Author

J. M. Sheltzer

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· 7 Cell Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Organism:human· 9 Approach:experimental assay· 7 Assay:bulk RNA-seq· 6 Research Focus:differential expression· 5 Research Focus:cancer & tumor microenvironment· 3 Research Focus:cell type annotation· 3 Approach:statistical model· 3 Research Focus:cell signaling & trafficking· 2

Frequent Co-Authors

J. C. Smith· 7 shared E. L. Sausville· 5 shared M. L. Yuan· 3 shared V. Girish· 3 shared A. Vasudevan· 2 shared B. E. Mendelson· 2 shared D. A. Lukow· 2 shared J. Kendall· 2 shared

Activity by Year

2017-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 34 mutual co-author links

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7 shared papersCancer Biology

J. C. Smith

Mutual co-authors in cluster

Author profile →

9 papers

Recent·Most cited

A drug's most potent target is not necessarily the source of its anti-cancer activity

D. Bhattacharjee, J. Bakar, E. L. Sausville, B. E. Mendelson, K. Long, J. C. Smith, J. M. Sheltzer

This study shows that ralimetinib's anti-cancer effect is due to EGFR inhibition, not p38, and highlights the need for comprehensive profiling to determine drug mechanisms.

Cell Chemical Biology · Oct 1, 2023Peer-reviewedCancer Biology

Oncogene-like addiction to aneuploidy in human cancers

V. Girish, A. A. Lakhani, C. M. Scaduto, S. L. Thompson, L. M. Brown, R. A. Hagenson, E. L. Sausville, B. E. Mendelson, D. A. Lukow, M. L. Yuan, P. K. Kandikuppa, E. C. Stevens, S. N. Lee, B. Salovska, W. Li, , J. M. Sheltzer

This study demonstrates that trisomy of chromosome 1q is essential for malignant growth in cancers and shows that TP53 mutations are mutually exclusive with 1q aneuploidy.

bioRxiv · Jan 9, 2023Cancer Biology

Genome-wide identification and analysis of prognostic features in human cancers

J. C. Smith, J. M. Sheltzer

The paper constructs genome-wide survival models using multi-omics data from 10,884 cancer patients to identify prognostic biomarkers and reveals that adverse biomarkers are not enriched for oncogenes or therapeutic targets.

Cell Reports · Mar 1, 2022Peer-reviewedCancer Biology

Combustible and electronic cigarette exposures increase ACE2 activity and SARS-CoV-2 Spike binding

A. Ghosh, V. Girish, M. L. Yuan, R. D. Coakley, N. E. Alexis, E. L. Sausville, A. Vasudevan, A. R. Chait, J. M. Sheltzer, R. Tarran

This study shows that combustible and electronic cigarette exposures increase ACE2 activity and SARS-CoV-2 Spike binding, potentially increasing infection risk.

American Journal of Respiratory and Critical Care Medicine · Jan 1, 2022Peer-reviewedPhysiology

Chromosomal instability accelerates the evolution of resistance to anti-cancer therapies

D. A. Lukow, E. L. Sausville, P. Suri, N. K. Chunduri, J. Leu, J. Kendall, Z. Wang, Z. Storchova, J. M. Sheltzer

This study shows that chromosomal instability accelerates cancer cell adaptation to anti-cancer therapies by enabling specific aneuploidy events that reduce drug sensitivity.

bioRxiv · Sep 25, 2020Cancer Biology

Cigarette smoke exposure and inflammatory signaling increase the expression of the SARS-CoV-2 receptor ACE2 in the respiratory tract

J. C. Smith, E. L. Sausville, V. Girish, M. L. Yuan, K. M. John, J. M. Sheltzer

This study shows cigarette smoke increases ACE2 expression in lung cells, making smokers more susceptible to severe SARS-CoV-2 infections.

bioRxiv · Mar 28, 2020Cell Biology

Single chromosome gains can function as metastasis suppressors and metastasis promoters

A. Vasudevan, P. S. Baruah, J. C. Smith, Z. Wang, N. M. Sayles, P. Andrews, J. Kendall, J. Leu, N. K. Chunduri, D. Levy, M. Wigler, Z. Storchova, J. M. Sheltzer

The paper investigates how single chromosome gains can either suppress or promote metastasis in cancer, showing that specific aneuploidies are linked to distinct clinical outcomes.

bioRxiv · Oct 10, 2019Cancer Biology

Combining CRISPR/Cas9 mutagenesis and a small-molecule inhibitor to probe the function of MELK in cancer

C. J. Giuliano, A. Lin, J. C. Smith, A. C. Palladino, J. M. Sheltzer

This study uses CRISPR/Cas9 and a MELK inhibitor to show that MELK knockout cancer cells grow normally, suggesting anti-MELK therapies may not be effective as monotherapies.

bioRxiv · Oct 16, 2017Cancer Biology

An integrated analysis of the epigenetic, genetic, and transcriptional patterns associated with outcome across cancer types

J. C. Smith, J. M. Sheltzer

The paper analyzes genomic data from 33,036 tumors to identify prognostic patterns, finding that copy number changes and methylation are more predictive of survival than mutations.

bioRxiv · Sep 8, 2017Cancer Biology