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We have carried out SEREX (serological identification of antigens by recombinant cDNA expression cloning), and identified SLC2A1 (solute carrier family 2/facilitated glucose transporter, member 1) as an antigen recognized by serum IgG antibodies in patients with esophageal squamous cell carcinoma (SCC). The levels of serum anti-SLC2A1 antibodies (s-SLC2A1-Abs), examined by enzyme-linked immunosorbent assay using bacterially expressed glutathione-S-transferase-SLC2A1 fusion protein, were significantly higher in patients with esophageal SCC than in healthy donors. When using a cutoff level as the mean + 2x standard deviations of healthy donors, a total of 12 (21%) out of 57 SCC patients were revealed as positive for s-SLC2A1-Abs. The presence of s-SLC2A1-Abs was not associated with either clinicopathological factors or survival. Because s-SLC2A1-Abs were not associated with the positivity of other conventional serum markers, a combination assay of s-SLC2A1-Abs with these conventional serum markers may be useful for the diagnosis and monitoring of esophageal SCC.

To investigate the e ect of p33 ING1 on wild-type p53 gene therapy, T.Tn human esophageal carcinoma cells were stably transfected with p33 ING1 cDNA. Infection with Adp53 (recombinant adenovirus containing wild-type p53) into p33-transfected cells reduced cell viability, while infection with empty vector had little e ect. This reduced viability was shown to be due to apoptotic cell death by the TUNEL (terminal deoxynucleotidyl transferasemediated nick end-labeling) assay. Following infection with Ad-p53, levels of p53 were similar in p33-expressing cells and in the parental line. However, levels of p21 and Mdm2 were elevated in p33-transfected cells. Nonetheless, this enhanced expression of Mdm2 appeared to be ine ective in downregulating p53. Transient transfection with mutant Mdm2 prior to Ad-p53 infection provided a signi®cant protection as compared with cells transfected with wild-type Mdm2. These results imply a synergistic e ect between p33 and p53 in the induction of apoptosis of human esophageal carcinoma cells. A role for Mdm2 in this synergism is suggested.

BACKGROUND Angiogenesis plays a crucial role in tumor growth and metastasis. Recently, some studies have focused on the angiogenesis inhibitor endostatin. However, the biologic role of the precursor of endostatin, collagen XVIII, in human malignancy is unknown. The purpose of the current study was to evaluate whether the expression of collagen XVIII has additional prognostic value for survival in patients with nonsmall cell lung carcinoma (NSCLC). METHODS The authors investigated the expression of collagen XVIII in 221 patients using immunohistochemical methods. To confirm the specificity of the collagen XVIII polyclonal antibody used in the current study and to test the expression of collagen XVIII in human lung carcinoma, Western blot analysis was performed on a panel of human lung carcinoma cell lines. RESULTS Collagen XVIII expression was detected in 162 of 221 patients with NSCLC (73%), primarily in the tumor cell cytoplasm. Low collagen XVIII expression levels were found in 75 tumor specimens, while high collagen XVIII expression levels were noted in 87 tumor specimens. The prevalence of positive collagen XVIII expression was greater in T2–4 tumors than in T1 tumors (P = 0.0235). The prognosis for patients with strongly collagen XVIII–positive NSCLC was significantly worse than the prognosis for patients with collagen XVIII–positive or collagen XVIII–negative NSCLC (P = 0.0010). Multivariate analysis indicated that T status, lymph node status, and the overexpression of collagen XVIII were independent prognostic factors. CONCLUSIONS The results of the current study indicated that the overexpression of collagen XVIII was associated with NSCLC progression and poor outcome. Thus, collagen XVIII expression may serve as a useful prognostic marker in patients with NSCLC. Cancer 2004. © 2004 American Cancer Society.

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