Author

V. Anastas

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· 5

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 4 Assay:proteomics· 3 Assay:bulk RNA-seq· 2 Research Focus:cell signaling & trafficking· 2 Organism:human· 2 Assay:ATAC-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

E. Chavdoula· 5 shared P. N. Tsichlis· 5 shared L. Sehgal· 4 shared A. La Ferlita· 3 shared G. I. Laliotis· 3 shared A. Orlacchio· 2 shared B. Soysal· 2 shared C. Tsatsanis· 2 shared

Activity by Year

2020-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 40 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

5 shared papersCancer Biology

E. Chavdoula

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Transcriptional regulation of amino acid metabolism by KDM2B, in the context of ncPRC1.1 and in concert with MYC and ATF4

E. Chavdoula, V. Anastas, A. La Ferlita, J. Aldana, G. Carota, M. Spampinato, B. Soysal, I. Cosentini, S. Parashar, A. Sircar, G. Nigita, L. Sehgal, M. A. Freitas, P. N. Tsichlis

This study identifies KDM2B's role in regulating amino acid metabolism through interactions with ncPRC1.1, MYC, and ATF4, revealing a metabolic network linked to poor prognosis in TNBC.

bioRxiv · Jul 7, 2023Cancer Biology

Overexpression of the SETD2 WW domain inhibits the phosphor-IWS1/SETD2 interaction and the oncogenic AKT/IWS1 RNA splicing program.

G. I. Laliotis, E. Chavdoula, V. Anastas, S. Singh, A. I. Kenney, S. Achaya, J. S. Yount, L. Sehgal, P. N. Tsichlis

The paper was withdrawn due to concerns about the integrity of the reported results on alternative splicing of U2AF2.

bioRxiv · Aug 12, 2021 · PreprintCancer Biology

IWS1 phosphorylation by AKT3 controls nuclear export of type I IFN mRNAs and sensitivity to oncolytic viral infection, by regulating the alternative RNA splicing of U2AF2.

G. I. Laliotis, A. Kenney, E. Chavdoula, A. Orlacchio, A. K. Kaba, A. La Ferlita, V. Anastas, C. Tsatsanis, J. D. Beane, L. Sehgal, V. Coppola, J. S. Yount, P. N. Tsichlis

The paper was withdrawn due to concerns about the validity of the reported alternative splicing mechanism of U2AF2 and potential data manipulation.

bioRxiv · Dec 26, 2020Cancer Biology

IWS1 phosphorylation promotes cell proliferation and predicts poor prognosis in EGFR mutant lung adenocarcinoma patients, through the cell cycle-regulated U2AF2 RNA splicing.

G. I. Laliotis, E. Chavdoula, M. D. Paraskevopoulou, A. D. Kaba, A. La Ferlita, S. Singh, V. Anastas, S. Alaimo, A. Orlacchio, K. A. Nair, V. Taraslia, I. Vlachos, M. Capece, A. Hatzigeorgiou, D. I. Palmieri, , P. N. Tsichlis

The paper was withdrawn due to concerns about the validity of the reported splicing mechanism and data integrity.

bioRxiv · Jul 14, 2020Cancer Biology

KDM2B Silencing Elicits a Paracrine Mechanism Which Destabilizes SLUG, Promoting Differentiation of Basal-Like Breast Cancer Cells.

E.-A. Fraile, B. Soysal, V. Anastas, Z. T. Soysal, O. Serebrennikova, M. D. Paraskevopoulou, E. Chavdoula, P. N. Tsichlis

This paper shows that silencing KDM2B triggers a paracrine mechanism that inactivates GSK3, leading to SLUG degradation and differentiation of basal-like breast cancer cells.

bioRxiv · May 21, 2020 · PreprintCancer Biology