PURPOSE: DCAMLK-1, a marker of colonic crypt stem cells, is a Ca++-calmodulin dependent protein kinase that is highly expressed in most colorectal carcinomas. Even though, the lung develops from the embryological foregut, DCAMLK-1 is not expressed in normal respiratory epithelium. We hypothesized that DCAMLK-1 would also be upregulated in lung cancers.
METHODS: After IRB approval, informed consent was obtained from prospectively identified patients undergoing diagnostic bronchoscopy for suspected lung cancer at the Oklahoma City VA Medical Center. DCAMLK-1 message expression was determined in cells obtained by BAL while protein levels were determined by the immunoreactivity of biopsy specimens.
RESULTS: Six males (age 57-80 years, all smokers, FEV1/FVC ratio 55-61%) were ultimately diagnosed with non-small cell carcinoma (n=3) or benign disease (n=3). DCAMLK-1 message expression was detected in BAL from all subjects. Weak (1+) DCAMLK-1 protein expression was observed in those without cancer, whereas markedly increased (4+) DCAMLK-1 protein expression was noted in the biopsies from the patients with endobronchial malignancy.
CONCLUSION: DCAMLK-1 message is upregulated in the lungs of smokers with COPD, and DCAMLK-1 is highly expressed in the cancers of patients with non-small cell lung carcinoma.
CLINICAL IMPLICATIONS: Upregulation of DCAMLK-1 in the lungs of smokers may contribute to the subsequent development of lung cancer.
DISCLOSURE: Mazen Zouwayhed, No Financial Disclosure Information; No Product/Research Disclosure Information