Mariana Ferreira Leal

Royal Marsden Hospital

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Marı́lia de Arruda Cardoso Smith

Universidade Federal de São Paulo

Rommel Mário Rodríguez Burbano

Universidade Federal do Pará

Paulo Pimentel de Assumpção

Universidade Federal do Pará

Danielle Queiroz Calcagno

Universidade Federal do Pará

Sâmia Demachki

Universidade Federal do Pará

Mitch Dowsett

Royal Marsden Hospital

Eugene F. Schuster

Institute of Cancer Research

Benno Ejnisman

Universidade Federal de São Paulo

André Salim Khayat

Universidade Federal do Pará

Carolina Oliveira Gigek

Universidade Federal de São Paulo

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Universidade Federal do Pará

Universidade Federal de São Paulo

Universidade de São Paulo

Institute of Cancer Research

Institut Curie

Université Paris Sciences et Lettres

Royal Marsden Hospital

Inserm

Breast Cancer Now

Fundação de Apoio à Universidade Federal de São Paulo

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Hepatitis E: Update on Prevention and Control

BioMed Research International (2018)

Juliana Gil Melgaço Noemi Rovaris Gardinali Vinicius M. Mello Mariana Ferreira Leal Lia Laura Lewis‐Ximenez

Hepatitis E virus (HEV) is a common etiology of acute viral hepatitis worldwide. Recombinant HEV vaccines have been developed, but only one is commercially available and licensed in China since 2011. Epidemiological studies have identified genotype 3 as the major cause of chronic infection in immunocompromised individuals. Ribavirin has been shown to be effective as a monotherapy to induce HEV clearance in chronic patients who have undergone solid organ transplant (SOT) under immunosuppressive therapy. Efforts and improvements in prevention and control have been made to reduce the instances of acute and chronic hepatitis E in endemic and nonendemic countries. However, this review shows that further studies are required to demonstrate the importance of preventive vaccination and treatment worldwide, with emphasis on hepatitis E infection in the public health system.

Hepatitis E Virus

Hepatitis E

Viral Hepatitis

10.1155/2018/5769201

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Citations (57)

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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Supplementary Figure from Impact of Duration of Neoadjuvant Aromatase Inhibitors on Molecular Expression Profiles in Estrogen Receptor–positive Breast Cancers

M.A. Bergamino Gabriele Morani Joel S. Parker Eugene F. Schuster Mariana Ferreira Leal

Supplementary Figure from Impact of Duration of Neoadjuvant Aromatase Inhibitors on Molecular Expression Profiles in Estrogen Receptor–positive Breast Cancers

Aromatase inhibitor

10.1158/1078-0432.22483100.v1

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[Supply of blood to heart surgery patients. Can transfusion habits be changed?].

PubMed (1996)

Mariana Ferreira Leal Jiménez Pi Márquez Bustos Ja Flores Jm Muñoz Jm

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MYC Deregulation in Gastric Cancer and Its Clinicopathological Implications

PLoS ONE (2013)

Carolina Rosal Teixeira de Souza Mariana Ferreira Leal Danielle Queiroz Calcagno Eliana Kelly Costa Sozinho Bárbara do Nascimento Borges

Our study investigated the relationship between MYC alterations and clinicopathological features in gastric cancers. We evaluated the effect of MYC mRNA expression and its protein immunoreactivity, as well as copy number variation, promoter DNA methylation, and point mutations, in 125 gastric adenocarcinoma and 67 paried non-neoplastic tissues. We observed that 77% of the tumors presented MYC immunoreactivity which was significantly associated with increased mRNA expression (p<0.05). These observations were associated with deeper tumor extension and the presence of metastasis (p<0.05). MYC protein expression was also more frequently observed in intestinal-type than in diffuse-type tumors (p<0.001). Additionally, MYC mRNA and protein expression were significantly associated with its copy number (p<0.05). The gain of MYC copies was associated with late-onset, intestinal-type, advanced tumor stage, and the presence of distant metastasis (p<0.05). A hypomethylated MYC promoter was detected in 86.4% of tumor samples. MYC hypomethylation was associated with diffuse-type, advanced tumor stage, deeper tumor extension, and the presence of lymph node metastasis (p<0.05). Moreover, eighteen tumor samples presented at least one known mutation. The presence of MYC mutations was associated with diffuse-type tumor (p<0.001). Our results showed that MYC deregulation was mainly associated with poor prognostic features and also reinforced the presence of different pathways involved in intestinal-type and diffuse-type gastric carcinogenesis. Thus, our findings suggest that MYC may be a useful marker for clinical stratification and prognosis.

10.1371/journal.pone.0064420

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Clinical implication of 14-3-3 epsilon expression in gastric cancer

World Journal of Gastroenterology (2012)

Mariana Ferreira Leal

To evaluate for the first time the protein and mRNA expression of 14-3-3ε in gastric carcinogenesis.14-3-3ε protein expression was determined by western blotting, and mRNA expression was examined by real-time quantitative RT-PCR in gastric tumors and their matched non-neoplastic gastric tissue samples.Authors observed a significant reduction of 14-3-3ε protein expression in gastric cancer (GC) samples compared to their matched non-neoplastic tissue. Reduced levels of 14-3-3ε were also associated with diffuse-type GC and early-onset of this pathology. Our data suggest that reduced 14-3-3ε may have a role in gastric carcinogenesis process.Our results reveal that the reduced 14-3-3ε expression in GC and investigation of 14-3-3ε interaction partners may help to elucidate the carcinogenesis process.

10.3748/wjg.v18.i13.1531

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Changes in the expression of matrix extracellular genes and TGFB family members in rotator cuff tears

Journal of Orthopaedic Research® (2018)

Paulo Santoro Belangero Eduardo Antônio de Figueiredo Carina Cohen Felipe de Seixas Alves Wânia Hiromi Yanaguizawa

ABSTRACT Lack of synthesis of extracellular matrix compounds may contribute to degeneration of the tendons. Thus, we aimed to evaluate the expression of extracellular matrix and TGFB family members in ruptured and non‐ruptured tendons of the rotator cuff, as well as the effect of clinical factors on gene expression in tendon samples, and the relationship between histological findings and altered gene expression. Injured and non‐injured supraspinatus tendon samples and subscapular non‐injured tendon samples were collected from 38 patients with rotator cuff tears. Non‐injured supraspinatus tendons were obtained from eight controls. Specimens were used for histological evaluation, quantification of collagen fibers, and mRNA and protein expression analyses. Increased COL1A1 , COL1A2 , COL3A1 , COL5A1 , FN1 , TNC , and TGFBR1 mRNA expression was observed in the tear samples ( p < 0.05). Duration of symptoms was correlated with the levels of collagen type I/III fibers ( p = 0.032; ρ = 0.0447) and FN1 immunostaining ( p = 0.031; ρ = 0.417). Smoking was associated with increased frequency of microcysts, myxoid degeneration, and COL5A1 , FN1 , TNC , and TGFB1 mRNA expression ( p < 0.05). FN1 immunostaining was correlated with the number of years of smoking ( p = 0.048; ρ = 0.384). Lower levels of collagen type I/III fibers were detected in samples with fissures (0 = 0.046). High frequency of microcysts was associated with increased COL5A1 , FN1 , and TNC expression ( p < 0.05, for all comparisons). Neovascularization was associated with reduced FN1 ( p = 0.035) and TGFBR1 expression ( p = 0.034). Our findings show differential expression of matrix extracellular genes and TGFB family members in the degeneration process involved in rotator cuff tears. These molecular alterations are influenced by clinical factors. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2542–2553, 2018.

Immunostaining

Matrix (chemical analysis)

10.1002/jor.23907

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Lymphocyte proliferation stimulated by activated Cebus apella macrophages treated with a complex homeopathic immune response modifiers

Homeopathy (2012)

Carlos Onete Coelho Moreira Joana de Fátima Ferreira Borges da Costa Mariana Ferreira Leal Edilson Andrade Alexandre Pingarilho Rezende

Canova is a complex homeopathic medicine that enhances a specific immunologic responses against several exogenous and endogenous conditions. Canova activates macrophages both in vivo and in vitro. We evaluated the effects of macrophages activated by Canova in vivo and ex vitro in the proliferation of lymphocytes. Canova was used to activate Cebus apella macrophages in vivo or ex vitro with Canova. Lymphocytes were cultured with the macrophage culture medium. The analysis of Canova effects in cultured lymphocytes was performed according to the cell cycle phase using flow cytometry. The Interferon gamma and Interleukin-5 cytokines quantification in these lymphocyte culture media was performed by Enzyme-linked immunosorbent assay (ELISA). We observed that Canova actives macrophages in vivo and ex vitro. The lymphocytes cultured in a supplemented medium with macrophages activated by Canova treatment presented a higher number of proliferation cells than lymphocytes not exposed to macrophages activated by Canova. The Interferon gamma and Interleukin-5 cytokines were only observed in the medium of lymphocytes exposed to macrophages activated by Canova. Thus, Canova has potential as a new adjuvant therapy.

Homeopathic medicine

Ex vivo

10.1016/j.homp.2011.09.001

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Citations (14)

MYC and gastric adenocarcinoma carcinogenesis

世界胃肠病学杂志：英文版（电子版） (2008)

Danielle Queiroz Calcagno Mariana Mariana J.A.M. Ferreira

MYC 是涉及房间周期规定，房间生长拘捕，房间粘附，新陈代谢，核糖体生物的续生说，蛋白质合成，和 mitochondrial 的 oncogene 功能。它在人被描述了为几个致癌作用过程的一个关键元素。许多研究显示出在 MYC 解除管制和胃的癌症之间的一个协会。MYC 解除管制也在胃的肿瘤前损害被看见，因此，它可以在早胃的致癌作用有一个角色。几研究建议了那扩大是在胃的癌症的 MYC 解除管制的主要机制。在现在的评论，我们在胃的腺癌致癌作用集中于 MYC oncogene 的解除管制，包括它有 Helicobacter pylori (H pylori ) 和临床的应用的协会。

Gastric adenocarcinoma

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SMARCA5Methylation and Expression in Gastric Cancer

Cancer Investigation (2011)

Carolina Oliveira Gigek Luara Carolina Frias Lisboa Mariana Ferreira Leal Patrícia Natália Silva Eleonidas Moura Lima

Here, we first evaluated SMARCA5 expression and promoter DNA methylation in gastric carcinogenesis. Immunohistochemistry and methylation-specific PCR were analyzed in 19 and 48 normal mucosa and in 52 and 92 gastric cancer samples, respectively. We observed higher immunoreactivity of SMARCA5 in gastric cancer samples than in normal mucosa. Moreover, SMARCA5 promoter methylation was associated with the absence of protein expression. Our findings suggest that SMARCA5 has a potential role in proliferation and malignancy in gastric carcinogenesis.

10.3109/07357907.2010.543365

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Citations (41)