Breadcrumb

Metastasis Susceptibility Section

Kent W. Hunter, Ph.D.

Team

Staff Scientist
Christina Ross, Ph.D.
Staff Scientist
Ruhul Amin, Ph.D.
Predoctoral Fellow
Megan Majocha, B.S.
Postdoctoral Fellow
Wan-Ning (Chloe) Li, Ph.D.
Postdoctoral Fellow
Nirupama Kotian, Ph.D.
Postdoctoral Fellow
Xi Chen, Ph.D.
Postbaccalaureate Fellow
Nthabeleng MacDonald
Biologist
Larry Pearce, B.S.

Covers

Nature Genetics cover:  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.
 

Mammalian Genome cover: 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.
 

Alumni

Ngoc-Han Ha
Ngoc-Han Ha, Ph.D.
2012 - 2020
Staff Scientist
Devin Jackson
Devin Jackson
2014 - 2021
Predoctoral Fellow
Aashni Kamra photo
Aashni Kamra, B.S.
2021-2022
Postbaccalaureate Fellow
Marie Pangracova photo
Marie Pangracova
2021-2022
Special Volunteer
Alina Kenina photo
Alina Kenina
2022-2023
Postbaccalaureate Fellow

Lab Life

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The Hunter lab 2019
The Hunter lab 2019
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Emmanuel Perrodin-Njoku
Emmanuel Perrodin-Njoku, B.S., Rochester Institute of Technology (Deaf Student Training Program Alumnus)
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Megan Majocha
Megan Majocha, B.S., Gallaudet University (Deaf Student Training Program Alumnus) 
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Anthony Laucevicius
Anthony Laucevicius, B.S., Gallaudet University (Deaf Student Training Program Alumnus)
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Kenneth Peters
Kenneth Peters, B.S., Gallaudet University (Deaf Student Training Program Alumnus)
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Aashni Kamra
Aashni Kamra, B.S., Gallaudet University (Deaf Student Training Program Alumnus)