F. Grunert et al., CD66B, CD66C AND CARCINOEMBRYONIC ANTIGEN (CEA) ARE INDEPENDENTLY REGULATED MARKERS IN SERA OF TUMOR PATIENTS, International journal of cancer, 63(3), 1995, pp. 349-355
Non-specific cross-reacting antigens (NCA-95 = CD66b and NCA-50/90 = C
D66c) are members of the CEA (carcinoembryonic antigen = CD66e) family
. Analysis of mRNA levels of CD66c in colon tumors suggests that this
antigen is strongly up-regulated compared to its normal counterpart an
d could, therefore, be of clinical interest. CD66c is also expressed i
n normal lung and spleen tissues and, above all, on granulocytes. The
appearance of CD66b in serum, the only strictly granulocyte-specific a
ntigen, could point to the involvement of granulocytes in disease. Spe
cific sandwich ELISAs have been established to determine CEA, CD66b an
d CD66c levels in serum. Controls have been carried out by testing ser
a from patients with benign tumors or inflammatory diseases and from h
ealthy individuals. In sera of most patients suffering from solid tumo
rs, sensitivities for CD66c are comparable to or lower than those for
CEA. CD66c showed a much higher sensitivity in early colon tumor stage
s. Sensitivities over 40% have been determined for CD66b in sera of pa
tients with uterine and kidney carcinomas. CML patients revealed sensi
tivities of 84% for CD66c and 47% for CD66b. investigations of sera fr
om patients with inflammatory colon diseases which are negative for CE
A showed high sensitivity for CD66c but not for the granulocyte-specif
ic CD66b. Patients with mastopathy revealed sensitivities of over 40%
for both CD66c and CD66b. CD66b, CD66c and CEA are independently regul
ated proteins in a high percentage of patients. The simultaneous deter
mination of CEA and CD66b/c can increase the sensitivities for maligna
nt tumors but high sensitivities of CD66b/c for benign diseases limit
their usefulness as tumor markers. CD66b may be interesting as a marke
r for kidney and corpus carcinomas, for which good markers are not yet
available. (C) 1995 Wiley-Liss, Inc.