Imperial College London

ProfessorJesusGil

Faculty of MedicineInstitute of Clinical Sciences

Professor of Cell Proliferation
 
 
 
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Contact

 

+44 (0)20 3313 8263jesus.gil

 
 
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Location

 

CRB room 5005CRB (Clinical Research Building)Hammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

108 results found

Gil J, Blunting senescence boosts liver regeneration, Genes and Development, ISSN: 0890-9369

Journal article

Gil J, Prostate Carcinogenesis: Actionable Inflammatory Storms?, Nature Reviews Cancer, ISSN: 1474-175X

Journal article

Calimport SRG, Bentley BL, Stewart CE, Pawelec G, Scuteri A, Vinciguerra M, Slack C, Chen D, Harries LW, Marchant G, Fleming GA, Conboy M, Antebi A, Small GW, Gil J, Lakatta EG, Richardson A, Rosen C, Nikolich K, Wyss-Coray T, Steinman L, Montine T, de Magalhães JP, Campisi J, Church Get al., 2019, To help aging populations, classify organismal senescence, Science, Vol: 366, Pages: 576-578, ISSN: 0036-8075

Globally, citizens exist for sustained periods in states of aging-related disease and multimorbidity. Given the urgent and unmet clinical, health care, workforce, and economic needs of aging populations, we need interventions and programs that regenerate tissues and organs and prevent and reverse aging-related damage, disease, and frailty (1). In response to these challenges, the World Health Organization (WHO) has called for a comprehensive public-health response within an international legal framework based on human rights law (1). Yet for a clinical trial to be conducted, a disease to be diagnosed, intervention prescribed, and treatment administered; a corresponding disease classification code is needed, adopted nationally from the WHO International Classification of Diseases (ICD). Such classifications and staging are fundamental for health care governance among governments and intergovernmental bodies. We describe a systematic and comprehensive approach to the classification and staging of organismal senescence and aging-related diseases at the organ and tissue levels in order to guide policy and practice and enable appropriate interventions and clinical guidance, systems, resources, and infrastructure.

Journal article

Gorgoulis V, Adams PD, Alimonti A, Bennett DC, Bischof O, Bishop C, Campisi J, Collado M, Evangelou K, Ferbeyre G, Gil J, Hara E, Krizhanovsky V, Jurk D, Maier AB, Narita M, Niedernhofer L, Passos JF, Robbins PD, Schmitt CA, Sedivy J, Vougas K, von Zglinicki T, Zhou D, Serrano M, Demaria Met al., 2019, Cellular senescence: defining a path forward, Cell, Vol: 179, Pages: 813-827, ISSN: 0092-8674

Cellular senescence is a cell state implicated in various physiological processes and a wide spectrum of age-related diseases. Thus, accurate detection of senescent cells, especially in vivo, is essential especially since the field of senotherapeutics is growing rapidly. Here, we present a consensus from the International Cell Senescence Association (ICSA), defining and discussing key cellular and molecular features of senescence and offering recommendation on how to use them as biomarkers. We also present a resource tool to facilitate the identification of genes linked with senescence (SeneQuest, available at http://Senequest.net). Lastly, we propose an algorithm to accurately assess and quantify senescence, both in cultured cells and in vivo.

Journal article

Guerrero A, Herranz N, Sun B, Wagner V, Gallage S, Guiho R, Wolter K, Pombo J, Irvine EE, Innes AJ, Birch J, Glegola J, Manshaei S, Heide D, Dharmalingam G, Harbig J, Olona A, Behmoaras J, Dauch D, Uren AG, Zender L, Vernia S, Martínez-Barbera JP, Heikenwalder M, Withers DJ, Gil Jet al., 2019, Cardiac glycosides are broad-spectrum senolytics, Nature Metabolism, Vol: 1, Pages: 1074-1088, ISSN: 2522-5812

Senescence is a cellular stress response that results in the stable arrest of old, damaged or pre-neoplastic cells. Oncogene-induced senescence is tumour suppressive but can also exacerbate tumorigenesis through the secretion of proinflammatory factors from senescent cells. Drugs that selectively kill senescent cells, termed ‘senolytics’, have proved beneficial in animal models of many age-associated diseases. In the present study, we show that the cardiac glycoside ouabain is a senolytic agent with broad activity. Senescent cells are sensitized to ouabain-induced apoptosis, a process mediated in part by induction of the proapoptotic Bcl-2 family protein NOXA. We demonstrate that cardiac glycosides synergize with anti-cancer drugs to kill tumour cells and eliminate senescent cells that accumulate after irradiation or in old mice. Ouabain also eliminates senescent pre-neoplastic cells. The findings of the present study suggest that cardiac glycosides may be effective anti-cancer drugs by acting through multiple mechanisms. Given the broad range of senescent cells targeted by cardiac glycosides, their use against age-related diseases warrants further exploration.

Journal article

Gil J, 2019, Cellular senescence causes ageing, Nature Reviews Molecular Cell Biology, Vol: 20, Pages: 388-388, ISSN: 1471-0072

Journal article

Sogaard P, Gil J, 2019, NAD+: A metabolic knob fine-tuning inflammation during senescence, Nature Metabolism, Vol: 1, Pages: 310-311, ISSN: 2522-5812

The senescence-associated secretory phenotype (SASP) is responsible for the deleterious effects of senescent cells in ageing and cancer. A new study shows that NAD+ metabolism can regulate the pro-inflammatory SASP, thereby promoting tumorigenesis.

Journal article

Bagnati M, Moreno-Moral A, Ko J-H, Nicod J, Harmston N, Imprialou M, Game L, Gil J, Petretto E, Behmoaras Jet al., 2019, Systems-genetics identifies a macrophage cholesterol network associated with physiological wound healing, JCI insight, Vol: 4, ISSN: 2379-3708

Among other cells, macrophages regulate the inflammatory and reparative phases during wound healing but genetic determinants and detailed molecular pathways that modulate these processes are not fully elucidated. Here, we took advantage of normal variation in wound healing in 1,378 genetically outbred mice, and carried out macrophage RNA-sequencing profiling of mice with extreme wound healing phenotypes (i.e., slow and fast healers, n = 146 in total). The resulting macrophage coexpression networks were genetically mapped and led to the identification of a unique module under strong trans-acting genetic control by the Runx2 locus. This macrophage-mediated healing network was specifically enriched for cholesterol and fatty acid biosynthetic processes. Pharmacological blockage of fatty acid synthesis with cerulenin resulted in delayed wound healing in vivo, and increased macrophage infiltration in the wounded skin, suggesting the persistence of an unresolved inflammation. We show how naturally occurring sequence variation controls transcriptional networks in macrophages, which in turn regulate specific metabolic pathways that could be targeted in wound healing.

Journal article

Innes AJ, Gil J, 2019, IMR90 ER:RAS: A cell model of oncogene-induced senescence, Methods in Molecular Biology, Vol: 1896, Pages: 83-92, ISSN: 1940-6029

Oncogene-induced senescence (OIS) is a cellular response that limits the replication of cells expressing oncogenes. As a result, OIS is a potent tumor suppressor mechanism limiting cancer progression. Here we describe IMR90 ER:RAS, a widely used model to study OIS in cell culture. This model takes advantage of IMR90 human primary fibroblast infected with a 4-hydroxy-tamoxifen (4-OHT) inducible ER:RAS construct. RAS activation upon 4-OHT treatment results in a coordinated induction of senescence, recapitulating different aspects of the phenotype such as the growth arrest and the establishment of a senescence-associated secretory phenotype (SASP).

Journal article

Bowling S, Di Gregorio A, Sancho M, Pozzi S, Aarts M, Signore M, Schneider MD, Martinez-Barbera JP, Gil J, Rodriguez TAet al., 2018, Author correction: P53 and mTOR signalling determine fitness selection through cell competition during early mouse embryonic development, Nature Communications, Vol: 9, ISSN: 2041-1723

The original version of this Article contained an error in the spelling of Juan Pedro Martinez-Barbera, which was incorrectly given as Juan Pedro Martinez Barbera. This error has now been corrected in both the PDF and HTML versions of the Article.

Journal article

Georgilis A, Klotz S, Hanley CJ, Herranz N, Weirrich B, Morancho B, Leote AC, D'Artista L, Gallage S, Seehawer M, Carroll T, Dharmalingam G, Wee KB, Mellone M, Pombo J, Heide D, Guccione E, Arribas J, Barbosa-Morais NL, Heikenwalder M, Thomas GJ, Zender L, Gil Jet al., 2018, PTBP1-mediated alternative splicing regulates the inflammatory secretome and the pro-tumorigenic effects of senescent cells, Cancer Cell, Vol: 34, Pages: 85-102.e9, ISSN: 1535-6108

Oncogene-induced senescence is a potent tumor-suppressive response. Paradoxically, senescence also induces an inflammatory secretome that promotes carcinogenesis and age-related pathologies. Consequently, the senescence-associated secretory phenotype (SASP) is a potential therapeutic target. Here, we describe an RNAi screen for SASP regulators. We identified 50 druggable targets whose knockdown suppresses the inflammatory secretome and differentially affects other SASP components. Among the screen candidates was PTBP1. PTBP1 regulates the alternative splicing of genes involved in intracellular trafficking, such as EXOC7, to control the SASP. Inhibition of PTBP1 prevents the pro-tumorigenic effects of the SASP and impairs immune surveillance without increasing the risk of tumorigenesis. In conclusion, our study identifies SASP inhibition as a powerful and safe therapy against inflammation-driven cancer.

Journal article

Bowling S, Di Gregorio A, Sancho M, Pozzi S, Aarts M, Signore M, Schneider M, Martinez Barbera JP, Gil J, Rodriguez TAet al., 2018, P53 and mTOR signalling determine fitness selection through cell competition during early mouse embryonic development, Nature Communications, Vol: 9, ISSN: 2041-1723

Ensuring the fitness of the pluripotent cells that will contribute to future development is important both for the integrity of the germline and for proper embryogenesis. Consequently, it is becoming increasingly apparent that pluripotent cells can compare their fitness levels and signal the elimination of those cells that are less fit than their neighbours. In mammals the nature of the pathways that communicate fitness remain largely unknown. Here we identify that in the early mouse embryo and upon exit from naive pluripotency, the confrontation of cells with different fitness levels leads to an inhibition of mTOR signalling in the less fit cell type, causing its elimination. We show that during this process, p53 acts upstream of mTOR and is required to repress its activity. Finally, we demonstrate that during normal development around 35% of cells are eliminated by this pathway, highlighting the importance of this mechanism for embryonic development.

Journal article

Apps JR, Carreno G, Gonzalez-Meljem JM, Haston S, Guiho R, Cooper JE, Manshaei S, Jani N, Holsken A, Pettorini B, Beynon RJ, Simpson DM, Fraser HC, Hong Y, Hallang S, Stone TJ, Virasami A, Donson AM, Jones D, Aquilina K, Spoudeas H, Joshi AR, Grundy R, Storer LCD, Korbonits M, Hilton DA, Tossell K, Thavaraj S, Ungless MA, Gil J, Buslei R, Hankinson T, Hargrave D, Goding C, Andoniadou CL, Brogan P, Jacques TS, Williams HJ, Martinez-Barbera JPet al., 2018, Tumour compartment transcriptomics demonstrate the activation of inflammatory and odontogenic programmes in human adamantinomatous craniopharyngioma and identify the MAPK/ERK pathway as a novel therapeutic target, Acta Neuropathologica, Vol: 135, Pages: 757-777, ISSN: 1432-0533

Adamantinomatous craniopharyngiomas (ACPs) are clinically challenging tumours, the majority of which have activating mutations in CTNNB1. They are histologically complex, showing cystic and solid components, the latter comprised of different morphological cell types (e.g. β-catenin-accumulating cluster cells and palisading epithelium), surrounded by a florid glial reaction with immune cells. Here, we have carried out RNA sequencing on 18 ACP samples and integrated these data with an existing ACP transcriptomic dataset. No studies so far have examined the patterns of gene expression within the different cellular compartments of the tumour. To achieve this goal, we have combined laser capture microdissection with computational analyses to reveal groups of genes that are associated with either epithelial tumour cells (clusters and palisading epithelium), glial tissue or immune infiltrate. We use these human ACP molecular signatures and RNA-Seq data from two ACP mouse models to reveal that cell clusters are molecularly analogous to the enamel knot, a critical signalling centre controlling normal tooth morphogenesis. Supporting this finding, we show that human cluster cells express high levels of several members of the FGF, TGFB and BMP families of secreted factors, which signal to neighbouring cells as evidenced by immunostaining against the phosphorylated proteins pERK1/2, pSMAD3 and pSMAD1/5/9 in both human and mouse ACP. We reveal that inhibiting the MAPK/ERK pathway with trametinib, a clinically approved MEK inhibitor, results in reduced proliferation and increased apoptosis in explant cultures of human and mouse ACP. Finally, we analyse a prominent molecular signature in the glial reactive tissue to characterise the inflammatory microenvironment and uncover the activation of inflammasomes in human ACP. We validate these results by immunostaining against immune cell markers, cytokine ELISA and proteome analysis in both solid tumour and cystic fluid from ACP pat

Journal article

Herranz N, Gil J, 2018, Mechanisms and functions of cellular senescence, Journal of Clinical Investigation, Vol: 128, Pages: 1238-1246, ISSN: 0021-9738

Cellular senescence is a highly stable cell cycle arrest that is elicited in response to different stresses. By imposing a growth arrest, senescence limits the replication of old or damaged cells. Besides exiting the cell cycle, senescent cells undergo many other phenotypic alterations such as metabolic reprogramming, chromatin rearrangement, or autophagy modulation. In addition, senescent cells produce and secrete a complex combination of factors, collectively referred as the senescence-associated secretory phenotype, that mediate most of their non–cell-autonomous effects. Because senescent cells influence the outcome of a variety of physiological and pathological processes, including cancer and age-related diseases, pro-senescent and anti-senescent therapies are actively being explored. In this Review, we discuss the mechanisms regulating different aspects of the senescence phenotype and their functional implications. This knowledge is essential to improve the identification and characterization of senescent cells in vivo and will help to develop rational strategies to modulate the senescence program for therapeutic benefit.

Journal article

Wagner V, Gil J, 2018, An epigenetic switch: from senescent melanocytes to malignant melanoma (and back), Cancer Cell, Vol: 33, Pages: 162-163, ISSN: 1535-6108

Oncogene-induced senescence is an important barrier during melanomagenesis. In this issue of Cancer Cell, Yu et al. show how elevated expression of structurally unrelated H3K9 demethylases disables senescence and constitutes a liability that can be exploited to restore senescence in melanoma by pharmacological inhibition of these epigenetic regulators.

Journal article

Gonzalez-Meljem JM, Haston S, Carreno G, Apps J, Pozzi S, Stache C, Kaushal G, Virasami A, Panousopoulos L, Mousavy-Gharavy SN, Guerrero A, Rashid M, Jani N, Goding CR, Jacques TS, Adams DJ, Gil J, Andoniadou CL, Martinez-Barbera JPet al., 2017, Stem cell senescence drives age-attenuated induction of pituitary tumours in mouse models of paediatric craniopharyngioma, Nature Communications, Vol: 8, ISSN: 2041-1723

Senescent cells may promote tumour progression through the activation of a senescence-associated secretory phenotype (SASP), whether these cells are capable of initiating tumourigenesis in vivo is not known. Expression of oncogenic β-catenin in Sox2+ young adult pituitary stem cells leads to formation of clusters of stem cells and induction of tumours resembling human adamantinomatous craniopharyngioma (ACP), derived from Sox2− cells in a paracrine manner. Here, we uncover the mechanisms underlying this paracrine tumourigenesis. We show that expression of oncogenic β-catenin in Hesx1+ embryonic precursors also results in stem cell clusters and paracrine tumours. We reveal that human and mouse clusters are analogous and share a common signature of senescence and SASP. Finally, we show that mice with reduced senescence and SASP responses exhibit decreased tumour-inducing potential. Together, we provide evidence that senescence and a stem cell-associated SASP drive cell transformation and tumour initiation in vivo in an age-dependent fashion.

Journal article

Aarts M, Georgilis A, Beniazza M, Beolchi P, Banito A, Carroll T, Kulisic M, Kaemena DF, Dharmalingam G, Martin N, Reik W, Zuber J, Kaji K, Chandra T, Gil Jet al., 2017, Coupling shRNA screens with single-cell RNA-Seq identifies a dual role for mTOR in reprogramming-induced senescence, Genes and Development, Vol: 31, Pages: 2085-2098, ISSN: 0890-9369

Expression of the transcription factors OCT4, SOX2, KLF4, and cMYC (OSKM) reprograms somatic cells into induced pluripotent stem cells (iPSCs). Reprogramming is a slow and inefficient process, suggesting the presence of safeguarding mechanisms that counteract cell fate conversion. One such mechanism is senescence. To identify modulators of reprogramming-induced senescence, we performed a genome-wide shRNA screen in primary human fibroblasts expressing OSKM. In the screen, we identified novel mediators of OSKM-induced senescence and validated previously implicated genes such as CDKN1A. We developed an innovative approach that integrates single-cell RNA sequencing (scRNA-seq) with the shRNA screen to investigate the mechanism of action of the identified candidates. Our data unveiled regulation of senescence as a novel way by which mechanistic target of rapamycin (mTOR) influences reprogramming. On one hand, mTOR inhibition blunts the induction of cyclin-dependent kinase (CDK) inhibitors (CDKIs), including p16INK4a, p21CIP1, and p15INK4b, preventing OSKM-induced senescence. On the other hand, inhibition of mTOR blunts the senescence-associated secretory phenotype (SASP), which itself favors reprogramming. These contrasting actions contribute to explain the complex effect that mTOR has on reprogramming. Overall, our study highlights the advantage of combining functional screens with scRNA-seq to accelerate the discovery of pathways controlling complex phenotypes.

Journal article

McHugh D, Gil J, 2017, Senescence and aging – causes, consequences, and therapeutic avenues, Journal of Cell Biology, Vol: 217, Pages: 65-77, ISSN: 0021-9525

Aging is the major risk factor for cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. Although we are far from understanding the biological basis of aging, research suggests that targeting the aging process itself could ameliorate many age-related pathologies. Senescence is a cellular response characterized by a stable growth arrest and other phenotypic alterations that include a proinflammatory secretome. Senescence plays roles in normal development, maintains tissue homeostasis, and limits tumor progression. However, senescence has also been implicated as a major cause of age-related disease. In this regard, recent experimental evidence has shown that the genetic or pharmacological ablation of senescent cells extends life span and improves health span. Here, we review the cellular and molecular links between cellular senescence and aging and discuss the novel therapeutic avenues that this connection opens.

Journal article

Young HL, Rowling EJ, Bugatti M, Giurisato E, Luheshi N, Arozarena I, Acosta JC, Kamarashev J, Frederick DT, Cooper ZA, Reuben A, Gil J, Flaherty KT, Wargo JA, Vermi W, Smith MP, Wellbrock C, Hurlstone Aet al., 2017, An adaptive signaling network in melanoma inflammatory niches confers tolerance to MAPK signaling inhibition, Journal of Experimental Medicine, Vol: 214, Pages: 1691-1710, ISSN: 1540-9538

Mitogen-activated protein kinase (MAPK) pathway antagonists induce profound clinical responses in advanced cutaneous melanoma, but complete remissions are frustrated by the development of acquired resistance. Before resistance emerges, adaptive responses establish a mutation-independent drug tolerance. Antagonizing these adaptive responses could improve drug effects, thereby thwarting the emergence of acquired resistance. In this study, we reveal that inflammatory niches consisting of tumor-associated macrophages and fibroblasts contribute to treatment tolerance through a cytokine-signaling network that involves macrophage-derived IL-1β and fibroblast-derived CXCR2 ligands. Fibroblasts require IL-1β to produce CXCR2 ligands, and loss of host IL-1R signaling in vivo reduces melanoma growth. In tumors from patients on treatment, signaling from inflammatory niches is amplified in the presence of MAPK inhibitors. Signaling from inflammatory niches counteracts combined BRAF/MEK (MAPK/extracellular signal–regulated kinase kinase) inhibitor treatment, and consequently, inhibiting IL-1R or CXCR2 signaling in vivo enhanced the efficacy of MAPK inhibitors. We conclude that melanoma inflammatory niches adapt to and confer drug tolerance toward BRAF and MEK inhibitors early during treatment

Journal article

Mellone M, Hanley CJ, Thirdborough S, Mellows T, Garcia E, Woo J, Tod J, Frampton S, Venei V, Moutasim KA, Kabir TD, Brennan PA, Venturi G, Ford K, Herranz N, Lim KP, Clarke J, Lambert DW, Prime SS, Underwood TJ, Vijayanand P, Eliceiri KW, Woelk C, King EV, Gil J, Ottensmeier CH, Thomas GJet al., 2016, Induction of fibroblast senescence generates a non-fibrogenic myofibroblast phenotype that differentially impacts on cancer prognosis, Aging, Vol: 9, Pages: 114-132, ISSN: 1945-4589

Cancer-associated fibroblasts (CAF) remain a poorly characterized, heterogeneous cell population. Here we characterized two previously described tumor-promoting CAF sub-types, smooth muscle actin (SMA)-positive myofibroblasts and senescent fibroblasts, identifying a novel link between the two.

Journal article

Wong CL, Innes AJ, Ma B, Gerrard G, Norziha ZA, Cheong SK, Leong CF, Bee PC, Sathar J, Lye SF, Foroni L, Aitman T, Liang L, Gil J, Laffan Met al., Differential Expression of Genes Associated with Oncogene-Induced Senescence and Senescence Associated Secretory Phenotype in the Absence of Differential Expression of High Molecular Risk Genes and Genes Associated with JAK-STAT Pathway in Sorted Cells of Patients with Polycythemia Vera and Primary Myelofibrosis, 59th Annual Meeting and Exposition of the American-Society-of-Hematology (ASH)/Symposium on the Basic Science of Hemostasis and Thrombosis, Publisher: American Society of Hematology, Pages: 4283-4283, ISSN: 0006-4971

Conference paper

guerrero a, Gil J, 2016, HMGB2 holds the key to the senescence-associated secretory phenotype, Journal of Cell Biology, Vol: 215, Pages: 297-299, ISSN: 1540-8140

The senescence-associated secretory phenotype (SASP) isahallmark of senescencewithimportantphysiologicalimpact, but how it is established is unclear. In this issue, Aird and colleagues(2016. J Cell Biol.xx-xx) describe how chromatin-bound HMGB2 fine-tunesSASP expressionby avoiding heterochromatin spreading.

Journal article

Tordella L, Khan S, Hohmeyer A, Banito A, Klotz S, Raguz S, Martin N, Ghamarlingam G, Carroll T, Gonzalez Meljem JM, Deswal S, Pedro J, Martinez-Barbero JP, Garcia-Escudero R, Zuber J, Zender L, Gil Jet al., 2016, SWI/SNF regulates a transcriptional programme that induces senescence to prevent liver cancer, Genes & Development, Vol: 30, Pages: 2187-2198-2187-2198, ISSN: 1549-5477

Oncogene-induced senescence (OIS) is a potent tumour suppressor mechanism. Toidentify senescence regulators relevant to cancer, we screened an shRNA librarytargeting genes deleted in hepatocellular carcinoma (HCC). Here, we describe howknockdown of the SWI/SNF component ARID1B prevents OIS and cooperates withRAS to induce liver tumours. ARID1B controls p16INK4a and p21CIP1a transcription butalso regulates DNA damage, oxidative stress and p53 induction, suggesting thatSWI/SNF uses additional mechanisms to regulate senescence. To systematicallyidentify SWI/SNF targets regulating senescence, we carried out a focused shRNAscreen. We discovered several new senescence regulators including ENTPD7, anenzyme that hydrolyses nucleotides. ENTPD7 affects oxidative stress, DNA damageand senescence. Importantly, expression of ENTPD7 or inhibition of nucleotidesynthesis in ARID1B-depleted cells results in re-establishment of senescence. Ourresults identify novel mechanisms by which epigenetic regulators can affect tumorprogression and suggest that pro-senescence therapies could be employed againstSWI/SNF-mutated cancers.

Journal article

Georgilis A, Gil J, 2016, Controlling secretion to limit chemoresistance, Genes & Development, Vol: 30, Pages: 1791-1792, ISSN: 1549-5477

The tumor microenvironment influences cancer progression and therapy outcome bymechanisms not yet fully understood. In this issue, Bent et al. (2016) show howchemotherapy causes endothelial senescence. Interestingly, senescent endothelial cells donot mount a typical senescence-associated secretory phenotype but instead acutely secreteIL-6, promoting chemoresistance. This study unveils a physiological switch involvingPI3K/AKT/mTOR signaling that restrains the senescence secretory responses to limit thedetrimental consequences of persistent inflammation.

Journal article

Gil J, Herranz N, 2016, Mitochondria and senescence: new actors for an old play, EMBO Journal, Vol: 35, Pages: 701-702, ISSN: 0261-4189

Mitochondrial dysfunction has been linked to both cellular senescence and ageing. Despite the relationship, it is still unclear whether mitochondria have a causal role in senescence. In this issue of The EMBO Journal, Correia-Melo et al (2016) combine targeted depletion of mitochondria with impairment of their biogenesis to demonstrate that decreased numbers of mitochondria impair the senescence response. Their results suggest that targeting mitochondria could reduce the detrimental effects of senescence during ageing.

Journal article

Gallage S, Gil J, 2016, Mitochondrial Dysfunction Meets Senescence, TRENDS IN BIOCHEMICAL SCIENCES, Vol: 41, Pages: 207-209, ISSN: 0968-0004

Journal article

Apps JR, Jani N, Gonzalez-Meljem JM, Tossell K, Carroll T, Ungless MA, Gil J, Williams H, Jacques TS, Martinez-Barbera JPet al., 2016, Clusters of Nuclear Beta-Catenin Accumulating Cells Form Secretory Hubs in Adamantinomatous Craniopharyngioma, 205th Meeting of the Pathological-Society-of-Great-Britain-and-Ireland, Publisher: WILEY-BLACKWELL, Pages: S5-S5, ISSN: 0022-3417

Conference paper

Gil J, Rodriguez T, 2016, Cancer: The Transforming Power of Cell Competition, CURRENT BIOLOGY, Vol: 26, Pages: R164-R166, ISSN: 0960-9822

Journal article

Gil J, Withers DJ, 2016, Ageing: out with the old, Nature, Vol: 530, Pages: 164-165, ISSN: 0028-0836

The selective elimination of cells that have adopted an irreversible, senescent state has now been shown to extend the lifespan of mice and to ameliorate some age-related disease processes.

Journal article

Herranz N, Gallage S, Gil J, 2015, TORn about SASP regulation, CELL CYCLE, Vol: 14, Pages: 3771-3772, ISSN: 1538-4101

Journal article

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