Allison Hall

Positions:

Assistant Professor of Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

MD./PhD. 2007

Duke University School of Medicine

Resident, Pathology

Duke University School of Medicine

Grants:

Anti-HPV RNA Interference Using Modified RNA's

Administered By
Pediatrics, Infectious Diseases
Awarded By
National Institutes of Health
Role
Research Assistant
Start Date
End Date

Publications:

The Lineage Determining Factor GRHL2 Collaborates with FOXA1 to Establish a Targetable Pathway in Endocrine Therapy-Resistant Breast Cancer.

Notwithstanding the positive clinical impact of endocrine therapies in estrogen receptor-alpha (ERα)-positive breast cancer, de novo and acquired resistance limits the therapeutic lifespan of existing drugs. Taking the position that resistance is nearly inevitable, we undertook a study to identify and exploit targetable vulnerabilities that were manifest in endocrine therapy-resistant disease. Using cellular and mouse models of endocrine therapy-sensitive and endocrine therapy-resistant breast cancer, together with contemporary discovery platforms, we identified a targetable pathway that is composed of the transcription factors FOXA1 and GRHL2, a coregulated target gene, the membrane receptor LYPD3, and the LYPD3 ligand, AGR2. Inhibition of the activity of this pathway using blocking antibodies directed against LYPD3 or AGR2 inhibits the growth of endocrine therapy-resistant tumors in mice, providing the rationale for near-term clinical development of humanized antibodies directed against these proteins.
Authors
Cocce, KJ; Jasper, JS; Desautels, TK; Everett, L; Wardell, S; Westerling, T; Baldi, R; Wright, TM; Tavares, K; Yllanes, A; Bae, Y; Blitzer, JT; Logsdon, C; Rakiec, DP; Ruddy, DA; Jiang, T; Broadwater, G; Hyslop, T; Hall, A; Laine, M; Phung, L; Greene, GL; Martin, L-A; Pancholi, S; Dowsett, M; Detre, S; Marks, JR; Crawford, GE; Brown, M; Norris, JD; Chang, C-Y; McDonnell, DP
MLA Citation
Cocce, Kimberly J., et al. “The Lineage Determining Factor GRHL2 Collaborates with FOXA1 to Establish a Targetable Pathway in Endocrine Therapy-Resistant Breast Cancer..” Cell Rep, vol. 29, no. 4, Oct. 2019, pp. 889-903.e10. Pubmed, doi:10.1016/j.celrep.2019.09.032.
URI
https://scholars.duke.edu/individual/pub1416479
PMID
31644911
Source
pubmed
Published In
Cell Reports
Volume
29
Published Date
Start Page
889
End Page
903.e10
DOI
10.1016/j.celrep.2019.09.032

Metastatic breast cancers have reduced immune cell recruitment but harbor increased macrophages relative to their matched primary tumors.

The interplay between the immune system and tumor progression is well recognized. However, current human breast cancer immunophenotyping studies are mostly focused on primary tumors with metastatic breast cancer lesions remaining largely understudied. To address this gap, we examined exome-capture RNA sequencing data from 50 primary breast tumors (PBTs) and their patient-matched metastatic tumors (METs) in brain, ovary, bone and gastrointestinal tract. We used gene expression signatures as surrogates for tumor infiltrating lymphocytes (TILs) and compared TIL patterns in PBTs and METs. Enrichment analysis and deconvolution methods both revealed that METs had a significantly lower abundance of total immune cells, including CD8+ T cells, regulatory T cells and dendritic cells. An exception was M2-like macrophages, which were significantly higher in METs across the organ sites examined. Multiplex immunohistochemistry results were consistent with data from the in-silico analysis and showed increased macrophages in METs. We confirmed the finding of a significant reduction in immune cells in brain METs (BRMs) by pathologic assessment of TILs in a set of 49 patient-matched pairs of PBT/BRMs. These findings indicate that METs have an overall lower infiltration of immune cells relative to their matched PBTs, possibly due to immune escape. RNAseq analysis suggests that the relative levels of M2-like macrophages are increased in METs, and their potential role in promoting breast cancer metastasis warrants further study.
Authors
Zhu, L; Narloch, JL; Onkar, S; Joy, M; Broadwater, G; Luedke, C; Hall, A; Kim, R; Pogue-Geile, K; Sammons, S; Nayyar, N; Chukwueke, U; Brastianos, PK; Anders, CK; Soloff, AC; Vignali, DAA; Tseng, GC; Emens, LA; Lucas, PC; Blackwell, KL; Oesterreich, S; Lee, AV
MLA Citation
Zhu, Li, et al. “Metastatic breast cancers have reduced immune cell recruitment but harbor increased macrophages relative to their matched primary tumors..” J Immunother Cancer, vol. 7, no. 1, Oct. 2019. Pubmed, doi:10.1186/s40425-019-0755-1.
URI
https://scholars.duke.edu/individual/pub1417146
PMID
31627744
Source
pubmed
Published In
Journal for Immunotherapy of Cancer
Volume
7
Published Date
Start Page
265
DOI
10.1186/s40425-019-0755-1

Efficient transplacental IgG transfer in women infected with Zika virus during pregnancy.

Zika virus (ZIKV) is a newly-identified infectious cause of congenital disease. Transplacental transfer of maternal IgG to the fetus plays an important role in preventing many neonatal infections. However, antibody transfer may also have negative consequences, such as mediating enhancement of flavivirus infections in early life, or trafficking of virus immune complexes to the fetal compartment. ZIKV infection produces placental pathology which could lead to impaired IgG transfer efficiency as occurs in other maternal infections, such as HIV-1 and malaria. In this study, we asked whether ZIKV infection during pregnancy impairs transplacental transfer of IgG. We enrolled pregnant women with fever or rash in a prospective cohort in Vitoria, Brazil during the recent ZIKV epidemic. ZIKV and dengue virus (DENV)-specific IgG, ZIKV and DENV neutralizing antibodies, and routine vaccine antigen-specific IgG were measured in maternal samples collected around delivery and 20 paired cord blood samples. We concluded that 8 of these mothers were infected with ZIKV during pregnancy and 12 were ZIKV-uninfected. The magnitude of flavivirus-specific IgG, neutralizing antibody, and vaccine-elicited IgG were highly correlated between maternal plasma and infant cord blood in both ZIKV-infected and -uninfected mother-infant pairs. Moreover, there was no difference in the magnitude of plasma flavivirus-specific IgG levels between mothers and infants regardless of ZIKV infection status. Our data suggests that maternal ZIKV infection during pregnancy does not impair the efficiency of placental transfer of flavivirus-specific, functional, and vaccine-elicited IgG. These findings have implications for the neonatal outomes of maternal ZIKV infection and optimal administration of antibody-based ZIKV vaccines and therapeutics.
Authors
Singh, T; Lopez, CA; Giuberti, C; Dennis, ML; Itell, HL; Heimsath, HJ; Webster, HS; Roark, HK; Merçon de Vargas, PR; Hall, A; Corey, RG; Swamy, GK; Dietze, R; Lazear, HM; Permar, SR
MLA Citation
Singh, Tulika, et al. “Efficient transplacental IgG transfer in women infected with Zika virus during pregnancy..” Plos Negl Trop Dis, vol. 13, no. 8, Aug. 2019. Pubmed, doi:10.1371/journal.pntd.0007648.
URI
https://scholars.duke.edu/individual/pub1406435
PMID
31449521
Source
pubmed
Published In
Plos Neglected Tropical Diseases
Volume
13
Published Date
Start Page
e0007648
DOI
10.1371/journal.pntd.0007648

Bimodally Expressed Genes in Ovarian Carcinoma.

Authors
Hall, AHS; Kernagis, DN; Datto, MB
MLA Citation
Hall, A. H. S., et al. “Bimodally Expressed Genes in Ovarian Carcinoma..” Modern Pathology, vol. 24, NATURE PUBLISHING GROUP, 2011, pp. 443A-443A.
URI
https://scholars.duke.edu/individual/pub873935
Source
wos
Published In
Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc
Volume
24
Published Date
Start Page
443A
End Page
443A

Minocycline-induced black thyroid.

Authors
Hall, AHS; Bean, SM
MLA Citation
Hall, Allison H. S., and Sarah M. Bean. “Minocycline-induced black thyroid..” Diagn Cytopathol, vol. 38, no. 8, Aug. 2010, pp. 579–80. Pubmed, doi:10.1002/dc.21227.
URI
https://scholars.duke.edu/individual/pub717851
PMID
19890835
Source
pubmed
Published In
Diagn Cytopathol
Volume
38
Published Date
Start Page
579
End Page
580
DOI
10.1002/dc.21227