Poor treatment outcome of Philadelphia chromosome-positive pediatric acute lymphoblastic leukemia despite intensive chemotherapy.

Children with Philadelphia (Ph) chromosome positive (+) acute lymphoblastic leukemia (ALL) represent a subgroup at very high risk for treatment failure. This study included 1322 children enrolled between 1988 and 1994 on CCG risk-adjusted studies for ALL who had centrally reviewed cytogenetic data. Thirty patients had a t(9;22) and are referred to as Ph+; 1292 were Ph-. 23 of these 30 patients were treated on the CCG-1882 high risk ALL protocol. The event-free survival (EFS) outcome in CCG-1882 was significantly worse for Ph+ compared with Ph- patients, with 4-year estimates of 11.3% (SD = 9.8%) and 73.4% (SD = 2.3%), respectively (p < 0.0001).

[1]  N. Heerema,et al.  Clinical significance of translocation t(1;19) in childhood acute lymphoblastic leukemia in the context of contemporary therapies: a report from the Children's Cancer Group. , 1998, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[2]  H. Sather,et al.  Augmented Berlin-Frankfurt-Munster therapy abrogates the adverse prognostic significance of slow early response to induction chemotherapy for children and adolescents with acute lymphoblastic leukemia and unfavorable presenting features: a report from the Children's Cancer Group. , 1997, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  B. Calabretta,et al.  Treatment of Philadelphia leukemia in severe combined immunodeficient mice by combination of cyclophosphamide and bcr/abl antisense oligodeoxynucleotides. , 1997, Journal of the National Cancer Institute.

[4]  H. Sather,et al.  Improved clinical outcome for children with T-lineage acute lymphoblastic leukemia after contemporary chemotherapy: a Children's Cancer Group Study. , 1996, Leukemia & lymphoma.

[5]  C. Almici,et al.  Selection of myeloid progenitors lacking BCR/ABL mRNA in chronic myelogenous leukemia patients after in vitro treatment with the tyrosine kinase inhibitor genistein. , 1996, Blood.

[6]  Jürg Zimmermann,et al.  Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells , 1996, Nature Medicine.

[7]  S. Ōmura,et al.  Treatment of Philadelphia‐chromosome‐positive human leukemia in scid mouse model with herbimycin A, bcr‐abl tyrosine kinase activity inhibitor , 1995, International journal of cancer.

[8]  A. Burkhardt,et al.  Biotherapy of B-cell precursor leukemia by targeting genistein to CD19-associated tyrosine kinases , 1995, Science.

[9]  Denis R. Miller,et al.  Lymphomatous presentation of childhood acute lymphoblastic leukemia. A subgroup at high risk of early treatment failure , 1991, Cancer.

[10]  J. Fletcher,et al.  Translocation (9;22) is associated with extremely poor prognosis in intensively treated children with acute lymphoblastic leukemia. , 1991, Blood.

[11]  F. Behm,et al.  Philadelphia chromosome positive childhood acute lymphoblastic leukemia: clinical and cytogenetic characteristics and treatment outcome. A Pediatric Oncology Group study , 1990 .

[12]  J. Rowley,et al.  Unexpected heterogeneity of BCR-ABL fusion mRNA detected by polymerase chain reaction in Philadelphia chromosome-positive acute lymphoblastic leukemia. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[13]  S. Raimondi,et al.  Comparative biochemical and cytogenetic studies of childhood acute lymphoblastic leukemia with the Philadelphia chromosome and other 22q 11 variants , 1989 .

[14]  B. Koller,et al.  Biphenotypic leukemic lymphocyte precursors in CD2+CD19+ acute lymphoblastic leukemia and their putative normal counterparts in human fetal hematopoietic tissues. , 1989, Blood.

[15]  N. Heisterkamp,et al.  Unique fusion of bcr and c-abl genes in Philadelphia chromosome positive acute lymphoblastic leukemia , 1987, Cell.

[16]  F. Behm,et al.  Clinical and biologic hallmarks of the Philadelphia chromosome in childhood acute lymphoblastic leukemia. , 1987, Blood.

[17]  O. Witte,et al.  Unique forms of the abl tyrosine kinase distinguish Ph1-positive CML from Ph1-positive ALL. , 1987, Science.

[18]  N. Heerema,et al.  Karyotypic and clinical findings in a consecutive series of children with acute lymphocytic leukemia. , 1985, Cancer genetics and cytogenetics.

[19]  E. Canaani,et al.  An 8-kilobase abl RNA transcript in chronic myelogenous leukemia. , 1984, Proceedings of the National Academy of Sciences of the United States of America.

[20]  E. Canaani,et al.  ALTERED TRANSCRIPTION OF AN ONCOGENE IN CHRONIC MYELOID LEUKAEMIA , 1984, The Lancet.

[21]  Rowley Jd Ph1-positive leukaemia, including chronic myelogenous leukaemia. , 1980 .

[22]  M. Pike,et al.  Design and analysis of randomized clinical trials requiring prolonged observation of each patient. II. analysis and examples. , 1977, British Journal of Cancer.

[23]  N. Mantel Evaluation of survival data and two new rank order statistics arising in its consideration. , 1966, Cancer chemotherapy reports.

[24]  P. Nowell,et al.  Chromosome studies on normal and leukemic human leukocytes. , 1960, Journal of the National Cancer Institute.

[25]  E. Kaplan,et al.  Nonparametric Estimation from Incomplete Observations , 1958 .

[26]  C. Pui,et al.  Uniform approach to risk classification and treatment assignment for children with acute lymphoblastic leukemia. , 1996, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[27]  Iscn International System for Human Cytogenetic Nomenclature , 1978 .