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目的 :证明鸡原始红细胞增多症逆病毒癌基因 V - erb B在人类白血病和骨髓增生异常综合征 (MDS)患者基因组内的存在。方法 :应用 V- erb B PCR,V - erb B寡核苷酸 (Oligo)原位杂交技术和 PCR产物 DNA测序 ,对 84例 MDS、可疑 MDS和 4 9例其他相关血液病进行检测。结果 :2例患者骨髓细胞基因组内均存在 V- erb B亚基因片段 ,同源性占 99.5 % ,它们具有相同的限制性酶切位点 ,因此可以在 Southern印迹杂交条件下发生骨髓细胞 C- erb B重排和重排 /扩增。白前 P1 P2 PCR产物有 4 2 0 bp,P1 P3产物有 6 5 0 bp,而白血病 (AL- M4 ) P1 P2 PCR产物仅 390 bp,P1 P3PCR因 P3无模板序列而无结果。提示从白前发展为白血病 ,可能发生 V- erb B亚基因序列的缺失 ,即缺失突变。结论 :大鼠和人白血病和食管癌等可能均起源于其基因组内存在 V- erb B亚基因及其缺失突变。白血病发病中除了上述病因以外 ,骨髓细胞染色体不稳定性可能起协同作用
PURPOSE: To demonstrate the presence of retroviral oncogene V - erb B in the genome of human leukemia and myelodysplastic syndromes (MDS) in chicken polygophism. Methods: Eighty - four MDS, suspicious MDS and forty - nine other related blood diseases were detected by V - erb B PCR, V - erb B in situ hybridization and DNA sequencing of PCR products. Results: The two V - erb B subunit fragments were found in the genome of bone marrow cells from two patients. Their homology was 99.5%. They shared the same restriction sites and could be used in Southern blot hybridization. erb B rearrangement and rearrangement / amplification. The P1 P2 PCR products were 420 bp in length, 650 bp in P1 P3, and 390 bp in P1-PCR products in leukemia (AL-M4). Prompt development from white to leukemia, the deletion of the V-erb B subunit sequence may occur, ie the deletion mutation. Conclusion: Both rat and human leukemia and esophageal cancer may originate from the presence of V-erb B subunit in their genome and their deletion mutations. Leukemia In addition to the above etiology, chromosomal instability of bone marrow cells may play a synergistic role