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

Assistant 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
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
Role
Principal Investigator
Start Date
End Date

Lung Squamous Cell Carcinoma: Validation of Molecular Signatures of Prognosis

Administered By
Surgery, Cardiovascular and Thoracic Surgery
Role
Pathologist
Start Date
End Date

Publications:

Glycogenic Hepatopathy Causing Elevated Lactic Acid and Liver Enzymes.

Authors
Regan, JA; Golubski, B; Gilbert, EB; Sullivan, B; McCall, SJ; Sata, SS
MLA Citation
Regan, Jessica A., et al. “Glycogenic Hepatopathy Causing Elevated Lactic Acid and Liver Enzymes..” Am J Med, July 2019. Pubmed, doi:10.1016/j.amjmed.2019.07.018.
URI
https://scholars.duke.edu/individual/pub1402333
PMID
31369721
Source
pubmed
Published In
Am J Med
Published Date
DOI
10.1016/j.amjmed.2019.07.018

Characterization of tumor mutational burden (TMB), PD-L1, and DNA repair genes to assess correlation with immune checkpoint inhibitors (ICIs) response in metastatic renal cell carcinoma (mRCC).

Authors
Labriola, M; Zhu, J; Gupta, R; McCall, S; Jackson, J; White, JR; Weingartner, E; Kong, E; Simone, P; Papp, E; Gerding, K; Simmons, J; George, DJ; Zhang, T
MLA Citation
Labriola, Matthew, et al. “Characterization of tumor mutational burden (TMB), PD-L1, and DNA repair genes to assess correlation with immune checkpoint inhibitors (ICIs) response in metastatic renal cell carcinoma (mRCC)..” Journal of Clinical Oncology, vol. 37, no. 15_suppl, American Society of Clinical Oncology (ASCO), 2019, pp. e16079–e16079. Crossref, doi:10.1200/jco.2019.37.15_suppl.e16079.
URI
https://scholars.duke.edu/individual/pub1415115
Source
crossref
Published In
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
Volume
37
Published Date
Start Page
e16079
End Page
e16079
DOI
10.1200/jco.2019.37.15_suppl.e16079

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

Authors
Zhu, J; Pabla, S; Labriola, M; Gupta, RT; McCall, S; George, DJ; Dressman, D; Glenn, S; George, S; Morrison, C; Zhang, T
MLA Citation
Zhu, Jason, et al. “Evaluation of tumor microenvironment and biomarkers of immune checkpoint inhibitor (ICI) response in metastatic renal cell carcinoma (mRCC)..” Journal of Clinical Oncology, vol. 37, no. 15_suppl, American Society of Clinical Oncology (ASCO), 2019, pp. 2595–2595. Crossref, doi:10.1200/jco.2019.37.15_suppl.2595.
URI
https://scholars.duke.edu/individual/pub1415279
Source
crossref
Published In
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
Volume
37
Published Date
Start Page
2595
End Page
2595
DOI
10.1200/jco.2019.37.15_suppl.2595

Concordance between PD-L1 assays for metastatic renal cell carcinoma (mRCC) and metastatic urothelial carcinoma (mUC).

Authors
Labriola, M; Zhu, J; Cheris, S; Liu, X; Perkinson, K; Su, Z; McCall, S; Huang, J; Gupta, RT; Armstrong, AJ; George, DJ; Zhang, T
MLA Citation
Labriola, Matthew, et al. “Concordance between PD-L1 assays for metastatic renal cell carcinoma (mRCC) and metastatic urothelial carcinoma (mUC)..” Journal of Clinical Oncology, vol. 37, no. 15_suppl, American Society of Clinical Oncology (ASCO), 2019, pp. e14259–e14259. Crossref, doi:10.1200/jco.2019.37.15_suppl.e14259.
URI
https://scholars.duke.edu/individual/pub1415282
Source
crossref
Published In
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
Volume
37
Published Date
Start Page
e14259
End Page
e14259
DOI
10.1200/jco.2019.37.15_suppl.e14259

Cell proliferation as a biomarker for response to immune checkpoint inhibitors in highly inflamed renal cell carcinoma.

<jats:p> 61 </jats:p><jats:p> Background: Cell proliferation is an important marker of survival in many tumors and we hypothesized that this attribute could be related to response to immune checkpoint inhibitors in RCC. Previously we reported (SITC 2018) moderately proliferative lung cancer has a much higher response rate than either poorly or highly proliferative tumors. Methods: 69 FFPE tumor samples of RCC were evaluated by RNA-seq to measure transcript levels of 394 immune related genes, including 10 related to cell proliferation (BUB1, CCNB2, CDK1, CDKN3, FOXM1, KIAA0101, MAD2L1, MELK, MKI67, TOP2A). Cell proliferation, defined as the mean mRNA expression of these 10 genes was evaluated for association with ORR to ICIs by RECIST v1.1 criteria for both PD-L1 IHC positive and negative cases. Cell proliferation for each case was split into 3 tertiles of poorly ( &lt; 33), moderately (33-66) and highly ( &gt; 66) proliferative compared to a reference population. Poorly and highly proliferative were grouped for comparison to moderately proliferative tumors. Tumors were inflamed or non-inflamed based upon RNA‐seq analysis of CD8 compared to a reference population of more than 500 cases of multiple tumors. Non-inflamed, or immune desert tumors, defined as the lower 25<jats:sup>th</jats:sup> percentile of rank for CD8<jats:sup>+</jats:sup> T-cells, and greater than 75<jats:sup>th</jats:sup> percentile of rank as inflamed. Results: In our cohort of 69 patient the overall ORR was 18.8%. 15.9% of tumors were non-inflamed with an ORR of 9.1%. For 36.2% inflamed tumor the ORR was 32%. For cell proliferation 62.2% were poorly proliferative, 8.7% were highly proliferative, and 29% were moderately. ORR in moderately proliferative tumors was 30% versus 14.2% in poorly/highly proliferative tumors. In inflamed tumors, ORR in moderately proliferative tumors was 37.5% as opposed to 17.6% in poorly/highly proliferative tumors. In 11 non-inflamed tumors, there was only one responder, which was a poorly/highly proliferative tumor. Conclusions: Cell proliferation may play a crucial role in distinguishing RCC patients who may have a clinical benefit to ICI, including the important subgroup of inflamed tumors. Moderately proliferative tumors have a higher ORR than their poorly/highly counterparts. </jats:p>
Authors
Pabla, S; Zhu, J; Labriola, M; Gupta, R; George, DJ; McCall, S; Yau, E; Conroy, JM; Glenn, ST; Nesline, M; Papanicolau-Sengos, A; Burgher, B; Lenzo, FL; Zhang, T; Morrison, C
MLA Citation
Pabla, Sarabjot, et al. “Cell proliferation as a biomarker for response to immune checkpoint inhibitors in highly inflamed renal cell carcinoma..” Journal of Clinical Oncology, vol. 37, no. 8_suppl, American Society of Clinical Oncology (ASCO), 2019, pp. 61–61. Crossref, doi:10.1200/jco.2019.37.8_suppl.61.
URI
https://scholars.duke.edu/individual/pub1416787
Source
crossref
Published In
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
Volume
37
Published Date
Start Page
61
End Page
61
DOI
10.1200/jco.2019.37.8_suppl.61

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