In the treatment of tumor patients introduction of multidrug resistance genes into hematopoietic cells has been reported as an approach for reducing myelotoxicity created by antitumor drugs. However, the nonspecific expression of the genes can also increase the chemoresistance of the tumor cells invaded into bone marrow, which influences seriously the effectiveness of chemotherapy. In this study, a new strategy is described for specific myeloprotection. The recombinant retroviral vector containing multidrug resistance 1 (MDR1) gene regulated by aminopeptidase N (APN) myeloid promoter was constructed and then introduced into myeloblastic cells KGla and tumor cell line BEL7402. The specific transcript of MDR1 was detected in KGla cells transduced with MDR1 gene and rhodamine 123 was effectively extruded by Pgp, the protein of MDR1 gene. The resistance elevated markedly by 10.6, 10.4, 11.2, 4.2 and 14.2 folds in MDR1 gene-transduced KGla cells to chemothera-peutic drugs such as cochicine, VP-16, vincristine In the treatment of tumor patients introduction of multidrug resistance genes into hematopoietic cells has been reported as an approach for reducing myelotoxicity created by antitumor drugs. However, the nonspecific expression of the genes can also increase the chemoresistance of the tumor cells invaded into bone marrow, which leads seriously the effectiveness of chemotherapy. In this study, a new strategy is described for specific myeloprotection. The recombinant retroviral vector containing multidrug resistance 1 (MDR1) gene regulated by aminopeptidase N (APN) myeloid promoter was constructed and then introduced into myeloblastic cells The specific transcript of MDR1 was detected in KGla cells transduced with MDR1 gene and rhodamine 123 was effectively extruded by Pgp, the protein of MDR1 gene. The resistance elevated markedly by 10.6, 10.4, 11.2, 4.2 and 14.2 folds in MDR1 gene-transduced KGla cells to chemothera-peutic drugs such as cochicine, VP-16, vincristine