Author

H. Katayama

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· 3

Signature Assays, Organisms & Methods

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Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Assay:metabolomics· 1 Organism:mouse· 1

Frequent Co-Authors

E. Irajizad· 2 shared F. C. Hsiao· 2 shared J. B. Dennison· 2 shared J. F. Fahrmann· 2 shared J. Vykoukal· 2 shared M. J. Hong· 2 shared S. M. Hanash· 2 shared S. Park· 2 shared

Activity by Year

2021-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersCancer Biology

E. Irajizad

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Vesicle-mediated mitochondrial clearance underlies an actionable metabolic vulnerability in triple-negative breast cancer

J. Vykoukal, Y. Chen, M. J. Hong, M. Zuo, H. Krishna, H. Katayama, E. Irajizad, R. Wu, R. Leon-Letelier, J. B. Dennison, A. Gutierrez, A. Paulucci-Holthauzen, T. C. Thompson, L. Rusling, Y. Cai, , J. F. Fahrmann

The paper identifies a metabolic vulnerability in triple-negative breast cancer through sphingolipid metabolism, showing that targeting this pathway with eliglustat reduces tumor growth and improves survival.

bioRxiv · Apr 4, 2024 · PreprintCancer Biology

EGFR inhibition in lung adenocarcinoma upregulates cell surface expression of the placental antigen ALPP and enhances efficacy of ALPP-ADC therapy

y. chen, M. J. Hong, H. Xu, J. Vykoukal, S. Park, y. Cai, R. A. Leon-Letelier, E. Irajizad, F. C. Hsiao, J. B. Dennison, E. J. Ostrin, J. F. Fahrmann, H. Katayama, S. M. Hanash

The paper shows EGFR inhibition increases ALPP surface expression in lung adenocarcinoma, enhancing the effectiveness of ALPP-ADC therapy.

bioRxiv · Mar 27, 2023 · PreprintCancer Biology

P4HA2-induced prolyl hydroxylation suppresses YAP1-mediated prostate cancer cell migration, invasion, and metastasis

M. Zhu, R. Peng, X. Liang, Z. Lan, M. Tang, P. Hou, J. H. Song, C. S. L. Mak, J. Park, S.-e. Zheng, A. Huang, X. Ma, R. Chen, Q. Chang, C. J. Logothetis, , G. Wang

This study identifies P4HA2-dependent prolyl hydroxylation of YAP1 as a suppressor of prostate cancer cell migration, invasion, and metastasis.

bioRxiv · Jan 24, 2021Cancer Biology