Author

H. L. Ford

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· 2

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

A. Chung· 1 shared A. D. Durbin· 1 shared A. E. Goodspeed· 1 shared A. Ganesan· 1 shared E. P. Danis· 1 shared E. P. Souto· 1 shared J. C. Black· 1 shared J. C. Costello· 1 shared

Activity by Year

2021-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCancer Biology

A. Chung

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Author profile →

2 papers

Recent·Most cited

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

E. P. Souto, P. Gong, J. D. Landua, R. R. Srinivasan, A. Ganesan, L. E. Dobrolecki, S. C. Purdy, X. Pan, M. Zeosky, A. Chung, S. S. Yi, H. L. Ford, M. T. Lewis

The paper identifies an IFN/STAT1 transcriptional state in tumor-initiating cells (TIC) of breast cancer using single-cell RNA sequencing, showing it differs from bulk RNA-seq derived TIC signatures.

bioRxiv · Sep 15, 2023 · PreprintCancer Biology

SIX1 Reprograms Myogenic Transcription Factors to Maintain the Rhabdomyosarcoma undifferentiated state

J. Y. Hsu, E. P. Danis, S. Nance, J. O'Brien, V. M. Wessells, A. E. Goodspeed, J. C. Talbot, S. L. Amacher, P. Jedlicka, J. C. Black, J. C. Costello, A. D. Durbin, K. B. Artinger, H. L. Ford

This study shows that SIX1 maintains the undifferentiated state of rhabdomyosarcoma cells by altering MYOD1 activity and enhancer regulation, and a SIX1 loss gene signature predicts RMS progression.

bioRxiv · Apr 25, 2021Cancer Biology