Fabrício G. Sousa

ORCID: 0000-0003-0444-754X
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About
Contact & Profiles
Research Areas
  • Cancer Genomics and Diagnostics
  • Estrogen and related hormone effects
  • Genomics and Chromatin Dynamics
  • PARP inhibition in cancer therapy
  • DNA Repair Mechanisms
  • Cancer therapeutics and mechanisms
  • Chromatin Remodeling and Cancer
  • Epigenetics and DNA Methylation
  • Bioinformatics and Genomic Networks
  • Protein Degradation and Inhibitors
  • RNA modifications and cancer
  • Cell death mechanisms and regulation
  • Colorectal Cancer Treatments and Studies
  • Signaling Pathways in Disease
  • Advanced Breast Cancer Therapies
  • Gene expression and cancer classification
  • Cardiac tumors and thrombi
  • Microbial Natural Products and Biosynthesis
  • Semiconductor materials and devices
  • Chemical Reactions and Isotopes
  • Advancements in Semiconductor Devices and Circuit Design
  • RNA Research and Splicing
  • HER2/EGFR in Cancer Research
  • Genetic factors in colorectal cancer
  • Caveolin-1 and cellular processes

Universidade Federal de Mato Grosso do Sul
2014-2018

Universidade Federal de Mato Grosso
2018

Center for Cancer Research
2014-2016

National Cancer Institute
2014-2016

National Institutes of Health
2014

Universidade Federal do Rio Grande do Sul
2008-2013

Centre de Recherche Saint-Antoine
2012

Inserm
2012

Sorbonne Université
2012

Community University of Chapecó Region - Unochapecó
2007

CellMinerCDB provides a web-based resource (https://discover.nci.nih.gov/cellminercdb/) for integrating multiple forms of pharmacological and genomic analyses, unifying the richest cancer cell line datasets (the NCI-60, NCI-SCLC, Sanger/MGH GDSC, Broad CCLE/CTRP). enables data queries genomics gene regulatory network exploration pharmacogenomic determinants drug signatures. It leverages overlaps lines drugs across databases to examine reproducibility expand pathway analyses. We illustrate...

10.1016/j.isci.2018.11.029 article EN cc-by-nc-nd iScience 2018-12-01

SLFN11 was identified as a critical determinant of response to DNA-targeted therapies by analyzing gene expression and drug sensitivity NCI-60 CCLE datasets. However, how is regulated in cancer cells remained unknown. Ewing sarcoma, which characterized the chimeric transcription factor EWS-FLI1, has notably high expression, leading us investigate whether EWS-FLI1 drives role sarcoma cells.Binding sites on promoter were analyzed chromatin immunoprecipitation sequencing promoter-luciferase...

10.1158/1078-0432.ccr-14-2112 article EN Clinical Cancer Research 2015-03-17

Abstract 5‐Fluorouracil (5‐FU) is an antineoplasic drug widely used to treat cancer. Its cytotoxic effect has been principally ascribed the misincorporation of fluoronucleotides into DNA and RNA during their synthesis, inhibition thymidylate synthase (TS) by FdUMP (one 5‐FU active metabolites), which leads nucleotide pool imbalance. In present study, we compared ability induce apoptosis influence cell cycle progression in human colon SW620 adenocarcinoma cells regards genotoxic clastogenic...

10.1002/jat.1411 article EN Journal of Applied Toxicology 2008-12-29

The rcellminer R package provides a wide range of functionality to help users access and explore molecular profiling drug response data for the NCI-60. enables flexible programmatic CellMiner's unparalleled breadth NCI-60 data, including gene protein expression, copy number, whole exome mutations, as well activity ∼21K compounds, with information on their structure, mechanism action repeat screens. Functions are available easily visualize compound structures, patterns feature profiles....

10.1093/bioinformatics/btv701 article EN public-domain Bioinformatics 2015-12-03

Exome sequencing provides unprecedented insights into cancer biology and pharmacological response. Here we assess these two parameters for the NCI-60, which is among richest genomic publicly available cell line databases. Homozygous genetic variants that putatively affect protein function were identified in 1,199 genes (approximately 6% of all genes). Variants are either enriched or depleted compared to non-cancerous genomes, thus may be influential progression differential drug response...

10.1371/journal.pone.0101670 article EN cc-by PLoS ONE 2014-07-17

The limited capacity to predict a patient's response distinct chemotherapeutic agents is major hurdle in cancer management. efficiency of large fraction current therapeutics (radio- and chemotherapies) influenced by chromatin structure. Reciprocally, alterations organization may affect resistance mechanisms. Here, we explore how the misexpression regulators-factors involved establishment maintenance functional domains-can inform about extent docetaxel response. We exploit Affymetrix...

10.1158/1535-7163.mct-15-1008 article EN Molecular Cancer Therapeutics 2016-05-17

Abstract The essential oil composition obtained from the leaves of Casearia sylvestris has been investigated by GC and GC/MS. Thirty-seven compounds were identified in oil. major constituents which β-caryophyllene (27.5%) bicyclogermacrene (24.2%). clastogenic anticlastogenic effect was tested chromosome aberration cells tissue hepatoma Rattus novergicus. three different concentrations C. showed effects. However, tests anticlastogenicity, same protective activity when associated with ethyl...

10.1080/10412905.2007.9699309 article EN Journal of Essential Oil Research 2007-07-01

Chromatin is thought to modulate access of repair proteins DNA lesions, and may be altered by chromatin remodelers facilitate repair.We investigated the participation in 5-fluorouracil (5-FU) cytotoxicity Saccharomyces cerevisiae.5-FU an antineoplastic drug commonly used clinical settings.Among several strains tested, only those ©FUNPEC-RP www.funpecrp.com.br

10.4238/2013.april.26.6 article EN Genetics and Molecular Research 2013-01-01

Abstract As precision medicine demands molecular determinants of drug response, CellMinerCDB provides ( https://discover.nci.nih.gov/cellminercdb/ ) a web-based portal for multiple forms pharmacological, molecular, and genomic analyses, unifying the richest cancer cell line datasets (NCI-60, NCI-SCLC, Sanger/MGH GDSC, Broad CCLE/CTRP). enables pharmacological data queries identifying pharmacogenomic determinants, signatures, gene regulatory networks researchers without requiring specialized...

10.1101/292904 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-04-02

Abstract The limited capacity to predict the response of a given patient cancer therapy is major hurdle in management. To date, many standard-of-care chemotherapy agents act by directly binding or modifying DNA indirectly during processes that rely on chromatin architecture, as exemplified with docetaxel. Therefore, alterations organization may impact resistance mechanisms for these drugs. Here, we explore mis-regulation regulators—factors involved establishment and maintenance functional...

10.1158/1538-7445.am2016-lb-129 article EN Cancer Research 2016-07-15

<p>Supplementary figure 1. The protein levels of SLFN11 in 25 EWS-FLI1-expressing cells (black) and 4 EWS-ERG-expressing (red) were detected by Western blotting using antibodies against (98 kDa) actin (42 kDa, loading control). relative each cell line normalized to the SLFN11/actin ratio TC-106 was set as 1.</p>

10.1158/1078-0432.22457172 preprint EN cc-by 2023-03-31

<p>Supplementary figure 1. The protein levels of SLFN11 in 25 EWS-FLI1-expressing cells (black) and 4 EWS-ERG-expressing (red) were detected by Western blotting using antibodies against (98 kDa) actin (42 kDa, loading control). relative each cell line normalized to the SLFN11/actin ratio TC-106 was set as 1.</p>

10.1158/1078-0432.22457172.v1 preprint EN cc-by 2023-03-31

<p>Supplementary figure 2. Scatterplots showing correlations between FLI1 expression (x axis, Log2 normalized intensity) and ETS1 (y in breast prostate cancers. n, number of samples; r, correlation coefficient.</p>

10.1158/1078-0432.22457169.v1 preprint EN cc-by 2023-03-31

<div>Abstract<p><b>Purpose:</b> SLFN11 was identified as a critical determinant of response to DNA-targeted therapies by analyzing gene expression and drug sensitivity NCI-60 CCLE datasets. However, how <i>SLFN11</i> is regulated in cancer cells remained unknown. Ewing sarcoma, which characterized the chimeric transcription factor EWS-FLI1, has notably high expression, leading us investigate whether EWS-FLI1 drives role sarcoma...

10.1158/1078-0432.c.6523521.v1 preprint EN 2023-03-31

<div>Abstract<p><b>Purpose:</b> SLFN11 was identified as a critical determinant of response to DNA-targeted therapies by analyzing gene expression and drug sensitivity NCI-60 CCLE datasets. However, how <i>SLFN11</i> is regulated in cancer cells remained unknown. Ewing sarcoma, which characterized the chimeric transcription factor EWS-FLI1, has notably high expression, leading us investigate whether EWS-FLI1 drives role sarcoma...

10.1158/1078-0432.c.6523521 preprint EN 2023-03-31

<p>Supplementary figure 2. Scatterplots showing correlations between FLI1 expression (x axis, Log2 normalized intensity) and ETS1 (y in breast prostate cancers. n, number of samples; r, correlation coefficient.</p>

10.1158/1078-0432.22457169 preprint EN cc-by 2023-03-31
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