Zhang Li-Hong, Wang Hui-Jun, Zhang Li, Zhou Kang, Yang Dong-Lin, Yan Zhang-Song, Li Hong-Qiang, Liu Qing-Guo, Qi Jun-Yuan, Liu Qiang, Chu Yu-Lin, Zhang Feng-Kui
Institute of Hematology and Blood Diseases Hospital, CAMS & PUMC, Tianjin 300020, China.
Zhonghua Xue Ye Xue Za Zhi. 2010 Apr;31(4):219-22.
To evaluate bone marrow hematopoietic cells genetic instability (BMHCGI) in patients with aplastic anemia (AA) and to explore its influence on immunosupressive therapy for AA and significance on late clonal hematologic disorders.
Genetic instability of bone marrow mononuclear cells (BMMNC) was measured by Comet assay. The relationship between bone marrow failure parameters and genetic instability results was evaluated. The reciprocity of genetic instability and treatment responses to immunosuppressive therapy (IST) was investigated.
Comet assay parameters [tail moment (TM), olive TM (OTM), comet %] of AA patients were significantly higher than that of control group (P < 0.05). There was no statistic correlation of comet parameters of severe AA (SAA) BM hematopoietic cells with age, gender and peripheral blood cell count (P > 0.05). For the treatment response rate at six months after IST there was no statistical difference between comet cells of < 21.64% and of >/= 21.64%, and so did between OTM < 1.58 and >/= 1.58 in SAA patients. IST had no effect on SAA BMHCGI, whereas, the Comet%, TM and OTM in SAA PR patients and Comet% in CR patients were significantly decreased than those before treatment. Comet parameters of two SAA patients were significantly increased before the development of clonal cytogenetic abnormalities.
Increased BMHCGI may be one of the elements in the pathogenetic mechanisms in AA. The genetic instability is irrelevant to the SAA patients overall response rate of IST at six months, but IST can alleviate the genetic instabilities in responded SAA patients.
