Treatment of Childhood Acute Lymphoblastic Leukemia: the Results of the Tokyo Children’s Cancer Study Group L84-11 Treatment Protocol Study

Nakazawa, Shinpei; Kinoshita, Akitoshi; Tsuchida, Masahiro; Hosoya, Ryota; Nishmura, Kozo; Yamamoto, Masao; Ueda, Yutaka; Hoshi, Nobutaka; Akatsuka, J; Bessho, Fumio; Tsunematus, Yukiko; Koide, R; Taguchi, Nobuyuki; Yamamoto, Keiko; Nishihira, Koichi; Nagao, Toshiyasu; Ikuta, Koichiro; Matsuyama, Sho; Okimoto, Yuri; Sato, Takahiro; Yamada, Kazuo; Ishikawa, Akira; Tukada, Masashige; Akabane, T; Ohira, Masaichi; Chihara, Hiroshi; Yamada, Katsushi; Sugita, Kenichi; Furukawa, Toshiharu; Okawa, Yoji; Yata, J; Shibuya, Atushi; Kaneko, Takashi; Otsuki, Hitoshi; Inana, Ichiro; Wada, Mayuko; Ishimoto, Koichi; Kaneko, Masakatsu; Ito, Koreatsu; Gunji, Yuji; Kato, Shingo; Saito, Tomohiro

doi:10.1007/978-1-4615-3898-1_17

Cited by 5 publications

(6 citation statements)

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“…13 Recent observations, however, have indicated that the targets of G-CSF may include multipotential hematopoietic progenitors. [14][15][16][17][18][19]21 Acute leukemia with 11q23 translocations is also considered to arise from such a multipotential stem cell, 1,3-11 which might support the result shown in this paper that leukemic cells with 11q23 translocations are responsive to G-CSF. Kita et al 37 showed that mRNA of G-CSFR was expressed in the CD7-positive non-T ALL and some of these leukemic blasts were stimulated by G-CSF in vitro and in vivo.…”

Section: Discussionsupporting

confidence: 61%

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Leukemic cells with 11q23 translocations express granulocyte colony-stimulating factor (G-CSF) receptor and their proliferation is stimulated with G-CSF

et al. 1998

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We report a 20-month-old boy with acute lymphoblastic leukemia with the 11q23 translocation whose blasts markedly increased in peripheral blood after intravenous granulocyte colony-stimulating factor (G-CSF) administration, but disappeared after stopping G-CSF. The in vitro study showed that the leukemic cells separated from this patient expressed G-CSF receptor (G-CSFR) and an addition of G-CSF stimulated their proliferation by 3 H-thymidine incorporation assay (stimulation index, 4.9). To clarify whether or not leukemic cells with 11q23 translocations generally express G-CSFR and show proliferative response to G-CSF, we performed the similar in vitro experiments using eight leukemic cell lines with 11q23 translocations. We found that all cell lines examined expressed G-CSFR (20-98%) and proliferation of seven leukemic cell lines was significantly enhanced in response to G-CSF (stimulation index Ͼ1.5 in five cell lines), suggesting a possible participation of the G-CSF/G-CSFR interaction in the process of growth regulation of leukemic cells with 11q23 translocations.

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Section: Discussionsupporting

confidence: 61%

“…Cytogenetic study was carried out, but failed at this time. The combined chemotherapy for highrisk ALL according to the TCCSG regimen 21 was started, and 1 month later complete remission was achieved. At 4 months from the onset, G-CSF (5 g/kg/day) was administered intravenously for severe neutropenia after consolidation chemotherapy.…”

Section: Case Reportmentioning

confidence: 99%

Leukemic cells with 11q23 translocations express granulocyte colony-stimulating factor (G-CSF) receptor and their proliferation is stimulated with G-CSF

et al. 1998

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“…From 1981 to 1995, 1450 previously untreated children aged 1 to 15 with acute lymphoblastic leukemia (ALL) were entered and 1438 were eligible for the four consecutive studies of Tokyo Children's Cancer Study Group (TCCSG): L81-10 (1981-1984, 189 patients), (Table 1), 9 L84-11 (1984-1989, 484 patients) ( Table 2), [10][11][12] L89-12 (1989-1992, 418 patients) ( Table 3) [13][14][15][16] and L92-13 (1992-1995, 347 patients) EFS, event-free survival; s.e., standard error; CNS, central nervous system; NCI, National Cancer Institute criteria. Infants were treated differently and retrospectively analyzed in Table 5.…”

Section: Methodsmentioning

confidence: 99%

“…The details of the L84-11 protocol were given in earlier publications. [10][11][12] In the L89-12 protocol, [13][14][15][16] which enrolled 418 eligible patients, a main objective was to determine whether or not cranial irradiation was essential for standard risk patients. The SR group was randomized into two arms at CNS directed therapy (Table 6).…”

Section: Treatmentmentioning

confidence: 99%

Long-term follow-up of childhood acute lymphoblastic leukemia in Tokyo Children's Cancer Study Group 1981–1995

et al. 2000

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“…The results reported in western countries and by large group studies have indicated that the incidence of relapse among patients given cranial irradiation has been reduced to 5-10% [ 2 4 ] . The incidence of CNS-L was 3.7% among those receiving the combination of cranial irradiation and high-dose MTX therapy, which is specified by the protocol of the Tokyo Children's Cancer Study Group (L84-I I ) ( Table 3 ) [5].…”

Section: Discussionmentioning

confidence: 99%

Extramedullary Relapse in Childhood Leukemia

Tsukimoto

1991

Pediatrics International

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As long-term survival of children with leukemia is increasing, the prophylaxis of extramedullary leukemia has become a more important part of treatment. We studied the pattern of occurrence of extramedullary leukemia in a retrospective review. This review included a total of 2,317 childhood leukemia patients aged 15 years or less who had been treated at 38 institutes in Japan between 1976 and 1985. Extramedullary leukemia developed in 386 of 1,724 ALL patients (22.4%) and 63 of 544 patients with ANLL (163%). Among the ALL patients, CNS-L was the most common form and was observed in 315 cases (81.6%), followed by testicular leukemia in 89 (23.0%). In the case of ANLL, the most common form of extramedullary leukemia was CNS-L (45 cases, 71.4%), followed by cutaneous leukemia in 10 cases (15.9%). In addition, leukemia of the lymph nodes, ovaries, bones, kidneys and eyes was observed in 7, 5, 5, 4 and 4 cases, respectively. The survival rate of ALL patients with CNS-L was 40.170 for isolated relapse and 2.7% for bone marrow relapse, and no more deaths occurred after 6 years from relapse. The survival rate of patients with testicular leukemia was 40.1% for isolated relapse and 5.9% for complicating bone marrow relapse, and no deaths occurred after 7 years from relapse. Cutaneous leukemia tended to occur late in older children with ALL and early in infants with ANLL, and all these patients died. Infiltration into the kidney was observed in 4 patients, all of whom died. More than 7 3 4 of patients died after isolated relapse of leukemia of the bones, ovaries, lymph nodes and eyes. Prophylactic extramedullary leukemia therapy, of CNS-L in particular, has played an important role in the treatment of childhood leukemia. Careful development of more effective therapy and close observation of late effects are required when monitoring affected children who are still growing.

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Treatment of Childhood Acute Lymphoblastic Leukemia: the Results of the Tokyo Children’s Cancer Study Group L84-11 Treatment Protocol Study

Cited by 5 publications

References 1 publication

Leukemic cells with 11q23 translocations express granulocyte colony-stimulating factor (G-CSF) receptor and their proliferation is stimulated with G-CSF

Leukemic cells with 11q23 translocations express granulocyte colony-stimulating factor (G-CSF) receptor and their proliferation is stimulated with G-CSF

Long-term follow-up of childhood acute lymphoblastic leukemia in Tokyo Children's Cancer Study Group 1981–1995

Extramedullary Relapse in Childhood Leukemia

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