ROGER CHAMMAS
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Radiologia, Faculdade de Medicina - Docente
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder
19 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 19
- Exploring the Neandertal legacy of pancreatic ductal adenocarcinoma risk in Eurasians(2023) PICCARDI, Margherita; GENTILUOMO, Manuel; BERTONCINI, Stefania; PEZZILLI, Raffaele; EROSS, Balint; BUNDUC, Stefania; UZUNOGLU, Faik G.; TALAR-WOJNAROWSKA, Renata; VANAGAS, Tomas; SPERTI, Cosimo; OLIVERIUS, Martin; AOKI, Mateus Nobrega; ERMINI, Stefano; HUSSEIN, Tamas; BOGGI, Ugo; JAMROZIAK, Krzysztof; MAIELLO, Evaristo; MORELLI, Luca; VODICKOVA, Ludmila; FRANCO, Gregorio Di; LANDI, Stefano; SZENTESI, Andrea; LOVECEK, Martin; PUZZONO, Marta; TAVANO, Francesca; LAARHOVEN, Hanneke W. M. van; ZERBI, Alessandro; MOHELNIKOVA-DUCHONOVA, Beatrice; STOCKER, Hannah; COSTELLO, Eithne; CAPURSO, Gabriele; GINOCCHI, Laura; LAWLOR, Rita T.; VANELLA, Giuseppe; BAZZOCCHI, Francesca; IZBICKI, Jakob R.; LATIANO, Anna; BUENO-DE-MESQUITA, Bas; PISANI, Ruggero Ponz de Leon; SCHOETTKER, Ben; SOUCEK, Pavel; HEGYI, Peter; GAZOULI, Maria; HACKERT, Thilo; KUPCINSKAS, Juozas; POSKIENE, Lina; TACELLI, Matteo; ROTH, Susanne; CARRARA, Silvia; PERRI, Francesco; HLAVAC, Viktor; THEODOROPOULOS, George E.; BUSCH, Olivier R.; MAMBRINI, Andrea; EIJCK, Casper H. J. van; ARCIDIACONO, Paolo; SCARPA, Aldo; PASQUALI, Claudio; BASSO, Daniela; LUCCHESI, Maurizio; MILANETTO, Anna Caterina; NEOPTOLEMOS, John P.; CAVESTRO, Giulia Martina; JANCIAUSKAS, Dainius; CHEN, Xuechen; CHAMMAS, Roger; GOETZ, Mara; BRENNER, Hermann; ARCHIBUGI, Livia; DANNEMANN, Michael; CANZIAN, Federico; TOFANELLI, Sergio; CAMPA, DanieleBackgroundThe genomes of present-day non-Africans are composed of 1-3% of Neandertal-derived DNA as a consequence of admixture events between Neandertals and anatomically modern humans about 50-60 thousand years ago. Neandertal-introgressed single nucleotide polymorphisms (aSNPs) have been associated with modern human disease-related traits, which are risk factors for pancreatic ductal adenocarcinoma (PDAC), such as obesity, type 2 diabetes, and inflammation. In this study, we aimed at investigating the role of aSNPs in PDAC in three Eurasian populations.ResultsThe high-coverage Vindija Neandertal genome was used to select aSNPs in non-African populations from 1000 Genomes project phase 3 data. Then, the association between aSNPs and PDAC risk was tested independently in Europeans and East Asians, using existing GWAS data on more than 200 000 individuals. We did not find any significant associations between aSNPs and PDAC in samples of European descent, whereas, in East Asians, we observed that the Chr10p12.1-rs117585753-T allele (MAF = 10%) increased the risk to develop PDAC (OR = 1.35, 95%CI 1.19-1.54, P = 3.59 x 10(-6)), with a P-value close to a threshold that takes into account multiple testing.ConclusionsOur results show only a minimal contribution of Neandertal SNPs to PDAC risk.
- Aerobic exercise training mitigates tumor growth and cancer-induced splenomegaly through modulation of non-platelet platelet factor 4 expression(2023) TOBIAS, Gabriel C.; GOMES, Joao L. P.; FERNANDES, Larissa G.; VOLTARELLI, Vanessa A.; ALMEIDA, Ney R. de; JANNIG, Paulo R.; SOUZA, Rodrigo W. Alves de; NEGRAO, Carlos E.; OLIVEIRA, Edilamar M.; CHAMMAS, Roger; ALVES, Christiano R. R.; BRUM, Patricia C.Exercise training reduces the incidence of several cancers, but the mechanisms underlying these effects are not fully understood. Exercise training can affect the spleen function, which controls the hematopoiesis and immune response. Analyzing different cancer models, we identified that 4T1, LLC, and CT26 tumor-bearing mice displayed enlarged spleen (splenomegaly), and exercise training reduced spleen mass toward control levels in two of these models (LLC and CT26). Exercise training also slowed tumor growth in melanoma B16F10, colon tumor 26 (CT26), and Lewis lung carcinoma (LLC) tumor-bearing mice, with minor effects in mammary carcinoma 4T1, MDA-MB-231, and MMTV-PyMT mice. In silico analyses using transcriptome profiles derived from these models revealed that platelet factor 4 (Pf4) is one of the main upregulated genes associated with splenomegaly during cancer progression. To understand whether exercise training would modulate the expression of these genes in the tumor and spleen, we investigated particularly the CT26 model, which displayed splenomegaly and had a clear response to the exercise training effects. RT-qPCR analysis confirmed that trained CT26 tumor-bearing mice had decreased Pf4 mRNA levels in both the tumor and spleen when compared to untrained CT26 tumor-bearing mice. Furthermore, exercise training specifically decreased Pf4 mRNA levels in the CT26 tumor cells. Aspirin treatment did not change tumor growth, splenomegaly, and tumor Pf4 mRNA levels, confirming that exercise decreased non-platelet Pf4 mRNA levels. Finally, tumor Pf4 mRNA levels are deregulated in The Cancer Genome Atlas Program (TCGA) samples and predict survival in multiple cancer types. This highlights the potential therapeutic value of exercise as a complementary approach to cancer treatment and underscores the importance of understanding the exercise-induced transcriptional changes in the spleen for the development of novel cancer therapies.
- The PANcreatic Disease ReseArch (PANDoRA) consortium: Ten years' experience of association studies to understand the genetic architecture of pancreatic cancer(2023) CAMPA, Daniele; GENTILUOMO, Manuel; STEIN, Angelika; AOKI, Mateus Nobrega; OLIVERIUS, Martin; VODICKOVA, Ludmila; JAMROZIAK, Krzysztof; THEODOROPOULOS, George; PASQUALI, Claudio; GREENHALF, William; ARCIDIACONO, Paolo Giorgio; UZUNOGLU, Faik; PEZZILLI, Raffaele; LUCHINI, Claudio; PUZZONO, Marta; LOOS, Martin; GIACCHERINI, Matteo; KATZKE, Verena; MAMBRINI, Andrea; KIUDELIENE, Edita; FEDERICO, Kauffmann Emanuele; JOHANSEN, Julia; HUSSEIN, Tamas; MOHELNIKOVA-DUCHONOVA, Beatrice; EIJCK, Casper H. J. van; BRENNER, Hermann; FARINELLA, Riccardo; PEREZ, Juan Sainz; LOVECEK, Martin; BUECHLER, Markus W.; HLAVAC, Viktor; IZBICKI, Jakob R.; HACKERT, Thilo; CHAMMAS, Roger; ZERBI, Alessandro; LAWLOR, Rita; FELICI, Alessio; GOETZ, Mara; CAPURSO, Gabriele; GINOCCHI, Laura; GAZOULI, Maria; KUPCINSKAS, Juozas; CAVESTRO, Giulia Martina; VODICKA, Pavel; MOZ, Stefania; NEOPTOLEMOS, John P.; KUNOVSKY, Lumir; BOJESEN, Stig E.; CARRARA, Silvia; GIOFFREDA, Domenica; MORKUNAS, Egidijus; ABIAN, Olga; BUNDUC, Stefania; BASSO, Daniela; BOGGI, Ugo; WLODARCZYK, Barbara; SZENTESI, Andrea; VANELLA, Giuseppe; CHEN, Inna; BIJLSMA, Maarten F.; KIUDELIS, Vytautas; LANDI, Stefano; Ben Schoettker; CORRADI, Chiara; GIESE, Nathalia; KAAKS, Rudolf; PEDUZZI, Giulia; HEGYI, Peter; MORELLI, Luca; FURBETTA, Niccolo; SOUCEK, Pavel; LATIANO, Anna; TALAR-WOJNAROWSKA, Renata; LINDGAARD, Sidsel C.; DIJK, Frederik; MILANETTOJ, Anna Caterina; TAVANO, Francesca; CERVENA, Klara; EROSS, Balint; TESTONI, Sabrina G.; VERHAGEN-OLDENAMPSEN, Judith H. E.; MALECKA-WOJCIESKO, E.; COSTELLO, Eithne; SALVIA, Roberto; MAIELLO, Evaristo; ERMINI, Stefano; SPERTI, Cosimo; HOLLECZEK, Bernd; PERRI, Francesco; SKIECEVICIENE, Jurgita; ARCHIBUGI, Livia; LUCCHESI, Maurizio; RIZZATO, Cosmeri; CANZIAN, FedericoPancreatic cancer has an incidence that almost matches its mortality. Only a small number of risk factors and 33 susceptibility loci have been identified. so Moreover, the relative rarity of pancreatic cancer poses significant hurdles for research aimed at increasing our knowledge of the genetic mechanisms contributing to the disease. Additionally, the inability to adequately power research questions prevents small monocentric studies from being successful. Several consortia have been established to pursue a better understanding of the genetic architecture of pancreatic cancers. The Pancreatic disease research (PANDoRA) consortium is the largest in Europe. PANDoRA is spread across 12 European countries, Brazil and Japan, bringing together 29 basic and clinical research groups. In the last ten years, PANDoRA has contributed to the discovery of 25 susceptibility loci, a feat that will be instrumental in stratifying the population by risk and optimizing preventive strategies.
- Polymorphisms in transcription factor binding sites and enhancer regions and pancreatic ductal adenocarcinoma risk(2024) UENAL, Pelin; LU, Ye; BUENO-DE-MESQUITA, Bas; EIJCK, Casper H. J. van; TALAR-WOJNAROWSKA, Renata; SZENTESI, Andrea; GAZOULI, Maria; KREIVENAITE, Edita; TAVANO, Francesca; MALECKA-WOJCIESKO, Ewa; EROSS, Balint; OLIVERIUS, Martin; BUNDUC, Stefania; AOKI, Mateus Nobrega; VODICKOVA, Ludmila; BOGGI, Ugo; GIACCHERINI, Matteo; KONDRACKIENE, Jurate; CHAMMAS, Roger; PALMIERI, Orazio; THEODOROPOULOS, George E.; BIJLSMA, Maarten F.; BASSO, Daniela; MOHELNIKOVA-DUCHONOVA, Beatrice; SOUCEK, Pavel; IZBICKI, Jakob R.; KIUDELIS, Vytautas; VANELLA, Giuseppe; ARCIDIACONO, Paolo Giorgio; WLODARCZYK, Barbara; HACKERT, Thilo; SCHOETTKER, Ben; UZUNOGLU, Faik G.; BAMBI, Franco; GOETZ, Mara; HLAVAC, Viktor; BRENNER, Hermann; PERRI, Francesco; CARRARA, Silvia; LANDI, Stefano; HEGYI, Peter; DIJK, Frederike; MAIELLO, Evaristo; CAPRETTI, Giovanni; TESTONI, Sabrina Gloria Giulia; PETRONE, Maria Chiara; STOCKER, Hannah; ERMINI, Stefano; ARCHIBUGI, Livia; GENTILUOMO, Manuel; CAVESTRO, Giulia Martina; PEZZILLI, Raffaele; FRANCO, Gregorio Di; MILANETTO, Anna Caterina; SPERTI, Cosimo; NEOPTOLEMOS, John P.; MORELLI, Luca; VOKACOVA, Klara; PASQUALI, Claudio; LAWLOR, Rita T.; BAZZOCCHI, Francesca; KUPCINSKAS, Juozas; CAPURSO, Gabriele; CAMPA, Daniele; CANZIAN, FedericoGenome-wide association studies (GWAS) are a powerful tool for detecting variants associated with complex traits and can help risk stratification and prevention strategies against pancreatic ductal adenocarcinoma (PDAC). However, the strict significance threshold commonly used makes it likely that many true risk loci are missed. Functional annotation of GWAS polymorphisms is a proven strategy to identify additional risk loci. We aimed to investigate single-nucleotide polymorphisms (SNP) in regulatory regions [transcription factor binding sites (TFBSs) and enhancers] that could change the expression profile of multiple genes they act upon and thereby modify PDAC risk. We analyzed a total of 12,636 PDAC cases and 43,443 controls from PanScan/PanC4 and the East Asian GWAS (discovery populations), and the PANDoRA consortium (replication population). We identified four associations that reached study-wide statistical significance in the overall meta-analysis: rs2472632(A) (enhancer variant, OR 1.10, 95%CI 1.06,1.13, p = 5.5 x 10-8), rs17358295(G) (enhancer variant, OR 1.16, 95%CI 1.10,1.22, p = 6.1 x 10-7), rs2232079(T) (TFBS variant, OR 0.88, 95%CI 0.83,0.93, p = 6.4 x 10-6) and rs10025845(A) (TFBS variant, OR 1.88, 95%CI 1.50,1.12, p = 1.32 x 10-5). The SNP with the most significant association, rs2472632, is located in an enhancer predicted to target the coiled-coil domain containing 34 oncogene. Our results provide new insights into genetic risk factors for PDAC by a focused analysis of polymorphisms in regulatory regions and demonstrating the usefulness of functional prioritization to identify loci associated with PDAC risk.
- Insights from a Computational-Based Approach for Analyzing Autophagy Genes across Human Cancers(2023) CARRASCO, Alexis German Murillo; GIOVANINI, Guilherme; RAMOS, Alexandre Ferreira; CHAMMAS, Roger; BUSTOS, Silvina OdeteIn the last decade, there has been a boost in autophagy reports due to its role in cancer progression and its association with tumor resistance to treatment. Despite this, many questions remain to be elucidated and explored among the different tumors. Here, we used omics-based cancer datasets to identify autophagy genes as prognostic markers in cancer. We then combined these findings with independent studies to further characterize the clinical significance of these genes in cancer. Our observations highlight the importance of innovative approaches to analyze tumor heterogeneity, potentially affecting the expression of autophagy-related genes with either pro-tumoral or anti-tumoral functions. In silico analysis allowed for identifying three genes (TBC1D12, KERA, and TUBA3D) not previously described as associated with autophagy pathways in cancer. While autophagy-related genes were rarely mutated across human cancers, the expression profiles of these genes allowed the clustering of different cancers into three independent groups. We have also analyzed datasets highlighting the effects of drugs or regulatory RNAs on autophagy. Altogether, these data provide a comprehensive list of targets to further the understanding of autophagy mechanisms in cancer and investigate possible therapeutic targets.
- Extracellular Vesicle-Packaged miR-195-5p Sensitizes Melanoma to Targeted Therapy with Kinase Inhibitors(2023) SANTOS, Nathalia L.; BUSTOS, Silvina O.; REIS, Patricia P.; CHAMMAS, Roger; ANDRADE, Luciana N. S.Management of advanced melanoma remains challenging, with most BRAF (B-Raf proto-oncogene, serine/threonine kinase)-mutated metastatic patients relapsing within a few months upon MAPK inhibitors treatment. Modulation of tumor-derived extracellular vesicle (EVs) cargo with enrichment of antitumoral molecules is a promising strategy to impair tumor progression and increase treatment response. Herein, we report that restored expression of miR-195-5p, down-regulated in melanoma favoring drug resistance, increases the release of EVs enriched in the tumor suppressor miRNAs, miR-195-5p, miR-152-3p, and miR-202-3p. Incorporating these EVs by bystander tumor cells resulted in decreased proliferation and viability, accompanied by a reduction in CCND1 and YAP1 mRNA levels. Upon treatment with MAPK inhibitors, miR-195 EVs significantly decreased BCL2-L1 protein levels and increased cell death ratio and treatment efficacy. Additionally, EVs exogenously loaded with miR-195-5p by electroporation reduced tumor volume in vivo and impaired engraftment and growth of xenografts implanted with melanoma cells exposed to MAPK inhibitors. Our study shows that miR-195-5p antitumoral activity can be spread to bystander cells through EVs, improving melanoma response to targeted therapy and revealing a promising EV-based strategy to increase clinical response in patients harboring BRAF mutations.
- Potential of [C-11](R)-PK11195 PET Imaging for Evaluating Tumor Inflammation: A Murine Mammary Tumor Model(2022) SOUZA, Aline Morais de; REAL, Caroline Cristiano; JUNQUEIRA, Mara de Souza; SOUZA, Larissa Estessi de; MARQUES, Fabio Luiz Navarro; BUCHPIGUEL, Carlos Alberto; CHAMMAS, Roger; SAPIENZA, Marcelo Tatit; FARIA, Daniele de PaulaBackground: Breast tumor inflammation is an immunological process that occurs mainly by mediation of Tumor-Associated Macrophages (TAM). Aiming for a specific measurement of tumor inflammation, the current study evaluated the potential of Positron Emission Tomography (PET) imaging with [C-11](R)-PK11195 to evaluate tumor inflammation in a mammary tumor animal model. Methods: Female Balb/C mice were inoculated with 4T1 cells. The PET imaging with [C-11](R)-PK11195 and [F-18]FDG was acquired 3 days, 1 week, and 2 weeks after cell inoculation. Results: The [C-11](R)-PK11195 tumor uptake increased from 3 days to 1 week, and decreased at 2 weeks after cell inoculation, as opposed to the [F-18]FDG uptake, which showed a slight decrease in uptake at 1 week and increased uptake at 2 weeks. In the control group, no significant differences occurred in tracer uptake over time. Tumor uptake of both radiopharmaceuticals is more expressed in tumor edge regions, with greater intensity at 2 weeks, as demonstrated by [C-11](R)-PK11195 autoradiography and immunofluorescence with TSPO antibodies and CD86 pro-inflammatory phenotype. Conclusion: The [C-11](R)-PK11195 was able to identify heterogeneous tumor inflammation in a murine model of breast cancer and the uptake varied according to tumor size. Together with the glycolytic marker [F-18]FDG, molecular imaging with [C-11](R)-PK11195 may provide a better characterization of inflammatory responses in cancer.
- Data-driven, cross-disciplinary collaboration: lessons learned at the largest academic health center in Latin America during the COVID-19 pandemic(2024) RITTO, Ana Paula; ARAUJO, Adriana Ladeira de; CARVALHO, Carlos Roberto Ribeiro de; SOUZA, Heraldo Possolo De; FAVARETTO, Patricia Manga e Silva; SABOYA, Vivian Renata Boldrim; GARCIA, Michelle Louvaes; KULIKOWSKI, Leslie Domenici; KALLAS, Esper Georges; PEREIRA, Antonio Jose Rodrigues; COBELLO JUNIOR, Vilson; SILVA, Katia Regina; ABDALLA, Eidi Raquel Franco; SEGURADO, Aluisio Augusto Cotrim; SABINO, Ester Cerdeira; RIBEIRO JUNIOR, Ulysses; FRANCISCO, Rossana Pulcineli Vieira; MIETHKE-MORAIS, Anna; LEVIN, Anna Sara Shafferman; SAWAMURA, Marcio Valente Yamada; FERREIRA, Juliana Carvalho; SILVA, Clovis Artur; MAUAD, Thais; GOUVEIA, Nelson da Cruz; LETAIF, Leila Suemi Harima; BEGO, Marco Antonio; BATTISTELLA, Linamara Rizzo; DUARTE, Alberto Jose da Silva; SEELAENDER, Marilia Cerqueira Leite; MARCHINI, Julio; FORLENZA, Orestes Vicente; ROCHA, Vanderson Geraldo; MENDES-CORREA, Maria Cassia; COSTA, Silvia Figueiredo; CERRI, Giovanni Guido; BONFA, Eloisa Silva Dutra de Oliveira; CHAMMAS, Roger; BARROS FILHO, Tarcisio Eloy Pessoa de; BUSATTO FILHO, GeraldoIntroduction The COVID-19 pandemic has prompted global research efforts to reduce infection impact, highlighting the potential of cross-disciplinary collaboration to enhance research quality and efficiency.Methods At the FMUSP-HC academic health system, we implemented innovative flow management routines for collecting, organizing and analyzing demographic data, COVID-related data and biological materials from over 4,500 patients with confirmed SARS-CoV-2 infection hospitalized from 2020 to 2022. This strategy was mainly planned in three areas: organizing a database with data from the hospitalizations; setting-up a multidisciplinary taskforce to conduct follow-up assessments after discharge; and organizing a biobank. Additionally, a COVID-19 curated collection was created within the institutional digital library of academic papers to map the research output.Results Over the course of the experience, the possible benefits and challenges of this type of research support approach were identified and discussed, leading to a set of recommended strategies to enhance collaboration within the research institution. Demographic and clinical data from COVID-19 hospitalizations were compiled in a database including adults and a minority of children and adolescents with laboratory confirmed COVID-19, covering 2020-2022, with approximately 350 fields per patient. To date, this database has been used in 16 published studies. Additionally, we assessed 700 adults 6 to 11 months after hospitalization through comprehensive, multidisciplinary in-person evaluations; this database, comprising around 2000 fields per subject, was used in 15 publications. Furthermore, thousands of blood samples collected during the acute phase and follow-up assessments remain stored for future investigations. To date, more than 3,700 aliquots have been used in ongoing research investigating various aspects of COVID-19. Lastly, the mapping of the overall research output revealed that between 2020 and 2022 our academic system produced 1,394 scientific articles on COVID-19.Discussion Research is a crucial component of an effective epidemic response, and the preparation process should include a well-defined plan for organizing and sharing resources. The initiatives described in the present paper were successful in our aim to foster large-scale research in our institution. Although a single model may not be appropriate for all contexts, cross-disciplinary collaboration and open data sharing should make health research systems more efficient to generate the best evidence.
- Role of galectin-3 in the elastic response of radial growth phase melanoma cancer cells(2023) HERRERA-REINOZA, Nataly; TORTELLI JUNIOR, Tharcisio Citrangulo; TEIXEIRA, Fernanda de Sa; CHAMMAS, Roger; SALVADORI, Maria CeciliaMelanoma is originated from the malignant transformation of the melanocytes and is characterized by a high rate of invasion, the more serious stage compromising deeper layers of the skin and eventually leading to the metastasis. A high mortality due to melanoma lesion persists because most of melanoma lesions are detected in advanced stages, which decreases the chances of survival. The identification of the principal mechanics implicated in the development and progression of melanoma is essential to devise new early diagnosis strategies. Cell mechanics is related with a lot of cellular functions and processes, for instance motility, differentiation, migration and invasion. In particular, the elastic modulus (Young's modulus) is a very explored parameter to describe the cell mechanical properties; most cancer cells reported in the literature smaller elasticity modulus. In this work, we show that the elastic modulus of melanoma cells lacking galectin-3 is significantly lower than those of melanoma cells expressing galectin-3. More interestingly, the gradient of elastic modulus in cells from the nuclear region towards the cell periphery is more pronounced in shGal3 cells.
- Deciphering the Functional Status of Breast Cancers through the Analysis of Their Extracellular Vesicles(2023) CARRASCO, Alexis German Murillo; OTAKE, Andreia Hanada; MACEDO-DA-SILVA, Janaina; SANTIAGO, Veronica Feijoli; PALMISANO, Giuseppe; ANDRADE, Luciana Nogueira de Sousa; CHAMMAS, RogerBreast cancer (BC) accounts for the highest incidence of tumor-related mortality among women worldwide, justifying the growing search for molecular tools for the early diagnosis and follow-up of BC patients under treatment. Circulating extracellular vesicles (EVs) are membranous nanocompartments produced by all human cells, including tumor cells. Since minimally invasive methods collect EVs, which represent reservoirs of signals for cell communication, these particles have attracted the interest of many researchers aiming to improve BC screening and treatment. Here, we analyzed the cargoes of BC-derived EVs, both proteins and nucleic acids, which yielded a comprehensive list of potential markers divided into four distinct categories, namely, (i) modulation of aggressiveness and growth; (ii) preparation of the pre-metastatic niche; (iii) epithelial-to-mesenchymal transition; and (iv) drug resistance phenotype, further classified according to their specificity and sensitivity as vesicular BC biomarkers. We discuss the therapeutic potential of and barriers to the clinical implementation of EV-based tests, including the heterogeneity of EVs and the available technologies for analyzing their content, to present a consistent, reproducible, and affordable set of markers for further evaluation.