Author

C. R. Vakoc

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Cancer Biology· 11

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Organism:human· 11 Research Focus:cancer & tumor microenvironment· 6 Approach:experimental assay· 6 Approach:genetic perturbation / CRISPR· 6 Research Focus:cell type annotation· 5 Assay:bulk RNA-seq· 4 Research Focus:chromatin & epigenetic regulation· 3 Approach:statistical model· 3

Frequent Co-Authors

O. E. Demerdash· 5 shared O. Klingbeil· 5 shared X. S. Wu· 4 shared A. Alpsoy· 2 shared C. Tonelli· 2 shared D. A. Tuveson· 2 shared D. Maia-Silva· 2 shared D. Skopelitis· 2 shared

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2019-2024 · peak 3/yr

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10 top collaborators · 32 mutual co-author links

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5 shared papersCancer Biology

O. E. Demerdash

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11 papers

Recent·Most cited

MARK2/MARK3 kinases are catalytic co-dependencies of YAP/TAZ in human cancer

O. Klingbeil, D. Skopelitis, C. Tonelli, A. Alpsoy, F. Minicozzi, D. Aggarwal, S. Russo, T. Ha, O. E. Demerdash, D. L. Spector, D. A. Tuveson, P. Cifani, C. R. Vakoc

This study identifies MARK2/3 as essential kinases for YAP/TAZ function in cancer and shows their inhibition can restore Hippo pathway tumor suppression.

bioRxiv · Feb 26, 2024Cancer Biology

Targeting the mSWI/SNF Complex in POU2F-POU2AF Transcription Factor-Driven Malignancies

T. He, L. Xiao, Y. Qiao, O. Klingbeil, E. Young, X. S. Wu, R. Mannan, S. Mahapatra, S. Eyunni, J. C.-Y. Tien, X. Wang, Y. Zheng, N. Kim, H. Zheng, S. Hou, , A. M. Chinnaiyan

This study identifies a therapeutic vulnerability in POU2F-POU2AF-driven cancers by showing that targeting the mSWI/SNF complex with a PROTAC degrader reduces tumor growth in preclinical models.

bioRxiv · Jan 22, 2024Cancer Biology

Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer

L. Duplaquet, K. So, A. W. Ying, X. Li, Y. Li, X. Qiu, R. Li, S. Singh, X. S. Wu, Q. Liu, J. Qi, T. D. D. Somerville, H. Heiling, E. Mazzola, Y. Lee, , M. G. Oser

This study identifies mSWI/SNF complex activity as a targetable dependency in POU2F3-positive small cell lung cancer, showing that inhibiting mSWI/SNF or BRD9 reduces tumor growth and improves survival.

bioRxiv · Jan 21, 2024Cancer Biology

Marker-based CRISPR screening reveals a MED12-p63 interaction that activates basal identity in pancreatic ductal adenocarcinoma

D. Maia-Silva, A. C. Schier, D. Skopelitis, V. Kechejian, A. Alpsoy, J. Liverpool, D. J. Taatjes, C. R. Vakoc

The paper identifies MED12-p63 interaction as a driver of basal identity in PDAC through genetic screens and biochemical analysis.

bioRxiv · Oct 24, 2023 · PreprintCancer Biology

p73 activates transcriptional signatures of basal lineage identity and ciliogenesis in pancreatic ductal adenocarcinoma

S. K. Hur, T. D. D. Somerville, X. S. Wu, D. Maia-Silva, O. E. Demerdash, D. A. Tuveson, F. Notta, C. R. Vakoc

This study shows p73 activates basal lineage and ciliogenesis genes in PDAC, suggesting its role in lineage plasticity and tumor progression.

bioRxiv · Apr 20, 2023 · PreprintCancer Biology

SPDEF promotes the classical subtype of pancreatic ductal adenocarcinoma.

C. Tonelli, G. N. Yordanov, Y. Hao, A. Deschenes, O. Klingbeil, H.-C. Ting, E. Brosnan, A. Doshi, Y. Park, C. R. Vakoc, J. Preall, D. Tuveson

The paper identifies SPDEF as a key driver of the classical subtype of pancreatic ductal adenocarcinoma, showing its role in tumor progression and dependence on specific target genes.

bioRxiv · Mar 18, 2022 · PreprintCancer Biology

The SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia

S. A. Polyanskaya, R. Y. Moreno, B. Lu, R. Feng, Y. Yao, S. Irani, O. Klingbeil, Z. Yang, Y. Wei, O. E. Demerdash, L. A. Benjamin, M. J. Weiss, Y. Zhang, C. R. Vakoc

This study identifies the SCP4-STK35/PDIK1L phosphatase-kinase complex as a critical signaling dependency in AML, showing its role in proliferation and amino acid metabolism through dual regulatory mechanisms.

bioRxiv · May 9, 2021Cancer Biology

Transcriptional silencing of ALDH2 in acute myeloid leukemia confers a dependency on Fanconi anemia proteins

Z. Yang, Y. Wei, X. S. Wu, S. V. Iyer, M. Jung, E. R. Adelman, O. Klingbeil, M. Kramer, O. E. Demerdash, K. Chang, S. Goodwin, E. Hodges, W. R. McCombie, M. E. Figueroa, A. Smogorzewska, C. R. Vakoc

This study identifies ALDH2 transcriptional silencing in AML as a dependency on FA proteins, suggesting FA pathway targeting as a therapeutic strategy.

bioRxiv · Oct 23, 2020Cancer Biology

Convergent organization of aberrant MYB complex controls oncogenic gene expression in acute myeloid leukemia

S. Takao, L. Forbes, M. Uni, S. Cheng, J. M. B. Pineda, Y. Tarumoto, P. Cifani, G. Minuesa, C. Chen, M. G. Kharas, R. K. Bradley, C. R. Vakoc, R. P. Koche, A. Kentsis

This study identifies aberrant MYB complex assembly as a driver of oncogenic gene expression in AML and shows that targeting this complex can induce differentiation and apoptosis.

bioRxiv · May 5, 2020Cancer Biology

Miswired enhancer logic drives translocation positive rhabdomyosarcoma

B. E. Gryder, M. Wachtel, K. Chang, O. E. Demerdash, N. G. Aboreden, W. Ewert, S. Pomella, W. Mohammed, R. Rota, J. S. Wei, Y. Song, B. Schaefer, C. R. Vakoc, J. Khan

The paper identifies a miswired enhancer logic driven by PAX3-FOXO1 translocation in rhabdomyosarcoma, disrupting normal transcription factor regulation and promoting undifferentiated proliferation.

bioRxiv · Sep 6, 2019 · PreprintCancer Biology

Tankyrase inhibition sensitizes cells to CDK4 blockade

M. Foronda, Y. Tarumoto, E. M. Schatoff, B. I. Leach, B. J. Diaz, S. Goswami, M. Shusterman, C. R. Vakoc, L. Dow

This study identifies that combining TNKS inhibition with CDK4 loss drives G1 cell cycle arrest and senescence in epithelial cancers.

bioRxiv · Jun 21, 2019Cancer Biology