1[1]Flokman J. Tumor angiogenesis [J]. Cancer Biology, 1997, 10: 181-204.
2[2]Gasparini G. The rational and future potential of angiogenesis inhibitors in neoplasia[J]. Drugs, 1999,58 (1): 17-38.
3[3]Garmendia G, Miranda N, Borrnso S, et al. Regression of infancy hemangiomas with recombinant IFN-alpha-2b [J]. J-Interferen-Cytokine-Res, 2001,21(1):31-38.
4[4]Faderl S, Kantarjian HM, Talpaz M. Chronic myelagenons leukemia: update on biology and treatment [J]. Oncolngy-(Huntingt), 1999, 13(2): 169-180.
6[6]Steward WP, Thomas A. Murimastat:The clinical develpment of a matrix metalloproteinase inhibitor[J]. Expert Opin Investig Drugs, 2000,9 (12) :2913-2922.
7[7]Bramhall SR,Rosemurpy A,Brown PD,Marimastat as first-line therapy for patients with unresectable pancreatic cancor: a randomized trial[J]. J Clin Oncol,2001,19(15):3447-3455.
8[8]Zucker S, Cao J, Chan WT. Critical appraisal of the use of matrix metalloproteinase inhibitors in cancer teatment[J].Oncogene, 2000, 27:17(56):6642-6650.
9[9]Singhals,Mehta J.Thalidomide in cancer potential uses and limitations [J]. Bio Drugs,2001,15(3): 163-172.
10[10]Barlogie B, Desikan R, Eddlemon P, et al. Extended survival in advanced and refractory mutiple myeloma after single-agent thalidomide: identification of prognostic factors in a phase Ⅱ study of 169 patients [J]. Blood,2001,15;98(2):492-494.