[Histogenesis of lung adenocarcinoma induced by oral adminstration of mycotoxins in mice].
OBJECTIVE
To study the histogenesis and the putative mechanisms of adenocarcinoma induced by AFG1 and ST in NIH mice.


METHODS
Thirty-four cases of lung adenocarcinomas induced by AFG1 and ST in NIH mice were included in this study and 12 cases of normal lung tissues were used as control. The phenotype of the lung adenocarcinomas was determined by immunohistochemical expression of SP-C and CC-10 at protein level. The expression of P53, Ras P21 and PCNA was studied with immunohistochemical staining.


RESULTS
The positive expression of SP-C was found in all the lung adenocarcinomas, while no expression of CC-10 could be seen. The labelling index of PCNA in the adenocarcinomas were significantly higher than that of control (P < 0.01). No positive expression of mutant P53 and Ras at protein level could be found.


CONCLUSIONS
The lung adenocarcinomas induced by the two mycotoxins in NIH mice arise from alveolar type II cells and no expression of mutant P53 and Ras at protein level was found in the lung adenocarcinomas.
Shen
Hai-Tao
HT
Laboratory of Experimental Pathology, Hebei Medical University, Shijiazhuang 050017, China.
Zhang
Xiang-Hong
XH
Huang
Xiang-Hua
XH
Li
Yue-Hong
YH
Wang
Junling
J
Yan
Xia
X
Wang
Fengrong
F
D000230:Adenocarcinoma / Q000209:etiology* / Q000378:metabolism; D016604:Aflatoxin B1 / Q000633:toxicity*; D000818:Animals; D008175:Lung Neoplasms / Q000209:etiology* / Q000378:metabolism; D051379:Mice; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D013241:Sterigmatocystin / Q000633:toxicity*
D018809:Proliferating Cell Nuclear Antigen; D013241:Sterigmatocystin; D016604:Aflatoxin B1