Selective Pathology - Gastrointestinal Pathology Fellowship

Histology of a neuroendocrine tumor

About the Program

Next opening: 2027-2028
Number of positions: 1
Length: 1 year

This ACGME-accredited fellowship provides robust training in disorders of the luminal GI tract, pancreas and hepatic pathology (medical liver including liver transplantation), preparing trainees for a career in an academic or private practice setting. Five GI pathologists provide clinical service, contribute to the research program of the GI section, and support the GI Pathology training program across four distinct hospital and outpatient settings.

The GI pathology fellow will get exposure to a comprehensive spectrum of gastrointestinal surgical specimens, ranging from small biopsies to complex procedures, as well as hepatobiliary specimens. Training also includes reviewing consult digital slides from community practices in Texas. The fellow will have graduated responsibility in performing operating room consultations (frozen sections and gross examination). The fellow is expected to closely interact with surgeons/clinicians and pathology colleagues from community practice, actively participate in tumor boards, IBD/liver conferences, participate in research projects and will have the opportunity to attend and contribute to numerous didactic and clinical conferences.

Rotations

The fellow will rotate across two institutions: Baylor St. Luke’s Medical Center and Texas Children’s Hospital, with a one-month rotation at MD Anderson Cancer Center. Program strengths include extensive experience in routine and complex gastrointestinal pathology, pancreatic pathology, medical liver biopsies, liver transplantation, and pediatric pathology.

A one-week rotation in clinical gastroenterology is included, during which the fellow may observe advanced endoscopic procedures such as EMR/ESD and EUS-guided FNA/FNB performed by experienced gastroenterologists.

Stipends and Benefits

Visit the Graduate School of Biomedical Sciences page on stipends and benefits for fellows. 

Learn More

Admissions

Candidates must be board certified or eligible for certification in anatomic pathology or AP/CP.

All application materials, including recommendation letters, must be submitted online, and include the following:

  • Completed online House Staff Application
  • Current Curriculum Vitae
  • Personal Statement
  • Transcript from Medical School(s)
  • Three Recommendation Letters

Apply Online

Applications are accepted from mid-April to July 31 for positions beginning July 1 two years later. Interviews are conducted starting in July or August and are completed by the end of August of the application year.

Case of the Month

Gladson Scaria, M.D.
Oluwaseyi Olayinka, M.D.

View case images here.

An 80-year-old male with a history of colon adenocarcinoma (status post right hemicolectomy), prostate carcinoma (status post prostatectomy), remote gastric ulcer disease with Roux-en-Y gastrojejunostomy, COPD, and hypertension presented with chronic diarrhea and approximately 45-pound unintentional weight loss over several years.

Surveillance upper endoscopy performed for known gastric intestinal metaplasia demonstrated diffuse gastric atrophy and a non-bleeding ulcer involving the lesser curvature/body-incisura region. Biopsies revealed moderately differentiated adenocarcinoma.

Subsequent endoscopic ultrasound identified a small non-circumferential bleeding mass at the incisura in the setting of altered postsurgical anatomy. Endosonographic staging was T3N0. Biopsy demonstrated at least intramucosal adenocarcinoma with intact mismatch repair protein expression (pMMR).

Pathologic Findings

Histologic sections demonstrated gastric adenocarcinoma associated with a dense lymphoplasmacytic infiltrate.

EBER in situ hybridization demonstrated diffuse nuclear positivity within tumor cells, confirming Epstein-Barr virus-associated gastric carcinoma (EBVaGC).

Ancillary Studies

  • EBER ISH: Positive
  • Mismatch repair proteins: Intact (pMMR)

Questions

Question 1
Compared with conventional gastric adenocarcinoma, EBV-associated gastric carcinoma is generally associated with:

A) Higher rates of nodal metastasis
B) Worse overall survival
C) Lower rates of nodal metastasis and relatively favorable prognosis
D) Universal resistance to immunotherapy

Answer
C) Lower rates of nodal metastasis and relatively favorable prognosis

Explanation
Several studies have associated EBV-associated gastric carcinoma with lower rates of lymph node metastasis and relatively favorable outcomes compared with conventional gastric adenocarcinoma. However, prognosis remains stage-dependent, and reported outcomes vary across cohorts.

Question 2
Which of the following actionable molecular alterations is most characteristic of Epstein-Barr virus (EBV)-associated gastric carcinoma?

A) HER2 amplification and EGFR mutation
B) PD-L1/PD-L2 overexpression and PIK3CA/AKT/mTOR pathway activation
C) ALK rearrangement and ROS1 fusion
D) APC mutation and WNT pathway activation

Answer
B) PD-L1/PD-L2 overexpression and PIK3CA/AKT/mTOR pathway activation

Explanation
EBV-associated gastric carcinoma commonly demonstrates PD-L1/PD-L2 overexpression and activation of the PIK3CA/AKT/mTOR signaling pathway, supporting investigation of:

  • PD-1/PD-L1 inhibitors (nivolumab, pembrolizumab)
  • mTOR-targeted therapies (everolimus, temsirolimus)

HER2 amplification is more characteristic of chromosomal instability-type gastric carcinoma, whereas APC/WNT pathway alterations are classically associated with colorectal adenocarcinoma.

Discussion

EBV-associated gastric carcinoma represents one of the four molecular subtypes of gastric carcinoma recognized by The Cancer Genome Atlas (TCGA). This subtype accounts for approximately 8–10% of gastric carcinomas and is characterized by:

  • Prominent lymphoid stroma
  • Recurrent PIK3CA mutations
  • PD-L1/PD-L2 overexpression
  • CpG island hypermethylation
  • Potential responsiveness to immune checkpoint inhibition

Morphologically, these tumors often demonstrate syncytial growth and dense tumor-infiltrating lymphocytes, sometimes resembling lymphoepithelioma-like carcinoma. A major diagnostic consideration is MSI-high gastric carcinoma, which may also demonstrate brisk lymphocytic infiltration. In this setting, EBER in situ hybridization is essential for confirming EBV-associated disease.

EBVaGC has attracted increasing therapeutic interest because many tumors demonstrate high PD-L1 expression and an immune-rich microenvironment. Multiple recent studies have supported the biologic rationale for response to PD-1/PD-L1 checkpoint inhibitors such as nivolumab and pembrolizumab.

In addition, recurrent activation of the PIK3CA/AKT/mTOR pathway has generated interest in mTOR-directed therapeutic strategies.

Compared with conventional gastric adenocarcinoma, EBVaGC has been associated in several studies with lower rates of lymph node metastasis and relatively favorable prognosis, although outcomes may vary depending on stage and molecular co-alterations.

Selected References

  1. WHO Classification of Tumours Editorial Board. Digestive System Tumours. WHO Classification of Tumours, 5th ed, Vol 1. Lyon: IARC; 2019.
  2. Cancer Genome Atlas Research Network. Comprehensive molecular characterization of gastric adenocarcinoma. Nature. 2014;513:202–209.
  3. Shinozaki-Ushiku A, Kunita A, Fukayama M. Update on Epstein-Barr virus and gastric cancer. Int J Oncol. 2015;46:1421–1434.
  4. Nakano H, Saito M, Nakajima S, et al. PD-L1 overexpression in EBV-positive gastric cancer is caused by unique genomic or epigenomic mechanisms. Sci Rep. 2021;11:1982.
  5. Angerilli V, et al. Epstein-Barr Virus–Associated Gastric Cancer. Mod Pathol. 2025.