Gustavo de Campos Molina

AC Camargo Hospital

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Dirce Maria Carraro

AC Camargo Hospital

Elisa Napolitano Ferreira

Fleury S.A. (Brazil)

Helena Brentani

Universidade de São Paulo

Emmanuel Dias‐Neto

AC Camargo Hospital

Antônio Hugo José Fróes Marques Campos

D’Or Institute for Research and Education

Diana Noronha Nunes

AC Camargo Hospital

Wadih Arap

Rutgers, The State University of New Jersey

Renata Pasqualini

Rutgers, The State University of New Jersey

Renato Puga

Hospital Israelita Albert Einstein

Anya Rothenbühler

Swiss Federal Institute of Sport Magglingen SFISM

Cooperative Institutions

AC Camargo Hospital

Universidade de São Paulo

Hospital São Paulo

Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo

The University of Texas MD Anderson Cancer Center

Eunice Kennedy Shriver National Institute of Child Health and Human Development

National Institutes of Health

Assistance Publique – Hôpitaux de Paris

Inserm

Universidade Federal de São Paulo

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Correction: Poly (A)⁺Transcriptome Assessment of ERBB2-Induced Alterations in Breast Cell Lines

PLoS ONE (2011)

Dirce Maria Carraro Elisa Napolitano Ferreira Gustavo de Campos Molina Renato Puga Eduardo F. Abrantes

10.1371/annotation/b8888ae6-e402-43af-a425-6fd5e58deef6

Cite

Citations (1)

Poly (A)+ Transcriptome Assessment of ERBB2-Induced Alterations in Breast Cell Lines

PLoS ONE (2011)

Dirce Maria Carraro Elisa Napolitano Ferreira Gustavo de Campos Molina Renato Puga Eduardo F. Abrantes

We report the first quantitative and qualitative analysis of the poly (A)+ transcriptome of two human mammary cell lines, differentially expressing (human epidermal growth factor receptor) an oncogene over-expressed in approximately 25% of human breast tumors. Full-length cDNA populations from the two cell lines were digested enzymatically, individually tagged according to a customized method for library construction, and simultaneously sequenced by the use of the Titanium 454-Roche-platform. Comprehensive bioinformatics analysis followed by experimental validation confirmed novel genes, splicing variants, single nucleotide polymorphisms, and gene fusions indicated by RNA-seq data from both samples. Moreover, comparative analysis showed enrichment in alternative events, especially in the exon usage category, in ERBB2 over-expressing cells, data indicating regulation of alternative splicing mediated by the oncogene. Alterations in expression levels of genes, such as LOX, ATP5L, GALNT3, and MME revealed by large-scale sequencing were confirmed between cell lines as well as in tumor specimens with different ERBB2 backgrounds. This approach was shown to be suitable for structural, quantitative, and qualitative assessment of complex transcriptomes and revealed new events mediated by ERBB2 overexpression, in addition to potential molecular targets for breast cancer that are driven by this oncogene.

10.1371/journal.pone.0021022

Cite

Citations (18)

Linear mRNA amplification approach for RNAseq from limited amount of RNA

Gene (2015)

Elisa Napolitano Ferreira Gustavo de Campos Molina Renato Puga María Aparecida Nagai Antônio Hugo José Fróes Marques Campos

Whole-transcriptome evaluation by next-generation sequencing (NGS) has been widely applied in the investigation of diverse transcriptional scenarios. In many clinical situations, including needle biopsy samples or laser microdissected cells, limited amounts of RNA are usually available for the assessment of the whole transcriptome. Here, we describe an mRNA amplification protocol based on in vitro T7 transcription for transcriptome evaluation by NGS. Initially, we performed RNAseq from two human mammary epithelial cell lines and evaluated several aspects of the transcriptomes generated by linear amplification of Poly (A)(+) mRNA species, including transcript representation, variability and abundance. Our protocol showed to be efficient with respect to full-length transcript coverage and quantitative expression levels. We then evaluated the applicability of using this protocol in a more realistic research scenario, analyzing tumor tissue samples microdissected by laser capture. In order to increase the quantification power of the libraries only the 3' end of transcripts were sequenced. We found highly reproducible RNAseq data among amplified tumor samples, with a median Spearman's correlation of 80%, strongly suggesting that the amplification step and library protocol preparation lead to a consistent transcriptional profile. Altogether, we established a robust protocol for assessing the polyadenylated transcriptome derived from limited amounts of total RNA that is applicable to all NGS platforms.

10.1016/j.gene.2015.03.058

Cite

Citations (4)

Phosphodiesterase 11A (PDE11A) Genetic Variants May Increase Susceptibility to Prostatic Cancer

Molecular Endocrinology (2010)

Fábio R. Faucz Anélia Horvath Anya Rothenbühler Madson Q. Almeida Rossella Libé

Abstract Context: Among the genomic loci harboring potential candidate genes for prostatic cancer (PCa) is the 2q31-39 chromosomal region that harbors the gene encoding phosphodiesterase 11A (PDE11A). In addition, the combined cancer genome expression metaanalysis datasets included PDE11A among the top 1% down-regulated genes in PCa. Objective: In the present study, we screened 50 unrelated PCa patients of Brazilian descent for PDE11A coding defects. Design: The study consisted of sequencing of PDE11A, in vitro functional assays, and immunostaining analysis. Results: We identified eight different sequence alterations in 15 patients (30%): one stop-codon and seven missense mutations. Three of the variants (R202C, Y658C, and E840K) were novel, and the remaining five (Y727C, R804H, R867G, M878V, and R307X) have been associated with predisposition to adrenal or testicular tumors. The overall prevalence of PDE11A-inactivating sequence variants among PCa patients was significantly higher than in 287 healthy controls (0.16 vs. 0.051, respectively, P < 0.001, odds ratio 3.81, 95% confidence interval 1.86–7.81) and the R202C, Y658C, and E840K substitutions were not found in controls. All missense mutations led to decreased PDE11A activity in human embryonic kidney 293 and PC3M cells and immunostaining of PCa samples with sequence changes showed decreased PDE11A protein expression. Conclusion: Our data suggest that, like in the adrenal cortex and the testicular germ cells, PDE11A-inactivating genetic alterations may play a role in susceptibility to PCa.

Immunostaining

10.1210/mend.24.11.9997

Cite

Citations (2)

Phosphodiesterase 11A (PDE11A) Genetic Variants May Increase Susceptibility to Prostatic Cancer

The Journal of Clinical Endocrinology & Metabolism (2010)

Fábio R. Faucz Anélia Horvath Anya Rothenbühler Madson Q. Almeida Rossella Libé

Among the genomic loci harboring potential candidate genes for prostatic cancer (PCa) is the 2q31-33 chromosomal region that harbors the gene encoding phosphodiesterase 11A (PDE11A). In addition, the combined cancer genome expression metaanalysis datasets included PDE11A among the top 1% down-regulated genes in PCa.

Immunostaining

10.1210/jc.2010-1655

Cite

Citations (42)

IDENTIFICAÇÃO DE MARCADORES MOLECULARES DE PROGNÓSTICO PARA ADENOCARCINOMA DE PRÓSTATA UTILIZANDO ABORDAGEM QUANTITATIVA BASEADA EM SEQUÊNCIAS

Gustavo de Campos Molina

Source

Cite

Citations (0)