scholarly journals Pharmacological properties and clinical efficacy of dasatinib hydrate (Sprycel®), an anticancer drug for chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia

2009 ◽  
Vol 134 (3) ◽  
pp. 159-167 ◽  
Author(s):  
Yutaka Fujii ◽  
Manabu Amano ◽  
Taku Seriu
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Chronic Myelogenous Leukemia ◽  
Anticancer Drug ◽  
Clinical Efficacy ◽  
Lymphoblastic Leukemia ◽  
Philadelphia Chromosome ◽  
Myelogenous Leukemia ◽  
Pharmacological Properties ◽  
Philadelphia Chromosome Positive

Philadelphia chromosome and monosomy 7 in childhood acute lymphoblastic leukemia: a Pediatric Oncology Group study

Blood ◽  
1991 ◽  
Vol 77 (5) ◽  
pp. 1050-1056 ◽  
Author(s):  
C Russo ◽  
A Carroll ◽  
S Kohler ◽  
M Borowitz ◽  
M Amylon ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lymphoblastic Leukemia ◽  
Chronic Myelogenous Leukemia ◽  
Pediatric Oncology ◽  
Lymphoblastic Leukemia ◽  
Philadelphia Chromosome ◽  
Myelogenous Leukemia ◽  
Oncology Group ◽  
Monosomy 7 ◽  
Pediatric Oncology Group

Abstract During an 8-year period, 3,638 children from institutions of the Pediatric Oncology Group (POG) were diagnosed with acute lymphoblastic leukemia (ALL). Fifty-seven patients had Philadelphia chromosome- positive (Ph1) ALL. Blast cells obtained at diagnosis from 13 of these 57 cases (23%) were also found to have partial or complete monosomy 7 (- 7). This subgroup of children with Ph1/-7 ALL was comprised primarily of older males with early B-lineage ALL. Bone marrow specimens from six Ph1/-7 patients were studied further using the polymerase chain reaction and primers that flank the ALL, and chronic myelogenous leukemia breakpoints to determine the molecular characteristic of the 9;22 translocation. Rearrangements were detected in RNA from bone marrow and/or peripheral blood cells of six patients, although four were in hematologic remission at the time of the analysis. Five cases showed the ALL breakpoint, while one child with Ph1/-7 showed the chronic myelogenous leukemia breakpoint. The induction failure rate was much higher in this subgroup (31%) as compared with Ph1-negative cases, and the projected duration of event-free survival reflected the aggressive nature of this subgroup because no children are projected to remain in remission at 2 years. ALL with both the 9;22 translocation and -7 appears to represent a unique and previously undescribed subgroup of childhood ALL associated with a particularly adverse outcome. Leukemic transformation in such patients may involve the interaction of a dominant oncogene (Ph1) and a tumor suppressor gene (- 7).

Philadelphia-Chromosome-Positive T-Lymphoblastic Leukemia: Acute Leukemia or Chronic Myelogenous Leukemia Blastic Crisis

2005 ◽  
Vol 113 (3) ◽  
pp. 181-189 ◽  
Author(s):  
Pia Raanani ◽  
Luba Trakhtenbrot ◽  
Gideon Rechavi ◽  
Esther Rosenthal ◽  
Abraham Avigdor ◽  
...  
Keyword(s):  
Acute Leukemia ◽  
Chronic Myelogenous Leukemia ◽  
Lymphoblastic Leukemia ◽  
Philadelphia Chromosome ◽  
Myelogenous Leukemia ◽  
Blastic Crisis ◽  
Philadelphia Chromosome Positive

scholarly journals Philadelphia chromosome and monosomy 7 in childhood acute lymphoblastic leukemia: a Pediatric Oncology Group study

Blood ◽  
1991 ◽  
Vol 77 (5) ◽  
pp. 1050-1056
Author(s):  
C Russo ◽  
A Carroll ◽  
S Kohler ◽  
M Borowitz ◽  
M Amylon ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lymphoblastic Leukemia ◽  
Chronic Myelogenous Leukemia ◽  
Pediatric Oncology ◽  
Lymphoblastic Leukemia ◽  
Philadelphia Chromosome ◽  
Myelogenous Leukemia ◽  
Oncology Group ◽  
Monosomy 7 ◽  
Pediatric Oncology Group

During an 8-year period, 3,638 children from institutions of the Pediatric Oncology Group (POG) were diagnosed with acute lymphoblastic leukemia (ALL). Fifty-seven patients had Philadelphia chromosome- positive (Ph1) ALL. Blast cells obtained at diagnosis from 13 of these 57 cases (23%) were also found to have partial or complete monosomy 7 (- 7). This subgroup of children with Ph1/-7 ALL was comprised primarily of older males with early B-lineage ALL. Bone marrow specimens from six Ph1/-7 patients were studied further using the polymerase chain reaction and primers that flank the ALL, and chronic myelogenous leukemia breakpoints to determine the molecular characteristic of the 9;22 translocation. Rearrangements were detected in RNA from bone marrow and/or peripheral blood cells of six patients, although four were in hematologic remission at the time of the analysis. Five cases showed the ALL breakpoint, while one child with Ph1/-7 showed the chronic myelogenous leukemia breakpoint. The induction failure rate was much higher in this subgroup (31%) as compared with Ph1-negative cases, and the projected duration of event-free survival reflected the aggressive nature of this subgroup because no children are projected to remain in remission at 2 years. ALL with both the 9;22 translocation and -7 appears to represent a unique and previously undescribed subgroup of childhood ALL associated with a particularly adverse outcome. Leukemic transformation in such patients may involve the interaction of a dominant oncogene (Ph1) and a tumor suppressor gene (- 7).

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