A high-cholesterol diet promotes the intravasation of breast tumor cells through an LDL-LDLR axis.

Most metastases in breast cancer occur via the dissemination of tumor cells through the bloodstream. How tumor cells enter the blood (intravasation) is, however, a poorly understood mechanism at the cellular and molecular levels. Particularly uncharacterized is how intravasation is affected by systemic nutrients. High levels of systemic LDL-cholesterol have been shown to contribute to breast cancer progression and metastasis in various models, but the cellular and molecular mechanisms involved are still undisclosed. Here we show that a high- cholesterol diet promotes intravasation in two mouse models of breast cancer and that this could be reverted by blocking LDL binding to LDLR in tumor cells. Moreover, we show that LDL promotes vascular invasion in vitro and the intercalation of tumor cells with endothelial cells, a phenotypic change resembling vascular mimicry (VM). At the molecular level, LDL increases the expression of SERPINE2, previously shown to be required for both VM and intravasation. Overall, our manuscript unravels novel mechanisms by which systemic hypercholesterolemia may affect the onset of metastatic breast cancer by favouring phenotypic changes in breast cancer cells and increasing intravasation.

Mitochondrial Metabolism Drives Low-density Lipoprotein-induced Breast Cancer Cell Migration.

Most cancer-related deaths are due to metastases. Systemic factors, such as lipid-enriched environments [as low-density lipoprotein (LDL)-cholesterol], favor breast cancer, including triple-negative breast cancer (TNBC) metastasis formation. Mitochondria metabolism impacts TNBC invasive behavior but its involvement in a lipid-enriched setting is undisclosed. Here we show that LDL increases lipid droplets, induces CD36 and augments TNBC cells migration and invasion in vivo and in vitro. LDL induces higher mitochondrial mass and network spread in migrating cells, in an actin remodeling-dependent manner, and transcriptomic and energetic analyses revealed that LDL renders TNBC cells dependent on fatty acids (FA) usage for mitochondrial respiration. Indeed, engagement on FA transport into the mitochondria is required for LDL-induced migration and mitochondrial remodeling. Mechanistically, LDL treatment leads to mitochondrial long-chain fatty acid accumulation and increased reactive oxygen species (ROS) production. Importantly, CD36 or ROS blockade abolished LDL-induced cell migration and mitochondria metabolic adaptations. Our data suggest that LDL induces TNBC cells migration by reprogramming mitochondrial metabolism, revealing a new vulnerability in metastatic breast cancer. Significance: LDL induces breast cancer cell migration that relies on CD36 for mitochondrial metabolism and network remodeling, providing an antimetastatic metabolic strategy.

Use of scanning electron microscope to evaluate the marginal fit of protocol bars obtained through benchtop or intraoral digital scanners

Aim: To evaluate the marginal fit of protocol bars milled from digital models obtained by conventional molding followed by bench scanning or digital molding with an intraoral scanner. Methods: Four morse-cone implants and the mini-pillars were installed in a 3D printed mandible model (master model). Digital models of the master model were obtained by (n=10): (Group A - Conventional) conventional (analog) molding of the master model followed by bench scanning or (Group B - Digital) molding of the master model with an intraoral scanner. All-on-four protocol bars were designed and milled from the digital models for both groups and screwed into the master model. Scanning electron microscopy (SEM) images from the distal, central, and mesial regions of each implant were obtained and the implant-protocol bar marginal fit was measured in an image software (Image J). The mean misfit of each region was analyzed by two-factor ANOVA, Tukey test, and Student's t-test (0,05 = 0.05). Results: The digital approach (B) showed higher misadaptation than the conventional approach (A, p < 0.05), regardless of the region evaluated. In group A, the central region showed higher maladjustment than the mesial region (p<0.05), however, there were no differences among regions of group B (p>0.05). Conclusion: The conventional method of acquiring digital models using the bench scanner produced bars for the All-On-Four protocol with better marginal fit than the digital models obtained with an intraoral scanner

On the Relevance of Soft Tissue Sarcomas Metabolic Landscape Mapping.

Soft tissue sarcomas (STS) prognosis is disappointing, with current treatment strategies being based on a "fit for all" principle and not taking distinct sarcoma subtypes specificities and genetic/metabolic differences into consideration. The paucity of precision therapies in STS reflects the shortage of studies that seek to decipher the sarcomagenesis mechanisms. There is an urge to improve STS diagnosis precision, refine STS classification criteria, and increase the capability of identifying STS prognostic biomarkers. Single-omics and multi-omics studies may play a key role on decodifying sarcomagenesis. Metabolomics provides a singular insight, either as a single-omics approach or as part of a multi-omics strategy, into the metabolic adaptations that support sarcomagenesis. Although STS metabolome is scarcely characterized, untargeted and targeted metabolomics approaches employing different data acquisition methods such as mass spectrometry (MS), MS imaging, and nuclear magnetic resonance (NMR) spectroscopy provided important information, warranting further studies. New chromatographic, MS, NMR-based, and flow cytometry-based methods will offer opportunities to therapeutically target metabolic pathways and to monitorize the response to such metabolic targeting therapies. Here we provide a comprehensive review of STS omics applications, comprising a detailed analysis of studies focused on the metabolic landscape of these tumors.

Sarcoma Metabolomics: Current Horizons and Future Perspectives.

The vast array of metabolic adaptations that cancer cells are capable of assuming, not only support their biosynthetic activity, but also fulfill their bioenergetic demands and keep their intracellular reduction-oxidation (redox) balance. Spotlight has recently been placed on the energy metabolism reprogramming strategies employed by cancer cells to proliferate. Knowledge regarding soft tissue and bone sarcomas metabolome is relatively sparse. Further characterization of sarcoma metabolic landscape may pave the way for diagnostic refinement and new therapeutic target identification, with benefit to sarcoma patients. This review covers the state-of-the-art knowledge on cancer metabolomics and explores in detail the most recent evidence on soft tissue and bone sarcoma metabolomics.

Modulating the Metabolic Phenotype of Cancer Microenvironment.

This chapter provides a brief overview of the methods to study and modulate the metabolic phenotype of the tumor microenvironment, including own research work to demonstrate the impact that metabolic shifts in the host have on cancer. Firstly, we briefly discuss the relevance of using animal models to address this topic, and also the importance of acknowledging that animals have diverse metabolic phenotypes according to species, and even with strain, age or sex. We also present original data to highlight the impact that changes in metabolic phenotype of the microenvironment have on tumor progression. Using an acute leukemia mouse xenograft model and high-fat diet we show that a shift in the host metabolic phenotype, induced by high-fat feeding, significantly impacts on tumor progression. The mechanism through which this occurs involves a direct effect of the increased levels of circulating lipoproteins in both tumor and non-neoplastic cells.

An antisense transcript mediates MALAT1 response in human breast cancer.

BACKGROUND: Long non-coding RNAs (lncRNAs) represent a substantial portion of the human transcriptome. LncRNAs present a very stringent cell-type/tissue specificity being potential candidates for therapeutical applications during aging and disease. As example, targeting of MALAT1, a highly conserved lncRNA originally identified in metastatic non-small cell lung cancer, has shown promising results in cancer regression. Nevertheless, the regulation and specificity of MALAT1 have not been directly addressed. Interestingly, MALAT1 locus is spanned by an antisense transcript named TALAM1. METHODS: Here using a collection of breast cancer cells and in vitro and in vivo migration assays we characterized the dynamics of expression and demonstrated that TALAM1 regulates and synergizes with MALAT1 during tumorigenesis. RESULTS: Down-regulation of TALAM1 was shown to greatly impact on the capacity of breast cancer cells to migrate in vitro or to populate the lungs of immunocompromised mice. Additionally, we demonstrated that TALAM1 cooperates with MALAT1 in the regulation of the properties guiding breast cancer aggressiveness and malignancy. CONCLUSIONS: By characterizing this sense/anti-sense pair we uncovered the complexity of MALAT1 locus regulation, describing new potential candidates for cancer targeting.

Biomechanical Behavior of an Implant System Using Polyether Ether Ketone Bar: Finite Element Analysis.

AIM AND OBJECTIVES: This study assessed, through finite element analysis, the biomechanical behavior of an implant system using the All-on-Four® technique with nickel-chromium (M1) and polyether ether ketone (PEEK) bars (M2). MATERIALS AND METHODS: Implants and components were represented in three-dimensional (3D) geometric models and submitted to three types of load: axial, oblique, and load on all teeth. The 3D models were exported to a computer-aided design-like software such as Solidworks 2016 (Dassault Systemes, Solidworks Corps, USA) for editing and Nonuniform Rational Basis Splines parametrization. RESULTS: Data were analyzed according to system's areas of action: peri-implant bone, implant, intermediates, intermediates' screws, prostheses' screws, and bars. Largest peak stress was shown in M2. CONCLUSION: PEEK is a promising material for use in dentistry; however, further studies are necessary to evaluate its performance.

Meeting the needs of breast cancer: A nucleolin's perspective.

A major challenge in the management of breast cancer disease has been the development of metastases. Finding new molecular targets and the design of targeted therapeutic approaches to improve the overall survival and quality of life of these patients is, therefore, of great importance. Nucleolin, which is overexpressed in cancer cells and tumor-associated blood vessels, have been implicated in various processes supporting tumorigenesis and angiogenesis. Additionally, its overexpression has been demonstrated in a variety of human neoplasias as an unfavorable prognostic factor, associated with a high risk of relapse and low overall survival. Hence, nucleolin has emerged as a relevant target for therapeutic intervention in cancer malignancy, including breast cancer. This review focus on the contribution of nucleolin for cancer disease and on the development of therapeutic strategies targeting this protein. In this respect, it also provides a critical analysis about the potential and pitfalls of nanomedicine for cancer therapy.

Low-Density Lipoprotein Uptake Inhibits the Activation and Antitumor Functions of Human Vγ9Vδ2 T Cells.

Vγ9Vδ2 T cells, the main subset of γδ T lymphocytes in human peripheral blood, are endowed with antitumor functions such as cytotoxicity and IFNγ production. These functions are triggered upon T-cell receptor-dependent activation by non-peptidic prenyl pyrophosphates ("phosphoantigens") that are selective agonists of Vγ9Vδ2 T cells, and which have been evaluated in clinical studies. Because phosphoantigens have shown interindividual variation in Vγ9Vδ2 T-cell activities, we asked whether metabolic resources, namely lipids such as cholesterol, could affect phosphoantigen-mediated Vγ9Vδ2 T-cell activation and function. We show here that Vγ9Vδ2 T cells express the LDL receptor upon activation and take up LDL cholesterol. Resulting changes, such as decreased mitochondrial mass and reduced ATP production, correlate with downregulation of Vγ9Vδ2 T-cell activation and functionality. In particular, the expression of IFNγ, NKG2D, and DNAM-1 were reduced upon LDL cholesterol treatment of phosphoantigen-expanded Vγ9Vδ2 T cells. As a result, their capacity to target breast cancer cells was compromised both in vitro and in an in vivo xenograft mouse model. Thus, this study describes the role of LDL cholesterol as an inhibitor of the antitumor functions of phosphoantigen-activated Vγ9Vδ2 T cells. Our observations have implications for therapeutic applications dependent on Vγ9Vδ2 T cells. Cancer Immunol Res; 6(4); 448-57. ©2018 AACR.

Therapeutic Implications of the Molecular and Immune Landscape of Triple-Negative Breast Cancer.

Treatment and management of breast cancer imposes a heavy burden on public health care, and incidence rates continue to increase. Breast cancer is the most common female neoplasia and primary cause of death among women worldwide. The recognition of breast cancer as a complex and heterogeneous disease, comprising different molecular entities, was a landmark in our understanding of this malignancy. Valuing the impact of the molecular characteristics on tumor behavior enabled a better assessment of a patient's prognosis and increased the predictive power to therapeutic response and clinical outcome. Molecular heterogeneity is also prominent in the triple-negative breast cancer subtype, and is reflected by the distinct prognostic and patient's sensitivity to treatment, being chemotherapy the only systemic treatment currently available. From a therapeutic perspective, gene expression profiling of triple-negative tumors has notably contributed to the exploration of new druggable targets and brought to light the need to align these patients to the various therapies according to their triple-negative subtype. Additionally, the higher amount of tumor infiltrating lymphocytes, and the prevalence of an increased expression of PD-1 receptor and its ligand, PD-L1, in triple-negative tumors, created a new treatment opportunity with immune checkpoint inhibitors. This manuscript addresses the current knowledge on the molecular and immune profiles of breast cancer, and its impact on the development of targeted therapies, with a particular emphasis on the triple-negative subtype.

VEGFR2-Mediated Reprogramming of Mitochondrial Metabolism Regulates the Sensitivity of Acute Myeloid Leukemia to Chemotherapy.

Metabolic reprogramming is central to tumorigenesis, but whether chemotherapy induces metabolic features promoting recurrence remains unknown. We established a mouse xenograft model of human acute myeloid leukemia (AML) that enabled chemotherapy-induced regressions of established disease followed by lethal regrowth of more aggressive tumor cells. Human AML cells from terminally ill mice treated with chemotherapy (chemoAML) had higher lipid content, increased lactate production and ATP levels, reduced expression of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α), and fewer mitochondria than controls from untreated AML animals. These changes were linked to increased VEGFR2 signaling that counteracted chemotherapy-driven cell death; blocking of VEGFR2 sensitized chemoAML to chemotherapy (re-)treatment and induced a mitochondrial biogenesis program with increased mitochondrial mass and oxidative stress. Accordingly, depletion of PGC-1α in chemoAML cells abolished such induction of mitochondrial metabolism and chemosensitization in response to VEGFR2 inhibition. Collectively, this reveals a mitochondrial metabolic vulnerability with potential therapeutic applications against chemotherapy-resistant AML.Significance: These findings reveal a mitochondrial metabolic vulnerability that might be exploited to kill chemotherapy-resistant acute myeloid leukemia cells. Cancer Res; 78(3); 731-41. ©2017 AACR.

Monocarboxylate transporter 1 (MCT1), a tool to stratify acute myeloid leukemia (AML) patients and a vehicle to kill cancer cells.

Dysregulation of glucose/lactate dynamics plays a role in cancer progression, and MCTs are key elements in metabolic remodeling. VEGF is a relevant growth factor in the maintenance of bone marrow microenvironment and it is also important in hematological diseases. Our aim was to investigate the role of VEGF in the metabolic adaptation of Acute myeloid leukemia (AML) cells by evaluating the metabolic profiles and cell features according to the AML lineage and testing lactate as a metabolic coin. Our in vitro results showed that AML promyelocytic (HL60) and monocytic (THP1) (but not erythroid- HEL) lineages are well adapted to VEGF and lactate rich environment. Their metabolic adaptation relies on high rates of glycolysis to generate intermediates for PPP to support cell proliferation, and on the consumption of glycolysis-generated lactate to supply biomass and energy production. VEGF orchestrates this metabolic network by regulating MCT1 expression. Bromopyruvic acid (BPA) was proven to be an effective cytotoxic in AML, possibly transported by MCT1. Our study reinforces that targeting metabolism can be a good strategy to fight cancer. MCT1 expression at the time of diagnosis can assist on the identification of AML patients that will benefit from BPA therapy. Additionally, MCT1 can be used in targeted delivery of conventional cytotoxic drugs.

Avaliação da resistência flexural em diferentes métodos de soldagem / Evaluation of flexural resistance in different welding methods

O objetivo do presente estudo foi avaliar três diferentes tipos de soldagem: Chama Direta a maçarico (convencional\brasagem), Solda Mista representada por fixação de dois pontos (Solda Elétrica Fixator - Kernit, Brasil), e completada com solda convencional, e o método de Solda a Laser (Soldadora Desktop - Sisma LM 500, Itália). Dois implantes plataforma Bränemark 4.1 mm (Neodent, Curitiba/Brasil) foram fixados em uma matriz de alumínio para simular uma ponte fixa implanto-suportada de três elementos. Os espécimes foram obtidos a partir de um bloco de cera CAD-CAM (Ceramill-Amammgirrbarch). Trinta e duas UCLAs hexágono externo foram fresadas e posteriormente unidas a uma barra pré-fabricada em cera com 2,5mm. Os corpos de prova foram fundidos em liga de cobalto-cromo simulando uma prótese fixa de três elementos. Esses espécimes foram divididos aleatoriamente e separados em três grupos (n=6): grupo A (solda chama direta), grupo B (solda mista), grupo C (solda laser). Os espécimes foram seccionados ao meio e unidos com resina acrílica para simular uma soldagem em prótese fixa. Os corpos foram soldados e tratados de acordo com a proposição. Após a soldagem os corpos de prova foram usinados e levados ao teste de flexão na técnica de três pontos. Os dados foram submetidos aos testes estatísticos de Tukey. Os cálculos estatísticos foram conduzidos adotando-se o nível de significância de 5% (α = 0,05). Houve diferença estatisticamente significativa entre os grupos soldados. Os resultados demonstraram valores mais elevados nos grupos A e B, solda convencional e solda mista, e menor valor no grupo C, solda a laser. No entanto, considerando a metodologia aplicada, a solda a laser mostrou uma menor resistência flexural comparada à soldagem convencional e mista, e a fixação prévia de solda elétrica com complemento de solda convencional (solda mista) não alterou a resistência flexural, produzindo resultado semelhante à solda convencional

The objective of this study was to evaluate three different types of welding, blowtorch; (conventional/brazing), welder Joint; represented by securing two points (Arc Welding Fixator - Kernit, Brazil), and supplemented with conventional welding), and Laser welding method (welder Desktop - Sisma LM 500, Italy). Two implants Bränemark 4.1 mm platform (Neodent, Curitiba/Brazil) were fixed in an aluminum matrix. Specimens were obtained from a CAD-CAM wax block (Ceramill - Amammgirrbarch) were milled 32 UCLAs (external hexagon, Bränemark platform), and subsequently joined to a prefabricated bar also wax 2.5 mm, the specimens were casted in cobalt-chromium alloy. These specimens were randomly divided and separated into 3 groups: group A (welding direct flame), Group B (mixed welding), C (laser welding), with 6 samples for each group. The specimens of each group were cut in half to simulate a fixed prosthesis in welding, and put together with acrylic resin. The bodies were welded and treated according to the statement. After the specimens were welded, they were manually grinded and submitted to the 3 points bending test technique. Data were subjected to statistical tests of Tukey. Statistical calculations were performed adopting the significance level of 5% (α = 0.05), using SPSS 20 (SPSS Inc., Chicago, IL, USA). There were differences between the soldered groups. The data showed the highest values obtained in groups A and B, conventional welding and soldering joint, and lower in group C, the laser welding. However, within the applied methodology, the laser welding showed a lower flexural strength compared to conventional and mixed welding, and that the advance fixing of electric welding, conventional welding complement (mixed welding), does not change its flexural strength, producing results similar to conventional welding

Does Hypoxic Response Mediate Primary Resistance to Sunitinib in Untreated Locally Advanced Breast Cancer?

BACKGROUND: The antiangiogenic drug sunitinib has never been evaluated as single agent in untreated breast cancer patients. OBJECTIVE: We aimed to characterize the activity of sunitinib, alone and with docetaxel, in untreated locally advanced or operable breast cancer and to uncover the mechanisms of response. METHOD: Patients were treated with an upfront window of sunitinib followed by four cycles of sunitinib plus docetaxel. Response, resistance and toxicity were evaluated according to standard clinical parameters, magnetic resonance imaging, positron emission tomography, standard pathology characterization, molecular pathology and gene expression profiling. RESULTS: Twelve patients were included. We detected primary resistance to sunitinib in the upfront window in untreated breast cancer, as evidenced by four non-responding patients. At surgery, five patients had viable tumor in the breast and axilla, four had viable tumor cells in the breast alone and three were taken off study and thus not evaluated, due to unacceptable toxicity. Early functional imaging was useful in predicting response. There were no clinical complete responses. Comparison of tumor gene expression profiling data between early responders and non-responders allowed us to identify the up-regulation of VEGF and angiogenic pathways in non-responders. Specifically, in tumors resistant to single-agent sunitinib we detected a transcriptional response to hypoxia characterized by over-expression of several HIF1α target genes. CONCLUSION: In this report of single-agent sunitinib treatment in untreated localized breast cancer patients, we found evidence of primary resistance to sunitinib, likely mediated by up-regulation of hypoxia responsive genes.

Inoculated Cell Density as a Determinant Factor of the Growth Dynamics and Metastatic Efficiency of a Breast Cancer Murine Model.

4T1 metastatic breast cancer model have been widely used to study stage IV human breast cancer. However, the frequent inoculation of a large number of cells, gives rise to fast growing tumors, as well as to a surprisingly low metastatic take rate. The present work aimed at establishing the conditions enabling high metastatic take rate of the triple-negative murine 4T1 syngeneic breast cancer model. An 87% 4T1 tumor incidence was observed when as few as 500 cancer cells were implanted. 4T1 cancer cells colonized primarily the lungs with 100% efficiency, and distant lesions were also commonly identified in the mesentery and pancreas. The drastic reduction of the number of inoculated cells resulted in increased tumor doubling times and decreased specific growth rates, following a Gompertzian tumor expansion. The established conditions for the 4T1 mouse model were further validated in a therapeutic study with peguilated liposomal doxorubicin, in clinical used in the setting of metastatic breast cancer. Inoculated cell density was proven to be a key methodological aspect towards the reproducible development of macrometastases in the 4T1 mouse model and a more reliable pre-clinical assessment of antimetastatic therapies.

LDL-Cholesterol Increases the Transcytosis of Molecules through Endothelial Monolayers.

Cholesterol has been identified as a causative factor in numerous pathologies including atherosclerosis and cancer. One of the frequent effects of elevated cholesterol levels in humans is the compromise of endothelial function due to activation of pro-inflammatory signalling pathways. While the mechanisms involved in endothelial activation by cholesterol during an inflammatory response are well established, less is known about the mechanisms by which cholesterol may affect endothelial barrier function, which were the subject of the present study. Here we show that low density lipoprotein (LDL) increases the permeability of endothelial monolayers to high molecular weight dextrans in an LDL receptor and cholesterol-dependent manner. The increased permeability seen upon LDL treatment was not caused by disruption of cell-to-cell junctions as determined by a normal localization of VE-Cadherin and ZO-1 proteins, and no major alterations in transendothelial electrical resistance or permeability to fluorescein. We show instead that LDL increases the level of high molecular weight transcytosis and that this occurs in an LDL receptor, cholesterol and caveolae-dependent way. Our findings contribute to our understanding of the systemic pathological effects of elevated cholesterol and the transport of cargo through endothelial monolayers.

Efeito de primer para zircônia sobre a resistência ao cisalhamento entre um cimento resinoso e a cerâmica de óxido de zircônio / Effect of primer on the bond strength between resin cement and zirconia

O objetivo deste estudo foi avaliar as influências acarretadas pelo tratamento das superfícies das zircônias com primer apropriado na resistência de união entre cimento resinoso e uma cerâmica de Zircônia. foram utilizados 20 corpos de prova em Zircônia VIPI BLOCK ZIRCONN (VIPI, São Paulo, Brasil) divididos em 2 grupos: Grupo 1 ­ tratamento de superfície da zircônia apenas com jateamento de óxido de alumínio e cimento resinoso PanaviaTF 2.0 (Kuraray, Kurashiki, Japão); e Grupo 2 ­ além do jateamento usou-se o primer Ceramic Primer (3M, São Paulo, Brasil). Os espécimes cerâmicos receberam o cimento manipulado na proporção de 1:1 e foram estocados em água destilada a 37ºC por 24 horas antes e após a termociclagem. O ensaio de cisalhamento foi realizado em máquina de ensaios EMIC DL2000 (EMIC, São Paulo, Brasil), os valores de resistência de união foram apresentados em Mpa e analisados através de Análise de Variância (ANOVA) e teste t Student para amostras independentes. Os valores resistência ao cisalhamento entre cimentos e cerâmica à base de zircônia utilizando os primers mencionados não foram estatisticamente diferentes, isto é, nenhuma diferença significativa foi encontrada entre os grupos G1 (8,70 ± 6,31) e G2 (8,18 ± 3,75). Os testes realizados com o primer não mostraram aumento considerável na resistência de união ao cisalhamento entre cimentos e cerâmica à base de zircônia.

The aim of this study was to evaluate the influence of the use of primer to treat zirconia surfaces on the bond strength between resin cement and zirconia ceramics. The 20 specimens were divided into 2 groups: group 1 ­ zirconia surface treatment with sandblasting with aluminum oxide and Panavia T f 2.0 (Kuraray); Group 2 ­ in addition to the sandblasting Ceramic Primer (3M) was used. Each specimen of the ceramic material received manipulated cement in the proportion 1:1. The specimens were stored in distilled water at 37 ° C for 24 hours before and after thermocycling. Shear test was performed in testing EMIC DL2000 (EMIC, São Paulo, Brazil) and the values of bond strength in MPa were analyzed using Analysis of Variance (ANOVA) and Student t test for independent samples machine. There was no significant difference between the values for shear strength between both studied groups: G1 (8.70 ± 6 groups, 31) and G2 (8.18 ± 3.75). The tests performed with the primer used in this study showed no significant increase on shear bond strength between cement and ceramics based on zirconia.