Sarah Sammons

Positions:

Assistant Professor of Medicine

Medicine, Medical Oncology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 2012

Jefferson Medical College of Thomas Jefferson University

Internal Medicine Residency

University of Maryland School of Medicine

Hematology-Oncology Fellowship

Duke University School of Medicine

Grants:

Phase II Multicenter Study of Durvalumab (MEDI4736) and Olaparib in PlatinumTreated Advanced Triple Negative Breast Cancer ¿ DORA

Administered By
Duke Cancer Institute
Awarded By
Duke University
Role
Principal Investigator
Start Date
End Date

Determining the clinical efficacy and predictive biomarkers of mirvetuximab soravtansine (IMGN853) in folate receptor alpha (FRA) expressing, chemotherapy refractory triple negative breast cance

Administered By
Medicine, Medical Oncology
Role
Principal Investigator
Start Date
End Date

TNBC Study

Administered By
Duke Clinical Research Institute
Role
Principal Investigator
Start Date
End Date

BMS CA2097FL (CheckMate)

Administered By
Duke Cancer Institute
Role
Principal Investigator
Start Date
End Date

Publications:

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

Practical Treatment Strategies and Future Directions After Progression While Receiving CDK4/6 Inhibition and Endocrine Therapy in Advanced HR+/HER2- Breast Cancer.

Cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) in combination with backbone endocrine therapy have markedly improved progression-free survival and overall survival over endocrine therapy alone in advanced hormone receptor-positive, HER2-negative (HR+/HER2-) breast cancer and are the standard of care in the first- or second-line setting. There are few data to drive decision making for subsequent treatment strategies after inevitable disease progression after CDK4/6i. Information about the genomic landscape of CDK4/6i-resistant disease is emerging. Resistance mechanisms appear to be varied, but mutations in PIK3CA and ESR1, which can be acquired while receiving treatment, are frequent. Activating PIK3CA mutations are present in up to 35% of patients and are now the most actionable genomic alteration in HR+/HER2- advanced breast cancer with the recent approval of alpelisib and fulvestrant. Everolimus-based combinations and chemotherapy appear to have continued efficacy after progression while receiving CDK4/6i, although historical data on benefit include CDK4/6i-naive patients. Use of selective estrogen down-regulators over aromatase inhibitors is best once the patient has an acquired ESR1 mutation. Tumor biopsy with genomic sequencing and repeat biomarker analysis in patients with CDK4/6i- and endocrine-resistant disease will be integral to guide subsequent treatment strategies and to inform clinical trial eligibility. Promising novel therapeutics in CDK4/6i-resistant disease including oral selective estrogen down-regulators, fibroblast growth factor receptor antagonists, and immunotherapy will be discussed.
Authors
Sammons, S; Shastry, M; Dent, S; Anders, C; Hamilton, E
MLA Citation
URI
https://scholars.duke.edu/individual/pub1422662
PMID
31780379
Source
pubmed
Published In
Clin Breast Cancer
Published Date
DOI
10.1016/j.clbc.2019.06.017

The Promise of Immunotherapy for Breast Cancer Brain Metastases

© 2019, Springer Science+Business Media, LLC, part of Springer Nature. Purpose of Review: The goal of our review is to describe the rationale for immunotherapy in the treatment of breast cancer brain metastases (BCBM), the current landscape of clinical trials for this disease process, and possible future directions based on anticipated results. Recent Findings: Immune checkpoint inhibition has shown efficacy in the treatment of several solid tumor brain metastases (i.e., melanoma and non-small cell lung cancer), but data specific to BCBM is relatively sparse. Preclinical studies in BCBM have illustrated a lower immune content in the brain microenvironment measured by tumor-infiltrating lymphocytes (TILs) in brain metastases compared to primary tumors. Yet, improved outcomes are associated with higher TIL content in the BCBM, and strategies to understand and alter the complex brain immune microenvironment are needed. Summary of Findings: Based on observations in the non-breast cancer setting and early results in advanced breast cancer, it is likely that novel, strategic combination immunotherapy strategies will be needed to yield meaningful outcomes for BCBM patients. Some exciting concepts underway include novel immunotherapy combinations, concurrent stereotactic radiosurgery, bi-specific antibody armed activated T cells, and HER2-chimeric antigen receptor T cells for leptomeningeal disease.
MLA Citation
Sammons, S., et al. “The Promise of Immunotherapy for Breast Cancer Brain Metastases.” Current Breast Cancer Reports, Jan. 2019. Scopus, doi:10.1007/s12609-019-00335-1.
URI
https://scholars.duke.edu/individual/pub1422666
Source
scopus
Published In
Current Breast Cancer Reports
Published Date
DOI
10.1007/s12609-019-00335-1

Loss of stromal caveolin-1 expression predicts poor clinical outcome in triple negative and basal-like breast cancers

Here, we investigated the possible predictive value of stromal caveolin-1 (Cav-1) as a candidate biomarker for clinical outcome in triple negative (TN) breast cancer patients. a cohort of 85 TN breast cancer patients was available, with the necessary annotation and nearly 12 years of follow-up data. Our primary outcome of interest in this study was overall survival. Interestingly, TN patients with high-levels of stromal Cav-1 had a good clinical outcome, with >50% of the patients remaining alive during the follow-up period. In contrast, the median survival for TN patients with moderate stromal Cav-1 staining was 33.5 months. similarly, the median survival for TN patients with absent stromal Cav-1 staining was 25.7 months. a comparison of 5-year survival rates yields a similar pattern. TN patients with high stromal Cav-1 had a good 5-year survival rate, with 75.5% of the patients remaining alive. In contrast, TN patients with moderate or absent stromal Cav-1 levels had progressively worse 5-year survival rates, with 40% and 9.4% of the patients remaining alive. In contrast, in a parallel analysis, the levels of tumor epithelial Cav-1 had no prognostic significance. as such, the prognostic value of Cav-1 immunostaining in TN breast cancer patients is compartment-specific, and selective for an absence of Cav-1 staining in the stromal fibroblast compartment. a recursive-partitioning algorithm was used to assess which factors are most predictive of overall survival in TN breast cancer patients. In this analysis, we included tumor size, histologic grade, whether the patient received surgery, radiotherapy or chemotherapy, CK5/6, eGFR, p53 and Ki67 status, as well as the stromal Cav-1 score. This analysis indicated that stromal loss of Cav-1 expression was the most important prognostic factor for overall survival in TN breast cancer. Virtually identical results were obtained with CK5/6 (+) and/or eGFR (+) TN breast cancer cases, demonstrating that a loss of stromal Cav-1 is also a strong prognostic factor for basal-like breast cancers. Our current findings may have important implications for the close monitoring and treatment stratification of TN and basal-like breast cancer patients. © 2010 Landes Bioscience.
Authors
Witkiewicz, AK; Dasgupta, A; Sammons, S; Er, O; Potoczek, MB; Guiles, F; Sotgia, F; Brody, JR; Mitchell, EP; Lisanti, MP
MLA Citation
Witkiewicz, A. K., et al. “Loss of stromal caveolin-1 expression predicts poor clinical outcome in triple negative and basal-like breast cancers.” Cancer Biology and Therapy, vol. 10, no. 2, July 2010, pp. 135–43. Scopus, doi:10.4161/cbt.10.2.11983.
URI
https://scholars.duke.edu/individual/pub1407299
Source
scopus
Published In
Cancer Biology & Therapy
Volume
10
Published Date
Start Page
135
End Page
143
DOI
10.4161/cbt.10.2.11983

Immune checkpoint inhibition

© Springer International Publishing AG, part of Springer Nature 2018. All rights reserved. Immune checkpoint inhibitors (ICI) represent a class of immuno-oncology drugs consisting of monoclonal antibodies occurring against inhibitory receptors or ligands within the immune system including CTLA-4, PD-1, and PD-L1. ICI has transformed oncology in the last decade leading to increased response rates and improved overall survival across several advanced malignancies. ICI is associated with a unique array of toxicities termed immune-related adverse events (IrAEs) which are T-cell-mediated autoimmune toxicities reported in nearly every organ system; most commonly affecting the skin, liver, gastrointestinal tract, and endocrine system. Most IrAEs are manageable with prompt recognition and initiation of appropriate management. General treatment of IrAEs is based on immunosuppression using varying strengths of glucocorticoids. Severe steroid-refractory IrAEs have required nonsteroidal immunosuppressive agents. In this chapter, we describe IrAEs observed with CTLA-4 and PD-1/PDL-1 inhibition by system describing clinical presentation, grading, incidence, time of onset, management, and time to resolution.
MLA Citation
Sammons, S., et al. “Immune checkpoint inhibition.” Side Effects of Medical Cancer Therapy: Prevention and Treatment: Second Edition, 2018, pp. 315–53. Scopus, doi:10.1007/978-3-319-70253-7_12.
URI
https://scholars.duke.edu/individual/pub1353932
Source
scopus
Published Date
Start Page
315
End Page
353
DOI
10.1007/978-3-319-70253-7_12