• Biomedical Science Letters
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• v.17 no.3
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• pp.197-202
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• 2011

Mitosis count is one of the most helpful morphologic features for distinguishing pulmonary typical carcinoid (TC) from atypical carcinoid (AC). However, identifying areas of highest mitotic activity is tedious and time-consuming, and mitosis count may vary substantially among pathologists. Anti-phosphohistone H3 (PHH3) is an antibody that specifically detects histone H3 only when phosphorylated at serine 10 or serine 28, an event that is concurrent with mitotic chromatin condensation and not observed during apoptosis. In this study, immunohistochemical staining for PHH3 was performed to determine whether PHH3 was a reliable and objective mitosis-specific marker for pulmonary carcinoid tumors. Seventeen cases of surgically resected pulmonary carcinoid tumors (12 TCs and 5 ACs) were obtained and classified according to the 2004 World Health Organization classification. Mitotic counts determined by PHH3 correlated to ones determined by hematoxylin and eosin (H&E) staining; however, PHH3 mitotic counts (mean mitotic counts: 1 in TCs and 3.2 in ACs) were slightly higher than H&E mitotic counts (mean mitotic counts: 0.25 in TCs and 1.8 in ACs). The mitotic counts determined by experienced observer were more correlated to those determined by inexperienced observer with the PHH3-based method (R=0.968, P<0.001) rather than H&E staining (R=0.658, P<0.001). These results suggest that the PHH3 mitotic counting method was more sensitive and simple for detecting mitoses compared to traditional H&E staining. Therefore, PHH3 immunohistochemistry may contribute to more accurate and reproducible diagnosis of pulmonary carcinoid tumors and may be a valuable aid for administrating appropriate clinical treatment.

• Radiation Oncology Journal
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• v.19 no.3
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• pp.259-264
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• 2001

Purpose : We investigated the temporal alterations of apoptosis and mitotic death following irradiation in the rat's small intestinal crypts. Materials and methods : Male Sprague-Dawley rats were irradiated 2 Gy by 6 MV linear accelerator and sacrified at 2, 4, 8, 24, 48 hours after irradiation. The mean numbers of the apoptotic cells and mitotic cells per their small intestinal crypts were measured in the unirradiated control and irradiated groups. To compare with H & E staining, ISEL (In Situ End Labelling) were peformed in the group having the highest apoptotic count. Results : The mean number of the apoptosis per crypt in the control group was 0.14 and those at 2, 4, 8, 24, 48 hours after irradiation were 1.43, 3.19, 1.15, 0.26, 0.17, respectively. So the apoptosis development was increased upto 4 hours and then normalized around 24 hours following irradiation. The mean number of the mitotic cells per crypt in the control group was 1.29 and those at 2, 4, 8, 24, 48 hours after irradiation were 0.56, 0.47, 0.23, 0.65, 1.19, respectively. The mitotic cell counts following irradiation was decreased to 8 hours and recovered to the normal level about 48 hours. So the increment of apoptotic cell count was occurred earlier and more remarkable than the decrement of mitotic cell count after irradiation. According to the staining time, false positivity was found in the ISEL staining. Conclusions : The cell death in the small intestinal crypt developed by acute radiation damage was usually decreased to the normal level within $24\~48\;hours$ after irradiation and the apoptosis was thought to be more important process than the mitotic death.