Katarina Bačević

ORCID: 0000-0003-3919-2858
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About
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Research Areas
  • Cancer-related Molecular Pathways
  • DNA Repair Mechanisms
  • Microtubule and mitosis dynamics
  • Cancer Genomics and Diagnostics
  • Mathematical Biology Tumor Growth
  • Telomeres, Telomerase, and Senescence
  • Ubiquitin and proteasome pathways
  • Cancer Research and Treatments

Université de Montpellier
2017-2022

Centre National de la Recherche Scientifique
2017-2022

Institut de Génétique Moléculaire de Montpellier
2017-2021

Adaptive therapy (AT) aims to control tumour burden by maintaining therapy-sensitive cells exploit their competition with resistant cells. This relies on the assumption that have impaired cellular fitness. Here, using a model of resistance pharmacological cyclin-dependent kinase inhibitor (CDKi), we show this is valid when between spatially structured. We generate CDKi-resistant cancer and find they reduced proliferative fitness stably rewired cell cycle pathways. Low-dose CDKi outperforms...

10.1038/s41467-017-01516-1 article EN cc-by Nature Communications 2017-12-04

Abstract Although cyclin-dependent kinase 2 (Cdk2) controls the G1/S transition and promotes DNA replication, it is dispensable for cell cycle progression due to redundancy with Cdk1. Yet Cdk2 also has non-redundant functions that can be revealed in certain genetic backgrounds was reported promote G2/M damage response checkpoint TP53 (p53)-deficient cancer cells. However, p53-proficient cells subjected damage, inactivated by CDK inhibitor p21. We therefore investigated whether differentially...

10.1038/s41598-017-12868-5 article EN cc-by Scientific Reports 2017-10-12

ABSTRACT Senescence is an irreversible withdrawal from cell proliferation that can be initiated after DNA damage-induced cycle arrest in G2 phase to prevent genomic instability. onset requires p53 (also known as TP53) and retinoblastoma protein (RB, also RB1) family tumour suppressors, but how they are regulated convert a temporary into permanent one remains unknown. Here, we show previously unrecognised balance between the cyclin-dependent kinase (CDK) inhibitor p21 checkpoint Chk1 controls...

10.1242/jcs.259114 article EN Journal of Cell Science 2022-03-28

Abstract Hepatocellular carcinoma (HCC) is a common cancer with high mortality. The limited therapeutic options for advanced disease include treatment Sorafenib, multi-kinase inhibitor whose targets the Mediator kinase CDK8. Since CDK8 has reported oncogenic activity in Wnt-dependent colorectal cancer, we investigated whether it also involved HCC. We find that and its paralogue CDK19 are significantly overexpressed HCC patients, where levels correlate poor prognosis. Liver-specific genetic...

10.1101/789586 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2019-10-01

ABSTRACT Senescence is an irreversible proliferation withdrawal that can be initiated after DNA damage-induced cell cycle arrest in G2 phase to prevent genomic instability. onset not well understood; it requires p53 and RB family tumour suppressors, but how they are regulated convert a temporary into permanent one remains unknown. Here, we show previously unrecognised balance between the CDK inhibitor p21 Chk1 controls D-type cyclin-CDK activity during arrest. In non-transformed cells,...

10.1101/2021.08.17.452482 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-08-17
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