ResearcherUniversidade Federal do Rio Grande do SulActive in the last 2 years
Alessandro Bersch Osvaldt
Matched on ORCID iD 0000-0002-5863-6656; OpenAlex author ID A5022040472.
Their work
- Papers
- 8 (first author 0, last author 1)
- Trials
- 0
- Grants
- 0
- Collaborators
- 10
2014: 1 paper · 2015: none · 2016: 2 papers · 2017: none · 2018: 1 paper · 2019: none · 2020: 1 paper · 2021: none · 2022: none · 2023: none · 2024: none · 2025: 1 paper · 2026: 2 papers
Papers 8
- International survey on neoadjuvant treatments in anatomically resectable pancreatic adenocarcinoma (INSPIRA): a real-life snapshot. Co-author DOI 10.1016/j.suronc.2026.102580↗
- Mutational signature landscape of pancreatic cancer genomes from nine countries Co-author DOI 10.64898/2026.10.21.26365999↗
- Single-cell and spatially resolved atlas of pancreatic cancer reveals immunophenotypes associated with clinical outcome Co-author DOI 10.1101/2025.02.08.637283↗
- Calcium Signaling Alterations Caused by Epigenetic Mechanisms in Pancreatic Cancer: From Early Markers to Prognostic Impact. Co-author DOI 10.3390/cancers12071735↗
- THE ROLE OF IMMUNOINFLAMMATORY MARKERS IN THE PROGNOSIS AND RESECTABILITY OF PANCREATIC ADENOCARCINOMA. Last author DOI 10.1590/0102-672020180001e1366↗
- miRNA-21 and miRNA-34a Are Potential Minimally Invasive Biomarkers for the Diagnosis of Pancreatic Ductal Adenocarcinoma. Co-author DOI 10.1097/mpa.0000000000000383↗
- H4K12 and H3K18 Acetylation Associates With Poor Prognosis in Pancreatic Cancer. Co-author DOI 10.1097/pai.0000000000000194↗
- PRIMA-1, a mutant p53 reactivator, induces apoptosis and enhances chemotherapeutic cytotoxicity in pancreatic cancer cell lines. Co-author DOI 10.1007/s10637-014-0090-9↗
Closest collaborators
The 10 strongest of 10 ranked by shared papers, trials and grants, with recent and small-team work weighing most.
- Cristina Bonorino · 1 shared paper, 2025
- Gabriel F. Pozo de Mattos P. · 1 shared paper, 2025
- Patrícia Ashton-Prolla · 4 shared papers, 2014–2020
- Paper Calcium Signaling Alterations Caused by Epigenetic Mechanisms in Pancreatic Cancer: From Early Markers to Prognostic Im… DOI 10.3390/cancers12071735↗
- Paper miRNA-21 and miRNA-34a Are Potential Minimally Invasive Biomarkers for the Diagnosis of Pancreatic Ductal Adenocarcinom… DOI 10.1097/mpa.0000000000000383↗
- Paper H4K12 and H3K18 Acetylation Associates With Poor Prognosis in Pancreatic Cancer. DOI 10.1097/pai.0000000000000194↗
- Bárbara Alemar · 3 shared papers, 2014–2020
- Paper Calcium Signaling Alterations Caused by Epigenetic Mechanisms in Pancreatic Cancer: From Early Markers to Prognostic Im… DOI 10.3390/cancers12071735↗
- Paper miRNA-21 and miRNA-34a Are Potential Minimally Invasive Biomarkers for the Diagnosis of Pancreatic Ductal Adenocarcinom… DOI 10.1097/mpa.0000000000000383↗
- Paper PRIMA-1, a mutant p53 reactivator, induces apoptosis and enhances chemotherapeutic cytotoxicity in pancreatic cancer ce… DOI 10.1007/s10637-014-0090-9↗
- Cleandra Gregório · 2 shared papers, 2016–2020
- Paper Calcium Signaling Alterations Caused by Epigenetic Mechanisms in Pancreatic Cancer: From Early Markers to Prognostic Im… DOI 10.3390/cancers12071735↗
- Paper miRNA-21 and miRNA-34a Are Potential Minimally Invasive Biomarkers for the Diagnosis of Pancreatic Ductal Adenocarcinom… DOI 10.1097/mpa.0000000000000383↗
- Patrícia Izetti · 3 shared papers, 2014–2016
- Paper miRNA-21 and miRNA-34a Are Potential Minimally Invasive Biomarkers for the Diagnosis of Pancreatic Ductal Adenocarcinom… DOI 10.1097/mpa.0000000000000383↗
- Paper H4K12 and H3K18 Acetylation Associates With Poor Prognosis in Pancreatic Cancer. DOI 10.1097/pai.0000000000000194↗
- Paper PRIMA-1, a mutant p53 reactivator, induces apoptosis and enhances chemotherapeutic cytotoxicity in pancreatic cancer ce… DOI 10.1007/s10637-014-0090-9↗
- Luís Felipe Ribeiro Pinto · 1 shared paper, 2020
- Tatiana Falcão Eyff · 1 shared paper, 2018
- Camila Juliano · 1 shared paper, 2016
- Maria I.Albano Edelweiss · 1 shared paper, 2016
How to reach this person
A chain of introductions through people who have published, run trials or held grants together (the fewest links first, then the links with the most shared work). Built from public records only; no contact details are kept.