A novel ALL-L3 cell line, BALM-16, lacking expression of immunoglobulin chains derived from a patient with hypercalcemia

Matsuo, Yoshinobu; MacLeod, Roderick A.F.; Kojima, Kensuke; Kuwahara, K.; Sakata, Atsuko; Drexler, Hans; Nishizaki, C; Fukuda, Shoichiro; Inoue, Yuko; Sezaki, T; Sakaguchi, Nobuki; Orita, Kunzo

doi:10.1038/sj.leu.2400867

Cited by 17 publications

(7 citation statements)

References 26 publications

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“…MOLM14 cells were generously provided by Dr. Yoshinobu Matsuo (Fujisaki Cell Center, Hayashibara Biochemical Labs, Okayama, Japan) (19). BAF3 cells with retrovirally introduced FLT3-ITD were created as previously described (20), and then retrovirally transfected with empty pMX vector or human FGFR1 in pMX.…”

Section: Methodsmentioning

confidence: 99%

FGF2 from Marrow Microenvironment Promotes Resistance to FLT3 Inhibitors in Acute Myeloid Leukemia

et al. 2016

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Potent FLT3 inhibitors such as quizartinib (AC220) have shown promise in treating acute myeloid leukemia (AML) containing FLT3 internal tandem duplication (ITD) mutations. However, responses are not durable and resistance develops within months. In this study, we outline a two-step model of resistance whereby extrinsic microenvironmental proteins FLT3 ligand (FL) and fibroblast growth factor 2 (FGF2) protect FLT3-ITD+ MOLM14 cells from AC220, providing time for subsequent accumulation of ligand-independent resistance mechanisms. FL directly attenuated AC220 inhibition of FLT3, consistent with previous reports. Conversely, FGF2 promoted resistance through activation of FGFR1 and downstream MAPK effectors; these resistant cells responded synergistically to combinatorial inhibition of FGFR1 and FLT3. Removing FL or FGF2 from ligand-dependent resistant cultures transiently restored sensitivity to AC220, but accelerated acquisition of secondary resistance via reactivation of FLT3 and RAS/MAPK signaling. FLT3-ITD AML patients treated with AC220 developed increased FGF2 expression in marrow stromal cells, which peaked prior to overt clinical relapse and detection of resistance mutations. Overall, these results support a strategy of early combination therapy to target early survival signals from the bone marrow microenvironment, in particular FGF2, to improve the depth of response in FLT3-ITD AML.

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Section: Methodsmentioning

confidence: 99%

FGF2 from Marrow Microenvironment Promotes Resistance to FLT3 Inhibitors in Acute Myeloid Leukemia

et al. 2016

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“…The smears were observed by three hematologists (Drs Kaneda, Kojima, and Tekeuchi). Immunophenotyping of fresh leukemia cells was performed by flow cytometry using a panel of monoclonal antibodies, and was confirmed by fluorescence microscopy in some cases, as described previously (20). The following antibodies were used: CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD13, CD14, CD19, CD20, CD33, CD34, CD56, and HLA‐DR.…”

Section: Cell Morphology and Immunophenotypingmentioning

confidence: 99%

Can t(8;21) oligoblastic leukemia be called a myelodysplastic syndrome?

Kaneda¹,

Kojima²,

Takeuchi³

et al. 2002

European J of Haematology

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The new World Health Organization (WHO) classification of hematologic malignancies has incorporated t(8;21) myelodysplastic syndromes (MDS) according to the French-American-British classification into the category of acute myeloid leukemia (AML) with t(8;21)(q22;q22), while our knowledge about clinicopathological features of t(8;21) oligoblastic leukemia is still limited. We present our experience with 12 patients meeting the FAB diagnostic criteria of MDS and having t(8;21), who were compared to 43 t(8;21) AML patients. The MDS and AML patients shared most hematomorphologic, immunophenotypic, and clinical features, whereas the differences lay along myeloid maturation. The MDS patients had higher percentages of circulating neutrophils and marrow myeloid cells beyond promyelocytes than the AML patients. The incidence of Auer rods in mature neutrophils in MDS was significantly higher than that in AML, and furthermore, the neutrophils in MDS more commonly contain t(8;21) than in AML. Our findings support the rationale for the WHO classification, and future studies on large patient populations should help clarify whether the spontaneous differentiation potential could be actively associated with a hematological manifestation of t(8;21) leukemias.

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“…Die häufigste Ursache der Hyperkalzämie bei Tumoren ist die HHM (80%). Ihr liegt meist die Produktion von PTH related Peptid (PTHrP) mit vermehrtem Knochenabbau und vermindertem Knochenaufbau zu Grunde (5,6,7,9,10). Sehr selten kommt es zur PTH-oder Vitamin D3-Produktion durch den Tumor selbst (13).…”

Section: Diskussionunclassified

Lebensbedrohliche Hyperkalzämie bei einem jungen Mann mit ALL

Schneider¹,

Seydlitz²,

Zimmermann³

et al. 2001

Dtsch med Wochenschr

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The acute treatment of hypercalcemia is independent of the underlying cause (rehydration with physiologic saline, renal excretion with furosemide, inhibition of osteoclastic activity). The main causes are hyperparathyreoidism or malignancys (90%). We describe TNF-alpha as a possible marker of tumoral load of a common ALL but we are not able to reveal a correlation between TNF-alpha and the calcium level.

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A novel ALL-L3 cell line, BALM-16, lacking expression of immunoglobulin chains derived from a patient with hypercalcemia

Cited by 17 publications

References 26 publications

FGF2 from Marrow Microenvironment Promotes Resistance to FLT3 Inhibitors in Acute Myeloid Leukemia

FGF2 from Marrow Microenvironment Promotes Resistance to FLT3 Inhibitors in Acute Myeloid Leukemia

Can t(8;21) oligoblastic leukemia be called a myelodysplastic syndrome?

Lebensbedrohliche Hyperkalzämie bei einem jungen Mann mit ALL

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