Alberto Martín
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Alberto Martín has a total of 113 co-authors. Here are the top co-authors by number of shared publications:
- Alberto Villanueva
Chemoresistance and Predictive Factors Group, Program Against Cancer Therapeutic Resistance (ProCURE), Catalan Institute of Oncology (ICO), Oncobell Program, Bellvitge Biomedical Research Institute (IDIBELL), L’Hospitalet del Llobregat, Barcelona, Spain
14 shared publications - Antoni Riera
Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Baldiri Reixac 10, Barcelona 08028, Spain
14 shared publications - Antonia Odena Caballol
Institute for Research in Biomedicine 2 (IRB Barcelona), the Barcelona Institute of Science and Technology (BIST), Barcelona, Spain
14 shared publications - Barbara M. G. Barbosa
CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria
14 shared publications - Camille Stephan-Otto Attolini
Institute for Research in Biomedicine, Barcelona Institute of Science and Technology, Barcelona, Spain
14 shared publications - Carlos Riego-Mejías
Institute for Research in Biomedicine 2 (IRB Barcelona), the Barcelona Institute of Science and Technology (BIST), Barcelona, Spain
14 shared publications
Latest Publications
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S4: Sanger sequencing dTAG-KRASG12V.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S4: Sanger sequencing dTAG-KRASG12V.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Effect of CD8+T cell immunodepletion in LUAD tumor regression upon KRASG12V degradation.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Effect of CD8+T cell immunodepletion in LUAD tumor regression upon KRASG12V degradation.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
LUAD resistance to targeted degradation in vivo is not mainly driven by efflux pump overactivation or point mutations in E3 machinery.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
LUAD resistance to targeted degradation in vivo is not mainly driven by efflux pump overactivation or point mutations in E3 machinery.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S2 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S2: Immunophenotyping strategy.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S2 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S2: Immunophenotyping strategy.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S5 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
LUAD tumor-derived cell lines resistant to PROTAC-induced KRASG12V degradation are sensitive to KRAS inhibitors.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S5 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
LUAD tumor-derived cell lines resistant to PROTAC-induced KRASG12V degradation are sensitive to KRAS inhibitors.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S1: antibodies cytometry.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S1: antibodies cytometry.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S5 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S5: SNV calling.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S5 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Table S5: SNV calling.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Data IVIS from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Data IVIS: representative IVIS images.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data IVIS from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Supplementary Data IVIS: representative IVIS images.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Selection of PROTACs compatible with the dTAG-KRASG12V LUAD model.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
Selection of PROTACs compatible with the dTAG-KRASG12V LUAD model.
- Open Access
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S6 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
KRAS degradation vs. inhibition.
- 14 August 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S6 from Targeted KRASG12V Degradation In Vivo Elicits Lung Adenocarcinoma Regression with Subsequent Relapse from Dysregulated Proteolysis
KRAS degradation vs. inhibition.