Shannon McCall

Overview:

As an anatomic pathologist, 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, a shared resource of the School of Medicine and the Duke Cancer Institute.  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

Resident, Pathology

Duke University

Grants:

Preoperative Breast Radiotherapy: A Tool to Provide Individualized and Biologically-Based Radiation Therapy

Administered By
Radiation Oncology
Role
Collaborator
Start Date
End Date

Characterization of Tumor Immunobiological Factors that Promote Lymphovascular Invasion and Dissemination in Locally Advanced Breast Cancer

Administered By
Surgery, Surgical Sciences
Awarded By
Department of Defense
Role
Co Investigator
Start Date
End Date

The role of gastrin in esophageal submucosal gland acinar ductal metaplasia

Administered By
Medicine, Gastroenterology
Awarded By
National Institutes of Health
Role
Biostatistician
Start Date
End Date

The role of gastrin in esophageal submucosal gland acinar ductal metaplasia

Administered By
Medicine, Gastroenterology
Awarded By
National Institutes of Health
Role
Biostatistician
Start Date
End Date

Project GENIE Steering Committee Resolution Part II

Administered By
Pathology
Awarded By
American Association for Cancer Research
Role
Principal Investigator
Start Date
End Date

Publications:

Comprehensive Analysis of Alternative Splicing Across Tumors from 8,705 Patients.

Our comprehensive analysis of alternative splicing across 32 The Cancer Genome Atlas cancer types from 8,705 patients detects alternative splicing events and tumor variants by reanalyzing RNA and whole-exome sequencing data. Tumors have up to 30% more alternative splicing events than normal samples. Association analysis of somatic variants with alternative splicing events confirmed known trans associations with variants in SF3B1 and U2AF1 and identified additional trans-acting variants (e.g., TADA1, PPP2R1A). Many tumors have thousands of alternative splicing events not detectable in normal samples; on average, we identified ≈930 exon-exon junctions ("neojunctions") in tumors not typically found in GTEx normals. From Clinical Proteomic Tumor Analysis Consortium data available for breast and ovarian tumor samples, we confirmed ≈1.7 neojunction- and ≈0.6 single nucleotide variant-derived peptides per tumor sample that are also predicted major histocompatibility complex-I binders ("putative neoantigens").
Authors
Kahles, A; Lehmann, K-V; Toussaint, NC; Hüser, M; Stark, SG; Sachsenberg, T; Stegle, O; Kohlbacher, O; Sander, C; Cancer Genome Atlas Research Network,; Rätsch, G
MLA Citation
Kahles, André, et al. “Comprehensive Analysis of Alternative Splicing Across Tumors from 8,705 Patients..” Cancer Cell, vol. 34, no. 2, Aug. 2018, pp. 211-224.e6. Pubmed, doi:10.1016/j.ccell.2018.07.001.
URI
https://scholars.duke.edu/individual/pub1353625
PMID
30078747
Source
pubmed
Published In
Cancer Cell
Volume
34
Published Date
Start Page
211
End Page
224.e6
DOI
10.1016/j.ccell.2018.07.001

Oncogenic Signaling Pathways in The Cancer Genome Atlas.

Genetic alterations in signaling pathways that control cell-cycle progression, apoptosis, and cell growth are common hallmarks of cancer, but the extent, mechanisms, and co-occurrence of alterations in these pathways differ between individual tumors and tumor types. Using mutations, copy-number changes, mRNA expression, gene fusions and DNA methylation in 9,125 tumors profiled by The Cancer Genome Atlas (TCGA), we analyzed the mechanisms and patterns of somatic alterations in ten canonical pathways: cell cycle, Hippo, Myc, Notch, Nrf2, PI-3-Kinase/Akt, RTK-RAS, TGFβ signaling, p53 and β-catenin/Wnt. We charted the detailed landscape of pathway alterations in 33 cancer types, stratified into 64 subtypes, and identified patterns of co-occurrence and mutual exclusivity. Eighty-nine percent of tumors had at least one driver alteration in these pathways, and 57% percent of tumors had at least one alteration potentially targetable by currently available drugs. Thirty percent of tumors had multiple targetable alterations, indicating opportunities for combination therapy.
Authors
Sanchez-Vega, F; Mina, M; Armenia, J; Chatila, WK; Luna, A; La, KC; Dimitriadoy, S; Liu, DL; Kantheti, HS; Saghafinia, S; Chakravarty, D; Daian, F; Gao, Q; Bailey, MH; Liang, W-W; Foltz, SM; Shmulevich, I; Ding, L; Heins, Z; Ochoa, A; Gross, B; Gao, J; Zhang, H; Kundra, R; Kandoth, C; Bahceci, I; Dervishi, L; Dogrusoz, U; Zhou, W; Shen, H; Laird, PW; Way, GP; Greene, CS; Liang, H; Xiao, Y; Wang, C; Iavarone, A; Berger, AH; Bivona, TG; Lazar, AJ; Hammer, GD; Giordano, T; Kwong, LN; McArthur, G; Huang, C; Tward, AD; Frederick, MJ; McCormick, F; Meyerson, M; Cancer Genome Atlas Research Network,; Van Allen, EM; Cherniack, AD; Ciriello, G; Sander, C; Schultz, N
MLA Citation
Sanchez-Vega, Francisco, et al. “Oncogenic Signaling Pathways in The Cancer Genome Atlas..” Cell, vol. 173, no. 2, Apr. 2018, pp. 321-337.e10. Pubmed, doi:10.1016/j.cell.2018.03.035.
URI
https://scholars.duke.edu/individual/pub1314293
PMID
29625050
Source
pubmed
Published In
Cell
Volume
173
Published Date
Start Page
321
End Page
337.e10
DOI
10.1016/j.cell.2018.03.035

Scalable Open Science Approach for Mutation Calling of Tumor Exomes Using Multiple Genomic Pipelines.

The Cancer Genome Atlas (TCGA) cancer genomics dataset includes over 10,000 tumor-normal exome pairs across 33 different cancer types, in total >400 TB of raw data files requiring analysis. Here we describe the Multi-Center Mutation Calling in Multiple Cancers project, our effort to generate a comprehensive encyclopedia of somatic mutation calls for the TCGA data to enable robust cross-tumor-type analyses. Our approach accounts for variance and batch effects introduced by the rapid advancement of DNA extraction, hybridization-capture, sequencing, and analysis methods over time. We present best practices for applying an ensemble of seven mutation-calling algorithms with scoring and artifact filtering. The dataset created by this analysis includes 3.5 million somatic variants and forms the basis for PanCan Atlas papers. The results have been made available to the research community along with the methods used to generate them. This project is the result of collaboration from a number of institutes and demonstrates how team science drives extremely large genomics projects.
Authors
Ellrott, K; Bailey, MH; Saksena, G; Covington, KR; Kandoth, C; Stewart, C; Hess, J; Ma, S; Chiotti, KE; McLellan, M; Sofia, HJ; Hutter, C; Getz, G; Wheeler, D; Ding, L; MC3 Working Group,; Cancer Genome Atlas Research Network,
MLA Citation
Ellrott, Kyle, et al. “Scalable Open Science Approach for Mutation Calling of Tumor Exomes Using Multiple Genomic Pipelines..” Cell Syst, vol. 6, no. 3, Mar. 2018, pp. 271-281.e7. Pubmed, doi:10.1016/j.cels.2018.03.002.
URI
https://scholars.duke.edu/individual/pub1311452
PMID
29596782
Source
pubmed
Published In
Cell Systems
Volume
6
Published Date
Start Page
271
End Page
281.e7
DOI
10.1016/j.cels.2018.03.002

Serum Amyloid A (SAA) and C-Reactive Protein (CRP) Are Commonly Positive in Hepatocellular Carcinoma and Expression Levels Stratify According to Etiology and the Absence of Cirrhosis

Authors
Shaar, M; Suzuki, A; Poster, C; de Ridder, G; Zhang, X; Cronin, MK; McCall, S; Cardona, D; Abdelmalek, M; Pizzo, S; Jiang, XS; Lefaivre, M; Guy, C
MLA Citation
URI
https://scholars.duke.edu/individual/pub1243592
Source
wos
Published In
Laboratory Investigation
Volume
97
Published Date
Start Page
424A
End Page
425A

Primary high-grade neuroendocrine carcinoma emerging from an adenomatous polyp in the setting of familial adenomatous polyposis.

Familial adenomatous polyposis (FAP) is a rare inherited syndrome that is characterised by innumerable adenomas of the colon and rectum, a high risk of colorectal cancer and a variety of extracolonic manifestations. FAP presents as hundreds to thousands of colonic adenomas beginning in adolescence. The syndrome is associated with less than 1% of all colorectal cancer cases, but there is a nearly 100% lifetime risk of colorectal cancer in individuals with FAP. This case demonstrates a 60-year-old man with FAP who developed high-grade neuroendocrine carcinoma with glandular and squamous differentiation, and regional lymph node and liver metastases. Early diagnosis of FAP is of the utmost importance to start screening colonoscopies to assess disease burden, perform polypectomies and to make management decisions. Neuroendocrine carcinomas rarely occur in patients with FAP, and awareness of this association among general medical physicians and pathologists is essential for the diagnosis and care of these patients.
Authors
Detweiler, CJ; Cardona, DM; Hsu, DS; McCall, SJ
MLA Citation
Detweiler, Claire J., et al. “Primary high-grade neuroendocrine carcinoma emerging from an adenomatous polyp in the setting of familial adenomatous polyposis..” Bmj Case Rep, vol. 2016, Feb. 2016. Pubmed, doi:10.1136/bcr-2015-214206.
URI
https://scholars.duke.edu/individual/pub1121334
PMID
26884076
Source
pubmed
Published In
Bmj Case Reports
Volume
2016
Published Date
DOI
10.1136/bcr-2015-214206

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