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  • Laboratorio 13

Dr. Isidro Sánchez-García

Experimental and Translational Oncology Laboratory: Stem Cells, Cancer Stem Cells and Cancer


Biography

Isidro Sánchez-García’s biographical sketch

Isidro Sánchez-García is a Senior Staff Scientist at the Instituto de Biologia Molecular y Celular del Cancer (IBMCC) of the Spanish National Research Council (CSIC). He learnt and practiced Medicine before completing his Ph.D. at University of Salamanca. Isidro was a postdoctoral fellow for five years at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge (UK) before appointment to his current position in 1997.

My research is focused on attaining a better understanding of the initiation, maintenance, and progression of leukemia, toward improving current treatment and/or prevention strategies. In this effort, I employ tools from functional genomics, computational biology, molecular genetics, and mouse models.

I hope to apply this knowledge to change the way we approach leukemia, from diagnosis and treatment to prevention first.

This work has allowed to establish both a pioneer relationship between stem cells and cancer and a causal link between infection and leukemia. The novel scientific achievements and ideas have not only resulted in high quality publications during his career but also they have crystallized into the first European patent granted in the field of Leukemia/Cancer Stem Cells.

This work has been awarded by the International Carreras Foundation (http://www.carrerasfoundation.org/fellow_bio.htm), and by the Eurosystem prize in 2010.

His research group hopes this investigation will result not only in new concepts in cancer biology and development, but also it  will provide the basis for the development of both a new strategy in cancer therapy and new methods for assessing treatment efficacy.

Isidro

POSICIONES DE MASTER Y TESIS:
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Dr. Isidro  Sánchez-García
Contact


Isidro Sánchez-García
Senior Staff Researcher CSIC, Laboratorio 13, Instituto de Biologia Molecular y Celular del Cancer (IBMCC), CSIC/Universidad de Salamanca, Campus Unamuno s/n, 37007-Salamanca, (Spain).

923 294 813
923 294813
isg(arroba)usal(.)es

Laboratorio 13, Instituto de Biologia Molecular y Celular del Cancer (IBMCC), CSIC/Universidad de Salamanca, Campus Unamuno s/n, 37007-Salamanca, (Spain).

Areas of Research

Our group is mainly interested in two main areas:

1-Infectious trigger in childhoodpB-ALL – deciphering the mechanisms responsible for clonal evolution with the aim of leukemia prevention 

2-Epigenetic priming in cancer initiation

1-Infectious trigger in childhoodpB-ALL – deciphering the mechanisms responsible for clonal evolution with the aim of leukemia prevention 

Leukemia accounts for a third of all cancers in children and its incidence has increased in the last 20 years. Recent results have khown that around 5% of healthy children carry a preleukemic clone. These preleukemic cells can persist for years, without harm for the individual and it is the exposure to an oncogenic environment, which provides the necessary selection pressure for the leukemia outgrowth. However, these oncogenic environments are not known. Recently, our group, in collaboration with Prof. Arndt Borkhardt’s group, has discovered for the first time the causal relationship between childhood B-cell leukemia (B-ALL) and exposure to natural infections, implying that B-ALL may be a preventable cancer (CancerDiscovery-2015; Nature-2017; CancerResearch-2017; CancerResearch-2018; EMBOJ-2018, Leukemia-2018; TrendsInCancer-2018).

These findings have been highlighted in:
+How infection can cause leukaemia. Nature 526, 167.
+ Infection causes childhood leukemia. Aging (Albany NY). 2015
+ Infection and the perils of B cell activation. Cancer Discovery December 2015 5:1244-1246.
+ Leukaemia: The part played by pathogens in pB-ALL. Nature Reviews Cancer 2015, 15, p637.
+ F1000Prime Recommendation in F1000Prime, 21 Nov. 2017.
+ A casual mechanism for childhood acute lymphoblastic leukemia. Nature Reviews Cancer 2018; 18(8): 471-484

The need for the clarification how genetic predisposition and exposure to infection act synergistically in B-ALL development is one of the current major goals and challenges in Oncology. Preclinical models of childhood B-ALL have been an essential unmet need to prevent the occurrence of this disease. A novel and unique feature of this proposal is the availability of mouse models for both the ETV6-RUNX1 and the Pax5-inherited susceptibility which only develop human-like B-ALL as a result of natural infection exposure. These mouse models have anticipated the second hit in childhood B-ALL and they will be used by our research team as the basis for understanding the molecular mechanisms that govern the development of B-ALL as a result of natural infection exposure. Now, state-of-the-art genetic and genomic approaches will be used to define the (epi)genetic and inmune events arising from leukemic reprogramming of pre-leukemic cells by the genetic predisposition–infection exposure interaction. The conceptual and mechanistic insights obtained in this experimental system represent an entirely novel strategy and the results of these endeavours will inform approaches for preventing childhood B-ALL.

2-Epigenetic priming in cancer initiation

Recent evidence from hematopoietic and epithelial tumors revealed that the contribution of oncogenes to cancer development is mediated mainly through epigenetic priming of cancer-initiating cells, suggesting that genetic lesions that initiate the cancer process might be dispensable for the posterior tumor progression and maintenance. Epigenetic priming may remain latent until it is later triggered by endogenous or environmental stimuli. Our group study the impact of epigenetic priming in cancer development and in the development of new therapeutic approaches.

Figura 1

Figure 1. Gene–environment interactions in cancer development. Tumoral epigenetic priming can take place at any point in life and can remain dormant in the cancer cell-of-origin unless other posterior events trigger further tumor progression. This priming will be preserved through tumor evolution, even if the initiating hit is not anymore present or expressed. A) Sometimes the second events can arise randomly B) However, a given epigenetic priming may be particularly sensitive to certain environmental factor (“gene–environment interaction”) so that exposure to this factor will favor the emergence of second hit(s) which will in turn drive cancer development. C) In other cases, the exposure to a certain environmental factor causes an epigenetic reprogramming that increases the cancer susceptibility of the primed cell.

Figura 2

Figure 2. Cancer epigenetic priming. A) In the current view of the initiation and progression of cancer, an initiating hit is required to immortalize a target cell. These cells are then predisposed to acquire additional genetics hits over time. The acquisition of additional hits further deregulates cell behaviour leading to subclonal genetic heterogeneity. Specific subclones may contribute to the initiation of cancer, resistance to therapy, or to relapse. In human cancers and in most animal models of cancer, oncogenic alterations are expressed in all malignant cells, from target cells to terminal differentiated cells. B) Epigenetic priming model. The cancer-initiating effect of the oncogenic hit takes place in the stem/progenitor compartment, where the oncogene imposes an epigenetic regulatory state that doesn’t interfere with normal differentiation, but may become active at later developmental stages in response to external of internal factors, leading to the appearance of tumor differentiated cells. C) Can epigenetic priming be the sole driver of cancer? A key open question is how the normal epigenetic mechanisms that regulate physiological development and cellular identity are destabilized in such a way that oncogenic priming can persist and be propagated.

Figura 3

Figure 3. Molecular underpinnings of tumor epigenetic priming. In the initial stages of cancer development, a normal cell (A, the cancer cell-of-origin, which initially presents normal chromatin modifications according to its identity and developmental stage) is going to become a pre-cancer cell (B) by the action of a given oncogenic hit (for example, ETV6-RUNX1 chimeric fusion gene in B-ALL, IDH1 mutation in AML, Pax5 haploinsuficiency in family cases of B-ALL, BRCA1 mutations in breast cancer) or by the exposure to an environmental factor (tobacco smoke in lung adenocarcinoma); both can “reset” the epigenetic and/or transcriptome status and reprogram the epigenome to give rise to a pre-cancer cell. Once its role in oncogenic reprogramming is performed, the initiating hit is not anymore necessary for tumor progression. C) The malignant epigenetic priming will remain silent until specific second events will trigger cancer appearance. These second hits can happen randomly or be triggered by environmental exposures (infections in childhood B-ALL, K-RAS mutations in lung adenocarcinoma). Blue cylinders represent nucleosomes, red and white circles symbolize changes in DNA methylation, green and orange curved lines denote histone modifications.

Projects
  • (2001-2016)

    The group's research program is funded by the following national and international agencies

Junta de Castilla y León Ministerio de economía y competitividad Fundación José Carreras ARIMMORA consortium European Federation for Systematic Stem Cell Biology National institutes of health Seventh framework programme Inbiomed Pharmacyclics Grifols Telefonica móviles Decision-making within cells and differentiation entity therapies Fondo europeo de desarrollo regional
Publications

(*) Means equal contribution as senior authors.



2018

Lmo2 expression defines tumor cell identity during T-cell leukemogenesis.

García-Ramírez I, Bhatia S, Rodríguez-Hernández G, González-Herrero I, Walter C, González de Tena-Dávila S, Parvin S, Haas O, Woessmann W, Stanulla M, Schrappe M, Dugas M, Natkunam Y, Orfao A, Domínguez V, Pintado B, Blanco O, Alonso-López D, De Las Rivas J, Martín-Lorenzo A, Jiménez R, García Criado FJ, García Cenador MB, Lossos IS, Vicente-Dueñas C, Borkhardt A, Hauer J, Sánchez-García I, 
EMBO J.; 2018-Jun; 1460-2075; e98783; 29880602

The Making of Leukemia.

González-Herrero I, Rodríguez-Hernández G, Luengas-Martínez A, Isidro-Hernández M, Jiménez R, García-Cenador MB, García-Criado FJ, Sánchez-García I, Vicente-Dueñas C, 
Int J Mol Sci; 2018-May; 1422-0067; E1494; 29772764


2017

Infection exposure promotes ETV6-RUNX1 precursor B cell leukemia via impaired H3K4 demethylases.

Rodríguez-Hernández G, Hauer J, Martín-Lorenzo A, Schafer D, Bartenhagen C, García-Ramírez I, Auer F, González-Herrero I, Ruiz-Roca L, Gombert M, Okpanyi V, Fischer U, Chen C, Dugas M, Bhatia S, Linka RM, Garcia-Suquia M, Rascón-Trincado MV, Garcia-Sanchez A, Blanco O, García-Cenador MB, García-Criado FJ, Cobaleda C, Alonso-López D, De Las Rivas J, Müschen M, Vicente-Dueñas C, Sánchez-García I, Borkhardt A, 
Cancer Res.; 2017-Jun; 1538-7445; canres.0; 28630052

Crebbp loss cooperates with Bcl2 over-expression to promote lymphoma in mice.

García-Ramírez I, Tadros S, González-Herrero I, Martín-Lorenzo A, Rodríguez-Hernández G, Moore D, Ruiz-Roca L, Blanco O, Alonso-López D, De Las Rivas J, Hartert K, Duval R, Klinkebiel D, Bast M, Vose J, Lunning M, Fu K, Greiner T, Rodrigues-Lima F, Jiménez R, García Criado FJ, García Cenador MB, Brindle P, Vicente-Dueñas C, Alizadeh A, Sánchez-García I, Green MR, 
Blood; 2017-Mar; (); ; 28288979

Metabolic gatekeeper function of B-lymphoid transcription factors.

Chan LN, Chen Z, Braas D, Lee JW, Xiao G, Geng H, Cosgun KN, Hurtz C, Shojaee S, Cazzaniga V, Schjerven H, Ernst T, Hochhaus A, Kornblau SM, Konopleva M, Pufall MA, Cazzaniga G, Liu GJ, Milne TA, Koeffler HP, Ross TS, Sánchez-García I, Borkhardt A, Yamamoto KR, Dickins RA, Graeber TG, Müschen M, 
Nature; 2017-Feb; (); ; 28192788


2015

Designing a broad-spectrum integrative approach for cancer prevention and treatment.

Block KI, Gyllenhaal C, Lowe L, Amedei A, Amin AR, Amin A, Aquilano K, Arbiser J, Arreola A, Arzumanyan A, Ashraf SS, Azmi AS, Benencia F, Bhakta D, Bilsland A, Bishayee A, Blain SW, Block PB, Boosani CS, Carey TE, Carnero A, Carotenuto M, Casey SC, Chakrabarti M, Chaturvedi R, Chen GZ, Chen H, Chen S, Chen YC, Choi BK, Ciriolo MR, Coley HM, Collins AR, Connell M, Crawford S, Curran CS, Dabrosin C, Damia G, Dasgupta S, DeBerardinis RJ, Decker WK, Dhawan P, Diehl AM, Dong JT, Dou QP, Drew JE, Elkord E, El-Rayes B, Feitelson MA, Felsher DW, Ferguson LR, Fimognari C, Firestone GL, Frezza C, Fujii H, Fuster MM, Generali D, Georgakilas AG, Gieseler F, Gilbertson M, Green MF, Grue B, Guha G, Halicka D, Helferich WG, Heneberg P, Hentosh P, Hirschey MD, Hofseth LJ, Holcombe RF, Honoki K, Hsu HY, Huang GS, Jensen LD, Jiang WG, Jones LW, Karpowicz PA, Keith WN, Kerkar SP, Khan GN, Khatami M, Ko YH, Kucuk O, Kulathinal RJ, Kumar NB, Kwon BS, Le A, Lea MA, Lee HY, Lichtor T, Lin LT, Locasale JW, Lokeshwar BL, Longo VD, Lyssiotis CA, MacKenzie KL, Malhotra M, Marino M, Martinez-Chantar ML, Matheu A, Maxwell C, McDonnell E, Meeker AK, Mehrmohamadi M, Mehta K, Michelotti GA, Mohammad RM, Mohammed SI, Morre DJ, Muralidhar V, Muqbil I, Murphy MP, Nagaraju GP, Nahta R, Niccolai E, Nowsheen S, Panis C, Pantano F, Parslow VR, Pawelec G, Pedersen PL, Poore B, Poudyal D, Prakash S, Prince M, Raffaghello L, Rathmell JC, Rathmell WK, Ray SK, Reichrath J, Rezazadeh S, Ribatti D, Ricciardiello L, Robey RB, Rodier F, Rupasinghe HP, Russo GL, Ryan EP, Samadi AK, Sánchez-García I, Sanders AJ, Santini D, Sarkar M, Sasada T, Saxena NK, Shackelford RE, Shantha Kumara HM, Sharma D, Shin DM, Sidransky D, Siegelin MD, Signori E, Singh N, Sivanand S, Sliva D, Smythe C, Spagnuolo C, Stafforini DM, Stagg J, Subbarayan PR, Sundin T, Talib WH, Thompson SK, Tran PT, Ungefroren H, Vander Heiden MG, Venkateswaran V, Vinay DS, Vlachostergios PJ, Wang Z, Wellen KE, Whelan RL, Yang ES, Yang H, Yang X, Yaswen P, Yedjou C, Yin X, Zhu J, Zollo M, 
Semin. Cancer Biol.; 2015-Dec; 35S(); S276-S30; 26590477


2016
2015

Sustained proliferation in cancer: Mechanisms and novel therapeutic targets.

Feitelson MA, Arzumanyan A, Kulathinal RJ, Blain SW, Holcombe RF, Mahajna J, Marino M, Martinez-Chantar ML, Nawroth R, Sánchez-García I, Sharma D, Saxena NK, Singh N, Vlachostergios PJ, Guo S, Honoki K, Fujii H, Georgakilas AG, Amedei A, Niccolai E, Amin A, Ashraf SS, Boosani CS, Guha G, Ciriolo MR, Aquilano K, Chen S, Mohammed SI, Azmi AS, Bhakta D, Halicka D, Nowsheen S, 
Semin. Cancer Biol.; 2015-Apr; (); ; 25892662


2014

Transient expression of Bcl6 is sufficient for oncogenic function and induction of mature B-cell lymphoma.

Green MR, Vicente-Dueñas C, Romero-Camarero I, Long Liu C, Dai B, González-Herrero I, García-Ramírez I, Alonso-Escudero E, Iqbal J, Chan WC, Campos-Sánchez E, Orfao A, Pintado B, Flores T, Blanco O, Jiménez R, Martínez-Climent JA, Criado FJ, Cenador MB, Zhao S, Natkunam Y, Lossos IS, Majeti R, Melnick A, Cobaleda C, Alizadeh AA, Sánchez-García I, 
Nat Commun; 2014-; 5(); 3904; 24887457


2013
2012

Expression of MALT1 oncogene in hematopoietic stem/progenitor cells recapitulates the pathogenesis of human lymphoma in mice.

Vicente-Dueñas C, Fontán L, González-Herrero I, Romero-Camarero I, Segura V, Aznar MA, Alonso-Escudero E, Campos-Sánchez E, Ruiz-Roca L, Barajas-Diego M, Sagardoy A, Martinez-Ferrandis JI, Abollo-Jiménez F, Bertolo C, Peñuelas I, García-Criado FJ, García-Cenador MB, Tousseyn T, Agirre X, Prosper F, Garcia-Bragado F, McPhail ED, Lossos IS, Du MQ, Flores T, Hernandez-Rivas JM, González M, Salar A, Bellosillo B, Conde E, Siebert R, Sagaert X, Cobaleda C, Sánchez-García I, Martínez-Climent JA, 
Proc. Natl. Acad. Sci. U.; 2012-06; 109(26); 10534-9; 22689981


2011
2010
2009
2008
2007
2006

SLUG (SNAI2) overexpression in embryonic development.

Pérez-Mancera PA, González-Herrero I, Maclean K, Turner AM, Yip MY, Sánchez-Martín M, García JL, Robledo C, Flores T, Gutiérrez-Adán A, Pintado B, Sánchez-García I, 
Cytogenet. Genome Res.; 2006-05; 114(1); 24-9; 16717446


2005

SLUG in cancer development.

Pérez-Mancera PA, González-Herrero I, Pérez-Caro M, Gutierrez-Cianca N, Flores T, Gutiérrez-Adán A, Pintado B, Sánchez-Martín M, Sánchez-García I, 
Oncogene; 2005-04; 24(19); 3073-82; 15735690

Patents
  • POLINUCLÉOTIDO QUE LIMITA LA EXPRESIÓN DEL ONCOGEN HUMANO TEL-AML1 A CÉLULAS MADRE HEMATOPOYÉTICAS Y MODELO ANIMAL QUE LO CONTIENE
    SOLICITUD PATENTE EUROPEA No: FECHA DE PRESENTACION: el 17 de mayo de 2013 El número de solicitud: 201330704 Sánchez García, Isidro / Cobaleda Hernández, César José / Vicente Dueñas, Carolina.
    201330704; 2013-05-17

  • A new polynucleotide comprising a hematopoietic stem cell–specific transcriptional regulatory sequence, and mucosa-associated lymphoid tissue; useful for producing a transgenic nonhuman animal.
    DESCRIPTION: A new polynucleotide comprising a hematopoietic stem cell–specific transcriptional regulatory sequence, and mucosa-associated lymphoid tissue; useful for producing a transgenic nonhuman animal. Assignee: CSIC, USAL and PROYECTO BIOMEDICINA CIMA Priority application date: 10/11/2011 Publication date: 4/18/2013 Highlighted in Nature Biotechnology 2013, 31 (7), 607 :“Recent patent applications in hematopoietic stem cells” Sánchez García, Isidro / Martínez Climent, José Ángel / Cobaleda Hernández, César José / Fontán Gabás, Lorena / Vicente Dueñas, Carolina
    WO 2013053765; 2013-04-18

  • A non-human animal model of HGAL-linked lymphoma, US Provisional Patent Application number 61/569,377
    Patent file with the US Patent and Trademark Office (USPTO) FECHA DE PRESENTACION: 11/12/2011 CSIC and University of Miami LICENCIADA a Pharmacyclics (Stanford, USA) Sánchez García, Isidro / Lossos, Izidore.
    Patent file with the US Patent and Trademark Office (USPTO); 2011-11-12

  • A non-human animal model of mucosa-associated lymphoid tissue (MALT) lymphoma
    SOLICITUD PATENTE EUROPEA No: EP 11382319; FECHA DE PRESENTACION: 11/10/2011 CSIC and INSTITUTO CIENTIFICO Y TECNOLOGICO DE NAVARRA, S.A. (ICTDP) Sánchez García, Isidro / Martínez Climent, José Ángel / Cobaleda Hernández, César José / Fontán Gabás, Lorena / Vicente Dueñas, Carolina.
    EP 11382319; 2011-10-11

  • Empleo del gen Slug, sus productos o expresión, y/o compuestos inhibidores o estimuladores de la expresión de Slug para conferir radiosensibilización o radioprotección celular
    Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / M. Sánchez-Martín
    ES2253028; 2007-08-01

  • Método para el screening in vitro de agentes
    (arising from Spanisn Patent Application No. P200202633,5 divisional of Spanisn Patent Application No. P200100151) Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García
    ES2241402B1; 2007-03-08

  • Methods of treating disorders associated with fat storage
    SOLICITADA: EP06076886.8 (16-X-2006) International Patent Application No. PCT/IB2007/003736 (WO 2008/047235). Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / Pedro A. Perez-Mancera (CSIC and USAL)
    PCT/IB2007/003736 (WO 2008/047235) EP06076886.8; 2006-10-16

  • IDENTIFICATION OF CANCER STEM CELLS using genetic markers
    SOLICITADA: 06017630.2 (7-IX-2006) International Patent Application No. PCT/IB2007/003648 (WO 2008/029290). Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / M. Pérez-Caro (CSIC and USAL)
    PCT/IB2007/003648 (WO 2008/029290) 06017630.2; 2006-09-07

  • Mouse model of a sustained cancer conditionally expressing an oncogene
    SOLICITADA: EPO6017630.2 (24-VIII-2006) Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / M. Pérez-Caro (CSIC and USAL)
    EPO6017630.2; 2006-08-24

  • Use of the slug gene, or of the transcription or expression products thereof in the detection and/or treatment of cancerous cells.
    I. Sánchez-García / J. Pérez-Losada / A. Orfao.
    US2006141454; 2006-06-29

  • Composición farmacéutica para el tratamiento del cáncer
    Presentada: 15-11-2002 (nº solicitud inicial200100151; nº solicitud: P200202634) Publicación de la solicitud: 01.11.2005 Fecha de concesión: 14.06.2006 (nº publicación: ES 2 242 469 B1). Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / J. Pérez-Losada / A. Orfao.
    US2006141454; 2006-06-14

  • Use of the slug gene or the replication, transcription or expression products thereof in the identification, diagnosis, prevention or treatment of the spread of cancer and/or the development of metastasis
    SOLICITADA Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / F. Voces
    WO2006045874; 2006-05-04

  • MURINE STEM CELLS AND APPLICATIONS THEREOF
    SOLICITADA Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / María Pérez-Caro / F. Voces
    PCT/IB2006/001969 WO06/136951; 2005-05-24

  • Use of the slug gene as a genetic marker comprising using a stem cell factor technique for treating transplant patients.
    Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / J. Pérez-Losada
    ES2213429; 2004-08-16

  • Non-human transgenic mammals used as models for human pathologies originating from stem cells
    Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / J. Pérez-Losada
    ES2195751 WO03046181; 2003-06-05

  • Patent 1 and Derivatives

    U.S. Patent No. 6,007,988 issued December 28, 2999 (RE39,229) RELATING TO BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.

    U.S. Patent No. 6,013,453 issued January 11, 2000 BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.

    U.S. Patent Application No. 10/309,578 filed December 3, 2002 RELATING TO BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.

    U.S. Patent Application No. 10/397,930 filed March 25, 2003 RELATING TO BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.

      U.S. Patent Application No. 10/400,017 filed March 25, 2003 RELATING TO BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.  

    U.S. Patent Application No. 11/500,162 filed August 7, 2006 BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.  

    EP Patent Application No. 08015286.1 filed August 17, 1995 IMPROVEMENTS IN OR RELATING TO BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.  

    U.S. Patent Application No. 09/478,513 filed January 6, 2000 (case is abandoned) DNA LIBRARY Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.

    U.S. Patent Application No. 09/718,538 filed November 22, 2000 (case is abandoned) BINDING PROTEINS FOR RECOGNITION OF DNA Inventores: A. Klug, Y. Choo y I. Sánchez-García. EN EXPLOTACION BY Sangamo BioSciences, Inc.  

    -Esta tecnología ha sido considerada por Nature y Nature Biotechnology como una revolución en biología: -Pearson H. Protein engineering: The fate of fingers. Nature. 2008 Sep 11;455(7210):160-4. -Chandrasekharan S, Kumar S, Valley CM, Rai A. Proprietary science, open science and the role of patent disclosure: the case of zinc-finger proteins. Nat Biotechnol. 2009 Feb;27(2):140-4. -Esta tecnología fue seleccionada como Method of the year 2011 by Nature Methods (Monya Baker, Technology editor for Nature and Nature Methods. Nature Methods 2012, 9(1), 23-26.)

    A. Klug / Y. Choo / I. Sánchez-García
    ;

  • GRADED EXPRESSION OF SNAIL AS A MARKER OF CANCER DEVELOPMENT
    Solicitada: PCT/IB2006/002571 (publication No. WO 2007/012970; claiming priority from EP application No 05076753.2) Agencia: Carpmales & Ransford, 43-45 Bloomsbury Square, London WC1A 2RA I. Sánchez-García / Pedro Antonio Pérez-Mancera / F. Voces
    PCT/IB2006/002571;

Group
  • Dr. Isidro  Sánchez-García Dr. Isidro Sánchez-García

    Dr. Isidro Sánchez-García

    Experimental and Translational Oncology Laboratory: Stem Cells, Cancer Stem Cells and Cancer

    Telf.:

    Fax:

    Email: isg@usal.es


    Contact

    Dr. Isidro Sánchez-García
    Senior Staff Researcher CSIC, Laboratorio 13, Instituto de Biologia Molecular y Celular del Cancer (IBMCC), CSIC/Universidad de Salamanca, Campus Unamuno s/n, 37007-Salamanca, (Spain).

    923 294 813
    923 294813
    isg(arroba)usal(.)es

    Laboratorio 13, Instituto de Biologia Molecular y Celular del Cancer (IBMCC), CSIC/Universidad de Salamanca, Campus Unamuno s/n, 37007-Salamanca, (Spain).


    Biography

    Isidro Sánchez-García’s biographical sketch

    Isidro Sánchez-García is a Senior Staff Scientist at the Instituto de Biologia Molecular y Celular del Cancer (IBMCC) of the Spanish National Research Council (CSIC). He learnt and practiced Medicine before completing his Ph.D. at University of Salamanca. Isidro was a postdoctoral fellow for five years at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge (UK) before appointment to his current position in 1997.

    My research is focused on attaining a better understanding of the initiation, maintenance, and progression of leukemia, toward improving current treatment and/or prevention strategies. In this effort, I employ tools from functional genomics, computational biology, molecular genetics, and mouse models.

    I hope to apply this knowledge to change the way we approach leukemia, from diagnosis and treatment to prevention first.

    This work has allowed to establish both a pioneer relationship between stem cells and cancer and a causal link between infection and leukemia. The novel scientific achievements and ideas have not only resulted in high quality publications during his career but also they have crystallized into the first European patent granted in the field of Leukemia/Cancer Stem Cells.

    This work has been awarded by the International Carreras Foundation (http://www.carrerasfoundation.org/fellow_bio.htm), and by the Eurosystem prize in 2010.

    His research group hopes this investigation will result not only in new concepts in cancer biology and development, but also it  will provide the basis for the development of both a new strategy in cancer therapy and new methods for assessing treatment efficacy.

    Isidro

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