Author

S. Hanash

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· 6

Signature Assays, Organisms & Methods

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Organism:human· 5 Research Focus:cell type annotation· 4 Research Focus:differential expression· 4 Approach:experimental assay· 4 Approach:statistical model· 4 Assay:bulk RNA-seq· 3 Research Focus:drug response / drug discovery· 2 Assay:metabolomics· 2

Frequent Co-Authors

J. F. Fahrmann· 3 shared M. K. Jolly· 3 shared S. C. Tripathi· 3 shared A. Maitra· 2 shared E. Irajizad· 2 shared F. Bocci· 2 shared H. Levine· 2 shared J. B. Dennison· 2 shared

Activity by Year

2017-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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3 shared papersCancer Biology

J. F. Fahrmann

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6 papers

Recent·Most cited

A Rigorous Multi-Laboratory Study of Known PDAC Biomarkers Identifies Increased Sensitivity and Specificity Over CA19-9 Alone

B. Haab, L. Qian, B. Staal, M. Jain, J. F. Fahrmann, C. Worthington, D. Prosser, L. Velikokhatnaya, C. Lopez, R. Tang, M. Hurd, N. Gopalakrishnan, S. Kumar, L. Smith, S. Hanash, , R. Brand

This study evaluates combinations of PDAC biomarkers across multiple labs, finding improved sensitivity and specificity for early-stage detection compared to CA19-9 alone.

bioRxiv · May 22, 2024Cancer Biology

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

Integrated spatial transcriptomics and lipidomics of precursor lesions of pancreatic cancer identifies enrichment of long chain sulfatide biosynthesis as an early metabolic alteration

M. Sans, Y. Chen, F. I. Thege, R. Dou, J. Min, M. Yip-Schneider, J. Zhang, R. Wu, E. Irajizad, Y. Makino, K. I. Rajapakshe, M. W. Hurd, R. A. Leon, J. Vykoukal, J. B. Dennison, , J. F. Fahrmann

bioRxiv · Aug 14, 2023 · PreprintCancer Biology

NFATc acts as a non-canonical phenotypic stability factor for a hybrid epithelial/mesenchymal phenotype

A. R. Subbalakshmi, D. Kundnani, K. Biswas, A. Ghosh, S. Hanash, S. C. Tripathi, M. K. Jolly

This study identifies NFATc as a non-canonical phenotypic stability factor that stabilizes hybrid epithelial/mesenchymal phenotypes by enabling coexistence and transitions between epithelial, mesenchymal, and hybrid states.

bioRxiv · Apr 18, 2020Cancer Biology

NRF2 activates a partial Epithelial-Mesenchymal Transition and is maximally present in a hybrid Epithelial/Mesenchymal phenotype

F. Bocci, S. C. Tripathi, S. Vilchez Mercedes, J. T. George, J. Casabar, P. K. Wong, S. Hanash, H. Levine, J. N. Onuchic, M. K. Jolly

This study shows NRF2 stabilizes a hybrid epithelial/mesenchymal phenotype by upregulating both E-cadherin and ZEB, and correlates this phenotype with poor survival in cancer.

bioRxiv · May 10, 2019Cancer Biology

Numb prevents a complete EMT by modulating Notch signalling

F. Bocci, M. K. Jolly, S. C. Tripathi, M. Aguilar, S. Hanash, H. Levine, J. N. Onuchic

This study shows Numb stabilizes a hybrid E/M phenotype by inhibiting Notch-driven full EMT, correlates with poor cancer survival, and predicts its role in tumor-initiation.

bioRxiv · Sep 2, 2017Cancer Biology