Marco Bolis
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
Research Subjects
Marco Bolis has a total of 388 co-authors. Here are the top co-authors by number of shared publications:
- Giada Andrea Cassanmagnago
Laboratory of Integrative Biomedicine, Department of Oncology, Istituto di Ricerche Farmacologiche ‘Mario Negri’ IRCCS, Via Mario Negri 2, 20156 Milano, Italy
20 shared publications - Mark A. Rubin
Department for BioMedical Research, University of Bern, Bern, Switzerland
19 shared publications - Alden King-Yung Leung
School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China
16 shared publications - Alina Naveed
University of Bern 1 Department for Biomedical Research Bern, Switzerland
16 shared publications - Andrej Benjak
Department for BioMedical Research (DBMR), University of Bern, Bern, Switzerland
16 shared publications - Bence Daniel
Department of Proteomic and Genomic Technologies, Genentech, South San Francisco, USA
16 shared publications
Latest Publications
- Open Access
Age-driven miR-29 trades youthful plasticity for epigenetic fidelity
Summary: Throughout life, somatic cells must preserve their identity while retaining the capacity to adapt. How this balance shifts with ageing and rejuvenation remains unclear. Here we identify miR-29 as a central point of convergence between the transcriptional programmes of physiological ageing and two routes to rejuvenation: induced reprogramming and the natural reset of early development. miR-29 rises with ageing, falls in both rejuvenation settings and shows the most conserved age-associated increase across vertebrates. miR-29 inhibition opposes transcriptional ageing, whereas mimics promote an older transcriptional state. Methylome analysis reveals a broader function: inhibition releases the miR-29 brake on remodelling, and mimic treatment reinforces it. This release increases methylation at repeat-associated CpGs and lowers epigenetic-clock estimates through unequal contributions in opposite directions. Inhibition also amplifies stimulus-induced methylation changes but reduces fidelity to lineage-specific methylation patterns. We extend this relationship to cancer, where low miR-29 expression marks tumours with younger epigenetic-age estimates yet greater methylation divergence from their tissue of origin. These findings identify miR-29 as a control point linking ageing, rejuvenation and cancer, and support a maladaptive trade-off model in which epigenetic fidelity is preserved at the expense of the plasticity needed for methylome maintenance and adaptation.
Open AccessAge-driven miR-29 trades youthful plasticity for epigenetic fidelity
Summary: Throughout life, somatic cells must preserve their identity while retaining the capacity to adapt. How this balance shifts with ageing and rejuvenation remains unclear. Here we identify miR-29 as a central point of convergence between the transcriptional programmes of physiological ageing and two routes to rejuvenation: induced reprogramming and the natural reset of early development. miR-29 rises with ageing, falls in both rejuvenation settings and shows the most conserved age-associated increase across vertebrates. miR-29 inhibition opposes transcriptional ageing, whereas mimics promote an older transcriptional state. Methylome analysis reveals a broader function: inhibition releases the miR-29 brake on remodelling, and mimic treatment reinforces it. This release increases methylation at repeat-associated CpGs and lowers epigenetic-clock estimates through unequal contributions in opposite directions. Inhibition also amplifies stimulus-induced methylation changes but reduces fidelity to lineage-specific methylation patterns. We extend this relationship to cancer, where low miR-29 expression marks tumours with younger epigenetic-age estimates yet greater methylation divergence from their tissue of origin. These findings identify miR-29 as a control point linking ageing, rejuvenation and cancer, and support a maladaptive trade-off model in which epigenetic fidelity is preserved at the expense of the plasticity needed for methylome maintenance and adaptation.
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S5 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment consistently modulates lineage-defining CRPCWNT signature and master TFs
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S5 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment consistently modulates lineage-defining CRPCWNT signature and master TFs
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S7 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment leads to decreased chromatin accessibility in CRPC-WNT
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S7 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
A947-treatment leads to decreased chromatin accessibility in CRPC-WNT
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
Drug screen with SMARCA2/4 degrader
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
Drug screen with SMARCA2/4 degrader
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S11 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 chromatin binding is reduced upon treatment with A947 in CRPC-WNT
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S11 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 chromatin binding is reduced upon treatment with A947 in CRPC-WNT
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids are SMARCA4 but not SMARCA2 dependent
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids are SMARCA4 but not SMARCA2 dependent
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S6 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids become deregulated in multiple proliferative pathways upon SMARCA2/4 degradation
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S6 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
CRPC-WNT organoids become deregulated in multiple proliferative pathways upon SMARCA2/4 degradation
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S12 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 regulates pro-proliferative pathways in CRPC-WNT
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S12 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
TCF7L2 regulates pro-proliferative pathways in CRPC-WNT
- Open Access
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S9 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
The TCF7L2 promoter interacts with an intragenic enhancer that is kept accessible by the SWI/SNF complex
- 2 April 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S9 from A Double-Negative Prostate Cancer Subtype Is Vulnerable to SWI/SNF-Targeting Degrader Molecules
The TCF7L2 promoter interacts with an intragenic enhancer that is kept accessible by the SWI/SNF complex