PrevenTest > For Providers

Tumor Molecular Testing > For Gastric Esophageal / Gastrointestinal Cancer

 

The Time Is Now

Personalized Treatment Designed For Cancer Patients

Gastric Esophageal Cancer

There are two main sites of gastric cancer: cardia (proximal, gastroesophageal junction) and noncardia (fundus, body, distal, and lesser or greater curvature). The incidence of noncardia tumors is decreasing, possibly due to lower incidence of H. Pylori infection caused by improved diet, food storage, and overall sanitation (Parsonnet et al. 1991). H. Pylori infection is a major etiologic factor in the development of intestinal type gastric cancer (Parsonnet et al. 1991). Nonetheless, the incidence of proximal tumors has been increasing since the 1970s, suggesting etiologic heterogeneity among gastric malignancies (Wu et al. 2009). Most patients with this tumor present with inoperable, locally advanced, or metastatic disease (SEER Stat Fact Sheet: Stomach, accessed 2012). Diagnosis is often delayed because many patients with early stage disease present with vague, non-specific symptoms or no symptoms at all. Late-stage disease at presentation, relative chemoresistance, and frequent co-morbidities causing poor functional status have contributed to poor overall survival (Okines and Cunningham 2010; Kim et al. 2012; Bang et al. 2010). Even patients with operable disease will only have about a one in three chance of surviving 5 years (McDonald et al. 2001; Cunningham et al. 2006). Metastatic disease is treated with systemic chemotherapy and supportive measures. 

HER2
ERCC1
TOPO1
TOP2A
TLE3
TUBB3
TS

Genes and Their Locations

Gastrointestinal Stromal Tumor (GIST)

Gastrointestinal stromal tumor (GIST) is the most common mesenchymal neoplasm of the gastrointestinal tract, if not the most common sarcoma overall (Reichardt et al. 2009). GIST is believed to arise from the interstitial cells of Cajal or their precursors. These pacemaker cells of the bowel have features of smooth muscle cells, fibroblasts, and neurons to various degrees (Huizinga et al. 1995).

GIST characteristically stains positive for the KIT receptor tyrosine kinase by immunohistochemistry. At the genomic level, mutations in KIT or the receptor tyrosine kinase PDGFRA are the hallmark of this diagnosis (Hirota et al. 1998). KIT and PDGFRA are mutated in ~85% and ~5%, respectively, of GIST. Mutations are also rarely found in the serine-threonine kinase, BRAF (<1%)

The incidence of GIST is on the order of 10–15/million (3000–4500 cases/year in the US) (Nilsson et al. 2005), although autopsy series may identify as many as 10% of people examined with microscopic GIST.

Genes and Their Locations

HER2
ERCC1
TOPO1

Why GeneID Molecular Tumor Testing?