Diego Serrano
A5068305884- Brain Metastases and Treatment
- Cancer Immunotherapy and Biomarkers
- PI3K/AKT/mTOR signaling in cancer
- Glioma Diagnosis and Treatment
- Mast cells and histamine
- Lung Cancer Research Studies
- RNA modifications and cancer
- Cancer Cells and Metastasis
- Immune cells in cancer
- Prostate Cancer Treatment and Research
- Immunotherapy and Immune Responses
- Cancer, Hypoxia, and Metabolism
- Lung Cancer Treatments and Mutations
- Adenosine and Purinergic Signaling
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- CAR-T cell therapy research
- Cancer Genomics and Diagnostics
- DNA Repair Mechanisms
- Nanoplatforms for cancer theranostics
- Telomeres, Telomerase, and Senescence
- Ferroptosis and cancer prognosis
- Microtubule and mitosis dynamics
- Epigenetics and DNA Methylation
- Radiomics and Machine Learning in Medical Imaging
- Genomics and Chromatin Dynamics
Universidad de Navarra
2009-2025
Centro de Investigación Biomédica en Red de Cáncer
2020-2024
Clinica Universidad de Navarra
2024
Instituto de Salud Carlos III
2023
Navarre Institute of Health Research
2021-2022
University of Ottawa
2020
Institute for Research in Immunology and Cancer
2016
Université de Montréal
2014-2016
In-Q-Tel
2012
University of Buenos Aires
2002
Background Tumor-associated macrophages (TAMs) play a key immunosuppressive role that limits the ability of immune system to fight cancer and hinder antitumoral efficacy most treatments currently applied in clinic. Previous studies have evaluated response triggered by (TLR) agonists, such as poly(I:C), imiquimod (R837) or resiquimod (R848) monotherapies; however, their combination for treatment has not been explored. This study investigates macrophage reprogramming poly(I:C) combined with...
Immunotherapy resistance in non-small cell lung cancer (NSCLC) may be mediated by an immunosuppressive microenvironment, which can shaped the mutational landscape of tumor. Here, we observed genetic alterations PTEN/PI3K/AKT/mTOR pathway and/or loss PTEN expression >25% patients with NSCLC, higher frequency squamous carcinomas (LUSC). Patients PTEN-low tumors had levels PD-L1 and PD-L2 showed worse progression-free survival when treated immunotherapy. Development a Pten-null LUSC mouse model...
Mortality rates for advanced lung cancer have not declined decades, even with the implementation of novel chemotherapeutic regimens or use tyrosine kinase inhibitors. Cancer Stem Cells (CSCs) are thought to be responsible resistance chemo/radiotherapy. Therefore, targeting CSCs compounds may an effective approach reduce tumor growth and metastasis. We isolated characterized from non-small cell (NSCLC) lines measured their telomerase activity, telomere length, sensitivity inhibitor MST312.The...
The use of immune-checkpoint inhibitors has drastically improved the management patients with non-small cell lung cancer (NSCLC), but innate and acquired resistances are hurdles needed to be solved. Immunomodulatory drugs that can reinvigorate immune cytotoxic activity, in combination antiprogrammed death 1 (PD-1) antibody, a great promise overcome resistance. We evaluated impact SRC family kinases (SFKs) on NSCLC prognosis, immunomodulatory effect SFK inhibitor dasatinib, anti-PD-1,...
Background One of the main difficulties adoptive cell therapies with chimeric antigen receptor (CAR)-T cells in solid tumors is identification specific target antigens. The tumor microenvironment can present suitable antigens for CAR design, even though they are not expressed by cells. We have generated a splice variant extra domain A (EDA) fibronectin, which highly stroma many types but healthy tissues. Methods EDA expression was explored RNA-seq data from different human and...
Abstract Immunotherapies against brain metastases have shown clinical benefits when applied to asymptomatic patients, but they are largely ineffective in symptomatic cases for unknown reasons. Here, we dissect the heterogeneity metastasis-associated astrocytes using single-cell RNA sequencing and report a population that blocks antitumoral activity of infiltrating T cells. This protumoral is mediated by secretion tissue inhibitor metalloproteinase-1 (TIMP1) from cluster pSTAT3+ acts on CD63+...
<p>Local immunosuppression could explain immunotherapy failure in high immune cluster symptomatic brain metastasis. Supplementary Figure 4 shows additional data corresponding to 3.</p>
<p>Patient-derived organotypic cultures as a surrogate to assess the potential of targeting local immunosuppression in brain metastasis. Supplementary Figure 9 shows additional data corresponding 7.</p>
<p>DEG cluster 3 brain metastasis-associated astrocytes. Differentially expressed genes (DEGs) found in number of metastasis associated-astrocytes. Significantly deregulated are highlighted. Red indicates upregulation and green downregulation respect to tumor free condition. The table contains information corresponding Figure 1D.</p>
<p>Antibodies used for multiplex immunohistochemistry. Detailed information of antibodies multiplex.</p>
<p>GSEA_comparision between cluster 3 and 5 of brain metastasis-associated astrocytes in human metastasis samples. Gene set enrichment analysis (GSEA) upregulated downregulated signatures comparing number associated-astrocytes. The table contains information corresponding to Figure 1I.</p>
<p>Overall survival according to TIMP1 in the CSF. Overall of brain metastasis patients with different primary tumors their levels cerebrospinal fluid (CSF). The table contains information corresponding Supplementary Figure 9B.</p>
<p>GSEA_comparision between STAT3+ clusters of brain metastasis-associated astrocytes in human metastasis samples. Gene set enrichment analysis (GSEA) upregulated and downregulated signatures comparing each cluster the other astrocytes. The table contains information corresponding to Figure 1F-I.</p>
<p>Antibodies used for flow cytometry analysis. Detailed information of antibodies cytometry.</p>
<p>GSEA_comparision between cluster 4 and 5 of brain metastasis-associated astrocytes in human metastasis samples. Gene set enrichment analysis (GSEA) upregulated downregulated signatures comparing number associated-astrocytes. The table contains information corresponding to Figure 1I.</p>
<p>Human brain metastases evaluated for pERK1/2 regarding their immune cluster. Information multiplex of cells in human metastasis samples used assessing status CD8+ T cells. The table contains information corresponding to Figure 6M.</p>
<p>Antibodies used for immunohistochemistry. Detailed information of antibodies immunohistochemistry stainings.</p>
<p>TIMP1 binding to CD63 modulates kinase signaling in CD8+ T cells. Supplementary Figure 7 shows additional data corresponding 6.</p>
<p>RENACER immune cluster evaluation. Immune and gene expression of markers in the RENACER cohort human brain metastasis samples. The table contains information corresponding to Supplementary Figure 4C-D.</p>
<p>Astrocyte signatures. Signatures used for astrocytes annotation in the single-cell RNA sequencing of brain metastasis-associated microenvironment using B16/F10-BrM model. The table contains information corresponding to Figure 1B and Supplementary 1C.</p>