Adriana Costa Guimarães

Universidade Federal do Pará

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Rommel Mário Rodríguez Burbano

Universidade Federal do Pará

André Salim Khayat

Universidade Federal do Pará

Paulo Pimentel de Assumpção

Universidade Federal do Pará

Marı́lia de Arruda Cardoso Smith

Universidade Federal de São Paulo

Mariana Ferreira Leal

Royal Marsden Hospital

Marcelo de Oliveira Bahia

Universidade Federal do Pará

Danielle Queiroz Calcagno

Universidade Federal do Pará

Aline Damasceno Seabra

Loyola Medicine

Sâmia Demachki

Universidade Federal do Pará

Plínio Cerqueira dos Santos Cardoso

Universidade Federal do Pará

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Universidade Federal do Pará

Universidade Federal de São Paulo

Weatherford College

Universidade de São Paulo

Instituto Evandro Chagas

Secretaria de Estado de Segurança Pública

Universidade Federal do Ceará

Centro de Genética Clínica

Instituto Biológico

Universidade Federal da Paraíba

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Chromosome Instability in Carcinomas

International Journal of Morphology (2006)

Paulo Pimentel de Assumpção Aline Damasceno Seabra Mariana Ferreira Leal Adriana Costa Guimarães Danielle Queiroz Calcagno

In the current carcinogenesis models, the occurrence of increasing mutations and selection mechanisms favoring cell survival and higher proliferation rates are taken into account.Epigenetic mechanisms, among which DNA methylation stands out, also take part in oncogenesis.The characteristic of tumor cells that allows the increase of mutations is named genetic instability, encompassing two mechanisms: microsatellite instability, characterized by nucleotide alterations with errors in the DNA repair systems; and chromosomal instability, represented by aberrations occurring in large chromosome segments.Carcinomas are characterized by complex cytogenetic alterations and large gene amalgamations.Telomeric alterations, inadequately repaired DNA breaks, and deficiencies in the mitotic spindle checking systems are events capable of generating the chromosomal instability and aneuploidy which characterize more aggressive neoplasias.A better understanding of the chromosomal instability mechanisms can show the way towards a clinical utilization of such information, like developing more adequate therapeutic strategies, targeted at specific sites involved in the malignization process.

10.4067/s0717-95022006000400007

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Citations (3)

Low frequency of human papillomavirus detection in prostate tissue from individuals from Northern Brazil

Memórias do Instituto Oswaldo Cruz (2009)

Rodrigo Vellasco Duarte Silvestre Mariana Ferreira Leal Sâmia Demachki Márcia Cristina de Souza Nahum Júlio Guilherme Balieiro Bernardes

The presence of human papillomavirus (HPV) was evaluated in 65 samples of prostate tumours and six samples of prostates with benign prostatic hyperplasia from individuals from Northern Brazil. We used a highly sensitive test, the Linear Array HPV Genotyping Test, to detect 37 high and low-risk HPV types. In this study, only 3% of tumour samples showed HPV infection. Our findings support the conclusion that, despite the high incidence of HPV infection in the geographic regions studied, HPV was not associated with a higher risk of prostate cancer. To our knowledge, this is the first study evaluating the frequency of HPV detection in prostatic tissue of individuals from Brazil.

10.1590/s0074-02762009000400024

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Citations (25)

Quantitative difference of oral pathogen between individuals with gastric cancer and individuals without cancer

Oncotarget (2021)

Gyselle Ribeiro de Carvalho Oliveira Carla de Castro Sant’ Anna Letícia Martins Lamarão Adriana Costa Guimarães Carlos Alberto Machado da Rocha

// Gyselle Ribeiro de Carvalho Oliveira 1 , Carla de Castro Sant' Anna 2 , 3 , Letícia Martins Lamarão 4 , Adriana Costa Guimarães 5 , Carlos Machado da Rocha 5 , Marcelo de Oliveira Bahia 6 , Carolina Rosal de Souza 6 , Danielle Queiroz Calcagno 2 , Paulo Pimentel de Assumpção 2 and Rommel Rodriguez Burbano 2 , 3 , 6 1 School of Dentistry, Federal University of Pará, Belém, Pará, Brazil 2 High Complexity Oncology Unit, Federal University of Pará, Rua dos Mundurucus, Hospital Universitário João de Barros Barreto, 2º piso da UNACOM, Belém, Pará, Brazil 3 Ophir Loyola Hospital, Av. Gov Magalhães Barata, Belem, Pará, Brazil 4 Foundation Center for Hemotherapy and Hematology, Travessa Padre Eutíquio, Belém, Pará, Brazil 5 Federal Institute of Pará, Belém, Pará, Brazil 6 Institute of Biological Sciences, Federal University of Pará, Belém, Pará, Brazil Correspondence to: Carla de Castro Sant' Anna, email: santannacarla@yahoo.com.br Keywords: periodontal disease; microbiome; gastric cancer; oral pathogens Received: December 08, 2020 Accepted: July 13, 2021 Published: August 17, 2021 Copyright: © 2021 Oliveira et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT The loss of teeth and lack of oral hygiene have been associated with the risk of developing gastric cancer (GC) in several populations evidenced in epidemiological studies. In this study, we quantitatively compared the proportion of oral pathogens in individuals with gastric cancer and individuals without cancer in a referral hospital in the city of Belém, Brazil. This study evaluated 192 patients with GC and 192 patients without cancer. Periodontal clinical examination was performed, and all individuals were submitted to the collection of salivary and dental biofilms. When comparing the median periodontal indexes in the gastric and cancer-free groups, it was statistically significant ( p < 0.001) in the gastric cancer group compared to the probing depth of the periodontal pocket. Levels of bacterial DNA were observed in saliva and dental plaque, with a statistically significant difference ( p < 0.001) between individuals with cancer and without neoplasia in all the bacteria surveyed. Significant relationships ( p < 0.001) between biological agents and GC have been found in bacterial species that cause high rates of periodontal pathology and caries. The results suggest a different quantitative association in the presence of oral pathogens between individuals without cancer and patients with GC. As noted, it cannot be said that the bacteria present in the oral cavity increase the risk of gastric cancer or are aggravating factors of the disease. However, it is worth mentioning that, as it is part of the digestive system, the lack of care for the oral cavity can negatively affect the treatment of patients with gastric cancer.

10.18632/oncotarget.28034

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O incrível mundo da fecundação

Adrian José Oliveira dos Reis Fabrielle Barbosa de Araújo Sandra Leticia Silva dos Santos Brenda Stefany dos Santos Braga Maria Luiza Cunha e Souza -Ferreira

10.22533/at.ed.248233008

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C-MYC locus amplification as metastasis predictor in intestinal-type gastric adenocarcinomas: CGH study in Brazil.

PubMed (2006)

Rommel Mário Rodríguez Burbano Paulo Pimentel de Assumpção Mariana Ferreira Leal Danielle Queiroz Calcagno Adriana Costa Guimarães

The genetic events involved in gastric cancer, the third most frequent cancer in the world with a high incidence in Pard State, Brazil, remain largely unknown.Twenty-one primary gastric adenocarcinomas were investigated by comparative genomic hybridization (CGH) and the relationships between genomic abnormalities and histopathological features were evaluated.Eighty-one percent of cases presented DNA copy-number changes. Chromosomal gains were the most frequent finding, losses occurring only in the diffuse type. The main copy-number gains were on chromosome 8, principally on 8q24.1 (8/21 cases), 8p21 (3/21) and 8p23.2-8p12 (2/21). Gain of region 8q24. 1, where C-MYC is located, was the main finding, exclusively in the intestinal type with metastasis.C-MYC locus amplification may be predictor of aggressiveness in intestinal-type gastric cancer, playing an important role in its development and progression. Moreover, other genes on 8q24 should be investigated. Gastric adenocarcinomas of differing histopathological features were associated with distinct genetic alterations, supporting the hypothesis that they evolve through distinct genetic pathways.

Comparative genomic hybridization

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Interrelationships among chromosome aneuploidy, promoter hypermethylation, and protein expression of the CDKN2A gene in individuals from northern Brazil with gastric adenocarcinoma

Cancer Genetics and Cytogenetics (2007)

Adriana Costa Guimarães Eleonidas Moura Lima André Salim Khayat M. Faria Sílvia Helena Barem Rabenhorst

Monosomy

10.1016/j.cancergencyto.2007.07.019

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Citations (11)

MYC insertions in diffuse-type gastric adenocarcinoma.

PubMed (2009)

Danielle Queiroz Calcagno Adriana Costa Guimarães Mariana Ferreira Leal Aline Damasceno Seabra André Salim Khayat

MYC is important in gastric carcinogenesis. A few studies reported MYC translocation or insertion associated with gastric cancer.MYC copy number and its insertion, as well as the chromosomes in which MYC was inserted, were evaluated by fluorescence in situ hybridization assay in interphase and metaphase cells of 12 diffuse-type gastric cancer samples. MYC protein expression was evaluated by immunohistochemistry.The presence of 3 MYC signals was the most frequent alteration. All cases also presented 4 and 5 MYC signals. In all samples, we observed chromosome 8 trisomy with MYC copies and MYC insertion into the chromosomes 2, 7, 14, 17, 18 and 22. All samples presented nucleic and cytoplasmic immunoreactivity.MYC cytoplasmic immunoreactivity can be the result of MYC insertion with the breakpoints within or close to the regions that are able to target the nucleus. MYC insertion and cytoplasmatic immunoreactivity may be a common characteristic of diffuse-type gastric cancer.

Trisomy

Interphase

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Citations (33)

In vitro assessment of anticytotoxic and antigenotoxic effects of CANOVA®

Homeopathy (2016)

Henrique Fonseca Sousa do Nascimento Plínio Cerqueira dos Santos Cardoso Helem Ferreira Ribeiro Tatiane Cristina Mota Lorena Monteiro Gomes

CANOVA(®) (CA) is a homeopathic immunomodulator. It contains several homeopathic medicines prepares according to the Brazilian Pharmacopoeia. CA is indicated in clinical conditions in which the immune system is impaired and against tumors. N-methyl-N-nitrosourea (NMU) is an N-nitroso compound, with genotoxic/mutagenic properties. Although several studies have shown promising results in the use of CA, there are no studies reporting possible antigenotoxic effects.This study evaluated the in vitro antigenotoxic and anticytotoxic effects of CA in human lymphocytes exposed to NMU. Samples of human lymphocytes that were subjected to different concentrations of a mixture containing CA and NMU were used. The genotoxicity/antigenotoxicity of CA was evaluated by the comet assay, anticytotoxicity was assessed by quantification of apoptosis and necrosis using acridine orange/ethidium bromide.CA significantly reduced DNA damage induced by NMU and reduced significantly the frequency of NMU-induced apoptosis after 24 h of treatment.CA has an important cytoprotective effect significantly reducing the DNA damage and apoptosis induced by the carcinogen NMU.

Acridine orange

Comet Assay

Ethidium bromide

10.1016/j.homp.2016.04.003

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Citations (6)

Cytogenetic biomonitoring of inhabitants of a large uranium mineralization area: the municipalities of Monte Alegre, Prainha, and Alenquer, in the State of Pará, Brazil

Cell Biology and Toxicology (2010)

Adriana Costa Guimarães Lusânia Maria Greggi Antunes Helem Ferreira Ribeiro Ândrea Ribeiro‐dos‐Santos Plínio Cerqueira dos Santos Cardoso

Clastogen

10.1007/s10565-010-9152-8

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Citations (18)

High-density array comparative genomic hybridization detects novel copy number alterations in gastric adenocarcinoma.

PubMed (2014)

Aline Damasceno Seabra Taíssa Maíra Thomaz Araújo Fernando Augusto Rodrigues Mello Diego Di Felipe Ávila Alcântara Amanda Paiva De Barros

To investigate frequent quantitative alterations of intestinal-type gastric adenocarcinoma.We analyzed genome-wide DNA copy numbers of 22 samples and using CytoScan® HD Array.We identified 22 gene alterations that to the best of our knowledge have not been described for gastric cancer, including of v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 4 (ERBB4), SRY (sex determining region Y)-box 6 (SOX6), regulator of telomere elongation helicase 1 (RTEL1) and UDP-Gal:betaGlcNAc beta 1,4- galactosyltransferase, polypeptide 5 (B4GALT5). The most significant alterations related to peritoneal invasion involved the regions 13q21.1 (gain) and 15q15.1, 17q23.1, 19q13.2 and 20q11.22 (loss of heterozygozity; LOH), where we found LOH of erythrocyte membrane protein band 4.1-like 1 (EPB41L1) gene. In relation to early age of onset, the most significant alterations were gains in the regions Xq26 and Xp22.31 and a loss in the region 11p15.4.These quantitative changes may play a role in the development of this type of neoplasia and may be used as markers in evaluating poor prognosis, as well as act as potential therapeutic targets for gastric cancer.

Comparative genomic hybridization

Viral Oncogene

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Citations (14)