Mariana Pacheco‐Blanco

ORCID: 0000-0003-2930-342X
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About
Contact & Profiles
Research Areas
  • Cancer Mechanisms and Therapy
  • Lymphoma Diagnosis and Treatment
  • Synthesis and Biological Evaluation
  • Ubiquitin and proteasome pathways
  • Synthesis and biological activity
  • Chronic Lymphocytic Leukemia Research
  • Cell Adhesion Molecules Research
  • CAR-T cell therapy research
  • Peptidase Inhibition and Analysis
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • T-cell and Retrovirus Studies
  • PI3K/AKT/mTOR signaling in cancer
  • Immune Response and Inflammation
  • Single-cell and spatial transcriptomics
  • Cancer-related gene regulation
  • Advanced Biosensing Techniques and Applications
  • TGF-β signaling in diseases
  • Multiple Myeloma Research and Treatments
  • Immune cells in cancer
  • Erythrocyte Function and Pathophysiology
  • Advanced Fluorescence Microscopy Techniques
  • S100 Proteins and Annexins
  • Toxin Mechanisms and Immunotoxins

Charles University
2019-2024

The University of Texas MD Anderson Cancer Center
2024

Max Planck Institute for Molecular Biomedicine
2017-2019

Instituto Politécnico Nacional
2016

Center for Research and Advanced Studies of the National Polytechnic Institute
2016

Abstract Purpose: Mantle cell lymphoma (MCL) is an aggressive subtype of B-cell non-Hodgkin lymphomas characterized by (over)expression BCL2. A BCL2-targeting drug, venetoclax, has promising anticancer activity in MCL. We analyzed molecular mechanisms venetoclax resistance MCL cells and tested strategies to overcome it. Experimental Design: confirmed key roles proapoptotic proteins BIM NOXA mediating venetoclax-induced death Both are, however, differentially expressed lines compared with...

10.1158/1078-0432.ccr-18-3275 article EN Clinical Cancer Research 2019-04-19

Abstract Human CD14++CD16− and CD14+/loCD16+ monocyte subsets comprise 85 15% of blood monocytes, respectively, are thought to represent distinct stages in the differentiation pathway. However, fates both along macrophage (Mϕ) lineage have not yet been elucidated. We now evaluated potential CD14++ CD16− CD16+ monocytes differentiate be primed toward pro- or anti-inflammatory Mϕs upon culture with GM-CSF M-CSF, respectively (subsequently referred as GM14, M14, GM16, M16). Whereas GM16 GM14...

10.4049/jimmunol.1501177 article EN The Journal of Immunology 2016-01-05

Abstract The family of PIM serine/threonine kinases includes three highly conserved oncogenes, PIM1, PIM2, and PIM3, which regulate multiple prosurvival pathways cooperate with other oncogenes such as MYC. Recent genomic CRISPR-Cas9 screens further highlighted oncogenic functions PIMs in diffuse large B-cell lymphoma (DLBCL) cells, justifying the development small-molecule inhibitors therapeutic targeting lymphomas. However, detailed consequences inhibition DLBCL remain undefined. Using...

10.1158/0008-5472.can-21-1023 article EN Cancer Research 2021-10-08

Assays based on Förster resonance energy transfer (FRET) can be used to study many processes in cell biology. Although this is most often done with microscopy for fluorescence detection, we report two ways measure FRET living cells by flow cytometry. Using a conventional cytometer and the "3-cube method" intensity-based calculation of efficiency, measured enzymatic activity specific kinases expressing genetically-encoded reporter. For both AKT protein kinase A, method time-course,...

10.1002/cyto.a.24472 article EN Cytometry Part A 2021-06-15

Arrest of rapidly flowing neutrophils in venules relies on capturing through selectins and chemokine-induced integrin activation. Despite a long-established concept, we show here that gene inactivation activating paired immunoglobulin-like receptor (PILR)-β1 nearly halved the efficiency neutrophil arrest mouse cremaster muscle. We found this binds to CD99, an interaction which flow-induced shear forces boosts β2-integrin-activation, leading attachment endothelium. Upon arrest, binding...

10.7554/elife.47642 article EN cc-by eLife 2019-08-06

<title>Abstract</title> The phosphatidylinositol 3‑kinase/protein kinase B (PI3K/AKT) signaling pathway is critically active in many cell types, both normal and neoplastic. Many small-molecule inhibitors targeting different levels of the PI3K/AKT have been developed for cancer therapy, but their efficacy reduced by compensatory re-activation mechanisms, tolerability side effects attributable to “on-target, off-tumor” inhibition. We studied this problem using lines representing diffuse large...

10.21203/rs.3.rs-4646815/v1 preprint EN cc-by Research Square (Research Square) 2024-09-02

&lt;p&gt;Supplemental Figure 1. Next-generation sequencing of PDXs and primary MCL cells Supplemental 2. IHC analysis samples murine xenografts 3. Array comparative genomic hybridization 24 4. Sensitivity HBL2 MAVER-1 resistant to venetoclax BCL-XL inhibitors WEHI-539 A1155463 Table Complete list protein coding variants FISH analyses the established Baseline characteristics patients 5. Tumor spleen weights at end in vivo experiments&lt;/p&gt;

10.1158/1078-0432.22471799.v1 preprint EN cc-by 2023-03-31

&lt;div&gt;AbstractPurpose:&lt;p&gt;Mantle cell lymphoma (MCL) is an aggressive subtype of B-cell non-Hodgkin lymphomas characterized by (over)expression BCL2. A BCL2-targeting drug, venetoclax, has promising anticancer activity in MCL. We analyzed molecular mechanisms venetoclax resistance MCL cells and tested strategies to overcome it.&lt;/p&gt;Experimental Design:&lt;p&gt;We confirmed key roles proapoptotic proteins BIM NOXA mediating venetoclax-induced death Both are, however,...

10.1158/1078-0432.c.6528017 preprint EN 2023-03-31

&lt;div&gt;AbstractPurpose:&lt;p&gt;Mantle cell lymphoma (MCL) is an aggressive subtype of B-cell non-Hodgkin lymphomas characterized by (over)expression BCL2. A BCL2-targeting drug, venetoclax, has promising anticancer activity in MCL. We analyzed molecular mechanisms venetoclax resistance MCL cells and tested strategies to overcome it.&lt;/p&gt;Experimental Design:&lt;p&gt;We confirmed key roles proapoptotic proteins BIM NOXA mediating venetoclax-induced death Both are, however,...

10.1158/1078-0432.c.6528017.v1 preprint EN 2023-03-31

&lt;p&gt;Supplemental Figure 1. Next-generation sequencing of PDXs and primary MCL cells Supplemental 2. IHC analysis samples murine xenografts 3. Array comparative genomic hybridization 24 4. Sensitivity HBL2 MAVER-1 resistant to venetoclax BCL-XL inhibitors WEHI-539 A1155463 Table Complete list protein coding variants FISH analyses the established Baseline characteristics patients 5. Tumor spleen weights at end in vivo experiments&lt;/p&gt;

10.1158/1078-0432.22471799 preprint EN cc-by 2023-03-31

&lt;div&gt;Abstract&lt;p&gt;The family of PIM serine/threonine kinases includes three highly conserved oncogenes, &lt;i&gt;PIM1, PIM2,&lt;/i&gt; and &lt;i&gt;PIM3&lt;/i&gt;, which regulate multiple prosurvival pathways cooperate with other oncogenes such as &lt;i&gt;MYC&lt;/i&gt;. Recent genomic CRISPR-Cas9 screens further highlighted oncogenic functions PIMs in diffuse large B-cell lymphoma (DLBCL) cells, justifying the development small-molecule inhibitors therapeutic targeting lymphomas....

10.1158/0008-5472.c.6513748.v1 preprint EN 2023-03-31

&lt;div&gt;Abstract&lt;p&gt;The family of PIM serine/threonine kinases includes three highly conserved oncogenes, &lt;i&gt;PIM1, PIM2,&lt;/i&gt; and &lt;i&gt;PIM3&lt;/i&gt;, which regulate multiple prosurvival pathways cooperate with other oncogenes such as &lt;i&gt;MYC&lt;/i&gt;. Recent genomic CRISPR-Cas9 screens further highlighted oncogenic functions PIMs in diffuse large B-cell lymphoma (DLBCL) cells, justifying the development small-molecule inhibitors therapeutic targeting lymphomas....

10.1158/0008-5472.c.6513748 preprint EN 2023-03-31
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