An Innovative Diagnostic Tool for Barrett’s Esophagus Patients

BarreGEN® (Esophageal Cancer Risk Classifier) is a molecular based assay that helps resolve the risk of progression of Barrett’s Esophagus to esophageal cancer.

About Barrett's Esophagus

Barrett’s Esophagus (BE) is a precancerous condition typically caused by Gastroesophageal Reflux Disease (GERD) and is a major risk factor for esophageal cancer.1

Other risk factors for BE include age, male sex, white race, central obesity, tobacco use, and family history of GERD, BE, or esophageal cancer.1,2

Prevalence

The incidence of esophageal cancer is rising and it is estimated that 5.6% of the US adult population has BE (over 14 million US adults).1,3

While people with BE are at higher risk of esophageal cancer, progression to cancer is uncommon. Roughly, only 0.5% of people with BE develop esophageal cancer each year.3,4

Cellular Changes

While uncommon, there is potential for the progression of cellular changes that can lead to esophageal cancer5:

Intestinal Metaplasia

The abnormal presence of intestinal type cells found in the esophagus as a consequence of chronic tissue injury. Most often, there is no evidence of dysplasia and this condition is termed “nondysplastic BE.”

  • The risk of cancer progression for people with nondysplastic BE is ~0.20.5% per year5

Dysplasia​

Cells that look abnormal under a microscope but are not yet cancer. These precancerous changes can be classified as low-grade or high-grade based on the degree of change.

Low-grade dysplasia (LGD) means that some cells looked abnormal and high-grade dysplasia (HGD) refers to precancerous changes being seen in the cells of the esophagus when looked at under a microscope.

  • The risk of cancer progression for a patient with LGD is ~0.7% per year and the risk for patients with HGD is ~10x higher, at ~7% per year. The vast majority of people with BE, however, do not progress to esophageal cancer2

Cancer

Cells consistent with esophageal adenocarcinoma are present.

BarreGEN can help identify BE patients at higher risk of esophageal cancer

Triaging patients according to their risk of future progression to esophageal cancer would help to limit unnecessary repeat endoscopies in patients with low risk and justify more aggressive management in patients with higher risk, perhaps even supporting early means of cancer prevention such as ablation.1

However, differentiating the presence and stage of dysplasia remains a challenge for pathologists, resulting in high inter-observer variability in diagnosing the level of dysplasia and the associated risk of esophageal cancer.6

About BarreGEN®

BarreGEN® is a molecular based assay that quantifies the mutational load (ML) in esophageal specimens obtained from patients who have BE—a leading risk factor of esophageal cancer.

ML provides a measure of cumulative genomic instability (DNA damage). In looking at key genomic loci in patients with BE and assessing DNA damage in tumor suppressor genes associated with progression to HGD and esophageal cancer, the risk of more advanced disease can be determined.7

Use of BarreGEN can help support the need for cancer preventative treatments, such as ablation, and provide justification for when such treatments may not be necessary. It does so by helping physicians understand if dysplasia is present or if there is a risk for developing dysplasia or cancer in the future.

Ablation can be a cost-effective means of cancer prevention in patients with BE when BarreGEN is used to identify patients at higher risk of cancer.8

How to Order

Testing can be conducted using the original biopsy sample. There is no need for an additional tissue sample to be taken. However, testing can be initiated only upon receipt of a signed, completed test requisition form for BarreGEN. All available imaging or clinical data, such as cytology or histopathology reports, should be submitted. The clinical data will be included within the integrated report.

Turnaround Time

Less than 18 business days after receipt of specimen and a signed, completed test requisition form. Contact Client Services at (800) 495-9885 for additional details or assistance.

Specimens

  • Formalin-fixed Paraffin-embedded (FFPE) Blocks
  • Slide recuts from FFPE tissue blocks​
  • FFPE blocks require additional processing that may increase turnaround time
  • The pathology report for FFPE or submitted slides is required
  • Not Accepted: Decalcified tissue, bleached tissue, and tissues fixed in Zenker’s or Bouin’s fixatives
  • Acceptable Fixatives: 10% buffered formalin, paraformaldehyde, B6, and most common fixatives

Full instructions on specimen collection and shipping are included within the specimen collection kit, available from Client Services:

Contact Us

Interpace Diagnostics

300 Interpace Parkway, Building C
Morris Corporate Center 1
Parsippany, NJ 07054

800-495-9885
info@interpacedx.com

References

  1. Spechler SJ, Souza RF. Barrett’s esophagus. N Engl J Med. 2014;371(9):836-845.
  2. Shaheen NJ, et al. ACG Clinical Guideline: diagnosis and management of Barrett’s esophagus. Am J Gastroenterol. 2016;111:30-50.
  3. Wild CP, Hardle LJ. Reflux, Barrett’s oesophagus and adenocarcinoma: burning questions. Cancer. 2003;3(9):676-684.
  4. Odze RD. Update on the diagnosis and treatment of Barrett esophagus and related neoplastic precursor lesions. Arch Pathol Lab Med. 2008;132(10):1577-1585.
  5. J-F Flejou. Barrett’s oesophagus: from metaplasia to dysplasia and cancer. Gut. 2005;54(Suppl 1):i6-i12.
  6. Khara HS et al. Assessment of mutational load in biopsy tissue provides additional information about genomic instability to histological classifications of Barrett’s esophagus. J Gastrointest Cancer. 2014;45(2):137-145.
  7. Eluri S, et al. The presence of genetic mutations at key loci predicts progression to esophageal adenocarcinoma in barrett’s esophagus. Am J Gastroenterol. 2015;110(6):828-834.
  8. Das A, et al. Endoscopic ablation is a cost-effective cancer preventative therapy in patients with Barrett’s esophagus who have elevated genomic instability. Endosc Int Open. 2016;4(5):E549-E559.
Scroll to Top