Isidro Sánchez-Garcı́a

ORCID: 0000-0001-6989-9905
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About
Contact & Profiles
Research Areas
  • Acute Lymphoblastic Leukemia research
  • Chronic Myeloid Leukemia Treatments
  • Acute Myeloid Leukemia Research
  • Cancer Cells and Metastasis
  • Epigenetics and DNA Methylation
  • CAR-T cell therapy research
  • Childhood Cancer Survivors' Quality of Life
  • Pluripotent Stem Cells Research
  • Lymphoma Diagnosis and Treatment
  • Cancer-related gene regulation
  • Chronic Lymphocytic Leukemia Research
  • Protein Degradation and Inhibitors
  • Cancer-related Molecular Pathways
  • Immune Cell Function and Interaction
  • RNA Interference and Gene Delivery
  • Microtubule and mitosis dynamics
  • Sarcoma Diagnosis and Treatment
  • Multiple Myeloma Research and Treatments
  • Cancer Research and Treatments
  • RNA modifications and cancer
  • Cancer Genomics and Diagnostics
  • RNA Research and Splicing
  • Ubiquitin and proteasome pathways
  • RNA and protein synthesis mechanisms
  • DNA Repair Mechanisms

Universidad de Salamanca
2015-2024

Instituto de Investigación Biomédica de Salamanca
2015-2024

Centro de Investigación del Cáncer
2015-2024

Universidad Autónoma de Madrid
2012-2023

Hospital Universitario de La Princesa
2023

Centro de Biología Molecular Severo Ochoa
2012-2023

Consejo Superior de Investigaciones Científicas
2007-2023

St. Jude Children's Research Hospital
2022

Block Center
2015

Instituto de Biologia Molecular e Celular
2007-2014

Significance Follicular lymphoma (FL) is a disease characterized by multiple relapses that are linked common progenitor bearing only subset of the mutations found within tumor presents clinically. Inability to cure this may therefore be failure current therapies clear these early tumor-propagating clones. Here we further define genetic hallmarks and model steps in evolution through phylogenetic analysis serial biopsies. This identified CREBBP as events genome enriched cell progenitors...

10.1073/pnas.1501199112 article EN Proceedings of the National Academy of Sciences 2015-02-23

Abstract Background Tumor cell invasion into adjacent normal brain is a mesenchymal feature of GBM and major factor contributing to their dismal outcomes. Therefore, better understandings mechanisms that promote change in are great clinical importance address invasion. We previously showed the bHLH transcription TWIST1 which orchestrates carcinoma metastasis through an epithelial transition (EMT) upregulated promotes SF767 line vitro . Results To further define functions we tested impact...

10.1186/1476-4598-9-194 article EN cc-by Molecular Cancer 2010-07-20

Waardenburg syndrome (WS; deafness with pigmentary abnormalities) is a congenital disorder caused by defective function of the embryonic neural crest. Depending on additional symptoms, WS classified into four types: WS1, WS2, WS3 and WS4. WS1 are mutations in PAX3, whereas WS2 heterogenous, being microphthalmia (MITF) gene some but not all affected families. The identification Slugh, zinc-finger transcription factor expressed migratory crest cells, as responsible for disturbances mice...

10.1093/hmg/11.25.3231 article EN Human Molecular Genetics 2002-11-20

BCR-ABL is a chimeric oncogene generated by translocation of sequences from the c-abl protein-tyrosine kinase gene on chromosome 9 into BCR 22. Alternative proteins, p210BCR-ABL and p190BCR-ABL, are produced that characteristic chronic myelogenous leukemia acute lymphoblastic leukemia, respectively. Their role in etiology human remains to be defined. Transformed murine hematopoietic cells can used as model function since these made growth factor independent tumorigenic action oncogene. We...

10.1073/pnas.92.12.5287 article EN Proceedings of the National Academy of Sciences 1995-06-06

Significance K-RAS oncogene-driven lung adenocarcinomas is one of the most malignant human tumors for which there are no efficacious therapeutic strategies. Here, we have used a mouse tumor model that closely recapitulates this disease to illustrate adult cells uniquely sensitive transformation by oncogene. Monitoring at single-cell level revealed they respond differently K-Ras oncogenic signals. Whereas –expressing Clara required an inflammatory response yield hyperplasias and adenomas,...

10.1073/pnas.1320383110 article EN Proceedings of the National Academy of Sciences 2013-12-23

Abstract Earlier in the past century, infections were regarded as most likely cause of childhood B-cell precursor acute lymphoblastic leukemia (pB-ALL). However, there is a lack relevant biologic evidence supporting this hypothesis. We present vivo genetic mechanistically connecting inherited susceptibility to pB-ALL and postnatal by showing that was initiated Pax5 heterozygous mice only when they exposed common pathogens. Strikingly, these murine pB-ALLs closely resemble human disease....

10.1158/2159-8290.cd-15-0892 article EN Cancer Discovery 2015-09-26

A translocation involving human chromosome 10, band q24, in a subset of T-cell acute leukemias disrupts region surrounding the putative oncogene HOX11, which encodes protein with homeodomain. The HOX11 binds to specific DNA sequence, it localizes cell nucleus, and transactivates transcription reporter gene linked cis-regulatory element, suggesting that functions vivo as positive activator. PCR analysis shows homeodomain is member distinct class homeodomains, representatives occur murine...

10.1073/pnas.90.10.4431 article EN Proceedings of the National Academy of Sciences 1993-05-15

Abstract ETV6-RUNX1 is associated with the most common subtype of childhood leukemia. As few carriers develop precursor B-cell acute lymphocytic leukemia (pB-ALL), underlying genetic basis for development full-blown remains to be identified, but appearance cases in time-space clusters keeps infection as a potential causal factor. Here, we present vivo evidence mechanistically connecting preleukemic expression hematopoetic stem cells/precursor cells (HSC/PC) and postnatal infections...

10.1158/0008-5472.can-17-0701 article EN Cancer Research 2017-06-20
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