Chanjuan Shi

Overview:

Dr. Shi is a gastrointestinal (GI)/liver pathologist. Her particular areas of interest are GI and pancreatic neuroendocrine tumors and pancreatic pathology. Her research interests include 1)  Pathobiology of GI and pancreatic neuroendocrine tumors and 2) Identification of diagnostic, prognostic and therapeutic biomarkers for colorectal and pancreatic cancers


Positions:

Professor of Pathology

Pathology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 1989

Zhejiang University (China)

Ph.D. 2002

Dalhousie University (Canada)

Publications:

Primary hepatic neoplasms arising in cirrhotic livers can have a variable spectrum of neuroendocrine differentiation.

Primary hepatic neoplasms with neuroendocrine differentiation are extremely rare. Their clinicopathological features and molecular genetic basis are largely unknown. We identified four cases of primary hepatic neoplasms with neuroendocrine differentiation. Electronic medical records were reviewed for clinical history, imaging findings, laboratory results, and follow-up. Pathology slides, immunohistochemistry, and ancillary studies were reviewed. There were two females and two males with age ranging from 52 to 74 years. There was one amphicrine carcinoma with tumor cells simultaneously demonstrating both hepatocellular and neuroendocrine differentiation, one mixed hepatocellular-neuroendocrine carcinoma (NEC) with hepatocellular component intermingled with neuroendocrine component, one small cell NEC, and one well-differentiated neuroendocrine tumor. Next- generation sequencing of the mixed hepatocellular-NEC and small cell NEC showed molecular/genetic alterations commonly seen in hepatocellular carcinoma (HCC). All four cases arose in a background of cirrhosis. Primary hepatic neoplasms arising in cirrhotic livers can have a spectrum of neuroendocrine differentiation. Presence of a NEC component may be an indicator of aggressiveness. In addition, primary hepatic carcinomas with neuroendocrine differentiation likely share the same molecular pathways as HCC.
Authors
Shi, C; Jug, R; Bean, SM; Jeck, WR; Guy, CD
MLA Citation
Shi, Chanjuan, et al. “Primary hepatic neoplasms arising in cirrhotic livers can have a variable spectrum of neuroendocrine differentiation.Hum Pathol, vol. 116, Oct. 2021, pp. 63–72. Pubmed, doi:10.1016/j.humpath.2021.07.007.
URI
https://scholars.duke.edu/individual/pub1489710
PMID
34310982
Source
pubmed
Published In
Hum Pathol
Volume
116
Published Date
Start Page
63
End Page
72
DOI
10.1016/j.humpath.2021.07.007

Rectothecal Fistula Secondary to a Tailgut Cyst With Malignant Transformation: An Abnormal Connection and Unusual Pathology.

Authors
Stewart, MK; Kavalukas, SL; Bonfield, CM; Ciombor, KK; Shi, C; Kachnic, LA; Hawkins, AT
MLA Citation
Stewart, Melissa K., et al. “Rectothecal Fistula Secondary to a Tailgut Cyst With Malignant Transformation: An Abnormal Connection and Unusual Pathology.The American Surgeon, vol. 87, no. 7, July 2021, pp. 1126–28. Epmc, doi:10.1177/0003134820940733.
URI
https://scholars.duke.edu/individual/pub1470224
PMID
33338389
Source
epmc
Published In
The American Surgeon
Volume
87
Published Date
Start Page
1126
End Page
1128
DOI
10.1177/0003134820940733

Colonic Epithelial-Derived Selenoprotein P Is the Source for Antioxidant-Mediated Protection in Colitis-Associated Cancer.

BACKGROUND & AIMS: Patients with inflammatory bowel disease (IBD) demonstrate nutritional selenium deficiencies and are at greater risk of developing colon cancer. Previously, we determined that global reduction of the secreted antioxidant selenium-containing protein, selenoprotein P (SELENOP), substantially increased tumor development in an experimental colitis-associated cancer (CAC) model. We next sought to delineate tissue-specific contributions of SELENOP to intestinal inflammatory carcinogenesis and define clinical context. METHODS: Selenop floxed mice crossed with Cre driver lines to delete Selenop from the liver, myeloid lineages, or intestinal epithelium were placed on an azoxymethane/dextran sodium sulfate experimental CAC protocol. SELENOP loss was assessed in human ulcerative colitis (UC) organoids, and expression was queried in human and adult UC samples. RESULTS: Although large sources of SELENOP, both liver- and myeloid-specific Selenop deletion failed to modify azoxymethane/dextran sodium sulfate-mediated tumorigenesis. Instead, epithelial-specific deletion increased CAC tumorigenesis, likely due to elevated oxidative stress with a resulting increase in genomic instability and augmented tumor initiation. SELENOP was down-regulated in UC colon biopsies and levels were inversely correlated with endoscopic disease severity and tissue S100A8 (calprotectin) gene expression. CONCLUSIONS: Although global selenium status is typically assessed by measuring liver-derived plasma SELENOP levels, our results indicate that the peripheral SELENOP pool is dispensable for CAC. Colonic epithelial SELENOP is the main contributor to local antioxidant capabilities. Thus, colonic SELENOP is the most informative means to assess selenium levels and activity in IBD patients and may serve as a novel biomarker for UC disease severity and identify patients most predisposed to CAC development.
Authors
Short, SP; Pilat, JM; Barrett, CW; Reddy, VK; Haberman, Y; Hendren, JR; Marsh, BJ; Keating, CE; Motley, AK; Hill, KE; Zemper, AE; Washington, MK; Shi, C; Chen, X; Wilson, KT; Hyams, JS; Denson, LA; Burk, RF; Rosen, MJ; Williams, CS
MLA Citation
Short, Sarah P., et al. “Colonic Epithelial-Derived Selenoprotein P Is the Source for Antioxidant-Mediated Protection in Colitis-Associated Cancer.Gastroenterology, vol. 160, no. 5, Apr. 2021, pp. 1694-1708.e3. Pubmed, doi:10.1053/j.gastro.2020.12.059.
URI
https://scholars.duke.edu/individual/pub1471393
PMID
33388316
Source
pubmed
Published In
Gastroenterology
Volume
160
Published Date
Start Page
1694
End Page
1708.e3
DOI
10.1053/j.gastro.2020.12.059

Key histopathologic features in idiopathic noncirrhotic portal hypertension: an interobserver agreement study and proposal for diagnostic criteria.

Histologic features of idiopathic noncirrhotic portal hypertension (INCPH), loosely termed as obliterative portal venopathy (OPV), are heterogenous, often subtle, and overlap with other entities. To this date, no consensus histopathologic diagnostic criteria have been established for INCPH. For these reasons, rendering a reproducible consensus histologic diagnosis of OPV on a liver biopsy may often be challenging even for experienced hepatopathologists. We report herein a two-phase interobserver agreement study on the diagnosis of OPV and assessed the relative value of histologic features in 104 liver biopsies in distinguishing between INCPH and non-INCPH with the goal to obtain a consensus on specific practical diagnostic criteria. Six hepatopathologists blinded to clinical information and original pathologic diagnosis reviewed internet-based case study sets with high-resolution whole-slide images. The initial interobserver agreement on OPV was expectedly low, but significantly improved (moderate agreement in most categories) upon adopting a consensus view recognizing portal vein sclerosis as the only strong independent histologic predictor for INCPH, and that contrary to the conventional view, aberrant portal/periportal vessels does not significantly contribute to the positive assignment of OPV status. We propose a three-tiered classification with diagnostic criteria to facilitate the histologic assignment of OPV status for the evaluation of INCPH. Furthermore, we have validated the performance of the proposed criteria either based on histology alone or coupled with clinicopathologic correlation. This classification may aid in practical histologic assessment of liver biopsies with or without portal hypertension and help to improve diagnostic consistency and accuracy.
Authors
Liang, J; Shi, C; Dupont, WD; Salaria, SN; Huh, WJ; Correa, H; Roland, JT; Perri, RE; Washington, MK
MLA Citation
Liang, Jiancong, et al. “Key histopathologic features in idiopathic noncirrhotic portal hypertension: an interobserver agreement study and proposal for diagnostic criteria.Mod Pathol, vol. 34, no. 3, Mar. 2021, pp. 592–602. Pubmed, doi:10.1038/s41379-020-00676-8.
URI
https://scholars.duke.edu/individual/pub1461072
PMID
32958831
Source
pubmed
Published In
Modern Pathology
Volume
34
Published Date
Start Page
592
End Page
602
DOI
10.1038/s41379-020-00676-8

Amsterdam International Consensus Meeting: tumor response scoring in the pathology assessment of resected pancreatic cancer after neoadjuvant therapy.

Histopathologically scoring the response of pancreatic ductal adenocarcinoma (PDAC) to neoadjuvant treatment can guide the selection of adjuvant therapy and improve prognostic stratification. However, several tumor response scoring (TRS) systems exist, and consensus is lacking as to which system represents best practice. An international consensus meeting on TRS took place in November 2019 in Amsterdam, The Netherlands. Here, we provide an overview of the outcomes and consensus statements that originated from this meeting. Consensus (≥80% agreement) was reached on a total of seven statements: (1) TRS is important because it provides information about the effect of neoadjuvant treatment that is not provided by other histopathology-based descriptors. (2) TRS for resected PDAC following neoadjuvant therapy should assess residual (viable) tumor burden instead of tumor regression. (3) The CAP scoring system is considered the most adequate scoring system to date because it is based on the presence and amount of residual cancer cells instead of tumor regression. (4) The defining criteria of the categories in the CAP scoring system should be improved by replacing subjective terms including "minimal" or "extensive" with objective criteria to evaluate the extent of viable tumor. (5) The improved, consensus-based system should be validated retrospectively and prospectively. (6) Prospective studies should determine the extent of tissue sampling that is required to ensure adequate assessment of the residual cancer burden, taking into account the heterogeneity of tumor response. (7) In future scientific publications, the extent of tissue sampling should be described in detail in the "Materials and methods" section.
Authors
Janssen, BV; Tutucu, F; van Roessel, S; Adsay, V; Basturk, O; Campbell, F; Doglioni, C; Esposito, I; Feakins, R; Fukushima, N; Gill, AJ; Hruban, RH; Kaplan, J; Koerkamp, BG; Hong, S-M; Krasinskas, A; Luchini, C; Offerhaus, J; Sarasqueta, AF; Shi, C; Singhi, A; Stoop, TF; Soer, EC; Thompson, E; van Tienhoven, G; Velthuysen, M-LF; Wilmink, JW; Besselink, MG; Brosens, LAA; Wang, H; Verbeke, CS; Verheij, J; International Study Group of Pancreatic Pathologists (ISGPP),
MLA Citation
Janssen, Boris V., et al. “Amsterdam International Consensus Meeting: tumor response scoring in the pathology assessment of resected pancreatic cancer after neoadjuvant therapy.Mod Pathol, vol. 34, no. 1, Jan. 2021, pp. 4–12. Pubmed, doi:10.1038/s41379-020-00683-9.
URI
https://scholars.duke.edu/individual/pub1462229
PMID
33041332
Source
pubmed
Published In
Modern Pathology
Volume
34
Published Date
Start Page
4
End Page
12
DOI
10.1038/s41379-020-00683-9