Bio

Clinical Focus


  • Anatomic and Clinical Pathology
  • Gastrointestinal Pathology
  • Pancreatobiliary Pathology
  • Digital Pathology

Academic Appointments


  • Assistant Professor - Med Center Line, Pathology
  • Member, Bio-X

Honors & Awards


  • Pathology in Precision Health Research Award, Stanford University Department of Pathology (2017)
  • Best Abstract Award Runner-up, Rodger C. Haggitt GI Pathology Society (2013)
  • Joseph J. and Ernesta G. Mira Scholarship, Washington University, School of Medicine (2009)
  • George F. Gill Scholarship, Washington University, School of Medicine (2009)
  • E.A. Marquard Memorial Student Scholarship, Washington University, School of Medicine (2008)
  • Dr. Larry T. Chiang Scholarship, Washington University, School of Medicine (2006)
  • President’s Scholar Award, Stanford University (2001)

Boards, Advisory Committees, Professional Organizations


  • Abstract Review Committee Member, Gastrointestinal Pathology, United States and Canadian Academy of Pathology (USCAP) (2017 - Present)
  • Member, Center for Artificial Intelligence in Medical Imaging (AIMI), Stanford University (2017 - Present)
  • Member, College of American Pathologists (2012 - Present)
  • Member, United States and Canadian Academy of Pathology (USCAP) (2011 - Present)

Professional Education


  • Board Certification: Anatomic and Clinical Pathology, American Board of Pathology (2014)
  • Medical Education:Washington University in St Louis (2010) MO
  • Fellowship, Brigham and Women's Hospital, Harvard Medical School, Gastrointestinal and Hepatopancreatobiliary Pathology (2015)
  • Residency, Brigham and Women's Hospital, Harvard Medical School, Anatomic and Clinical Pathology (2014)
  • BS, Stanford University, Biological Sciences (2005)

Research & Scholarship

Current Research and Scholarly Interests


Gastrointestinal and pancreatobiliary pathology, with major emphasis on GI and pancreatic neoplasia, inflammatory bowel disease, and the application of artificial intelligence and other emerging technologies to digital pathology.

Publications

All Publications


  • Changes in the dielectric spectra of murine colon during neoplastic progression Biomedical Physics & Engineering Express Sabuncu*, A. C., Shen*, J., Zaki, M., Beskok, A., (*equal contribution) 2018; 4 (3): 035003

    View details for DOI 10.1088/2057-1976/aaad81

  • Clinical, pathologic, and outcome study of hyperplastic and sessile serrated polyps in inflammatory bowel disease HUMAN PATHOLOGY Shen, J., Gibson, J. A., Schulte, S., Khurana, H., Farraye, F. A., Levine, J., Burakoff, R., Cerda, S., Qazi, T., Hamilton, M., Srivastava, A., Odze, R. D. 2015; 46 (10): 1548-1556

    Abstract

    There is evidence that some cancers in patients with inflammatory bowel disease (IBD) develop via the serrated pathway of carcinogenesis. This study examined the clinicopathological features and outcome of 115 IBD patients (65 with ulcerative colitis, 50 with Crohn disease), all with at least 1 serrated polyp at endoscopy or colon resection, including the presence of synchronous and metachronous conventional neoplastic lesions (dysplasia or adenocarcinoma), over an average follow-up period of 56.4 months. Conventional neoplasia was categorized as flat dysplasia (low or high grade), sporadic adenoma, adenoma-like dysplasia-associated lesion or mass, or adenocarcinoma. Overall, 97% of patients had at least 1 hyperplastic polyp (HP), 6% had a sessile serrated adenoma/polyp, and none had a traditional serrated adenoma. Eight patients (7%) had a synchronous conventional neoplastic lesion; only 1 had flat dysplasia (1%) and 2 had adenocarcinoma (2%). Thirteen patients developed a metachronous conventional neoplastic lesion, with 8 developing their conventional neoplasm within an area of previous or concurrent colitis; only 1 patient developed flat dysplasia (1%), and none developed adenocarcinoma. A higher proportion of patients with both an HP and a synchronous conventional neoplastic lesion at index developed a metachronous conventional neoplastic lesion, compared with those with an index HP only (25% versus 7%). These results suggest that IBD patients (both ulcerative colitis and Crohn disease patients) with HP have a very low risk of developing a conventional neoplastic lesion (flat dysplasia or adenocarcinoma) that would warrant surgical resection.

    View details for DOI 10.1016/j.humpath.2015.16.019

    View details for Web of Science ID 000362061400017

    View details for PubMedID 26297256

  • SWI/SNF component ARID1A restrains pancreatic neoplasia formation. Gut Wang, S. C., Nassour, I., Xiao, S., Zhang, S., Luo, X., Lee, J., Li, L., Sun, X., Nguyen, L. H., Chuang, J., Peng, L., Daigle, S., Shen, J., Zhu, H. 2018

    Abstract

    OBJECTIVE: ARID1A is commonly mutated in pancreatic ductal adenocarcinoma (PDAC), but the functional effects of ARID1A mutations in the pancreas are unclear. Understanding the molecular mechanisms that drive PDAC formation may lead to novel therapies.DESIGN: Concurrent conditional Arid1a deletion and Kras activation mutations were modelled in mice. Small-interfering RNA (siRNA) and CRISPR/Cas9 were used to abrogate ARID1A in human pancreatic ductal epithelial cells.RESULTS: We found that pancreas-specific Arid1a loss in mice was sufficient to induce inflammation, pancreatic intraepithelial neoplasia (PanIN) and mucinous cysts. Concurrent Kras activation accelerated the development of cysts that resembled intraductal papillary mucinous neoplasm. Lineage-specific Arid1a deletion confirmed compartment-specific tumour-suppressive effects. Duct-specific Arid1a loss promoted dilated ducts with occasional cyst and PDAC formation. Heterozygous acinar-specific Arid1a loss resulted in accelerated PanIN and PDAC formation with worse survival. RNA-seq showed that Arid1a loss induced gene networks associated with Myc activity and protein translation. ARID1A knockdown in human pancreatic ductal epithelial cells induced increased MYC expression and protein synthesis that was abrogated with MYC knockdown. ChIP-seq against H3K27ac demonstrated an increase in activated enhancers/promoters.CONCLUSIONS: Arid1a suppresses pancreatic neoplasia in a compartment-specific manner. In duct cells, this process appears to be associated with MYC-facilitated protein synthesis.

    View details for DOI 10.1136/gutjnl-2017-315490

    View details for PubMedID 30315093

  • Continuity of transcriptomes among colorectal cancer subtypes based on meta-analysis GENOME BIOLOGY Ma, S., Ogino, S., Parsana, P., Nishihara, R., Qian, Z., Shen, J., Mima, K., Masugi, Y., Cao, Y., Nowak, J. A., Shima, K., Hoshida, Y., Giovannucci, E. L., Gala, M. K., Chan, A. T., Fuchs, C. S., Parmigiani, G., Huttenhower, C., Waldron, L. 2018; 19: 142

    Abstract

    Previous approaches to defining subtypes of colorectal carcinoma (CRC) and other cancers based on transcriptomes have assumed the existence of discrete subtypes. We analyze gene expression patterns of colorectal tumors from a large number of patients to test this assumption and propose an approach to identify potentially a continuum of subtypes that are present across independent studies and cohorts.We examine the assumption of discrete CRC subtypes by integrating 18 published gene expression datasets and > 3700 patients, and contrary to previous reports, find no evidence to support the existence of discrete transcriptional subtypes. Using a meta-analysis approach to identify co-expression patterns present in multiple datasets, we identify and define robust, continuously varying subtype scores to represent CRC transcriptomes. The subtype scores are consistent with established subtypes (including microsatellite instability and previously proposed discrete transcriptome subtypes), but better represent overall transcriptional activity than do discrete subtypes. The scores are also better predictors of tumor location, stage, grade, and times of disease-free survival than discrete subtypes. Gene set enrichment analysis reveals that the subtype scores characterize T-cell function, inflammation response, and cyclin-dependent kinase regulation of DNA replication.We find no evidence to support discrete subtypes of the CRC transcriptome and instead propose two validated scores to better characterize a continuity of CRC transcriptomes.

    View details for DOI 10.1186/s13059-018-1511-4

    View details for Web of Science ID 000445752300001

    View details for PubMedID 30253799

    View details for PubMedCentralID PMC6154428

  • HER2 mutated lung adenocarcinoma is a distinct molecular and clinicopathologic entity 101st Annual Meeting of the United States and Canadian Academy of Pathology (USCAP) Shen, J., Taneja, K., W, Z., Dillon, D. A., Gandhi, L., Sholl, L. M. : 490A
  • Clinicopathologic significance of macrocystic change in esophageal adenocarcinoma 103rd Annual Meeting, United States and Canadian Academy of Pathology (USCAP) Setia, N., Agoston, A., Shen, J., Tippawong, M., Bueno, R., Zheng, Y., Odze, R. D., Srivastava, A. : 203A
  • Acute glomerulitis with neutrophils may underscore the development of glomerular basement membrane multi-lamination in transplant glomerulopathy 100th Annual Meeting, United States and Canadian Academy of Pathology (USCAP) Gaut, J. P., Shen, J., DeGuire, M., Klein, C., Liapis, H. : 344A
  • Prognostic role of combined MSI and BRAF mutation status in colorectal cancer: Toward routine clinical use 101st Annual Meeting, United States and Canadian Academy of Pathology (USCAP) Shen, J., Morikawa, T., Kuchiba, A., Fuchs, C. S., Ogino, S. : 179A
  • Clinicopathological characteristics of invasive gastric Helicobacter pylori HUMAN PATHOLOGY Dudley, J., Wieczorek, T., Selig, M., Cheung, H., Shen, J., Odze, R., Deshpande, V., Zukerberg, L. 2017; 61: 19-25
  • Hermansky-pudlak syndrome complicated by pulmonary fibrosis: radiologic-pathologic correlation and review of pulmonary complications. Journal of clinical imaging science Kelil, T., Shen, J., O'Neill, A. C., Howard, S. A. 2014; 4: 59-?

    Abstract

    Hermansky-Pudlak syndrome (HPS) is a rare autosomal recessive disorder characterized by oculocutaneous hypopigmentation, platelet dysfunction, and in many cases, life-threatening pulmonary fibrosis. We report the clinical course, imaging, and postmortem findings of a 38-year-old female with HPS-related progressive pulmonary fibrosis, highlighting the role of imaging in assessment of disease severity and prognosis.

    View details for DOI 10.4103/2156-7514.143437

    View details for PubMedID 25379352

    View details for PubMedCentralID PMC4220421

  • Clinical, Pathologic, and Biologic Features Associated with BRAF Mutations in Non-Small Cell Lung Cancer CLINICAL CANCER RESEARCH Cardarella, S., Ogino, A., Nishino, M., Butaney, M., Shen, J., Lydon, C., Yeap, B. Y., Sholl, L. M., Johnson, B. E., Jaenne, P. A. 2013; 19 (16): 4532-4540

    Abstract

    BRAF mutations are found in a subset of non-small cell lung cancers (NSCLC). We examined the clinical characteristics and treatment outcomes of patients with NSCLC harboring BRAF mutations.Using DNA sequencing, we successfully screened 883 patients with NSCLC for BRAF mutations between July 1, 2009 and July 16, 2012. Baseline characteristics and treatment outcomes were compared between patients with and without BRAF mutations. Wild-type controls consisted of patients with NSCLC without a somatic alteration in BRAF, KRAS, EGFR, and ALK. In vitro studies assessed the biologic properties of selected non-V600E BRAF mutations identified from patients with NSCLC.Of 883 tumors screened, 36 (4%) harbored BRAF mutations (V600E, 18; non-V600E, 18) and 257 were wild-type for BRAF, EGFR, KRAS, and ALK negative. Twenty-nine of 36 patients with BRAF mutations were smokers. There were no distinguishing clinical features between BRAF-mutant and wild-type patients. Patients with advanced NSCLC with BRAF mutations and wild-type tumors showed similar response rates and progression-free survival (PFS) to platinum-based combination chemotherapy and no difference in overall survival. Within the BRAF cohort, patients with V600E-mutated tumors had a shorter PFS to platinum-based chemotherapy compared with those with non-V600E mutations, although this did not reach statistical significance (4.1 vs. 8.9 months; P = 0.297). We identified five BRAF mutations not previously reported in NSCLC; two of five were associated with increased BRAF kinase activity.BRAF mutations occur in 4% of NSCLCs and half are non-V600E. Prospective trials are ongoing to validate BRAF as a therapeutic target in NSCLC.

    View details for DOI 10.1158/1078-0432.CCR-13-0657

    View details for Web of Science ID 000323147700025

    View details for PubMedID 23833300

    View details for PubMedCentralID PMC3762878

  • Microsatellite Instability and BRAF Mutation Testing in Colorectal Cancer Prognostication JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE Lochhead, P., Kuchiba, A., Imamura, Y., Liao, X., Yamauchi, M., Nishihara, R., Qian, Z. R., Morikawa, T., Shen, J., Meyerhardt, J. A., Fuchs, C. S., Ogino, S. 2013; 105 (15): 1151-1156

    Abstract

    BRAF mutation in colorectal cancer is associated with microsatellite instability (MSI) through its relationship with high-level CpG island methylator phenotype (CIMP) and MLH1 promoter methylation. MSI and BRAF mutation analyses are routinely used for familial cancer risk assessment. To clarify clinical outcome associations of combined MSI/BRAF subgroups, we investigated survival in 1253 rectal and colon cancer patients within the Nurses' Health Study and Health Professionals Follow-up Study with available data on clinical and other molecular features, including CIMP, LINE-1 hypomethylation, and KRAS and PIK3CA mutations. Compared with the majority subtype of microsatellite stable (MSS)/BRAF-wild-type, MSS/BRAF-mutant, MSI-high/BRAF-mutant, and MSI-high/BRAF-wild-type subtypes showed multivariable colorectal cancer-specific mortality hazard ratios of 1.60 (95% confidence interval [CI] =1.12 to 2.28; P = .009), 0.48 (95% CI = 0.27 to 0.87; P = .02), and 0.25 (95% CI = 0.12 to 0.52; P < .001), respectively. No evidence existed for a differential prognostic role of BRAF mutation by MSI status (P(interaction) > .50). Combined BRAF/MSI status in colorectal cancer is a tumor molecular biomarker for prognosic risk stratification.

    View details for DOI 10.1093/jnci/djt173

    View details for Web of Science ID 000322976000013

    View details for PubMedID 23878352

    View details for PubMedCentralID PMC3735463

  • Neurocandidiasis: a case report and consideration of the causes of restricted diffusion. Journal of radiology case reports Lin, D. J., Sacks, A., Shen, J., Lee, T. C. 2013; 7 (5): 1-5

    Abstract

    Diffusion weighted magnetic resonance imaging has risen to the forefront of imaging for acute stroke. However, the differential diagnosis of restricted diffusion is wide and includes ischemia, metabolic derangements, infections, and highly-cellular masses. We present a case of central nervous system (CNS) candidiasis presenting radiographically as bilateral punctate areas of restricted magnetic resonance (MR) diffusion in the basal ganglia. This case illustrates the value of carefully considering the causes of restricted diffusion in the brain, notably to be broader than acute stroke and to include invasive fungal infections.

    View details for DOI 10.3941/jrcr.v7i5.1319

    View details for PubMedID 23705051

    View details for PubMedCentralID PMC3661417

  • The persistent problem of new-onset postoperative atrial fibrillation: A single-institution experience over two decades JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY Shen, J., Lall, S., Zheng, V., Buckley, P., Damiano, R. J., Schuessler, R. B. 2011; 141 (2): 559-570

    Abstract

    Postoperative atrial fibrillation is the most common complication after cardiac surgery. A variety of postoperative atrial fibrillation risk factors have been reported, but study results have been inconsistent or contradictory, particularly in patients with preexisting atrial fibrillation. The incidence of postoperative atrial fibrillation was evaluated in a group of 10,390 patients undergoing cardiac surgery among a comprehensive range of risk factors to identify reliable predictors of postoperative atrial fibrillation.This 20-year retrospective study examined the relationship between postoperative atrial fibrillation and demographic factors, preoperative health conditions and medications, operative procedures, and postoperative complications. Multivariate logistic regression models were used to evaluate potential predictors of postoperative atrial fibrillation.Increasing age, mitral valve surgery (odds ratio=1.91), left ventricular aneurysm repair (odds ratio=1.57), aortic valve surgery (odds ratio=1.52), race (Caucasian) (odds ratio=1.51), use of cardioplegia (odds ratio=1.36), use of an intraaortic balloon pump (odds ratio=1.28), previous congestive heart failure (odds ratio=1.28), and hypertension (odds ratio=1.15) were significantly associated with postoperative atrial fibrillation. The non-linear relationship between age and postoperative atrial fibrillation revealed the acceleration of postoperative atrial fibrillation risk in patients aged 55 years or more. In patients undergoing coronary artery bypass grafting, increasing age and previous congestive heart failure were the only factors associated with a higher risk of postoperative atrial fibrillation. There was no trend in incidence of postoperative atrial fibrillation over time. No protective factors against postoperative atrial fibrillation were detected, including commonly prescribed categories of medications.The persistence of the problem of postoperative atrial fibrillation and the modest predictability using common risk factors suggest that limited progress has been made in understanding its cause and treatment.

    View details for DOI 10.1016/j.jtcvs.2010.03.011

    View details for Web of Science ID 000286222800042

    View details for PubMedID 20434173

    View details for PubMedCentralID PMC2917532

  • Surgery for Lone Atrial Fibrillation: Present State-of-the-Art. Innovations (Philadelphia, Pa.) Shen, J., Bailey, M., Damiano, R. J. 2009; 4 (5): 248-255

    Abstract

    For two decades, the cut-and-sew Cox-Maze III procedure was the gold standard for the surgical treatment of atrial fibrillation (AF), and proved to be effective at curing lone AF and preventing its most dreaded complication, stroke. However, this procedure was not widely adopted due to its complexity and technical difficulty. Over the last 5-10 years, the introduction of new ablation technology has led to the development of the Cox-Maze IV procedure, as well as, more limited lesion sets, with the ultimate goal of performing a minimally-invasive lesion set on the beating heart, without the need for cardiopulmonary bypass. This review summarizes the current state of the art and future directions in the surgical treatment of lone atrial fibrillation. The hope is that as we learn more about the mechanisms of AF and develop preoperative diagnostic technologies capable of precisely locating the areas responsible for AF, it will become possible to tailor specific lesion sets and ablation modalities to individual patients, making the surgical treatment of lone AF available to a larger population of patients.

    View details for PubMedID 20473355

    View details for PubMedCentralID PMC2868583

  • The surgical treatment of atrial fibrillation HEART RHYTHM Shen, J., Bailey, M. S., Damiano, R. J. 2009; 6 (8): S45-S50

    Abstract

    For two decades, the cut-and-sew Cox-maze III procedure was the gold standard for the surgical treatment of atrial fibrillation (AF) and has proven to be effective at eliminating AF. The incidence of late stroke was also very low. However, this procedure was not widely adopted owing to its complexity and technical difficulty. Over the last 5-10 years, the introduction of new ablation technology has led to the development of the Cox-maze IV procedure as well as more limited lesion sets, with the ultimate goal of performing a minimally invasive lesion set on the beating heart without the need for cardiopulmonary bypass. This review summarizes the current state of the art and future directions in the stand-alone surgical treatment of AF. The hope is that as more is learned about the mechanisms of AF and with better preoperative diagnostic technologies capable of precisely locating the areas responsible for AF, it will become possible to tailor specific lesion sets and ablation modalities to individual patients, making the surgical treatment of AF available to a larger population of patients.

    View details for DOI 10.1016/j.hrthm.2009.05.019

    View details for Web of Science ID 000268867800009

    View details for PubMedID 19631907

    View details for PubMedCentralID PMC2760330

  • A temporal switch from Notch to Wnt signaling in muscle stem cells is necessary for normal adult myogenesis CELL STEM CELL Brack, A. S., Conboy, I. M., Conboy, M. J., Shen, J., Rando, T. A. 2008; 2 (1): 50-59

    Abstract

    The temporal switch from progenitor cell proliferation to differentiation is essential for effective adult tissue repair. We previously reported the critical role of Notch signaling in the proliferative expansion of myogenic progenitors in mammalian postnatal myogenesis. We now show that the onset of differentiation is due to a transition from Notch signaling to Wnt signaling in myogenic progenitors and is associated with an increased expression of Wnt in the tissue and an increased responsiveness of progenitors to Wnt. Crosstalk between these two pathways occurs via GSK3beta, which is maintained in an active form by Notch but is inhibited by Wnt in the canonical Wnt signaling cascade. These results demonstrate that the temporal balance between Notch and Wnt signaling orchestrates the precise progression of muscle precursor cells along the myogenic lineage pathway, through stages of proliferative expansion and then differentiation, during postnatal myogenesis.

    View details for DOI 10.1016/j.stem.2007.10.006

    View details for Web of Science ID 000252606400011

    View details for PubMedID 18371421