Browsing by Author "Ibáñez, Carolina"

Now showing 1 - 4 of 4
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    Access disparities and underutilization of germline genetic testing in Chilean breast cancer patients
    (2023) Acevedo Claros, Francisco Nicolás; Walbaum García, Benjamín Vicente; Camus Appuhn, Mauricio Gonzalo; Manzor Véliz, Manuel; Muñiz Muñoz, María Sabrina; Medina Araya, Lidia; Petric Guajardo, Militza Paulina; Reyes, Paula; Domínguez, Francisco; Puschel Illanes, Klaus; Merino Lara, Tomás Rodrigo; Bravo, M. Loreto; Pinto, Mauricio P.; Ibáñez, Carolina; Hughes, Kevin; Sánchez Rojel, César Giovanni
    Purpose Latin American reports on genetic cancer risk assessments are scarce. In Chile, current breast cancer (BC) guidelines do not define strategies for germline genetic testing. Our study sought to quantify the disparities in access to genetic testing in Chilean BC patients, according to international standards and their clinical characteristics to explore improvement strategies.Methods Retrospective analysis of invasive BC databases including patients treated in a Public Hospital (PH) and in an Academic Private Center (AC) in Santiago, Chile between 2012 and 2021.Results Of 5438 BC patients, 3955 had enough data for National Comprehensive Cancer Network (NCCN) categorization. From these, 1911 (48.3%) fulfilled NCCN criteria for germline testing, of whom, 300 were tested for germline mutations and 268 with multigene panels. A total of 65 pathogenic variants were found in this subset. As expected, BRCA1/2 mutations were the most frequent (17.7%). Access to genetic testing was higher in AC versus PH (19.6% vs. 10.3%, p = 0.0001). Other variables associated with germline genetic testing were BC diagnosis after 2018, being 45 years old or younger at diagnosis, BC family history (FH), FH of ovarian cancer, non-metastatic disease, and triple-negative subtype.Conclusion In our cohort, 15% of BC patients who met NCCN criteria for germline testing were effectively tested. This percentage was even lower at the PH. Current recommendations encourage universal genetic testing for BC patients; however, our findings suggest that Chile is far from reaching such a goal and national guidelines in this regard are urgently needed. To our knowledge, this is the first study of its kind in Chile and Latin America.
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    Diabetic concentrations of metformin inhibit platelet-mediated ovarian cancer cell progression
    (2017) Erices, R.; Cubillos, Sofía; Aravena, Raúl; Santoro, Felice; Márquez, Mónica; Orellana Walden, Renán Felipe; Ramírez, Carolina; González, Pamela; Fuenzalida, Patricia; Bravo Castillo, María Loreto; Oliva, Bárbara; Kato Cardemil, Sumie Rode; Ibáñez, Carolina; Brañes, Jorge; Bravo, Erasmo; Alonso, Catalina
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    Extracellular matrix protein signaling promotes multi-step cancer vasculogenic mimicry formation
    (2025) Mingo Orsini, Gabriel Antonio; Valdivia Román, Andrés Felipe; Santander Zambrano, Gema Nicolle; Babbitt Negrete, Nicole Anike; Aldana Villarroel, Varina Isabel; Pradenas Mateluna, Javiera Macarena Guillerm; González, Pamela; Canales Valenzuela, Cristóbal; Toledo, Jorge A.; Ibáñez, Carolina; Nualart, Francisco; Varas-Godoy, Manuel; Gejman, Roger; Roa, Juan Carlos; Ravasio, Andrea; Bertocchi, Cristina; Owen, Gareth Ivor
    Cancer vasculogenic mimicry (VM) is the formation of vasculature structures in the absence of endothelial cells. We previously established an in vitro model that facilitates the formation of a lumen-containing and fluid-conducting tubular structures after 4 days of cancer cell growth on Matrigel. Herein, we mechanistically characterize this model in breast and ovarian cancer cell lines demonstrating distinct phases of VM formation and the dependence of specific extracellular matrix proteins. We report that VM occurs in four distinct stages. Firstly, alignment, migration then clustering delineate the area of the future tubular structure. Secondly, contraction of aligned structures followed by loss of attachment of some cells and cellular blebbing. Thirdly, a phase of mass proliferation followed by the raising of specific areas of the cancer cell mass above the Matrigel (bridge). Finally, the formation of a cell monolayer closes the tubular structure, forms a glycoprotein-rich luminal lining, then elevates the structure. Only later stages of VM require AKT and FAK signaling, as confirmed by chemical inhibition and phosphorylation analysis. We demonstrate that the lining of the tubular lumen is rich in laminin. Furthermore, the presence of Laminin 111 (but not collagen I) is sufficient in the extracellular matrix (Matrigel) for VM to occur and we confirm that integrin β1, but not integrin β3, is required and this protein changes location during the formation process. RNASeq analysis suggests that VM formation principally occurs through post-transcriptional regulation. As VM is associated with poor patient survival VM, an understanding of the mechanism of VM may bring to light novel biomarkers and anticancer targets.
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    Radiation recall dermatitis: Report of two cases
    (2013) Acevedo Claros, Francisco Nicolás; Arriagada, Paula; Ibáñez, Carolina; Ortega Mogilevich, Claudia Beatriz; Muñoz Schuffenegger, Pablo; Borghero Ríos, Yerko Orestes; Bustos Carrasco, Marisa Orietta; Sánchez Rojel, César Giovanni