APOPTOSIS IN CANCER-THERAPY - CROSSING THE THRESHOLD

[1] ASKEW DS, 1991, ONCOGENE, V6, P1915

[2] ANAPLASTIC WILMS-TUMOR, A SUBTYPE DISPLAYING POOR-PROGNOSIS, HARBORS P53 GENE-MUTATIONS [J]. NATURE GENETICS, 1994, 7 (01) : 91 - 97

[3] P53-DEPENDENT APOPTOSIS IN THE ABSENCE OF TRANSCRIPTIONAL ACTIVATION OF P53-TARGET GENES [J]. NATURE, 1994, 370 (6486) : 220 - 223

[4] THYMOCYTE APOPTOSIS INDUCED BY P53-DEPENDENT AND INDEPENDENT PATHWAYS [J]. NATURE, 1993, 362 (6423) : 849 - 852

[5] DRUG-TARGET INTERACTIONS - ONLY THE 1ST STEP IN THE COMMITMENT TO A PROGRAMMED CELL-DEATH [J]. BRITISH JOURNAL OF CANCER, 1991, 64 (01) : 192 - 196

[6] EASTMAN A, 1990, CANCER CELL-MON REV, V2, P275

[7] INDUCTION OF APOPTOSIS IN FIBROBLASTS BY C-MYC PROTEIN [J]. CELL, 1992, 69 (01) : 119 - 128

[8] HALL EJ, 1994, RADIOBIOLOGY RADIOLO, P245

[9] CLINICAL IMPLICATIONS OF THE P53 TUMOR-SUPPRESSOR GENE [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1993, 329 (18) : 1318 - 1327

[10] DEFECTS IN A CELL-CYCLE CHECKPOINT MAY BE RESPONSIBLE FOR THE GENOMIC INSTABILITY OF CANCER-CELLS [J]. CELL, 1992, 71 (04) : 543 - 546

[1] ASKEW DS, 1991, ONCOGENE, V6, P1915

[2] ANAPLASTIC WILMS-TUMOR, A SUBTYPE DISPLAYING POOR-PROGNOSIS, HARBORS P53 GENE-MUTATIONS [J]. NATURE GENETICS, 1994, 7 (01) : 91 - 97

[3] P53-DEPENDENT APOPTOSIS IN THE ABSENCE OF TRANSCRIPTIONAL ACTIVATION OF P53-TARGET GENES [J]. NATURE, 1994, 370 (6486) : 220 - 223

[4] THYMOCYTE APOPTOSIS INDUCED BY P53-DEPENDENT AND INDEPENDENT PATHWAYS [J]. NATURE, 1993, 362 (6423) : 849 - 852

[5] DRUG-TARGET INTERACTIONS - ONLY THE 1ST STEP IN THE COMMITMENT TO A PROGRAMMED CELL-DEATH [J]. BRITISH JOURNAL OF CANCER, 1991, 64 (01) : 192 - 196

[6] EASTMAN A, 1990, CANCER CELL-MON REV, V2, P275

[7] INDUCTION OF APOPTOSIS IN FIBROBLASTS BY C-MYC PROTEIN [J]. CELL, 1992, 69 (01) : 119 - 128

[8] HALL EJ, 1994, RADIOBIOLOGY RADIOLO, P245

[9] CLINICAL IMPLICATIONS OF THE P53 TUMOR-SUPPRESSOR GENE [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1993, 329 (18) : 1318 - 1327

[10] DEFECTS IN A CELL-CYCLE CHECKPOINT MAY BE RESPONSIBLE FOR THE GENOMIC INSTABILITY OF CANCER-CELLS [J]. CELL, 1992, 71 (04) : 543 - 546