Shamit Soneji
John Radcliffe Hospital
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Publication
Featured researches published by Shamit Soneji.
Science | 2008
Dengli Hong; Rajeev Gupta; Philip Ancliff; Ann Atzberger; John Brown; Shamit Soneji; Joanne Green; Sue Colman; Wanda Piacibello; Veronica J. Buckle; Shinobu Tsuzuki; Mel Greaves; Tariq Enver
Understanding cancer pathogenesis requires knowledge of not only the specific contributory genetic mutations but also the cellular framework in which they arise and function. Here we explore the clonal evolution of a form of childhood precursor–B cell acute lymphoblastic leukemia that is characterized by a chromosomal translocation generating a TEL-AML1 fusion gene. We identify a cell compartment in leukemic children that can propagate leukemia when transplanted in mice. By studying a monochorionic twin pair, one preleukemic and one with frank leukemia, we establish the lineal relationship between these “cancer-propagating” cells and the preleukemic cell in which the TEL-AML1 fusion first arises or has functional impact. Analysis of TEL-AML1–transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this preleukemic cell with altered self-renewal and survival properties.
Cell Stem Cell | 2008
Gillian M. Morrison; Ifigenia Oikonomopoulou; Rosa Portero Migueles; Shamit Soneji; Alessandra Livigni; Tariq Enver; Joshua M. Brickman
The use of embryonic stem cell (ESC) differentiation to generate functional hepatic or pancreatic progenitors and as a tool for developmental biology is limited by an inability to isolate in vitro equivalents of regionally specified anterior definitive endoderm (ADE). To address this, we devised a strategy using a fluorescent reporter gene under the transcriptional control of the anterior endoderm marker Hex alongside the definitive mesendoderm marker Cxcr4. Isolation of Hex(+)Cxcr4(+) differentiating ESCs yielded a population expressing ADE markers that both can be expanded and is competent to undergo differentiation toward liver and pancreatic fates. Hex reporter ESCs were also used to define conditions for ADE specification in serum-free adherent culture and revealed an unexpected role for FGF signaling in the generation of ADE. Our findings in defined monolayer differentiation suggest FGF signaling is an important regulator of early anterior mesendoderm differentiation rather than merely a mediator of morphogenetic movement.
Nature Immunology | 2012
Sidinh Luc; Tiago C. Luis; Hanane Boukarabila; Iain C Macaulay; Natalija Buza-Vidas; Tiphaine Bouriez-Jones; Michael Lutteropp; Petter S. Woll; Stephen Loughran; Adam Mead; Anne Hultquist; John Brown; Takuo Mizukami; S Matsuoka; Helen Ferry; Kristina Anderson; Deborah Atkinson; Shamit Soneji; Aniela Domanski; Alison Farley; Alejandra Sanjuan-Pla; Cintia Carella; Roger Patient; Marella de Bruijn; Tariq Enver; Claus Nerlov; C. Clare Blackburn; Isabelle Godin; Sten Eirik W. Jacobsen
The stepwise commitment from hematopoietic stem cells in the bone marrow to T lymphocyte–restricted progenitors in the thymus represents a paradigm for understanding the requirement for distinct extrinsic cues during different stages of lineage restriction from multipotent to lineage-restricted progenitors. However, the commitment stage at which progenitors migrate from the bone marrow to the thymus remains unclear. Here we provide functional and molecular evidence at the single-cell level that the earliest progenitors in the neonatal thymus had combined granulocyte-monocyte, T lymphocyte and B lymphocyte lineage potential but not megakaryocyte-erythroid lineage potential. These potentials were identical to those of candidate thymus-seeding progenitors in the bone marrow, which were closely related at the molecular level. Our findings establish the distinct lineage-restriction stage at which the T cell lineage–commitment process transits from the bone marrow to the remote thymus.
BMC Biophysics | 2013
Ana Z Canals-Hamann; Ricardo Pires das Neves; Joyce Reittie; Carlos Iñiguez; Shamit Soneji; Tariq Enver; Veronica J. Buckle; Francisco J. Iborra
SummaryTranscription factories are nuclear domains where gene transcription takes placealthough the molecular basis for their formation and maintenance are unknown. In thisstudy, we explored how the properties of chromatin as a polymer may contribute to thestructure of transcription factories. We found that transcriptional active chromatincontains modifications like histone H4 acetylated at Lysine 16 (H4K16ac). Singlefibre analysis showed that this modification spans the entire body of the gene.Furthermore, H4K16ac genes cluster in regions up to 500 Kb alternating active andinactive chromatin. The introduction of H4K16ac in chromatin induces stiffness in thechromatin fibre. The result of this change in flexibility is that chromatin couldbehave like a multi-block copolymer with repetitions of stiff-flexible(active-inactive chromatin) components. Copolymers with such structure self-organizethrough spontaneous phase separation into microdomains. Consistent with such modelH4K16ac chromatin form foci that associates with nascent transcripts. We propose thattranscription factories are the result of the spontaneous concentration of H4K16acchromatin that are in proximity, mainly in cis.
Annals of the New York Academy of Sciences | 2007
Shamit Soneji; Sui Huang; Matthew Loose; Ian J. Donaldson; Roger Patient; Berthold Göttgens; Tariq Enver; Gillian May
Abstract:u2002 Identifying the transcription factor interactions that are responsible for cell‐specific gene expression programs is key to understanding the regulation of cell behaviors, such as self‐renewal, proliferation, differentiation, and death. The rapidly increasing availability of microarray‐derived global gene expression data sets, coupled with genome sequence information from multiple species, has driven the development of computational methods to reverse engineer and dynamically model genetic regulatory networks. An understanding of the architecture and behavior of transcriptional networks should lend insight into how the huge number of potential gene expression programs is constrained and facilitates efforts to direct or redirect cell fate.
Immunity | 2007
Robert Månsson; Anne Hultquist; Sidinh Luc; Liping Yang; Kristina Anderson; Shabnam Kharazi; Suleiman Al-Hashmi; Karina Liuba; Lina Thorén; Jörgen Adolfsson; Natalija Buza-Vidas; Hong Qian; Shamit Soneji; Tariq Enver; Mikael Sigvardsson; Sten Eirik W. Jacobsen
Blood | 2011
Sidinh Luc; Iain C Macaulay; Natalija Buza-Vidas; Tiphaine Bouriez-Jones; Michael Lutteropp; Petter S. Woll; Adam Mead; Hanane Boukarabila; Tiago C. Luis; T Mizukami; S Matsuoka; John Brown; Helen Ferry; Kristina Anderson; Debbie Atkinson; Shamit Soneji; A Domanski; A Farley; Alejandra Sanjuan-Pla; C Carella; Roger Patient; M de Bruijn; Tariq Enver; Claus Nerlov; C. Clare Blackburn; Isabelle Godin; Jacobsen Sew.
Archive | 2015
Rong Chen; Kang Liu; Michael Mindrinos; Ronald W. Davis; Minnie M. Sarwal; Li Li; Lihua Ying; Maarten Naesens; Wenzhong Xiao; Tara K. Sigdel; Sue Hsieh; Douglas R. Higgs; Veronica J. Buckle; Simon J. McGowan; Stephen Taylor; Asoke K. Nandi; William G. Wood; T. Merryweather-Clarke; Shamit Soneji; Nicki Gray; Kevin D. Clark
Archive | 2013
Tariq Enver; Göran Karlsson; Jonas Larsson; Christine Karlsson; Aurélie Baudet; Natsumi Miharada; Shamit Soneji; Rajeev Gupta
Archive | 2013
Marco De Gobbi; David Garrick; Magnus Lynch; Douglas Vernimmen; Jim R. Hughes; Nicolas Goardon; Sidinh Luc; Karen M. Lower; Jacqueline A. Sloane-Stanley; Cristina Pina; Shamit Soneji; Raffaele Renella; Tariq Enver; Stephen Taylor; Sten Eirik W. Jacobsen; Paresh Vyas; Richard J. Gibbons; Douglas R. Higgs