Montse Sánchez‐Céspedes

ORCID: 0000-0002-6045-5627
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About
Contact & Profiles
Research Areas
  • RNA modifications and cancer
  • Epigenetics and DNA Methylation
  • Lung Cancer Treatments and Mutations
  • Chromatin Remodeling and Cancer
  • Cancer Genomics and Diagnostics
  • Cancer-related gene regulation
  • Cancer-related Molecular Pathways
  • Cancer Mechanisms and Therapy
  • Genetic factors in colorectal cancer
  • Cancer Immunotherapy and Biomarkers
  • Cancer Research and Treatments
  • Protein Degradation and Inhibitors
  • Peptidase Inhibition and Analysis
  • Lung Cancer Research Studies
  • MicroRNA in disease regulation
  • Ferroptosis and cancer prognosis
  • Liver physiology and pathology
  • ATP Synthase and ATPases Research
  • 14-3-3 protein interactions
  • Cancer-related molecular mechanisms research
  • Mechanisms of cancer metastasis
  • Immunotherapy and Immune Responses
  • PI3K/AKT/mTOR signaling in cancer
  • Genomics and Chromatin Dynamics
  • Neuroendocrine Tumor Research Advances

Josep Carreras Leukaemia Research Institute
2020-2024

Fundación Josep Carreras Contra la Leucemia
2023

Institut d'Investigació Biomédica de Bellvitge
2011-2020

Cancer Genetics (United States)
2020

Institut Català d'Oncologia
2010-2019

Ajuntament de L’Hospitalet
2011-2019

Bellvitge University Hospital
2019

Universidad de Sevilla
2013

Hospital Universitario Virgen del Rocío
2013

Instituto de Biomedicina de Sevilla
2013

10.1038/nature14664 article EN Nature 2015-07-10

MicroRNAs (miRNAs) are small, noncoding RNAs that can contribute to cancer development and progression by acting as oncogenes or tumor suppressor genes. Recent studies have also linked different sets of miRNAs metastasis through either the promotion suppression this malignant process. Interestingly, epigenetic silencing with features CpG island hypermethylation is emerging a common hallmark human tumors. Thus, we wondered whether there was miRNA profile characteristic metastasis. We used...

10.1073/pnas.0803055105 article EN Proceedings of the National Academy of Sciences 2008-09-04

The mechanisms underlying microRNA (miRNA) disruption in human disease are poorly understood. In cancer cells, the transcriptional silencing of tumor suppressor genes by CpG island promoter hypermethylation has emerged as a common hallmark. We wondered if same epigenetic can "hit" miRNAs transformed cells. To address this issue, we have used cells genetically deficient for DNA methyltransferase enzymes combination with miRNA expression profiling. observed that hypomethylation induces release...

10.1158/0008-5472.can-06-4218 article EN Cancer Research 2007-02-15

BACKGROUND The majority of lung carcinoma cases occur in current or former smokers. K-ras gene mutations are common adenocarcinoma and have been associated with cigarette smoking, asbestos exposure, female gender. METHODS In the study, authors examined contribution smoking to patients primary adenocarcinoma. Smoking histories were obtained from 106 prospectively enrolled lung. RESULTS detected tumor using an allele-specific ligation assay. Ninety-two (87%) Nonsmokers this more likely be...

10.1002/1097-0142(20010915)92:6<1525::aid-cncr1478>3.0.co;2-h article EN Cancer 2001-09-15

Most of the studies characterizing DNA methylation patterns have been restricted to particular genomic loci in a limited number human samples and pathological conditions. Herein, we present compromise between an extremely comprehensive study sample population with intermediate level resolution CpGs at level. We obtained fingerprint 1628 which interrogated 1505 CpG sites. The revealed show this epigenetic mark be critical tissue-type definition stemness, particularly around transcription...

10.1101/gr.119867.110 article EN Genome Research 2011-05-25

Non-small-cell lung cancer (NSCLC) is a tumor in which only small improvements clinical outcome have been achieved. The issue critical for stage I patients whom there are no available biomarkers that indicate high-risk should receive adjuvant chemotherapy. We aimed to find DNA methylation markers could be helpful this regard.A microarray analyzes 450,000 CpG sites was used study tumoral obtained from 444 with NSCLC included 237 tumors. prognostic were validated by single-methylation...

10.1200/jco.2012.48.5516 article EN Journal of Clinical Oncology 2013-10-01

Werner syndrome (WS) is an inherited disorder characterized by premature onset of aging, genomic instability, and increased cancer incidence. The disease caused loss function mutations the WRN gene, a RecQ family member with both helicase exonuclease activities. However, despite its putative tumor-suppressor function, little known about contribution to human sporadic malignancies. Here, we report that abrogated in cells transcriptional silencing associated CpG island-promoter...

10.1073/pnas.0600645103 article EN Proceedings of the National Academy of Sciences 2006-05-25

Abstract Purpose: The DNA repair enzyme O6-methylguanine methyltransferase (MGMT) inhibits the killing of tumor cells by alkylating agents, and its loss in cancer is associated with hypermethylation MGMT CpG island. Thus, methylation has been correlated clinical response to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) primary gliomas. Here, we investigate whether presence gliomas also a good predictor another emergent agent, temozolomide. Experimental Design: Using methylation-specific PCR...

10.1158/1078-0432.ccr-04-0392 article EN Clinical Cancer Research 2004-08-01

Components of the SWI/SNF chromatin-remodeling complex, such as INI1, are inactivated in human cancer and, thus, act tumor suppressors. Here we screened for mutations entire coding sequence BRG1 (SMARCA4), which encodes ATPase 59 lung cell lines most common histopathological types. Mutations were detected 24% lines, many them cells commonly used research. All homozygous and predicted truncated proteins. The alterations significantly more frequent non-small-cell (NSCLC) type (13/37, 35%)...

10.1002/humu.20730 article EN Human Mutation 2008-04-03

Our knowledge of small cell lung cancer (SCLC) genetics is still very limited, amplification L-MYC, N-MYC, and C-MYC being some the well-established gene alterations. Here, we report our discovery tumor-specific inactivation MYC-associated factor X gene, MAX, in SCLC. MAX mutually exclusive with alterations MYC BRG1, latter coding for an ATPase switch/sucrose nonfermentable (SWI/SNF) complex. We demonstrate that BRG1 regulates expression through direct recruitment to promoter, depletion...

10.1158/2159-8290.cd-13-0799 article EN Cancer Discovery 2013-12-21
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