Shannon McCall

Overview:

As Vice Chair for Translational Research in the Department of Pathology, I am involved in numerous translational cancer research projects that rely on the study of human biological samples.  I am the director of the Duke BioRepository & Precision Pathology Center (Duke BRPC), a shared resource of the School of Medicine and the Duke Cancer Institute.  I serve as the PI for the National Cancer Institute's Cooperative Human Tissue Network Southern Division (a five-year UM1 grant), which lives in the Duke BRPC.  My own area of research interest is gastrointestinal tract metaplasias and their relationship to carcinogenesis, particularly in the upper GI tract.

Positions:

Associate Professor of Pathology

Pathology
School of Medicine

Associate Professor in Surgery

Surgery, Surgical Sciences
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 1996

North Carolina State University

M.D. 2000

Duke University

Anatomic and Clinical Pathology, American Board of Pathology (ABPath)

American Board of Pathology

Clinical Informatics, American Board of Pathology (ABPath)

American Board of Pathology

Resident, Pathology

Duke University

Chief Resident, Pathology

Duke University

Grants:

Mutation analysis of pap smear samples and associated tissues for ovarian cancer diagnostics

Administered By
Pathology
Awarded By
Genendeavor LLC
Role
Principal Investigator
Start Date
End Date

Cooperative Human Tissue Network Support through Duke's BioRepository & Precision Pathology Center

Administered By
Pathology
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

The genetics of hepatosplenic T cell lymphoma

Administered By
Medicine, Hematologic Malignancies and Cellular Therapy
Awarded By
National Institutes of Health
Role
Co Investigator
Start Date
End Date

Empowering Duke's Precision Pathology Center with Quantitative Image Analysis to Support Discovery, Diagnostic Assay Development, and Immune Cell Monitoring

Administered By
Pathology
Awarded By
North Carolina Biotechnology Center
Role
Principal Investigator
Start Date
End Date

Lung Squamous Cell Carcinoma: Validation of Molecular Signatures of Prognosis

Awarded By
University of Colorado - Denver
Role
Pathologist
Start Date
End Date

Publications:

Ensuring remote diagnostics for pathologists: an open letter to the US Congress.

Authors
Lennerz, JK; Pantanowitz, L; Amin, MB; Eltoum, I-E; Hameed, MR; Kalof, AN; Khanafshar, E; Kunju, LP; Lazenby, AJ; Montone, KT; Otis, CN; Reid, MD; Staats, PN; Whitney-Miller, CL; Abendroth, CS; Aron, M; Birdsong, GG; Bleiweiss, IJ; Bronner, MP; Chapman, J; Cipriani, NA; de la Roza, G; Esposito, MJ; Fadare, O; Ferrer, K; Fletcher, CD; Frishberg, DP; Garcia, FU; Geldenhuys, L; Gill, RM; Gui, D; Halat, S; Hameed, O; Hornick, JL; Huber, AR; Jain, D; Jhala, N; Jorda, M; Jorns, JM; Kaplan, J; Khalifa, MA; Khan, A; Kim, GE; Lee, EY; LiVolsi, VA; Longacre, T; Magi-Galluzzi, C; McCall, SJ; McPhaul, L; Mehta, V; Merzianu, M; Miller, SB; Molberg, KH; Moreira, AL; Naini, BV; Nosé, V; O'Toole, K; Picken, M; Prieto, VG; Pullman, JM; Quick, CM; Reynolds, JP; Rosenberg, AE; Schnitt, SJ; Schwartz, MR; Sekosan, M; Smith, MT; Sohani, A; Stowman, A; Vanguri, VK; Wang, B; Watts, JC; Wei, S; Whitney, K; Younes, M; Zee, S; Bracamonte, ER
MLA Citation
Lennerz, Jochen K., et al. “Ensuring remote diagnostics for pathologists: an open letter to the US Congress.Nat Med, vol. 28, no. 12, Dec. 2022, pp. 2453–55. Pubmed, doi:10.1038/s41591-022-02040-6.
URI
https://scholars.duke.edu/individual/pub1554695
PMID
36266514
Source
pubmed
Published In
Nat Med
Volume
28
Published Date
Start Page
2453
End Page
2455
DOI
10.1038/s41591-022-02040-6

Genomic analysis of early-stage lung cancer reveals a role for TP53 mutations in distant metastasis.

Patients with non-small cell lung cancer (NSCLC) who have distant metastases have a poor prognosis. To determine which genomic factors of the primary tumor are associated with metastasis, we analyzed data from 759 patients originally diagnosed with stage I-III NSCLC as part of the AACR Project GENIE Biopharma Collaborative consortium. We found that TP53 mutations were significantly associated with the development of new distant metastases. TP53 mutations were also more prevalent in patients with a history of smoking, suggesting that these patients may be at increased risk for distant metastasis. Our results suggest that additional investigation of the optimal management of patients with early-stage NSCLC harboring TP53 mutations at diagnosis is warranted in light of their higher likelihood of developing new distant metastases.
Authors
Van Egeren, D; Kohli, K; Warner, JL; Bedard, PL; Riely, G; Lepisto, E; Schrag, D; LeNoue-Newton, M; Catalano, P; Kehl, KL; Michor, F; AACR Project GENIE Consortium represented by Shawn Sweeney,
MLA Citation
Van Egeren, Debra, et al. “Genomic analysis of early-stage lung cancer reveals a role for TP53 mutations in distant metastasis.Sci Rep, vol. 12, no. 1, Nov. 2022, p. 19055. Pubmed, doi:10.1038/s41598-022-21448-1.
URI
https://scholars.duke.edu/individual/pub1556451
PMID
36351964
Source
pubmed
Published In
Scientific Reports
Volume
12
Published Date
Start Page
19055
DOI
10.1038/s41598-022-21448-1

Leveraging patient derived models of FGFR2 fusion positive intrahepatic cholangiocarcinoma to identify synergistic therapies.

Intrahepatic cholangiocarcinoma (ICC) remains a deadly malignancy lacking systemic therapies for advanced disease. Recent advancements include selective FGFR1-3 inhibitors for the 15% of ICC patients harboring fusions, although survival is limited by poor response and resistance. Herein we report generation of a patient-derived FGFR2 fusion-positive ICC model system consisting of a cell line, organoid, and xenograft, which have undergone complete histologic, genomic, and phenotypic characterization, including testing standard-of-care systemic therapies. Using these FGFR2 fusion-positive ICC models, we conducted an unbiased high-throughput small molecule screen to prioritize combination strategies with FGFR inhibition, from which HDAC inhibition together with pemigatinib was validated in vitro and in vivo as a synergistic therapy for ICC. Additionally, we demonstrate broad utility of the FGFR/HDAC combination for other FGFR fusion-positive solid tumors. These data are directly translatable and justify early phase trials to establish dosing, safety, and therapeutic efficacy of this synergistic combination.
Authors
Lidsky, ME; Wang, Z; Lu, M; Liu, A; Hsu, SD; McCall, SJ; Sheng, Z; Granek, JA; Owzar, K; Anderson, KS; Wood, KC
MLA Citation
Lidsky, Michael E., et al. “Leveraging patient derived models of FGFR2 fusion positive intrahepatic cholangiocarcinoma to identify synergistic therapies.Npj Precis Oncol, vol. 6, no. 1, Oct. 2022, p. 75. Pubmed, doi:10.1038/s41698-022-00320-5.
URI
https://scholars.duke.edu/individual/pub1554318
PMID
36274097
Source
pubmed
Published In
Npj Precis Oncol
Volume
6
Published Date
Start Page
75
DOI
10.1038/s41698-022-00320-5

Evaluation of tumor microenvironment and biomarkers of immune checkpoint inhibitor response in metastatic renal cell carcinoma.

BACKGROUND: Immunotherapy combinations including ipilimumab and nivolumab are now the standard of care for untreated metastatic renal cell carcinoma (mRCC). Biomarkers of response are lacking to predict patients who will have a favorable or unfavorable response to immunotherapy. This study aimed to use the OmniSeq transcriptome-based platform to develop biomarkers of response to immunotherapy. METHODS: Two cohorts of patients were retrospectively collected. These included an investigational cohort of patients with mRCC treated with immune checkpoint inhibitor therapy from five institutions, and a subsequent validation cohort of patients with mRCC treated with combination ipilimumab and nivolumab from two institutions (Duke Cancer Institute and Cleveland Clinic Taussig Cancer Center). Tissue-based RNA sequencing was performed using the OmniSeq Immune Report Card on banked specimens to identify gene signatures and immune checkpoints associated with differential clinical outcomes. A 5-gene expression panel was developed based on the investigational cohort and was subsequently evaluated in the validation cohort. Clinical outcomes including progression-free survival (PFS) and overall survival (OS) were extracted by retrospective chart review. Objective response rate (ORR) was assessed by Response Evaluation Criteria in Solid Tumors (RECIST) V.1.1. RESULTS: The initial investigation cohort identified 86 patients with mRCC who received nivolumab (80%, 69/86), ipilimumab/nivolumab (14%, 12/86), or pembrolizumab (6%, 5/86). A gene expression score was created using the top five genes found in responders versus non-responders (FOXP3, CCR4, KLRK1, ITK, TIGIT). The ORR in patients with high gene expression (GEhigh) on the 5-gene panel was 29% (14/48), compared with low gene expression (GElow) 3% (1/38, χ2 p=0.001). The validation cohort was comprised of 62 patients who received ipilimumab/nivolumab. There was no difference between GEhigh and GElow in terms of ORR (44% vs 38.5%), PFS (HR 1.5, 95% CI 0.58 to 3.89), or OS (HR 0.96, 95% CI 0.51 to 1.83). Similarly, no differences in ORR, PFS or OS were observed when patients were stratified by tumor mutational burden (high=top 20%), PD-L1 (programmed death-ligand 1) expression by immunohistochemistry or RNA expression, or CTLA-4 (cytotoxic T-lymphocytes-associated protein 4) RNA expression. The International Metastatic RCC Database Consortium (IMDC) risk score was prognostic for OS but not PFS. CONCLUSION: A 5-gene panel that was associated with improved ORR in a predominantly nivolumab monotherapy population of patients with mRCC was not predictive for radiographic response, PFS, or OS among patients with mRCC treated with ipilimumab and nivolumab.
Authors
Brown, LC; Zhu, J; Desai, K; Kinsey, E; Kao, C; Lee, YH; Pabla, S; Labriola, MK; Tran, J; Dragnev, KH; Tafe, LJ; Dayyani, F; Gupta, RT; McCall, S; George, DJ; Glenn, ST; Nesline, MK; George, S; Zibelman, M; Morrison, C; Ornstein, MC; Zhang, T
MLA Citation
Brown, Landon C., et al. “Evaluation of tumor microenvironment and biomarkers of immune checkpoint inhibitor response in metastatic renal cell carcinoma.J Immunother Cancer, vol. 10, no. 10, Oct. 2022. Pubmed, doi:10.1136/jitc-2022-005249.
URI
https://scholars.duke.edu/individual/pub1554101
PMID
36252996
Source
pubmed
Published In
Journal for Immunotherapy of Cancer
Volume
10
Published Date
DOI
10.1136/jitc-2022-005249

Truncated Caveolin-3 Mutation In Familial Barrett’s Esophagus

Authors
Garman, KS; Furstenberg, RV; Fecteau, R; Becker, TC; Purkayastha, BPD; Falk, GW; Dawson, D; Willis, JE; McCall, SJ; Blum, AE; Guda, K; Chak, A
MLA Citation
Garman, Katherine S., et al. “Truncated Caveolin-3 Mutation In Familial Barrett’s Esophagus.” Cold Spring Harbor Laboratory, 17 May 2021. Crossref, doi:10.1101/2021.05.15.444305.
URI
https://scholars.duke.edu/individual/pub1556751
Source
crossref
Published Date
DOI
10.1101/2021.05.15.444305

Research Areas:

Ampulla of Vater
Apoptosis
Bevacizumab
Bile Ducts
Biological Markers
Biopsy
Biopsy, Needle
Cell Differentiation
Cell Line
Cell Nucleus
Cell Proliferation
Cell Survival
Cells, Cultured
Colorectal Neoplasms
Colorectal Neoplasms, Hereditary Nonpolyposis
Cytochrome P-450 CYP2E1
Endocytosis
Epithelial Cells
Epithelial-Mesenchymal Transition
Gene Deletion
Gene Expression Profiling
Gene Expression Regulation
Gene Expression Regulation, Developmental
Gene Expression Regulation, Neoplastic
Genetic Predisposition to Disease
Hedgehog Proteins
Homeodomain Proteins
Humans
Hydroxyproline
Immunohistochemistry
Kruppel-Like Transcription Factors
Lasers
Mesenchymal Stromal Cells
Mesoderm
Microdissection
Mutation
Nuclear Proteins
Oligonucleotides, Antisense
Oligoribonucleotides, Antisense
Oncogenes
Organoplatinum Compounds
Pancreaticoduodenectomy
Pancreatitis
Pilot Projects
Prognosis
Protein Isoforms
Proteome
Proto-Oncogene Proteins
Proto-Oncogene Proteins B-raf
Pyrimidines
RNA, Messenger
Receptors, Cell Surface
Recombinant Proteins
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction
Stromal Cells
Thiazoles
Tissue Donors
Tumor Markers, Biological
Tumor Necrosis Factor-alpha
Wnt Proteins
Xenograft Model Antitumor Assays
ras Proteins