Proliferative Activity in Pulmonary Carcinoids

Overview

Aim.
On the basis of known Ki-67 dependence on tumor malignancy in some lesions, we comparedthis marker expression quantitatively in pulmonary typical and atypical carcinoid tumors andattempted to predict their biological behavior especially in cases associated with tumorous lym-phadenopathy, satellites, and carcinoid tumorlets.Method. Using material from surgically treated patients, we examined 54 cases of pulmonarycarcinoids divided into five groups. 1. Forty-two typical carcinoids (TC), 2. Twelve atypical car-cinoids (AC) diagnosed according to modified Arrigoni’s criteria (Travis et al., 1998), 3. Thirty-two TC without metastases, satellites, and tumorlets (M, S, T), 4. Eight AC without M, S, T, and 5.Fourteen TC and AC associated with M, S, T. Groups 3, 4, and 5 were formed of cases selectedfrom group 1 and 2.The proliferate activity was evaluated by Ki-67 (MIB-1, Immunotech France, 1:25). Its nuclearlabeling was counted in more than 50 HPF and calculated as a number of positive nuclei in 10HPF. The Fisher exact test was used for statistical analysis.Results. The Ki-67 nuclear expression was found in 19 (45%) out of 42 TC and in 9 (75%) out of 12AC. In the set of TC without metastases (M, S, T), the Ki-67 positive labeling was found in 14 (44%)out of 32 cases (group III) and in six (75%) out of eight AC (group IV). In all TC and AC tumorswith M, S, T (group V), the Ki-67 expression was encountered in 8 (57%) out of 14 cases. The Fisherexact test showed no significant difference between all examined groups.Conclusion. No statistically significant difference was found in Ki-67 expression in pulmonarytypical and atypical carcinoids. It appears to be a factor which can not be used for tumor progno-sis prediction or adjuvant therapy indication in surgically treated patients.

Key words:
carcinoid - atypical carcinoid - tumorlet - lung - Ki-67