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Latin America Cutaneous Oncology Management (LACOM) I: The Role of Skin Care in Oncology Patients and Survivors
(SanovaWorks, 2025-02-01)
Daniel Alcalá Pérez
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Ana Sofia Acosta Madiedo
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Sebastian Andreani
;
Anneke Andriessen
;
Hebert Cárdenas
2
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Maraviroc/cisplatin combination inhibits gastric cancer tumoroid growth and improves mice survival
(Springer Science and Business Media LLC, 2025-01-18)
Bárbara Mora-Lagos
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María Elena Reyes
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LOBOS GONZALEZ, LORENA DE LOURDES
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Matías del Campo
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Kurt Buchegger
<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Background</jats:title> <jats:p>Gastric cancer (GC) is a significant cancer-related cause of death worldwide. GC’s most used chemotherapeutic regimen is based on platinum drugs such as cisplatin (CDDP). However, CDDP chemoresistance reduces the survival rate of advanced GC. The immune C-C chemokine receptor type 5 (CCR5) have been proposed as a pivotal factor in cancer progression since its blockade has been linked with antineoplastic effects on tumor cell proliferation; nevertheless, its role in the chemoresistance of GC has not been elucidated. This study aimed to determine the effects induced by the CCR5 using Maraviroc (MVC), a highly selective CCR5 antagonist, on CDDP-resistant AGS cells (AGS R-CDDP), tumoroids (<jats:italic>3D</jats:italic> tumor spheroids), and animal models.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>The combined CDDP and MVC treatment reduced cell viability and inhibited tumoroid formation in AGS R-CDDP cells. The effects of the MVC/CDDP combination on apoptosis and cell cycle progression were correlated with the increase in CDDP (dose-dependent). The mRNA levels of C-C Motif Chemokine Ligand 5 (CCL5), the main ligand for CCR5, decreased significantly in cells treated with the MVC/CDDP combination. MVC in the MVC/CDDP combination improved the survival rate and biochemical parameters of CDDP-treated mice by reducing the side effects of CDDP alone.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>This finding suggests that MVC/CDDP combination could be a potential complementary therapy for GC.</jats:p> </jats:sec>
3Scopus© Citations 4
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The Ω-3 fatty acid docosahexaenoic acid selectively induces apoptosis in tumor-derived cells and suppress tumor growth in gastric cancer
(2021)
Lorena Ortega
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Lorena Lobos-González
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Mauricio Reyna-Jeldes
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Daniela Cerda
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Erwin De la Fuente-Ortega
Scopus© Citations 16 2
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Potential use of n-3 PUFAs to prevent oxidative stress-derived ototoxicity caused by platinum-based chemotherapy
(2020)
Ignacio A. Cortés Fuentes
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Mauricio Burotto
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Mauricio A. Retamal
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Michael Frelinghuysen
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Christian Caglevic
Scopus© Citations 4 1
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Identification of Rigosertib for the Treatment of Recessive Dystrophic Epidermolysis Bullosa-Associated Squamous Cell Carcinoma
(2019)
Velina S. Atanasova
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Celine Pourreyron
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Mehdi Farshchian
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Michael Lawler
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Christian A. Brown
<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Purpose:</jats:title> <jats:p>Squamous cell carcinoma (SCC) of the skin is the leading cause of death in patients with the severe generalized form of the genetic disease recessive dystrophic epidermolysis bullosa (RDEB). Although emerging data are identifying why patients suffer this fatal complication, therapies for treatment of RDEB SCC are in urgent need.</jats:p> <jats:p>Experimental Design: We previously identified polo-like kinase 1 (PLK1) as a therapeutic target in skin SCC, including RDEB SCC. Here, we undertake a screen of 6 compounds originally designated as PLK1 inhibitors, and detail the efficacy of the lead compound, the multipathway allosteric inhibitor ON-01910, for targeting RDEB SCC in vitro and in vivo.</jats:p> </jats:sec> <jats:sec> <jats:title>Results:</jats:title> <jats:p>ON-01910 (or rigosertib) exhibited significant specificity for RDEB SCC: in culture rigosertib induced apoptosis in 10 of 10 RDEB SCC keratinocyte populations while only slowing the growth of normal primary skin cells at doses 2 orders of magnitude higher. Furthermore, rigosertib significantly inhibited the growth of two RDEB SCC in murine xenograft studies with no apparent toxicity. Mechanistically, rigosertib has been shown to inhibit multiple signaling pathways. Comparison of PLK1 siRNA with MEK inhibition, AKT inhibition, and the microtubule-disrupting agent vinblastine in RDEB SCC shows that only PLK1 reduction exhibits a similar sensitivity profile to rigosertib.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions:</jats:title> <jats:p>These data support a "first in RDEB" phase II clinical trial of rigosertib to assess tumor targeting in patients with late stage, metastatic, and/or unresectable SCC.</jats:p> </jats:sec>
24Scopus© Citations 32
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Prevalence and management of condylomas in consulting population in Chile: "DIACON study" [Prevalencia y manejo de condilomas en poblacion consultante en Chile: estudio "DIACON"]
(2019)
Andrea Schilling R.
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Andrea Huneeus V.
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Alejandra Massoc P.
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Francisca Rivera M.
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Gabriel Cavada Ch.
1Scopus© Citations 3 1
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Epanorin, a lichen secondary metabolite, inhibits proliferation of MCF-7 breast cancer cells.
(2019)
Juan Palacios-Moreno
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Cecilia Rubio
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Wanda Quilhot
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M. Fernanda Cavieres
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Eduardo de la Peña
<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Background</jats:title> <jats:p>Epanorin (EP) is a secondary metabolite of the <jats:italic>Acarospora</jats:italic> lichenic species. EP has been found in lichenic extracts with antimicrobial activity, and UV-absorption properties have been described for closely related molecules; however, its antiproliferative activity in cancer cells has not yet been explored. It has been hypothesized that EP inhibits cancer cell growth. MCF-7 breast cancer cells, normal fibroblasts, and the non-transformed HEK-293 cell line were exposed to increasing concentrations of EP, and proliferation was assessed by the sulforhodamine-B assay.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>MCF-7 cells exposed to EP were examined for cell cycle progression using flow cytometry, and DNA fragmentation was examined using the TUNEL assay. In addition, EP’s mutagenic activity was assessed using the <jats:italic>Salmonella typhimurium</jats:italic> reverse mutation assay. The data showed that EP inhibits proliferation of MCF-7 cells, and it induces cell cycle arrest in G0/G1 through a DNA fragmentation-independent mechanism. Furthermore, EP’s lack of overt cytotoxicity in the normal cell line HEK-293 and human fibroblasts in cell culture is supported by the absence of mutagenic activity of EP.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion</jats:title> <jats:p>EP emerges as a suitable molecule for further studies as a potential antineoplastic agent.</jats:p> </jats:sec>
Scopus© Citations 7 20
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Gold nanoparticle based double-labeling of melanoma extracellular vesicles to determine the specificity of uptake by cells and preferential accumulation in small metastatic lung tumors
(2020)
Pablo Lara
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Sujey Palma-Florez
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Edison Salas-Huenuleo
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Iva Polakovicova
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Simón Guerrero
<jats:title>Abstract</jats:title><jats:sec> <jats:title>Background</jats:title> <jats:p>Extracellular vesicles (EVs) have shown great potential for targeted therapy, as they have a natural ability to pass through biological barriers and, depending on their origin, can preferentially accumulate at defined sites, including tumors. Analyzing the potential of EVs to target specific cells remains challenging, considering the unspecific binding of lipophilic tracers to other proteins, the limitations of fluorescence for deep tissue imaging and the effect of external labeling strategies on their natural tropism. In this work, we determined the cell-type specific tropism of B16F10-EVs towards cancer cell and metastatic tumors by using fluorescence analysis and quantitative gold labeling measurements. Surface functionalization of plasmonic gold nanoparticles was used to promote indirect labeling of EVs without affecting size distribution, polydispersity, surface charge, protein markers, cell uptake or in vivo biodistribution. Double-labeled EVs with gold and fluorescent dyes were injected into animals developing metastatic lung nodules and analyzed by fluorescence/computer tomography imaging, quantitative neutron activation analysis and gold-enhanced optical microscopy.</jats:p> </jats:sec><jats:sec> <jats:title>Results</jats:title> <jats:p>We determined that B16F10 cells preferentially take up their own EVs, when compared with colon adenocarcinoma, macrophage and kidney cell-derived EVs. In addition, we were able to detect the preferential accumulation of B16F10 EVs in small metastatic tumors located in lungs when compared with the rest of the organs, as well as their precise distribution between tumor vessels, alveolus and tumor nodules by histological analysis. Finally, we observed that tumor EVs can be used as effective vectors to increase gold nanoparticle delivery towards metastatic nodules.</jats:p> </jats:sec><jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Our findings provide a valuable tool to study the distribution and interaction of EVs in mice and a novel strategy to improve the targeting of gold nanoparticles to cancer cells and metastatic nodules by using the natural properties of malignant EVs.</jats:p> </jats:sec>
11 1Scopus© Citations 88

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