Background In Barrett’s esophagus (BE), the normal esophageal squamous epithelium is replaced by specialized metaplastic columnar epithelium. BE is a premalignant lesion which can progress to esophageal adenocarcinoma (EAC). Currently there are no early molecular indicators that would predict progression from BE to EAC. As the only permanent residents of the epithelium, stem cells have been implicated in this metaplastic progression. Aim To determine the expression of DCAMKL-1 and other putative gastrointestinal stem cell markers in normal esophageal mucosa (NEM), BE and EAC. Methods Human NEM, BE, EAC and multi-tissue microarrays were analyzed for DCAMKL-1 and immunohistochemically scored based on staining intensity and tissue involvement, with epithelia and stroma scored separately. Total RNA isolated from BE and paired NEM was subjected to real-time RT-PCR analysis for DCAMKL-1, LGR5 and Musashi-1 mRNA expression. Results DCAMKL-1 is minimally expressed in squamous NEM, but increased in BE (with and without dysplasia) and EAC tissues. In EAC, we found increased stromal DCAMKL-1 staining compared to adjacent epithelia. Within the sub-mucosa of dysplastic BE tissues, an increase in endothelial cell expression of DCAMKL-1 was observed. Finally, an upregulation of DCAMKL-1, LGR5 and Musashi-1 mRNA was seen in BE compared to squamous NEM. Conclusions Here we report progressive increase of DCAMKL-1 expression in BE from dysplasia to EAC. Furthermore, there was an increase in putative stem cell markers DCAMKL-1, LGR5 and Msi-1 mRNA. These data taken together suggest that regulation of resident stem cells may play an important role in progression of BE to EAC.

Increased expression of DCLK1 was observed in the epithelium, stroma and plasma of patients with BE/EAC. Furthermore, the presence of detectable DCLK1 in plasma of BE/EAC patients may provide a less invasive, detection tool in those patients as well as represent a novel molecular marker distinguishing between normal esophageal mucosa and BE or EAC.

A 68-year-old male presented with progressive abdominal pain, dyspnea, weight loss, and dysuria. Lab work revealed elevated creatine phosphokinase levels, prostate-specific antigen level (approximately 60 ng/mL), and elevated liver enzymes. He was admitted to the intensive care unit for worsening respiratory distress and confusion. He continued to deteriorate, and his bilirubin peaked at 8.5 mg/dL. The patient subsequently died, and an autopsy revealed extensive hepatic necrosis with diffuse intravascular and intraparenchymal permeation of metastatic prostatic carcinoma. Fulminant hepatic failure remains a rare presentation of metastatic prostatic carcinoma, with a rapidly progressive course toward hepatic coma and death. A high index of suspicion is needed to investigate the possibility of palliative chemotherapy.