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1. Pigment epithelium derived factor drives melanocyte proliferation and migration in neurofibromatosis café au lait macules.

Author

Lovatt, Charlotte, Williams, Megan, Gibbs, Alex, Mukhtar, Abdullahi, Morgan, Huw J., Lanfredini, Simone, Olivero, Carlotta, Spurlock, Gill, Davies, Sally, Philpott, Charlotte, Tovell, Hannah, Turnpenny, Peter, Baban, Dilair, Knight, Sam, Brems, Hilde, Sampson, Julian R., Legius, Eric, Upadhyaya, Meena, and Patel, Girish K.

Published
2024
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2. Foxp2 regulates gene networks implicated in neurite outgrowth in the developing brain.

Author

Vernes, Sonja C, Oliver, Peter L, Spiteri, Elizabeth, Lockstone, Helen E, Puliyadi, Rathi, Taylor, Jennifer M, Ho, Joses, Mombereau, Cedric, Brewer, Ariel, Lowy, Ernesto, Nicod, Jérôme, Groszer, Matthias, Baban, Dilair, Sahgal, Natasha, Cazier, Jean-Baptiste, Ragoussis, Jiannis, Davies, Kay E, Geschwind, Daniel H, and Fisher, Simon E

Subjects
Brain, Corpus Striatum, Neurites, Cell Line, Tumor, Animals, Mice, Inbred C57BL, Mice, Repressor Proteins, RNA, Messenger, Oligonucleotide Array Sequence Analysis, Chromatin Immunoprecipitation, Gene Expression Profiling, Gene Expression Regulation, Developmental, Mutation, Models, Biological, Forkhead Transcription Factors, Gene Regulatory Networks, Primary Cell Culture, Cell Line, Tumor, Gene Expression Regulation, Developmental, Inbred C57BL, Models, Biological, RNA, Messenger, Genetics, Developmental Biology
Abstract

Forkhead-box protein P2 is a transcription factor that has been associated with intriguing aspects of cognitive function in humans, non-human mammals, and song-learning birds. Heterozygous mutations of the human FOXP2 gene cause a monogenic speech and language disorder. Reduced functional dosage of the mouse version (Foxp2) causes deficient cortico-striatal synaptic plasticity and impairs motor-skill learning. Moreover, the songbird orthologue appears critically important for vocal learning. Across diverse vertebrate species, this well-conserved transcription factor is highly expressed in the developing and adult central nervous system. Very little is known about the mechanisms regulated by Foxp2 during brain development. We used an integrated functional genomics strategy to robustly define Foxp2-dependent pathways, both direct and indirect targets, in the embryonic brain. Specifically, we performed genome-wide in vivo ChIP-chip screens for Foxp2-binding and thereby identified a set of 264 high-confidence neural targets under strict, empirically derived significance thresholds. The findings, coupled to expression profiling and in situ hybridization of brain tissue from wild-type and mutant mouse embryos, strongly highlighted gene networks linked to neurite development. We followed up our genomics data with functional experiments, showing that Foxp2 impacts on neurite outgrowth in primary neurons and in neuronal cell models. Our data indicate that Foxp2 modulates neuronal network formation, by directly and indirectly regulating mRNAs involved in the development and plasticity of neuronal connections.

Published
2011

3. Supplementary Figure 6 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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4. Supplementary Figure 5 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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5. Supplementary Figure 8 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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6. Supplementary Figure 7 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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7. Supplementary Figure 3 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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8. Supplementary Figure 2 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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9. Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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10. Supplemetary Data from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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11. Supplementary Figure 4 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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12. Authorship Change Form from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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13. Supplementary Figure 1 from Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, primary, Zois, Christos E., primary, Albers, Patrick K., primary, Soga, Tomoyoshi, primary, Feldinger, Katharina, primary, Fischer, Roman, primary, Frejno, Martin, primary, McIntyre, Alan, primary, Bridges, Esther, primary, Haider, Syed, primary, Buffa, Francesca M., primary, Baban, Dilair, primary, Rodriguez, Miguel, primary, Yanes, Oscar, primary, Whittington, Hannah J., primary, Lake, Hannah A., primary, Zervou, Sevasti, primary, Lygate, Craig A., primary, Kessler, Benedikt M., primary, and Harris, Adrian L., primary

Published
2023
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21. Renal Cyst Formation in Fh1-Deficient Mice Is Independent of the Hif/Phd Pathway: Roles for Fumarate in KEAP1 Succination and Nrf2 Signaling

Author

Adam, Julie, Hatipoglu, Emine, O'Flaherty, Linda, Ternette, Nicola, Sahgal, Natasha, Lockstone, Helen, Baban, Dilair, Nye, Emma, Stamp, Gordon W., Wolhuter, Kathryn, Stevens, Marcus, Fischer, Roman, Carmeliet, Peter, Maxwell, Patrick H., Pugh, Chris W., Frizzell, Norma, Soga, Tomoyoshi, Kessler, Benedikt M., El-Bahrawy, Mona, Ratcliffe, Peter J., and Pollard, Patrick J.

Published
2011
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22. Mammalian γ2 AMPK regulates intrinsic heart rate

Author

Yavari, Arash, Bellahcene, Mohamed, Bucchi, Annalisa, Sirenko, Syevda, Pinter, Katalin, Herring, Neil, Jung, Julia J., Tarasov, Kirill V., Sharpe, Emily J., Wolfien, Markus, Czibik, Gabor, Steeples, Violetta, Ghaffari, Sahar, Nguyen, Chinh, Stockenhuber, Alexander, Clair, Joshua R. St., Rimmbach, Christian, Okamoto, Yosuke, Yang, Dongmei, Wang, Mingyi, Ziman, Bruce D., Moen, Jack M., Riordon, Daniel R., Ramirez, Christopher, Paina, Manuel, Lee, Joonho, Zhang, Jing, Ahmet, Ismayil, Matt, Michael G., Tarasova, Yelena S., Baban, Dilair, Sahgal, Natasha, Lockstone, Helen, Puliyadi, Rathi, de Bono, Joseph, Siggs, Owen M., Gomes, John, Muskett, Hannah, Maguire, Mahon L., Beglov, Youlia, Kelly, Matthew, dos Santos, Pedro P. N., Bright, Nicola J., Woods, Angela, Gehmlich, Katja, Isackson, Henrik, Douglas, Gillian, Ferguson, David J. P., Schneider, Jürgen E., Tinker, Andrew, Wolkenhauer, Olaf, Channon, Keith M., Cornall, Richard J., Sternick, Eduardo B., Paterson, David J., Redwood, Charles S., Carling, David, Proenza, Catherine, David, Robert, Baruscotti, Mirko, DiFrancesco, Dario, Lakatta, Edward G., Watkins, Hugh, and Ashrafian, Houman

Subjects
Adult, Magnetic Resonance Spectroscopy, Science, Magnetic Resonance Imaging, Cine, AMP-Activated Protein Kinases, Article, Mice, Sarcolemma, Microscopy, Electron, Transmission, Heart Rate, Physical Conditioning, Animal, MD Multidisciplinary, Bradycardia, Animals, Humans, lcsh:Science, Exercise, Sinoatrial Node, Myocardium, Heart, Ryanodine Receptor Calcium Release Channel, Mutation, Electrocardiography, Ambulatory, Physical Endurance, lcsh:Q, Calcium
Abstract

AMPK is a conserved serine/threonine kinase whose activity maintains cellular energy homeostasis. Eukaryotic AMPK exists as αβγ complexes, whose regulatory γ subunit confers energy sensor function by binding adenine nucleotides. Humans bearing activating mutations in the γ2 subunit exhibit a phenotype including unexplained slowing of heart rate (bradycardia). Here, we show that γ2 AMPK activation downregulates fundamental sinoatrial cell pacemaker mechanisms to lower heart rate, including sarcolemmal hyperpolarization-activated current (I f) and ryanodine receptor-derived diastolic local subsarcolemmal Ca2+ release. In contrast, loss of γ2 AMPK induces a reciprocal phenotype of increased heart rate, and prevents the adaptive intrinsic bradycardia of endurance training. Our results reveal that in mammals, for which heart rate is a key determinant of cardiac energy demand, AMPK functions in an organ-specific manner to maintain cardiac energy homeostasis and determines cardiac physiological adaptation to exercise by modulating intrinsic sinoatrial cell behavior., AMPK regulates cellular energy balance using its γ subunit as an energy sensor of cellular AMP and ADP to ATP ratios. Here, the authors show that γ2 AMPK activation lowers heart rate by reducing the activity of pacemaker cells, whereas loss of γ2 AMPK increases heart rate and prevents the adaptive bradycardia of endurance training in mice.

Published
2017

28. Adenoviral Vector Vaccination Induces a Conserved Program of CD8+ T Cell Memory Differentiation in Mouse and Man

Author

Bolinger, Beatrice, Sims, Stuart, Swadling, Leo, O’Hara, Geraldine, de Lara, Catherine, Baban, Dilair, Saghal, Natasha, Lee, Lian Ni, Marchi, Emanuele, Davis, Mark, Newell, Evan, Capone, Stefania, Folgori, Antonella, Barnes, Ellie, and Klenerman, Paul

Subjects
Genetic Vectors, Vaccination, Cytomegalovirus, Apoptosis, Cell Differentiation, CD8-Positive T-Lymphocytes, Lymphocyte Activation, Adenoviridae, Mice, Inbred C57BL, Mice, lcsh:Biology (General), Report, Animals, Humans, Immunologic Memory, lcsh:QH301-705.5, Transcription Factors
Abstract

Summary Following exposure to vaccines, antigen-specific CD8+ T cell responses develop as long-term memory pools. Vaccine strategies based on adenoviral vectors, e.g., those developed for HCV, are able to induce and sustain substantial CD8+ T cell populations. How such populations evolve following vaccination remains to be defined at a transcriptional level. We addressed the transcriptional regulation of divergent CD8+ T cell memory pools induced by an adenovector encoding a model antigen (beta-galactosidase). We observe transcriptional profiles that mimic those following infection with persistent pathogens, murine and human cytomegalovirus (CMV). Key transcriptional hallmarks include upregulation of homing receptors and anti-apoptotic pathways, driven by conserved networks of transcription factors, including T-bet. In humans, an adenovirus vaccine induced similar CMV-like phenotypes and transcription factor regulation. These data clarify the core features of CD8+ T cell memory following vaccination with adenovectors and indicate a conserved pathway for memory development shared with persistent herpesviruses., Graphical Abstract, Highlights • Adenovector vaccination induces two transcriptionally distinct CD8 memory responses • The sustained response induced by adenovectors and CMV is closely related • The core molecular features are shared tightly in mouse and man • Adenovaccines in humans induce a CD8 response that recapitulates these core features, Bolinger et al. define the transcriptional program associated with sustained CD8+ T cell memory induced by adenoviral vaccination. They relate these to memory “inflation” induced following infection by persistent CMVs. Core features are found to be shared by mouse and man, including a prominent role for TBX21.

Published
2015

29. Adaptation to HIF1α Deletion in Hypoxic Cancer Cells by Upregulation of GLUT14 and Creatine Metabolism

Author

Valli, Alessandro, primary, Morotti, Matteo, additional, Zois, Christos E., additional, Albers, Patrick K., additional, Soga, Tomoyoshi, additional, Feldinger, Katharina, additional, Fischer, Roman, additional, Frejno, Martin, additional, McIntyre, Alan, additional, Bridges, Esther, additional, Haider, Syed, additional, Buffa, Francesca M., additional, Baban, Dilair, additional, Rodriguez, Miguel, additional, Yanes, Oscar, additional, Whittington, Hannah J., additional, Lake, Hannah A., additional, Zervou, Sevasti, additional, Lygate, Craig A., additional, Kessler, Benedikt M., additional, and Harris, Adrian L., additional

Published
2019
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30. Chemokine gene expression in lung CD8 T cells correlates with protective immunity in mice immunized intra-nasally with Adenovirus-85A

Author

Beverley Peter CL, Ragoussis Jiannis, Ronan Edward O, Baban Dilair, Lee Lian N, and Tchilian Elma Z

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Immunization of BALB/c mice with a recombinant adenovirus expressing Mycobacterium tuberculosis (M. tuberculosis) antigen 85A (Ad85A) protects against aerosol challenge with M. tuberculosis only when it is administered intra-nasally (i.n.). Immunization with Ad85A induces a lung-resident population of activated CD8 T cells that is antigen dependent, highly activated and mediates protection by early inhibition of M. tuberculosis growth. In order to determine why the i.n. route is so effective compared to parenteral immunization, we used microarray analysis to compare gene expression profiles of pulmonary and splenic CD8 T cells after i.n. or intra-dermal (i.d.) immunization. Method Total RNA from CD8 T cells was isolated from lungs or spleens of mice immunized with Ad85A by the i.n. or i.d. route. The gene profiles generated from each condition were compared. Statistically significant (p ≤ 0.05) differentially expressed genes were analyzed to determine if they mapped to particular molecular functions, biological processes or pathways using Gene Ontology and Panther DB mapping tools. Results CD8 T cells from lungs of i.n. immunized mice expressed a large number of chemokines chemotactic for resting and activated T cells as well as activation and survival genes. Lung lymphocytes from i.n. immunized mice also express the chemokine receptor gene Cxcr6, which is thought to aid long-term retention of antigen-responding T cells in the lungs. Expression of CXCR6 on CD8 T cells was confirmed by flow cytometry. Conclusions Our microarray analysis represents the first ex vivo study comparing gene expression profiles of CD8 T cells isolated from distinct sites after immunization with an adenoviral vector by different routes. It confirms earlier phenotypic data indicating that lung i.n. cells are more activated than lung i.d. CD8 T cells. The sustained expression of chemokines and activation genes enables CD8 T cells to remain in the lungs for extended periods after i.n. immunization. This may account for the early inhibition of M. tuberculosis growth observed in Ad85A i.n. immunized mice and explain the effectiveness of i.n. compared to parenteral immunization with this viral vector.

Published
2010
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31. CpG methylation profiling in VHL related and VHL unrelated renal cell carcinoma

Author

Clarke Noel W, Ragoussis Jiannis, Baban Dilair, Winchester Laura, Gentle Dean, Morris Mark R, McRonald Fiona E, Brown Michael D, Kishida Takeshi, Yao Masahiro, Latif Farida, and Maher Eamonn R

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Renal cell carcinoma (RCC) is histopathologically heterogeneous with clear cell and papillary the most common subtypes. The most frequent molecular abnormality in clear cell RCC is VHL inactivation but promoter methylation of tumour suppressor genes is common in both subtypes of RCC. To investigate whether RCC CpG methylation status was influenced by histopathology and VHL status we performed high-throughput epigenetic profiling using the Illumina Goldengate Methylation Array in 62 RCC (29 RCC from von Hippel-Lindau (VHL) disease patients, 20 sporadic clear cell RCC with wild type VHL and 13 sporadic papillary RCC). Results 43 genes were methylated in >20% of primary RCC (range 20–45%) and most (37/43) of these had not been reported previously to be methylated in RCC. The distribution of the number of methylated CpGs in individual tumours differed from the expected Poisson distribution (p < 0.00001; log-likelihood G test) suggesting that a subset of RCC displayed a CpG Island Methylator Phenotype. Comparison of RCC subtypes revealed that, on average, tumour specific CpG methylation was most prevalent in papillary RCC and least in VHL RCC. Many of the genes preferentially methylated in pRCC were linked to TGFβ or ERK/Akt signalling. Conclusion These findings demonstrate differing patterns of tumour-specific CpG methylation in VHL and non VHL clear cell RCC and papillary RCC, and identify multiple novel potential CpG methylation biomarkers for RCC.

Published
2009
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32. TCR-Identical CD8+ T-Cells Can Have Distinct Killing Efficacy Determined By Events Beyond the T-Cell Receptor

Author

Glanville, Julie M, primary, Moody, Anne-Marie, additional, Peng, Yanchun, additional, Taylor, Stephan, additional, Ladell, Kristin, additional, Gillespie, Geraldine, additional, de Bree, Godelieve, additional, Baban, Dilair, additional, Stewart-Jones, Guillaume, additional, Cullen, Claire, additional, Mead, Adam J, additional, Repapi, Emmanuela, additional, Rowland-Jones, Sarah, additional, Simmons, Alison, additional, Price, David A, additional, Dong, Tao, additional, and McMichael, Andrew, additional

Published
2017
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33. Survival of metastatic melanoma patients after dendritic cell vaccination correlates with expression of leukocyte phosphatidylethanolamine-binding protein 1/Raf kinase inhibitory protein

Author

Buschow, Sonja I, Ramazzotti, Matteo, Reinieren-Beeren, Inge M J, Heinzerling, Lucie M, Westdorp, Harm, Stefanini, Irene, Beltrame, Luca, Hato, Stanleyson V, Ellebaek, Eva, Gross, Stefanie, Nguyen, Van Anh, Weinlich, Georg, Ragoussis, Jiannis, Baban, Dilair, Schuler-Thurner, Beatrice, Svane, Inge M, Romani, Nikolaus, Austyn, Jonathan M, De Vries, I Jolanda M, Schuler, Gerold, Cavalieri, Duccio, Figdor, Carl G, Buschow, Sonja I, Ramazzotti, Matteo, Reinieren-Beeren, Inge M J, Heinzerling, Lucie M, Westdorp, Harm, Stefanini, Irene, Beltrame, Luca, Hato, Stanleyson V, Ellebaek, Eva, Gross, Stefanie, Nguyen, Van Anh, Weinlich, Georg, Ragoussis, Jiannis, Baban, Dilair, Schuler-Thurner, Beatrice, Svane, Inge M, Romani, Nikolaus, Austyn, Jonathan M, De Vries, I Jolanda M, Schuler, Gerold, Cavalieri, Duccio, and Figdor, Carl G

Abstract

Immunotherapy for metastatic melanoma offers great promise but, to date, only a subset of patients have responded. There is an urgent need to identify ways of allocating patients to the most beneficial therapy, to increase survival and decrease therapy-associated morbidity and costs. Blood-based biomarkers are of particular interest because of their straightforward implementation in routine clinical care. We sought to identify markers for dendritic cell (DC) vaccine-based immunotherapy against metastatic melanoma through gene expression analysis of peripheral blood mononuclear cells. A large-scale microarray analysis of 74 samples from two treatment centers, taken directly after the first round of DC vaccination, was performed. We found that phosphatidylethanolamine binding protein 1 (PEBP1)/Raf Kinase inhibitory protein (RKIP) expression can be used to identify a significant proportion of patients who performed poorly after DC vaccination. This result was validated by q-PCR analysis on blood samples from a second cohort of 95 patients treated with DC vaccination in four different centers. We conclude that low PEBP1 expression correlates with poor overall survival after DC vaccination. Intriguingly, this was only the case for expression of PEBP1 after, but not prior to, DC vaccination. Moreover, the change in PEBP1 expression upon vaccination correlated well with survival. Further analyses revealed that PEBP1 expression positively correlated with genes involved in T cell responses but inversely correlated with genes associated with myeloid cells and aberrant inflammation including STAT3, NOTCH1, and MAPK1. Concordantly, PEBP1 inversely correlated with the myeloid/lymphoid-ratio and was suppressed in patients suffering from chronic inflammatory disease.

Published
2017

34. Survival of metastatic melanoma patients after dendritic cell vaccination correlates with expression of leukocyte phosphatidylethanolamine-binding protein 1/Raf kinase inhibitory protein

Author

Buschow, Sonja I., primary, Ramazzotti, Matteo, additional, Reinieren-Beeren, Inge M.J., additional, Heinzerling, Lucie M., additional, Westdorp, Harm, additional, Stefanini, Irene, additional, Beltrame, Luca, additional, Hato, Stanleyson V., additional, Ellebaek, Eva, additional, Gross, Stefanie, additional, Nguyen, Van Anh, additional, Weinlich, Georg, additional, Ragoussis, Jiannis, additional, Baban, Dilair, additional, Schuler-Thurner, Beatrice, additional, Svane, Inge M., additional, Romani, Nikolaus, additional, Austyn, Jonathan M., additional, De Vries, I. Jolanda M., additional, Schuler, Gerold, additional, Cavalieri, Duccio, additional, and Figdor, Carl G., additional

Published
2017
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36. Genomic clusters, putative pathogen recognition molecules, and antimicrobial genes are induced by infection of C. elegans with M. nematophilum

Author

O'Rourke, Delia, Baban, Dilair, Demidova, Maria, Hodgkin, Jonathan, and Mott, Richard

Subjects
DNA microarrays -- Research, Caenorhabditis elegans -- Research, Immunogenetics -- Research, Health
Abstract

Microarray expression data was used to analyze whole-genome changes in expression caused by the interaction between Caenorhabditis elegans and the Gram-positive bacterium Microbacteroim nematophilum. It was shown that C-type lectins and other putative pathogen-recognition molecules were important for innate immune defense in C. elegans.

Published
2006

37. Pattern recognition receptor mediated downregulation of microRNA-650 fine-tunes MxA expression in dendritic cells infected with influenza A virus

Author

Pichulik, Tica, primary, Khatamzas, Elham, additional, Liu, Xiao, additional, Brain, Oliver, additional, Delmiro Garcia, Magno, additional, Leslie, Alasdair, additional, Danis, Benedicte, additional, Mayer, Alice, additional, Baban, Dilair, additional, Ragoussis, Jiannis, additional, Weber, Alexander N. R., additional, and Simmons, Alison, additional

Published
2015
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39. CD161 Defines a Transcriptional and Functional Phenotype across Distinct Human T Cell Lineages

Author

Fergusson, Joannah R., Smith, Kira E., Fleming, Vicki M., Rajoriya, Neil, Newell, Evan W., Simmons, Ruth, Marchi, Emanuele, Björkander, Sophia, Kang, Yu-Hoi, Swadling, Leo, Kurioka, Ayako, Sahgal, Natasha, Lockstone, Helen, Baban, Dilair, Freeman, Gordon J., Sverremark-Ekström, Eva, Davis, Mark M., Davenport, Miles P., Venturi, Vanessa, Ussher, James E., Willberg, Christian B., Klenerman, Paul, Fergusson, Joannah R., Smith, Kira E., Fleming, Vicki M., Rajoriya, Neil, Newell, Evan W., Simmons, Ruth, Marchi, Emanuele, Björkander, Sophia, Kang, Yu-Hoi, Swadling, Leo, Kurioka, Ayako, Sahgal, Natasha, Lockstone, Helen, Baban, Dilair, Freeman, Gordon J., Sverremark-Ekström, Eva, Davis, Mark M., Davenport, Miles P., Venturi, Vanessa, Ussher, James E., Willberg, Christian B., and Klenerman, Paul

Abstract

The C-type lectin CD161 is expressed by a large proportion of human T lymphocytes of all lineages, including a population known as mucosal-associated invariant T (MAIT) cells. To understand whether different T cell subsets expressing CD161 have similar properties, we examined these populations in parallel using mass cytometry and mRNA microarray approaches. The analysis identified a conserved CD161++/MAIT cell transcriptional signature enriched in CD161+CD8+ T cells, which can be extended to CD161+ CD4+ and CD161+TCR gamma delta+ T cells. Furthermore, this led to the identification of a shared innate-like, TCR-independent response to interleukin (IL)-12 plus IL-18 by different CD161-expressing T cell populations. This response was independent of regulation by CD161, which acted as a costimulatory molecule in the context of T cell receptor stimulation. Expression of CD161 hence identifies a transcriptional and functional phenotype, shared across human T lymphocytes and independent of both T cell receptor (TCR) expression and cell lineage., AuthorCount:22

Published
2014
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41. CD161 Defines a Transcriptional and Functional Phenotype across Distinct Human T Cell Lineages

Author

Fergusson, Joannah R., primary, Smith, Kira E., additional, Fleming, Vicki M., additional, Rajoriya, Neil, additional, Newell, Evan W., additional, Simmons, Ruth, additional, Marchi, Emanuele, additional, Björkander, Sophia, additional, Kang, Yu-Hoi, additional, Swadling, Leo, additional, Kurioka, Ayako, additional, Sahgal, Natasha, additional, Lockstone, Helen, additional, Baban, Dilair, additional, Freeman, Gordon J., additional, Sverremark-Ekström, Eva, additional, Davis, Mark M., additional, Davenport, Miles P., additional, Venturi, Vanessa, additional, Ussher, James E., additional, Willberg, Christian B., additional, and Klenerman, Paul, additional

Published
2014
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42. Genome-wide expression analysis of a spinal muscular atrophy model : towards discovery of new drug targets

Author

Lee, Sheena, Sayin, Arzu, Cauchi, Ruben J., Grice, Stuart, Burdett, Howard, Baban, Dilair, and van den Heuvel, Marcel

Subjects
Oligonucleotides, lcsh:Medicine, SMN1, Molecular Biology/RNA Splicing, Nucleic acid hybridization, Polymerase Chain Reaction, 0302 clinical medicine, Gene expression, lcsh:Science, Cyclic AMP Response Element-Binding Protein, Genetics and Genomics/Genetics of Disease, Neurological Disorders/Movement Disorders, Oligonucleotide Array Sequence Analysis, Motor neurons, Regulation of gene expression, Genetics, Genetics and Genomics/Medical Genetics, 0303 health sciences, Multidisciplinary, Genome, RNA-Binding proteins, Nucleic Acid Hybridization, RNA-Binding Proteins, Genetics and Genomics/Gene Expression, SMN Complex Proteins, Diseases -- Animal models, SMA, Phenotype, 3. Good health, Polymerase chain reaction, Genetics and Genomics/Gene Function, Survival of Motor Neuron 2 Protein, Genetics and Genomics/Gene Discovery, Research Article, Nerve Tissue Proteins, Neurological Disorders/Neuromuscular Diseases, Biology, Muscular Atrophy, Spinal, 03 medical and health sciences, Nerve tissue proteins, medicine, Animals, Humans, Genomes, Gene, 030304 developmental biology, Diptera, lcsh:R, Proteins, Spinal muscular atrophy, medicine.disease, Survival of Motor Neuron 1 Protein, nervous system diseases, Disease Models, Animal, Genetics and Genomics/Disease Models, Neurological Disorders/Neurogenetics, nervous system, lcsh:Q, 030217 neurology & neurosurgery
Abstract

Spinal Muscular Atrophy is a recessive genetic disease and affects lower motor neurones and muscle tissue. A single gene is disrupted in SMA: SMN1 activity is abolished but a second copy of the gene (SMN2) provides limited activity. While the SMN protein has been shown to function in the assembly of RNA-protein complexes, it is unclear how the overall reduction in SMN activity specifically results in the neuromuscular phenotypes. Similar to humans, reduced smn activity in the fly causes earliest phenotypes in neuromuscular tissues. To uncover the effects of reduced SMN activity, we have studied gene expression in control and diseased fly tissues using whole genome micro-arrays. A number of gene expression changes are recovered and independently validated. Identified genes show trends in their predicted function: several are consistent with the function of SMN, in addition some uncover novel pathways. This and subsequent genetic analysis in the fly indicates some of the identified genes could be taken for further studies as potential drug targets for SMA and other neuromuscular disorders., peer-reviewed

Published
2008

45. Smooth Muscle Cells Differentiated From Reprogrammed Embryonic Lung Fibroblasts Through DKK3 Signaling Are Potent for Tissue Engineering of Vascular Grafts

Author

Karamariti, Eirini, primary, Margariti, Andriana, additional, Winkler, Bernhard, additional, Wang, Xiaocong, additional, Hong, Xuechong, additional, Baban, Dilair, additional, Ragoussis, Jiannis, additional, Huang, Yi, additional, Han, Jing-Dong J., additional, Wong, Mei Mei, additional, Sag, Can M., additional, Shah, Ajay M., additional, Hu, Yanhua, additional, and Xu, Qingbo, additional

Published
2013
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46. A Role for Cytosolic Fumarate Hydratase in Urea Cycle Metabolism and Renal Neoplasia

Author

Adam, Julie, primary, Yang, Ming, additional, Bauerschmidt, Christina, additional, Kitagawa, Mitsuhiro, additional, O’Flaherty, Linda, additional, Maheswaran, Pratheesh, additional, Özkan, Gizem, additional, Sahgal, Natasha, additional, Baban, Dilair, additional, Kato, Keiko, additional, Saito, Kaori, additional, Iino, Keiko, additional, Igarashi, Kaori, additional, Stratford, Michael, additional, Pugh, Christopher, additional, Tennant, Daniel A., additional, Ludwig, Christian, additional, Davies, Benjamin, additional, Ratcliffe, Peter J., additional, El-Bahrawy, Mona, additional, Ashrafian, Houman, additional, Soga, Tomoyoshi, additional, and Pollard, Patrick J., additional

Published
2013
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48. Antigen-sensitive CD8 T-cell clones with tough HIV-1 suppression

Author

Glanville, Julie M, primary, Taylor, Steve, additional, Baban, Dilair, additional, Gillespie, Geraldine, additional, Easterbrook, Philippa, additional, Stewart-Jones, Guillaume, additional, Simmons, Alison, additional, Rowland-Jones, Sarah, additional, Dong, Tao, additional, and McMichael, Andrew, additional

Published
2013
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49. Pattern recognition receptor mediated downregulation of microRNA-650 fine-tunes MxA expression in dendritic cells infected with influenza A virus.

Author

Pichulik, Tica, Khatamzas, Elham, Liu, Xiao, Brain, Oliver, Delmiro Garcia, Magno, Leslie, Alasdair, Danis, Benedicte, Mayer, Alice, Baban, Dilair, Ragoussis, Jiannis, Weber, Alexander N. R., and Simmons, Alison

Abstract

MicroRNAs are important posttranscriptional regulators of gene expression, which have been shown to fine-tune innate immune responses downstream of pattern recognition receptor (PRR) signaling. This study identifies miR-650 as a novel PRR-responsive microRNA that is downregulated upon stimulation of primary human monocyte-derived dendritic cells (MDDCs) with a variety of different microbe-associated molecular patterns. A comprehensive target search combining in silico analysis, transcriptional profiling, and reporter assays reveals that miR-650 regulates several well-known interferon-stimulated genes, including IFIT2 and MXA. In particular, downregulation of miR-650 in influenza A infected MDDCs enhances the expression of MxA and may therefore contribute to the establishment of an antiviral state. Together these findings reveal a novel link between miR-650 and the innate immune response in human MDDCs. [ABSTRACT FROM AUTHOR]

Published
2016
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50. Estrogen receptor-α directly regulates the hypoxiainducible factor 1 pathway associated with antiestrogen response in breast cancer.

Author

Jun Yang, AlTahan, Alaa, Jones, Dylan T., Buffa, Francesca M., Bridges, Esther, Interiano, Rodrigo B., Qu, Chunxu, Vogt, Nathan, Ji-Liang Li, Baban, Dilair, Ragoussis, Jiannis, Nicholson, Robert, Davidoff, Andrew M., and Harris, Adrian L.

Subjects
ESTROGEN receptors, ESTROGEN antagonists, GENETICS of breast cancer, HYPOXEMIA, CANCER cells
Abstract

A majority of breast cancers are driven by estrogen via estrogen receptor-α (ERα). Our previous studies indicate that hypoxia-inducible factor 1α (HIF-1α) cooperates with ERα in breast cancer cells. However, whether ERα is implicated in the direct regulation of HIF-1α and the role of HIF-1α in endocrine therapy response are unknown. In this study we found that a subpopulation of HIF-1α targets, many of them bearing both hypoxia response elements and estrogen response elements, are regulated by ERα in normoxia and hypoxia. Interestingly, the HIF-1α gene itself also bears an estrogen response element, and its expression is directly regulated by ERα. Clinical data revealed that expression of the HIF-1α gene or a hypoxia metagene signature is associated with a poor outcome to endocrine treatment in ERα+ breast cancer. HIF-1α was able to confer endocrine therapy resistance to ERα+ breast cancer cells. Our findings define, for the first time to our knowledge, a direct regulatory pathway between ERα and HIF-1α, which might modulate hormone response in treatment. [ABSTRACT FROM AUTHOR]

Published
2015
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