Author

Z. D. Nassar

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· 4

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

C. Y. Mah· 4 shared J. Dehairs· 4 shared J. V. Swinnen· 4 shared L. M. Butler· 4 shared D. J. Lynn· 3 shared L. A. Selth· 3 shared A. J. Hoy· 2 shared L. G. Horvath· 2 shared

Activity by Year

2019-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

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4 shared papersCancer Biology

C. Y. Mah

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4 papers

Recent·Most cited

Cancer BiologybioRxivNov 5, 2022

Peroxisomal β-oxidation enzyme, DECR2, regulates lipid metabolism and promotes treatment resistance in advanced prostate cancer

C. Y. Mah, A. D. T. Nguyen, T. Niijima…·L. M. Butler

This study identifies DECR2 as a key driver of treatment resistance in advanced prostate cancer by regulating lipid metabolism and cell cycle progression.

DOI 10.1038/s41416-023-02557-8

humanbulk RNA-seq

𝕏 PostBluesky

Cancer BiologybioRxivPreprintOct 13, 2022

ACSM1 and ACSM3 regulate prostate cancer fatty acid metabolism to promote tumour growth and constrain ferroptosis

R. Shrestha, Z. D. Nassar, A. R. Hanson…·L. A. Selth

This study identifies ACSM1 and ACSM3 as AR-regulated factors that promote prostate cancer growth by enhancing fatty acid metabolism and suppressing ferroptosis.

DOI 10.1101/2022.10.13.511039

humanproteomics

𝕏 PostBluesky

Cancer BiologybioRxivOct 27, 2020

Lipidomic profiling of clinical prostate cancer reveals targetable alterations in lipid composition

L. M. Butler, C. Y. Mah, J. Machiels…·J. V. Swinnen

The paper profiles lipidomes in prostate cancer tissues and identifies targetable lipid alterations linked to AR signaling and therapeutic response.

DOI 10.1158/0008-5472.can-20-3863

humanmetabolomics

𝕏 PostBluesky

Cancer BiologybioRxivDec 6, 2019

DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis

Z. D. Nassar, C. Y. Mah, J. Dehairs…·L. M. Butler

This study identifies DECR1 as an androgen-repressed gene that promotes prostate cancer cell survival by facilitating PUFA oxidation and preventing ferroptosis.

DOI 10.7554/elife.54166

humanbulk RNA-seq

𝕏 PostBluesky