- Cancer Genomics and Diagnostics
- Helicobacter pylori-related gastroenterology studies
- Caveolin-1 and cellular processes
- Eosinophilic Esophagitis
- Epigenetics and DNA Methylation
- Histone Deacetylase Inhibitors Research
- CRISPR and Genetic Engineering
- Chemical Reactions and Isotopes
- Renal and related cancers
- RNA Research and Splicing
- Glycosylation and Glycoproteins Research
- Peptidase Inhibition and Analysis
- Sarcoma Diagnosis and Treatment
- Gastric Cancer Management and Outcomes
- DNA Repair Mechanisms
- Extracellular vesicles in disease
- Ion channel regulation and function
- Gastroesophageal reflux and treatments
- PARP inhibition in cancer therapy
- Galectins and Cancer Biology
- RNA modifications and cancer
- Lung Cancer Treatments and Mutations
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto
2015-2022
Universidade do Porto
2015-2022
IPO Porto
2020
Instituto Português de Oncologia Francisco Gentil
2013
Advances in the treatment of triple-negative breast and ovarian cancer remain challenging. In particular, resistance to available therapy, by restoring or overexpressing DNA repair machinery, has often been reported. New strategies improve therapeutic outcomes these cancers are needed. Herein, we disclose dregamine 5-bromo-pyridin-2-ylhydrazone (BBIT20), a natural monoterpene indole alkaloid derivative, as an inhibitor homologous repair.To unveil BBIT20 antitumour activity underlying...
Deregulated expression of histone deacetylases (HDACs) has been implicated in tumorigenesis. Herein, we investigated class I HDACs bladder urothelial cell carcinoma (BUCC), its prognostic value and biological significance. Significantly increased transcript levels all were found BUCC compared to 20 normal mucosas, these higher lower grade stage tumors. Increased HDAC3 associated with improved patient survival. SiRNA experiments showed decrease viability motility, apoptosis. We concluded that...
Event Abstract Back to Chitosan microspheres can fight Helicobacter pylori gastric infection in mice Patrícia C. Henriques1, 2, Lia M. Costa1, Susana Junqueira-Neto1, Ricardo Carvalho1, Catarina L. Seabra1, 3, Bernardo P. Antunes1, Ana Magalhães2, 4, Celso A. Reis2, Fatima Gartner2, Elliete Touati5, Joana Gomes1, M Cristina Martins1, 3 and Inês Gonçalves1, 2 1 INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal i3S Investigação e Inovação em Saúde, Ciências Biomédicas...
Abstract Resistance to treatment is a major clinical problem and cause of cancer-related deaths. Understanding the biological basis resistance acquisition utmost importance improve management cancer patients. NGS analysis human lung (LC) tumors from patients that relapsed after with EGFR-tyrosine kinase inhibitors (TKI), revealed p.T790M mutation not present in all relapsing tumor cells, suggesting LC cells can become resistant even if carrying mutation. Using vitro treatments conditioned...
Abstract Despite initial benefit from anti-EGFR therapy, patients with EGFR-mutated lung cancer (LC) inevitably relapse. Knowing that the majority of relapsing cells do not carry resistance mutation, we hypothesized to therapy can be transferred horizontally between LC cells, through intercellular communication. Using a cell culture system allows communication secreted molecules and extracellular vesicles, performed indirect co-culture Erlotinib-sensitive HCC827 (S cells) Erlotinib-resistant...
Abstract Targeted therapies almost universally fail due to the development of resistance. EGFR-mutant non-small cell lung cancer (NSCLC) is a well characterized model such mechanism. In this model, treatment with anti-EGFR therapy leads resistance driven by presence EGFR T790M mutation in about 50% cases. However, clinical data shows present only subpopulation relapsing cells. How cells devoid become resistant not known. The aim study explore if T790M-mediated can spread horizontally,...