Journal of Clinical Oncology · 2002 · 167 citations · 28 references
MedicineOncologySurgeryChemotherapyMolecular OncologyNeoplasiaCancer CytogeneticsCancer ProgressionGerm Cell TumorsMalignant NeoplasmsRelapsed DiseaseApurinic EndonucleasesApyrimidinic EndonucleasesCytogenetic AberrationsCytogenetic AbnormalitiesGerm Cell Tumor ChemotherapyGerm Cell Tumor GeneticsLate RelapseRelapsed Germ Cell Tumors
PURPOSE: Analysis of patients with late relapse (LR) of germ cell tumor (GCT) with reports on clinical characteristics, outcomes, and molecular and cytogenetic features. PATIENTS AND METHODS: Eighty-three patients evaluated at Indiana University from 1993 through 2000 for relapse of GCT more than 2 years from initial therapy were reviewed. Available specimens were investigated for expression of the transcription regulator FoxD3 and apurinic/apyrimidinic endonuclease and the presence of chromosome 12 abnormalities. RESULTS: Median interval from initial presentation to LR was 85 months. Forty-three of 49 LR patients who underwent surgery were rendered disease free (NED), and 20 (46.5%) remain continuously NED. Thirty-two patients received chemotherapy, but only six (18.8%) obtained a complete remission. Five of these patients remain continuously NED after chemotherapy alone, including three who were chemotherapy naïve. Eighteen of these 32 patients were successfully rendered NED by postchemotherapy surgery, and 12 remain continuously NED. Two patients continue on observation with no treatment for their LR. Overall, 69 of the 81 treated patients (85.2%) ultimately achieved an NED state, and 38 (46.9%) remain continuously NED with median follow-up from LR therapy of 24.5 months (range, 1 to 83 months), whereas nine other patients are currently NED after therapy for subsequent relapses. Because of the small numbers of specimens tested, we were unable to draw any definitive conclusions from the molecular and cytogenetic analyses. CONCLUSION: GCT patients require lifetime follow-up. At the time of LR, surgical resection alone remains our preferred therapy.
28
Redox activation of Fos‐Jun DNA binding activity is mediated by a DNA repair enzyme.
Steven Xanthoudakis, Graham G. Miao, F. Wang et al. · The EMBO Journal · 1992 · 927 citations · Full text
Requirement of mammalian DNA polymerase-β in base-excision repair
Robert W. Sobol, Julie K. Horton, Ralf Kühn et al. · Nature · 1996 · 832 citations