Author

C. M. Lovly

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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Organism:human· 3 Approach:biophysical modeling· 1 Assay:bulk RNA-seq· 1 Research Focus:clustering· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

A. A. Jungbluth· 1 shared A. D. Jayaprakash· 1 shared A. L. Hartzler· 1 shared A. W. Smith· 1 shared B. P. Brown· 1 shared D. I. Lin· 1 shared E. J. Jordan· 1 shared E. M. Ebot· 1 shared

Activity by Year

2018-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperCancer Biology

A. A. Jungbluth

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3 papers

Recent·Most cited

Integrative analysis of a large real-world cohort of small cell lung cancer identifies distinct genetic subtypes and insights into histological transformation

S. Sivakumar, J. A. Moore, M. Montesion, R. Sharaf, D. I. Lin, Z. Fleischmann, E. M. Ebot, J. Newberg, J. M. Mills, P. S. Hedge, G. M. Frampton, J. Sage, C. M. Lovly

This study analyzes 3,600 SCLC cases to identify new genetic subtypes and insights into histological transformation, revealing associations between genetic alterations and survival outcomes.

bioRxiv · Jul 27, 2022Cancer Biology

Allele-specific activation, enzyme kinetics, and inhibitor sensitivities of EGFR exon 19 deletion mutations in lung cancer

B. P. Brown, Y. Zhang, S. Kim, P. Finneran, Y. Yan, Z. Du, J. Kim, A. L. Hartzler, M. L. LeNoue-Newton, A. W. Smith, J. Meiler, C. M. Lovly

The paper identifies allele-specific functional differences among EGFR exon 19 deletion variants, showing how sequence and structure motifs affect oncogenic activity, dimerization, and TKI sensitivity.

bioRxiv · Mar 16, 2022Cancer Biology

YES1 amplification: a mechanism of acquired resistance to EGFR inhibitors identified by transposon mutagenesis and clinical genomics

P.-D. Fan, G. Narzisi, A. D. Jayaprakash, E. Venturini, N. Robine, P. Smibert, S. Germer, H. A. Yu, E. J. Jordan, P. K. Paik, Y. Y. Janjigian, J. E. Chaft, L. Wang, A. A. Jungbluth, S. Middha, , M. Ladanyi

This study identifies YES1 amplification as a novel mechanism of resistance to EGFR inhibitors in lung cancer using transposon mutagenesis and clinical genomic analysis.

bioRxiv · Mar 17, 2018Cancer Biology