title: Post-induction residual disease in translocation t(12;21)-positive childhood ALL.
abstract: BACKGROUND
  t(12;21)(p1 3;q22), the most frequent chromosomal translocation found in childhood acute lymphoblastic leukemia (ALL), occurs in approximately 25% of B-lineage ALL cases and has been claimed to carry a good prognosis.
  
  
  METHODS
  As part of the Nordic Society of Pediatric Hematology and Oncology (NOPHO) ALL-MRD 95 study, which includes children from Iceland, Norway, and Denmark diagnose d with ALL, patients were screened for the presence of t(12; 21) by reverse transcriptase-polymerase chain reaction (RT-PCR) at diagnosis, and their residual disease was quantified after 4 weeks of induction therapy (prednisolone, vincristine, doxorubicin, i.t. methotrexate) by a competitive, clone-specific, semi-nested PCR analysis.
  
  
  RESULTS
  Among 96 children diagnosed with ALL, and quantified for post induction residual disease, 32 were t(12;21)-positive. The median residual disease was similar for B-precursor ALL patients with and without t(12;21) (0.009 vs. 0.03%, P = 0.12).
  
  
  CONCLUSIONS
  Al though patients with t(12;21)-positive ALL have been claimed to have a good outcome, these data indicate that this does not reflect a high sensitivity to prednisolone, vincristine, and doxorubicin given during induction therapy.
authors.affiliation: Department of Clinical Immunology, The National University Hospital, Rigshospitalet, Copenhagen, Denmark.
authors.forename: Jeanette
authors.initials: J
authors.lastname: Seyfarth
authors.forename: Hans O
authors.initials: HO
authors.lastname: Madsen
authors.forename: Charlotte
authors.initials: C
authors.lastname: Nyvold
authors.forename: Lars P
authors.initials: LP
authors.lastname: Ryder
authors.forename: Niels
authors.initials: N
authors.lastname: Clausen
authors.forename: Gudmundur K
authors.initials: GK
authors.lastname: Jonmundsson
authors.forename: Finn
authors.initials: F
authors.lastname: Wesenberg
authors.forename: Kjeld
authors.initials: K
authors.lastname: Schmiegelow
mesh_terms: D000293:Adolescent; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use*; D002648:Child; D002675:Child, Preschool; D002881:Chromosomes, Human, Pair 12 / Q000235:genetics*; D002891:Chromosomes, Human, Pair 21 / Q000235:genetics*; D050676:Core Binding Factor Alpha 2 Subunit; D017931:DNA Primers / Q000737:chemistry; D004317:Doxorubicin / Q000008:administration & dosage; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D007223:Infant; D008297:Male; D008727:Methotrexate / Q000008:administration & dosage; D018365:Neoplasm, Residual / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D015514:Oncogene Proteins, Fusion / Q000235:genetics / Q000378:metabolism; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology; D011239:Prednisolone / Q000008:administration & dosage; D012333:RNA, Messenger / Q000378:metabolism; D012334:RNA, Neoplasm / Q000378:metabolism; D012074:Remission Induction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014178:Translocation, Genetic; D014750:Vincristine / Q000008:administration & dosage; D000097764:ETS Translocation Variant 6 Protein
chemical_list: D050676:Core Binding Factor Alpha 2 Subunit; D017931:DNA Primers; D004317:Doxorubicin; D008727:Methotrexate; D015514:Oncogene Proteins, Fusion; D011239:Prednisolone; D012333:RNA, Messenger; D012334:RNA, Neoplasm; D014750:Vincristine; C102421:TEL-AML1 fusion protein; D000097764:ETS Translocation Variant 6 Protein