti, Mariateresa, additional, Samur, Mehmet K., additional, and Munshi, Nikhil C, additional

Published
2022
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5. Long Noncoding RNA RROL Provides Chromatin Scaffold for MYC-WDR82 Interaction to Impact Lipid Metabolism and Tumor Cell Growth in Multiple Myeloma

Author

Morelli, Eugenio, primary, Fulciniti, Mariateresa, additional, Samur, Mehmet Kemal, additional, Ribeiro, Caroline F, additional, Wert-Lamas, Leon, additional, Henninger, Jon E, additional, Gulla, Annamaria, additional, Aktas-Samur, Anil, additional, Todoerti, Katia, additional, Talluri, Srikanth, additional, Park, Woojun D, additional, Federico, Cinzia, additional, Scionti, Francesca, additional, Amodio, Nicola, additional, Bianchi, Giada, additional, Johnstone, Megan, additional, Liu, Na, additional, Gramegna, Doriana, additional, Russo, Nicola A, additional, Lin, Charles, additional, Tai, Yu-Tzu, additional, Neri, Antonino, additional, Chauhan, Dharminder, additional, Hideshima, Teru, additional, Shammas, Masood, additional, Tassone, Pierfrancesco, additional, Gryaznov, Sergei, additional, Young, Richard, additional, Anderson, Kenneth C, additional, Novina, Carl, additional, Loda, Massimo, additional, and Munshi, Nikhil C, additional

Published
2021
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6. Identifying Long Noncoding RNA Dependencies Using CRISPR Interference (CRISPRi)-Based Platform in Multiple Myeloma

Author

Morelli, Eugenio, primary, Aktas-Samur, Anil, additional, Samur, Mehmet K., additional, Gulla, Annamaria, additional, Wert-Lamas, Leon, additional, Ribeiro, Caroline, additional, Henninger, Jonathan E, additional, Park, Woojun D, additional, Amodio, Nicola, additional, Gramegna, Doriana, additional, Johnstone, Megan, additional, Tassone, Pierfrancesco, additional, Tai, Yu-Tzu, additional, Novina, Carl D., additional, Young, Richard A., additional, Loda, Massimo, additional, Shammas, Masood A., additional, Gryaznov, Sergei, additional, Fulciniti, Mariateresa, additional, Anderson, Kenneth C., additional, and Munshi, Nikhil C., additional

Published
2021
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7. OAB-009: Genome-wide CRISPR interference screen identifies RNA Regulator of Lipogenesis (RROL) as a leading LncRNA dependency in Multiple Myeloma

Author

Morelli, Eugenio, primary, Fulciniti, Mariateresa, additional, Samur, Mehmet K., additional, Ribeiro, Caroline, additional, Wert-Lamas, Leon, additional, Henninger, Jon, additional, Gulla, Annamaria, additional, Aktas-Samur, Anil, additional, Todoerti, Katia, additional, Talluri, Srikanth, additional, Park, Woojun D., additional, Amodio, Nicola, additional, Bianchi, Giada, additional, Lin, Charles, additional, Tai, Yu-Tzu, additional, Neri, Antonino, additional, Chauhan, Dharminder, additional, Hideshima, Teru, additional, Shammas, Masood, additional, Tassone, Pierfrancesco, additional, Young, Rick, additional, Anderson, Kenneth, additional, Novina, Carl, additional, Loda, Massimo, additional, and Munshi, Nikhil C., additional

Published
2021
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8. RNA Regulator of Lipogenesis (RROL) Is a Novel Lncrna Mediating Protein-Protein Interaction at Gene Regulatory Loci Driving Lipogenic Programs in Multiple Myeloma

Author

Morelli, Eugenio, primary, Fulciniti, Mariateresa, additional, Samur, Mehmet K., additional, Ribeiro, Caroline, additional, Wert-Lamas, Leon, additional, Gulla, Annamaria, additional, Aktas-Samur, Anil, additional, Todoerti, Katia, additional, Talluri, Srikanth, additional, Park, Woojun Daniel, additional, Henninger, Jonathan E, additional, Federico, Cinzia, additional, Bianchi, Giada, additional, Scionti, Francesca, additional, Yao, Yao, additional, Amodio, Nicola, additional, Lin, Charles Y, additional, Tai, Yu-Tzu, additional, Tassone, Pierfrancesco, additional, Neri, Antonino, additional, Chauhan, Dharminder, additional, Hideshima, Teru, additional, Young, Richard A., additional, Anderson, Kenneth, additional, Novina, Carl D., additional, Loda, Massimo, additional, and Munshi, Nikhil C., additional

Published
2020
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10. Targeting Myeloma Cell Metabolism Via Disruption of the Lnc-17-92 Transcriptional Program: Druggable New Vulnerability in Multiple Myeloma

Author

Morelli, Eugenio, primary, Fulciniti, Mariateresa, primary, Samur, Mehmet Kemal, primary, Ribeiro, Caroline, primary, Wert-Lamas, Leon, primary, Gulla, Annamaria, primary, Aktas Samur, Anil, primary, Federico, Cinzia, primary, Scionti, Francesca, primary, Yao, Yao, primary, Amodio, Nicola, primary, Bianchi, Giada, primary, Tai, Yu-Tzu, primary, Tassone, Pierfrancesco, primary, Anderson, Kenneth C., primary, Novina, Carl D., primary, Loda, Massimo, primary, and Munshi, Nikhil C., primary

Published
2019
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11. Discovery, Functional Characterization and Therapeutic Targeting of Lnc-17-92 Metabolic Signaling in Multiple Myeloma

Author

Morelli, Eugenio, primary, Fulciniti, Mariateresa, additional, Samur, Mehmet, additional, Ribeiro, Caroline, additional, Wert-Lamas, Leon, additional, Gullà, Annamaria, additional, Samur, Anil, additional, Federico, Cinzia, additional, Scionti, Francesca, additional, Yao, Yao, additional, Amodio, Nicola, additional, Bianchi, Giada, additional, Tai, Yu-Tzu, additional, Tassone, Pierfrancesco, additional, Anderson, Kenneth C., additional, Novina, Carl, additional, Loda, Massimo, additional, and Munshi, Nikhil, additional

Published
2019
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15. Identifying Long Noncoding RNA Dependencies Using CRISPR Interference(CRISPRi)-Based Platform in Multiple Myeloma

Author

Morelli, Eugenio, Aktas-Samur, Anil, Samur, Mehmet K., Gulla, Annamaria, Wert-Lamas, Leon, Ribeiro, Caroline, Henninger, Jonathan E, Park, Woojun D, Amodio, Nicola, Gramegna, Doriana, Johnstone, Megan, Tassone, Pierfrancesco, Tai, Yu-Tzu, Novina, Carl D., Young, Richard A., Loda, Massimo, Shammas, Masood A., Gryaznov, Sergei, Fulciniti, Mariateresa, Anderson, Kenneth C., and Munshi, Nikhil C.

Abstract

To identify therapeutically actionable genetic dependencies we have pursued various approaches to derive a deeper understanding of the oncogenic hallmarks of myelomagenesis. We have studied the long noncoding RNA (lncRNA) landscape in multiple myeloma (MM) and identified a large number of differentially expressed lncRNAs in MM versus normal plasma cells. These lncRNAs presumably drive the tumorigenesis and MM cell growth, and in turn be susceptible to therapeutic intervention. To this end, we have developed and utilized a CRISPR interference(CRISPRi)-based platform for decoding and targeting the lncRNA dependencies (LongDEPs) in MM.

Published
2021
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16. The lncRNA SLNCRRecruits the Androgen Receptor to EGR1-Bound Genes in Melanoma and Inhibits Expression of Tumor Suppressor p21

Author

Schmidt, Karyn, Carroll, Johanna S., Yee, Elaine, Thomas, Dolly D., Wert-Lamas, Leon, Neier, Steven C., Sheynkman, Gloria, Ritz, Justin, and Novina, Carl D.

Abstract

Melanoma is the deadliest form of skin cancer, affecting men more frequently and severely than women. Although recent studies suggest that differences in activity of the androgen receptor (AR) underlie the observed sex bias, little is known about AR activity in melanoma. Here we show that AR and EGR1 bind to the long non-coding RNA SLNCRand increase melanoma proliferation through coordinated transcriptional regulation of several growth-regulatory genes. ChIP-seq reveals that ligand-free AR is enriched on SLNCR-regulated melanoma genes and that AR genomic occupancy significantly overlaps with EGR1 at consensus EGR1 binding sites. We present a model in which SLNCRrecruits AR to EGR1-bound genomic loci and switches EGR1-mediated transcriptional activation to repression of the tumor suppressor p21Waf1/Cip1. Our data implicate the regulatory triad of SLNCR, AR, and EGR1 in promoting oncogenesis and may help explain why men have a higher incidence of and more rapidly progressive melanomas compared with women.

Published
2019
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17. Characterising Long Non-Coding RNAs (lncRNAs) Associated with a Protective Type 1 Interferon (IFN) Gene Signature in Tumour and Immune cells

Author

Morozova, Ksenia, Novina, Carl, and Wert-Lamas, Leon

Subjects
lncRNA, melanoma, ovarian cancer, type 1 IFN, Immunology
Abstract

Type 1 interferons have emerged as critical regulators of cancer immunity. By inducing the transcription of interferon-stimulated genes (ISGs), these cytokines can directly inhibit tumour proliferation and mediate apoptosis, as well as enhancing immunosurveillance through activation of innate and adaptive effectors. However, dose-dependent toxicities and tumour-promoting immunosuppression have limited their use in the clinic. Current efforts are aimed at modulating the endogenous type 1 IFN response with precision immunotherapies. One promising category of molecular targets is long non-coding (lncRNAs), which are aberrantly expressed in many tumour types. We analysed The Cancer Genome Atlas (TCGA) sequencing datasets and selected 38 abundant lncRNA transcripts that were expressed in most patients and had a significant association with the type 1 IFN response and survival. We subsequently validated them by siRNA knockdown in an ISG54/ISRE inducible luciferase reporter system and found 12 genes that differentially affected type 1 IFN signalling. Using NanoString, we profiled 59 IFN signature genes in tumour and immune cells overexpressing lncRNA transcripts to identify positive and negative regulators of the type 1 IFN response. This study presents a high-throughput approach for discovering potentially immunostimulatory lncRNA molecules and elucidating their regulatory roles in cancer.

Published
2021

18. lncRNA CRNDE204 regulates erythropoiesis and myelopoiesis by binding to PUS1

Author

Hu, Jingwen, Novina, Carl, and Wert-Lamas, Leon

Subjects
erythropoiesis, lncRNA, Immunology
Abstract

Hematopoiesis is a crucial process that produces all cells within the hematopoietic system. Mutations in genes that disrupt normal hematopoiesis can cause bone marrow failure disorders ranging from myelodysplastic syndromes (MDS) to leukemia. Recent studies have pointed out the association between ribosomopathy and hematopoietic failure, and hematopoietic deficiency is a common clinical manifestation of multiple ribosomopathies, including Shwachman Diamond Syndrome and Diamond-Blackfan anemia (DBA). Shwachman Diamond Syndrome (SDS) is a rare and inherited form of ribosomopathy that is caused by mutations in SBDS gene, and patients with SDS lack myeloid progenitor cells, which causes severe anemia and neutropenia, and have increased risk of developing MDS or acute myeloid leukemia in later stages of life. Although standard care for SDS and other forms of MDS can relieve the symptoms, patients usually require lifelong treatment and multiple hospital visits to monitor their current status. Until now, the only cure for SDS is hematopoietic stem cell transplantation, yet due to its high risk of side effects, this is not widely used for treating SDS patients and is only considered if the patient has severe symptoms or starting to develop malignancies. The absence of curative treatment of SDS suggests there is a need to understand the molecular mechanism of SDS pathogenesis. The Novina Lab published the first map of SDS hematopoiesis at single cell resolution. Analysis of this SDS patient data identified a lncRNA first described in colorectal cancers, called colorectal neoplasia differentially expressed (CRNDE), as the most downregulated genes during SDS hematopoiesis and the expression of it is increased in acute myeloid leukemia. Our data points out the role of CRNDE in promoting normal erythropoiesis. In vitro experiments show that one splice variant isoform of CRNDE, CRNDE204, can promote differentiation of erythrocytes and megakaryocytes in K562 cells. However, another isoform, CRNDE201, represses differentiation. Based on these observations, we performed RNA-seq and proteomics analysis and found that CRNDE204 regulates key erythropoiesis and myelopoiesis genes and pathways. In addition, a yeast three-hybrid screen identified 24 proteins that could bind to CRNDE204, including PUS1 which is the key regulator of erythrocyte development and its mutation causes sideroblastic anemia. This is further validated by computational analysis and knock-down assays, and knock-down of PUS1 result in a decrease in both erythroid and megakaryocyte differentiation in K562 cells. Collectively, our findings pinpoint that CRNDE204 regulates erythropoiesis and myelopoiesis by interacting with PUS1, which makes CRNDE204 reintroduction as promising genetic therapy target for bone marrow failure disorders.

Published
2021

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