Author

P. Cifani

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

Biology Disciplines

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Cancer Biology· 5 Biochemistry· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 7 Assay:proteomics· 6 Approach:experimental assay· 5 Research Focus:cancer & tumor microenvironment· 4 Research Focus:cell type annotation· 4 Research Focus:cell signaling & trafficking· 2 Approach:deep learning· 2 Research Focus:differential expression· 2

Frequent Co-Authors

A. Kentsis· 6 shared C. R. Vakoc· 2 shared S. Takao· 2 shared A. Alpsoy· 1 shared A. G. Henssen· 1 shared A. Habowski· 1 shared A. Krivtsov· 1 shared A. Letai· 1 shared

Activity by Year

2017-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 13 mutual co-author links

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6 shared papersCancer Biology

A. Kentsis

Mutual co-authors in cluster

Author profile →

8 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

Plasma cells in human pancreatic ductal adenocarcinoma secrete antibodies to self-antigens

M. Yao, J. Preall, J. Yeh, D. Pappin, P. Cifani, Y. Zhao, S. Shen, P. Moresco, B. He, H. Patel, A. Habowski, D. King, K. Raphael, A. Rishi, D. Sejpal, , D. Fearon

The paper identifies auto-antibodies secreted by plasma cells in PDAC against self-antigens, suggesting a link between chronic inflammation and autoimmunity.

bioRxiv · Mar 20, 2023 · PreprintCancer Biology

Quantitative Cell Proteomic Atlas: Pathway-scale targeted mass spectrometry for high-resolution functional profiling of cell signaling

P. Cifani, A. Kentsis

The paper introduces QCPA, a targeted mass spectrometry framework for quantifying signaling pathway activities by measuring post-translational modifications and protein abundance in human cells.

bioRxiv · Apr 14, 2022Biochemistry

Discovery of protein modifications using high resolution differential mass spectrometry proteomics

P. Cifani, Z. Li, D. Luo, M. Grivainis, A. M. Intlekofer, D. Fenyo, A. Kentsis

This paper introduces SAMPEI, a spectral alignment method for detecting protein modifications using high-resolution mass spectrometry, demonstrating its effectiveness in identifying sub-stoichiometric modifications in mouse macrophages.

bioRxiv · Jun 19, 2020Biochemistry

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

A cancer-associated missense mutation in PP2A-Aα increases centrosome clustering during mitosis

N. V. Antao, M. Marcet-Ortega, P. Cifani, A. Kentsis, E. A. Foley

This study shows that a cancer-associated mutation in PP2A-Aα enhances centrosome clustering during mitosis after whole-genome doubling, improving cell survival.

bioRxiv · Mar 7, 2019Cell Biology

Prohibitin is a prognostic marker of relapse and therapeutic target to block chemotherapy resistance in Wilms tumor

M. V. Ortiz, S. Ahmed, M. Burns, A. G. Henssen, T. Hollmann, I. MacArthur, S. Gunasekerea, L. Gaewsky, G. Bradwin, J. Ryan, A. Letai, Y. He, A. Naranjo, Y.-Y. Chi, M. LaQuaglia, , A. Kentsis

This study identifies prohibitin as a urine biomarker for Wilms tumor relapse and shows it promotes chemotherapy resistance by disrupting mitochondrial apoptosis.

bioRxiv · Dec 30, 2018Cancer Biology

MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

F. Brown, E. Still, P. Cifani, S. Takao, C. Reed, S. Ficarro, R. Koche, P. Romanienko, W. Mark, C. O'Donnell, B. Spitzer, C. Stutzke, A. Krivtsov, G. Pouliot, J. Marto, , A. Kentsis

This study identifies MEF2C phosphorylation as a marker of chemotherapy resistance in AML and shows that inhibiting this phosphorylation can overcome resistance in MEF2C-activated cells.

bioRxiv · Feb 9, 2017Cancer Biology