Research
The Litovchick laboratory studies how cells enter, maintain and escape quiescence, with a particular focus on the DREAM transcriptional repressor complex and its control of cell-cycle gene expression. The group connects the molecular assembly of DREAM—through RB-family proteins, E2F factors, the MuvB core and the DYRK1A kinase—to tumor suppression, cancer-cell dormancy and treatment response. Current work extends these mechanisms into lung cancer, ovarian cancer, HPV-associated disease and mutant-p53 non-small-cell lung cancer, seeking vulnerabilities that can convert growth arrest from a protective state into a therapeutic opportunity.
We investigate how failure of DREAM-mediated transcriptional repression enables lung cells to escape quiescence and acquire tumor-promoting growth programmes.
How does disruption of DREAM assembly alter lung epithelial cell fate, tumor initiation and the response of lung cancers to therapy?Explore this programme →
We define the biochemical decisions that assemble repressive DREAM or redirect the MuvB core toward B-MYB–FOXM1 activation.
Which phosphorylation, protein-interaction and dosage-sensitive mechanisms determine whether MuvB represses or activates cell-cycle genes?Explore this programme →
We study when growth arrest protects cancer cells from treatment and when disrupting quiescence creates a therapeutic liability.
Can the molecular machinery that preserves dormant cancer cells be targeted to prevent relapse or improve the response to cytotoxic and targeted therapies?Explore this programme →
We test whether reactivating DREAM or destabilizing oncogenic proteins can expose selective vulnerabilities in HPV-associated and TP53-mutant cancers.
Can tumors that disable RB-family control be forced back into a repressive cell-cycle state or selectively eliminated through their dependence on oncogenic protein stability?Explore this programme →
