Kent W. Hunter, Ph.D.

Kent W. Hunter, Ph.D.

  • Center for Cancer Research
  • National Cancer Institute


Dr. Hunter established the paradigm that metastatic progression of breast cancer has a significant inherited component. Using innovative strategies and cutting edge technologies he has identified a number of genes that contribute to inherited susceptibility to tumor dissemination. Dr. Hunter continues to pioneer the use of integrated genetic and genomic technologies to gain better understanding of the genes and cellular pathways that contribute to the metastatic process. Recent efforts include incorporating the knowledge gained from the genetic studies with novel therapeutic compounds or strategies to try to reduce metastatic burden in breast cancer patients.

Areas of Expertise

1) metastasis 2) breast cancer 3) genetics 4) genomics 5) systems biology 6) genetic susceptibility


Selected Key Publications

Integrated sequence and gene expression analysis of mouse models of breast cancer reveals critical events with human parallels

Rennhack JP, Swiatnicki M, Zhang Y, Caralynn L, Bylett E, Ross C, Szczepanek K, Hanrahan W, Jantissa M, Hunter K, and Andrechek E
Nature Communications. 22: 3261, 2019. [ Journal Article ]

The genomic landscape of metastasis in treatment-naïve breast cancer models

Ross C, Szczepanek K, Lee MP, Yang H, Qiu T, Sanford JD and Hunter KW
PLoS Genetics. 16(5): e1008743, 2020. [ Journal Article ]

Autophagy promotes the survival of dormant breast cancer cells and metastatic tumor recurrence

Vera-Ramirez L, Vodnala S, Nini R, Hunter KW*, and Green JE
Nature Communications. 22: 1944, 2018. [ Journal Article ]

Sipa1 is a candidate for underlying the metastasis efficiency modifier locus Mtes1

Park YG, Zhao X, Lesueur F, Lowy DR, Lancaster M, Pharoah P, Qian X, Hunter KW.
Nat Genet. 37: 1055-1062, 2005. [ Journal Article ]

Nuclear pore protein NUP210 depletion suppresses metastasis through heterochromatin-mediated disruption of tumor cell mechanical response

Ruhul Amin, Anjali Shukla, Jacqueline Jufen Zhu, Sohyoung Kim, Ping Wang, Simon Zhongyuan Tian, Andy D Tran , Debasish Paul, Steven D Cappell, Sandra Burkett, Huaitian Liu , Maxwell P Lee , Michael J Kruhlak , Jennifer E Dwyer, R Mark Simpson, Gordon L Hager, Yijun Ruan, Kent W Hunter
Nature Communications. 2021.
Full-Text Article
[ Journal Article ]

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Research Fellow
Ruhul Amin, Ph.D.
Postbaccalaureate Fellow (CRTA)
Aashni Kamra
Predoctoral Fellow (CRTA)
Megan Majocha, B.S.
Larry Pearce, B.S.
Tinghu Qiu, Ph.D.
Staff Scientist
Christina Ross, Ph.D.
Special Volunteer
Marie Pangracova
Postdoctoral Fellow
Wan-Ning (Chloe) Li, Ph.D.


Modifying Metastasis

Sipa1 is a candidate for underlying the metastasis efficiency Sipa1 is a candidate for underlying the metastasis efficiency modifier locus Mtes1modifier locus Mtes1

Published Date

Previously, we demonstrated the presence of loci in the mouse genome that significantly influenced mammary tumor metastatic efficiency. Here we present data supporting the signal transduction molecule, Sipa1, as a candidate for the metastasis efficiency modifier locus Mtes1.  Analysis of candidate genes revealed a non-synonymous animo acid polymorphism in Sipa1 which has a significant effect on the Sipa1 RapGAP function.  Spontaneous metastasis assays using cells ectopically expressing or knocked down for Sipa1 demonstrate that metastatic capacity is correlated with cellular Sipa1 levels.  Examination of human expression data is consistent with the role of Sipa1 concentration in metastasis.  Together these data suggest that the Sipa1 polymorphism is likely to be at least one of the genetic polymorphisms responsible for the Mtes1 locus.  This is also, to the best of our knowledge, the first demonstration of a constitutional genetic polymorphism having a significant impact on tumor metastasis.


Nature Genetics, 37, 1055-1062

Modifying breast cancer latency

An Epistatic Interaction Controls the Latency of a Transgene-Induced Mammary Tumor

Published Date

Previous studies from our laboratory demonstrated that the latency, tumor growth, and metastatic progression of polyoma middle T-induced mammary tumor in an FVB/NJ inbred mouse background could be significantly altered by the introduction of different genetic backgrounds. In this study we extend these findings by mapping a number of interacting quantitative trait loci responsible for the changes in phenotype. Introduction of the I/LnJ inbred genetic background into the FVB/NJ-PyMT animal significantly accelerated the appearance of the primary tumor (35 vs. 57 days postnatal, p < 10(-7)). A backcross mapping panel was established, and loci responsible for the tumor acceleration were detected on Chrs 15 and 9. Examination of the genotype/phenotype correlation revealed that the FVB/NJ but not the I/LnJ allele of the Chr 15 locus was associated with tumor acceleration and was conditional on the presence of I/LnJ allele on Chr 9. These loci, designated Apmt1 and Apmt2, map to homologous regions associated with LOH in human breast cancer. These results suggest that allelic variants of genes in these regions may contribute to age of onset in human breast cancer.


Mammalian Genome 11: 883-9.


Anthony Laucevicius, B.S.
Anthony Laucevicius, B.S.
Postbaccalaureate Fellow
Megan Majocha, B.S.
Megan Majocha, B.S.
Postbaccalaureate Fellow
Ngoc-Han Ha, Ph.D.
Ngoc-Han Ha, Ph.D.
Staff Scientist
Sarah Deasy, Ph.D.
Sarah Deasy, Ph.D.
Graduate Student, George Washington University
Devin Jackson
Devin Jackson
2014- 2021
Predoctoral Fellow
Emmanuel Perrodin-Njoku
Emmanuel Perrodin-Njoku, B.S.
June 2019-June 2022
Postbaccalaureate Fellow