Luminal epithelial antigen (LEA.135) expression in adenocarcinoma of the colon.

BACKGROUND: Luminal Epithelial Antigen (LEA.135) is a cell surface glycoprotein, whose expression has been shown to have prognostic significance in breast carcinoma and transitional cell carcinoma of the bladder, but has not been previously evaluated in adenocarcinoma of the colon. PATIENTS AND METHODS: This study examines LEA.135 expression in 134 archival cases of colon adenocarcinoma obtained from Wellington Hospital Pathology Department between 1985 and 1990 inclusive. The findings were compared with tumor grade, stage and survival, to determine whether LEA.135 could serve as a useful indicator of the progression of colonic adenocarcinoma. RESULTS: Analysis of results showed that LEA.135 expression was not related to depth of invasion (p = 0.097), grade (p = 0.14) or clinical outcome (p = 0.27). Both luminal and cytoplasmic labelling of LEA.135 was seen in tumor cells however there was no association between LEA.135 distribution and either tumor grade or patient survival. CONCLUSION: The results suggest that the expression of LEA.135 does not provide a useful indication of clinical progression or outcome in patients with colonic adenocarcinoma.

Immunodeficiency due to a unique protracted developmental delay in the B-cell lineage.

A unique immune deficiency in a 24-month-old male characterized by a transient but protracted developmental delay in the B-cell lineage is reported. Significant deficiencies in the number of B cells in the blood, the concentrations of immunoglobulins in the serum, and the titers of antibodies to T-dependent and T-independent antigens resolved spontaneously by the age of 39 months in a sequence that duplicated the normal development of the B-cell lineage: blood B cells followed by immunoglobulin M (IgM), IgG, IgA, and specific IgG antibodies to T-independent antigens (pneumococcal polysaccharides). Because of the sequence of recovery, the disorder could have been confused with other defects in humoral immunity, depending on when in the course of disease immunologic studies were conducted. Investigations of X-chromosome polymorphisms suggested that the disorder was not X linked in that the mother appeared to have identical X chromosomes. An autosomal recessive disorder involving a gene that controls B-cell development and maturation seems more likely. In summary, this case appears to be a novel protracted delay in the development of the B-cell lineage, possibly due to an autosomal recessive genetic defect.