Author

J. V. Forment

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 4 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:drug response / drug discovery· 5 Organism:human· 4 Approach:genetic perturbation / CRISPR· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Assay:DNA methylation· 2 Assay:proteomics· 2 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

J. Armenia· 2 shared M. J. O'Connor· 2 shared M. Liptay· 2 shared S. Rottenberg· 2 shared S. T. Durant· 2 shared A. A. Sartori· 1 shared A. Barros· 1 shared A. Bradley· 1 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersCancer Biology

J. Armenia

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

D. Dibitetto, M. Liptay, F. Vivalda, E. Gogola, H. Dogan, M. G. Fernandez, A. Duarte, J. A. Schmid, S. T. Durant, J. V. Forment, I. Klebic, M. Siffert, R. de Brujin, A. N. Kousholt, N. A. Marti, , S. Rottenberg

This study identifies H2AX's role in promoting replication fork degradation and chemosensitivity in BRCA-deficient tumours, independent of its classical DNA damage signalling function.

bioRxiv · May 22, 2023Cancer Biology

MND1 and PSMC3IP control PARP inhibitor sensitivity in mitotic cells

A. Zelceski, P. Francica, L. Lingg, M. Mutlu, C. Stok, M. Liptay, J. Alexander, J. S. Baxter, R. Brough, A. Gulati, S. Haider, M. Raghunandan, F. Song, S. Sridhar, J. V. Forment, , C. J. Lord

This study shows that PSMC3IP and MND1 depletion increases PARP inhibitor sensitivity in mitotic cells through impaired D-loop formation and homology-directed repair.

bioRxiv · Aug 24, 2022Cancer Biology

Drug-gene interaction screens coupled to tumour data analyses identify the most clinically-relevant cancer vulnerabilities driving sensitivity to PARP inhibition

K. Jamal, A. Galbiati, J. Armenia, G. Illuzzi, J. Hall, S. Bentouati, D. Barrell, M. Ahdesmäki, Functional Genomics Centre, M. J. O'Connor, E. Leo, J. V. Forment

The paper identifies 110 genes linked to PARP inhibitor sensitivity through CRISPR screens and tumor data analysis, highlighting XRCC3 as a potential biomarker for prostate cancer.

bioRxiv · Jul 29, 2022Cancer Biology

A meta-analysis of clinical cases of reversion mutations in BRCA genes identifies signatures of DNA end-joining repair mechanisms driving therapy resistance

L. Tobalina, J. Armenia, E. Irving, M. J. O'Connor, J. V. Forment

This study analyzes reversion mutations in BRCA genes from clinical cases to identify DNA end-joining repair mechanisms linked to therapy resistance and suggests targeting these pathways to improve treatment outcomes.

bioRxiv · Jul 22, 2020Cancer Biology

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

G. Balmus, D. Pilger, J. Coates, M. Demir, M. Sczaniecka-Clift, A. Barros, M. Woods, B. Fu, F. Yang, E. Chen, M. Ostermaier, T. Stankovic, H. Ponstingl, M. Herzog, K. Yusa, , S. P. P. Jackson

The paper identifies how ATM counteracts toxic non-homologous end-joining at broken replication forks by showing that loss of NHEJ components or BRCA1-A complex confers resistance to DNA-damaging agents in ATM-deficient cells.

bioRxiv · May 24, 2018Cell Biology