Human urinary macrophage colony-stimulating factor reduces the incidence and duration of febrile neutropenia and shortens the period required to finish three courses of intensive consolidation therapy in acute myeloid leukemia: a double-blind controlled study.

Ohno, Ryuzo; Miyawaki, Shuichi; Hatake, Kiyohiko; Kuriyama, Kazutaka; Saito, Kenji; Kanamaru, Akihisa; Kobayashi, Toshimitsu; Kodera, Yoshihisa; Nishikawa, Kiyoshi; Matsuda, Shin; Yamada, Osamu; Omoto, Eijiro; Takeyama, Hideo; Tsukuda, Koji; Asou, Norio; Tanimoto, Mitsune; Shiozaki, Hiroko; Tomonaga, Masao; Masaoka, T; Miura, Yasusada; Takaku, Fumimaro; Ohashi, Yasuo; Motoyoshi, Kazuo

doi:10.1200/jco.1997.15.8.2954

Cited by 56 publications

(39 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There were four protocols (AML87, AML89, AML92 and AML95) and 19, 28, 44 and 27 patients were treated with each, respectively. The first three protocols, which have been described in detail before, [7][8][9] had similar therapeutic regimens. The remission induction regimen consisted of daunorubicin (DNR; 40-50 mg/m 2 for 3 days) and cytosine arabinoside (Ara-C; 100 mg/m 2 for 7-10 days) or behenoyl cytarabine (BHAC; 200 mg/m 2 for 7-10 days) mainly.…”

Section: Chemotherapymentioning

confidence: 99%

Allogeneic bone marrow transplantation improves the outcome of de novo AML with trilineage dysplasia (AML-TLD)

et al. 2000

Self Cite

View full text Add to dashboard Cite

De novo acute myeloid leukemia (AML) with dysplastic features in erythroblasts, granulocytes and megakaryocytes, similar to those in myelodysplastic syndrome (MDS) has been described as AML with trilineage dysplasia (AML-TLD) since 1987. Several reports have suggested that AML-TLD is a subtype of de novo AML in adults and has a poor clinical outcome when treated by conventional chemotherapy. It is not certain whether allogeneic bone marrow transplantation (BMT) brings a favorable outcome for AML-TLD. To evaluate the therapeutic efficacy of allogeneic BMT for AML-TLD, we investigated the clinical data and outcomes of conventional chemotherapy and allogeneic BMT for 118 patients with de novo AML. These patients were registered consecutively for the Japan Adult Leukemia Study Group (JALSG) protocols at our institutes. We treated 28 AML-TLD patients and 90 AML-nonTLD patients with conventional chemotherapeutic protocols. AML-TLD patients did not have a significantly different complete remission (CR) rate (75.0% and 88.4% P = 0.1234), but had a significantly higher relapse rate than AML-nonTLD patients (94.1% and 49.3%, P = 0.0007). The outcome of chemotherapy for AML-TLD was significantly worse than that for AML-nonTLD. The overall survival (OS) and leukemia-free survival (LFS) at 6 years were 9.4% and 0% in AML-TLD group, and 51.9% (P = 0.0017) and 46.3% (P Ͻ 0.0001) in AML-nonTLD group, respectively. Meanwhile, among the patients who underwent allogeneic BMT, five of eight AML-TLD patients and eight of 14 AML-nonTLD patients were alive, and three and five patients survived more than 3 years, respectively. These results suggest that allogeneic BMT can improve the outcome for AML-TLD, which is poor when conventional chemotherapy is given alone. Allogeneic BMT before relapse may be the best therapeutic strategy for AML-TLD patients under 50 years of age if a donor is available.

show abstract

Section: Chemotherapymentioning

confidence: 99%

Allogeneic bone marrow transplantation improves the outcome of de novo AML with trilineage dysplasia (AML-TLD)

et al. 2000

Self Cite

View full text Add to dashboard Cite

show abstract

“…M-CSF stimulates the survival, proliferation, and differentiation of cells of the mononuclear phagocyte lineage (3). M-CSF reduced the incidence and duration of febrile neutropenia in acute myeloid leukemia patients and ovarian cancer patients during chemotherapy (1,4) and improved the long term prognosis of ovarian cancer patients with no residual tumors (5). Furthermore, M-CSF was reported to have an antitumor effect (2,6,7).…”

mentioning

confidence: 99%

“…The use of dose-intensive chemotherapeutic regimens and the expanding application of chemotherapy to older patients have made the management of myelosuppression increasingly important. M-CSF, which was the initially characterized hemopoietic growth factor, is used to treat these patients to ameliorate myelosuppression and prevent severe infections (1,2). M-CSF stimulates the survival, proliferation, and differentiation of cells of the mononuclear phagocyte lineage (3).…”

mentioning

confidence: 99%

Macrophage Colony-Stimulating Factor Induces Vascular Endothelial Growth Factor Production in Skeletal Muscle and Promotes Tumor Angiogenesis

Okazaki

Ebihara

Takahashi

et al. 2005

The Journal of Immunology

View full text Add to dashboard Cite

Although M-CSF has been used for myelosuppression due to chemotherapy in patients with solid tumors, the effect of exogenous M-CSF on tumor angiogenesis has not been studied. In this study we showed that M-CSF has the ability to accelerate solid tumor growth by enhancing angiogenesis with a novel mechanism. M-CSF accelerated intratumoral vessel density in tumors inoculated into mice, although it did not accelerate the proliferation of malignant cells and cultured endothelial cells in vitro. In both the absence and the presence of tumors, M-CSF significantly increased the circulating cells that displayed phenotypic characteristics of endothelial progenitor cells in mice. Moreover, M-CSF treatment induced the systemic elevation of vascular endothelial growth factor (VEGF). VEGFR-2 kinase inhibitor significantly impaired the effect of M-CSF on tumor growth. In vivo, M-CSF increased VEGF mRNA expression in skeletal muscles. Even after treatment with carageenan and anti-CD11b mAb in mice, M-CSF increased VEGF production in skeletal muscles, suggesting that systemic VEGF elevation was attributed to skeletal muscle VEGF production. In vitro, M-CSF increased VEGF production and activated the Akt signaling pathway in C2C12 myotubes. These results suggest that M-CSF promotes tumor growth by increasing endothelial progenitor cells and activating angiogenesis, and the effects of M-CSF are largely based on the induction of systemic VEGF from skeletal muscles.

show abstract

“…13) The clinical effects of M-CSF, such as reduction of the incidence and duration of febrile neutropenia during intensive consolidation chemotherapy and improvement of the long-term prognosis of ovarian cancer patients, [14][15][16] may be explained by improvement of immunological functions by M-CSF.…”

mentioning

confidence: 99%

Mirimostim (macrophage colony‐stimulating factor; M‐CSF) improves chemotherapy‐induced impaired natural killer cell activity, Th1/Th2 balance, and granulocyte function

Hidaka

Akada²,

Teranishi

et al. 2003

Cancer Science

View full text Add to dashboard Cite

Human urinary macrophage colony-stimulating factor reduces the incidence and duration of febrile neutropenia and shortens the period required to finish three courses of intensive consolidation therapy in acute myeloid leukemia: a double-blind controlled study.

Abstract: M-CSF significantly reduced the incidence and duration of febrile neutropenia during the intensive consolidation therapy, and shortened the time to complete consolidation chemotherapy in AML.

Cited by 56 publications

References 44 publications

Allogeneic bone marrow transplantation improves the outcome of de novo AML with trilineage dysplasia (AML-TLD)

Allogeneic bone marrow transplantation improves the outcome of de novo AML with trilineage dysplasia (AML-TLD)

Macrophage Colony-Stimulating Factor Induces Vascular Endothelial Growth Factor Production in Skeletal Muscle and Promotes Tumor Angiogenesis

Mirimostim (macrophage colony‐stimulating factor; M‐CSF) improves chemotherapy‐induced impaired natural killer cell activity, Th1/Th2 balance, and granulocyte function

Contact Info

Product

Resources

About