Nils L. Visser
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Nils L. Visser has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Carine Dufau
Division of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, the Netherlands
12 shared publications - Daniel S. Peeper
Division of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, the Netherlands
12 shared publications - Daniela Mercedes D’EMpaire Altimari
Division of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, the Netherlands
12 shared publications - Elisabeth H. Jin
Division of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, the Netherlands
12 shared publications - Hester H. Van Boven
The Netherlands Cancer Institute 13 Department of Pathology Amsterdam, the Netherlands
12 shared publications - Juan Simon Nieto
Division of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, the Netherlands
12 shared publications
Latest Publications
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S2 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
TCGA and DepMap data, related to Figure 5 and S4
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S2 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
TCGA and DepMap data, related to Figure 5 and S4
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Genome-wide drug-anchored CRISPR-Cas9 screens identify targetable pathways to sensitize to DDLPS therapies, related to Figure 1
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Genome-wide drug-anchored CRISPR-Cas9 screens identify targetable pathways to sensitize to DDLPS therapies, related to Figure 1
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Supplementary Table S3 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Supplementary Table S3 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S5 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
RNA seq data, related to Figure 3, S3, S4, and 5
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S5 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
RNA seq data, related to Figure 3, S3, S4, and 5
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
(non-)essential gene lists, readcounts CRISPR screens, MAGeCK output, related to Figure 1 and S1
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
(non-)essential gene lists, readcounts CRISPR screens, MAGeCK output, related to Figure 1 and S1
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S2 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Perturbation of NHEJ-related genes sensitizes specifically to low-dose doxorubicin, related to Figure 2
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S2 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Perturbation of NHEJ-related genes sensitizes specifically to low-dose doxorubicin, related to Figure 2
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
All sgRNA sequences used in this study
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
All sgRNA sequences used in this study
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Perturbation of TDP2 or DNA-PKcs strongly increases cell cycle arrest and senescence induction by low-dose doxorubicin, related to Figure 3
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Perturbation of TDP2 or DNA-PKcs strongly increases cell cycle arrest and senescence induction by low-dose doxorubicin, related to Figure 3
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
TDP2-/- plus low-dose doxorubicin activates p53 in MDM2 amplified DDLPS, related to Figure 5
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
TDP2-/- plus low-dose doxorubicin activates p53 in MDM2 amplified DDLPS, related to Figure 5
- Open Access
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S6 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Gene sets used in this study, related to Figure 3 and S3
- 1 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S6 from Targeting the Non-Homologous End Joining Pathway Sensitizes MDM2-Amplified Liposarcoma to Doxorubicin by Enhancing p53-Mediated Senescence
Gene sets used in this study, related to Figure 3 and S3