Kristen Atkins
· Professor of PathologyVerifiedUniversity of Virginia · Molecular Physiology and Biological Physics
Active 1998–2026
About
Kristen A. Atkins, M.D., is a Professor of Pathology at the University of Virginia School of Medicine. She received her medical degree from the University of Vermont in Burlington, VT. Her residency was completed at Stanford University, where she also completed fellowships in Surgical Pathology and Cytopathology, the latter at Virginia Commonwealth University. Dr. Atkins specializes in surgical and cytopathology with a particular interest in gynecologic and breast pathology. Her research focuses on prognostic features in smooth muscle tumors of the uterus and improving staging analysis in ovarian carcinoma. She has contributed to the understanding of histologic subclassification of endocervical adenocarcinoma, the clinical significance of tattoo ink within lymph nodes, metabolic vulnerabilities in endometrial cancer, and the response of ovarian cancer to treatment, among other topics. Her work includes numerous publications and book chapters, emphasizing her expertise in pathology and her contributions to advancing diagnostic and prognostic methods in her field.
Research topics
- Cancer research
- Biology
- Medicine
- Internal medicine
- Cell biology
- Chemistry
- Genetics
Selected publications
2026-02-06
articleOpen access<p>Table S2. Criteria for pathological features scored in MCF10DCIS.com intraductal xenografts.</p>
2026-02-06
articleOpen access<div>Abstract<p>The most widely used cell line for studying ductal carcinoma <i>in situ</i> (DCIS) premalignancy is the transformed breast epithelial cell line, MCF10DCIS.com. During its original clonal isolation and selection, MCF10DCIS.com acquired a heterozygous M452I mutation in the proprotein convertase PCSK5, which has never been reported in any human cancer. The mutation is noteworthy because PCSK5 matures GDF11, a TGFβ superfamily ligand that suppresses progression of triple-negative breast cancer. We asked here whether PCSK5<sup>M452I</sup> and its activity toward GDF11 might contribute to the unique properties of MCF10DCIS.com. Using an optimized in-cell GDF11 maturation assay, we found that overexpressed PCSK5<sup>M452I</sup> was measurably active but at a fraction of the wild-type enzyme. In a <i>PCSK5</i><sup><i>–/–</i></sup> clone of MCF10DCIS.com reconstituted with different PCSK5 alleles, PCSK5<sup>M452I</sup> was mildly defective in anterograde transport. However, the multicellular organization of PCSK5<sup>M452I</sup> addback cells in three-dimensional Matrigel cultures was significantly less circumscribed than wild-type and indistinguishable from a PCSK5<sup>T288P</sup>-null allele. Growth of intraductal MCF10DCIS.com xenografts was similarly impaired along with the frequency of comedo necrosis and stromal activation. In no setting did PCSK5<sup>M452I</sup> exhibit gain-of-function activity, leading us to conclude that it is hypomorphic and thus compensated by the remaining wild-type allele in MCF10DCIS.com.</p>Implications:<p>This work reassures that an exotic PCSK5 mutation is not responsible for the salient characteristics of the MCF10DCIS.com cell line.</p></div>
2026-02-06
articleOpen access<p>Figure S7. Longitudinal tumor bioluminescence and correlation with estimated tumor volume.</p>
2026-02-06
articleOpen access<p>DEseq2 analysis of 3D spheroids prepared from MCF10DCIS.com cells reconstituted with wild-type (WT), hypomorphic (M452I), or null (T288P) PCSK5, and PCSK5<sup>T288P</sup> cultured with 250 ng/mL GDF11 for 8 days. Worksheets compare GDF11 relative to T288P, WT relative to T288P, and WT relative to M452I. Each sheet reports the log<sub>2</sub> fold change, standard error (SE), DEseq2 statistics, and the mean and modeled counts for each condition from <i>N</i> = 4 biological replicates.</p>
2026-02-16
articleOpen access<p>Figure S6. PCSK5 genotypes and recombinant GDF11 do not detectably alter cell-cell adhesion of MCF10DCIS.com.</p>
2026-02-06
articleOpen access<p>Table S1. Categorical grouping of PCSK5 mutation predictions.</p>
2026-02-06
articleOpen access<p>Figure S5. Weak nuclear localization signals and observed nuclear localization of PCSK5.</p>
2026-02-16
articleOpen access<p>Table S2. Criteria for pathological features scored in MCF10DCIS.com intraductal xenografts.</p>
2026-02-16
articleOpen access<p>Figure S1. Affinity-purified PCSK5 antibody sensitivity and dynamic range.</p>
2026-02-06
articleOpen access<p>Figure S8. Other MCF10DCIS.com histologic phenotypes not detectably altered by PCSK5 activity.</p>
Frequent coauthors
- 44 shared
Kevin A. Janes
University of Virginia
- 34 shared
Jill K. Slack‐Davis
- 28 shared
Jennifer A. Harvey
University of Queensland
- 25 shared
Shambhavi Singh
Massachusetts General Hospital
- 23 shared
Kathy Repich
University of Virginia Health System
- 23 shared
Matthew D. Sutcliffe
- 18 shared
Krisztina Hanley
Emory University Hospital
- 14 shared
Susan C. Modesitt
Emory University
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