The administration of the nerve growth factor to children with widespread neuroblastoma

Kumar, Shant; Steward, J. K.; Waghe, M.; Pearson, D; Edwards, D. C.; Fenton, E. L.; Griffith, Ashley

doi:10.1016/0022-3468(70)90515-4

Cited by 16 publications

(5 citation statements)

References 10 publications

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“…Relapse after complete remission may reflect the ability of tumor cells to hide in sanctuaries (micrometastases) and elimination of these hidden tumor cells represents a major challenge of tumor therapy. An NGF-based treatment modality has previously been attempted with little success (Kumar et al, 1970); however, our data now demonstrate that a network of trophic signals is needed to achieve NB differentiation. Indeed, preliminary experiments with HTLA230 cells grown in nude mice demonstrated that NB tumors responded to growth factor treatment, since N-MYC expression was substantially decreased after treatment with GDNF, CNTF and NGF (data not shown), although the effect on micrometastases remains to be determined.…”

Section: Discussionmentioning

confidence: 75%

The RET and TRKA pathways collaborate to regulate neuroblastoma differentiation

Peterson

Bogenmann

2004

Oncogene

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Neuroblastoma (NB) is a childhood cancer that arises in the adrenal gland and often shows differentiated neuronal and glial elements. The RET receptor signal pathway is functional in most NB, while loss of nerve growth factor (NGF) receptor (trkA) gene expression correlates with an aggressive phenotype. Thus, we hypothesized that the RET and TRKA signal pathways collaborate to instruct NB differentiation, reminiscent of normal neuronal maturation. Here, we demonstrate that activation of the RET receptor by glial cell line-derived neurotrophic factor (GDNF) increases expression of the RET receptor complex in a panel of malignant human NB cell lines, indicative of a positive feedback mechanism. GDNF also induces growth cessation concomitant with an arrest of cells in the G 0 /G 1 phase of the cell cycle. Furthermore, GDNF synergizes with ciliary neurotrophic factor (CNTF) to enhance TRKA receptor expression, thereby strengthening the NGF-mediated differentiation signal. Differentiated NB cells downregulate expression of the amplified N-myc gene, concurrent with the arrest of cell proliferation, while expressing neuron-specific markers (i.e., SCG10). Interestingly, maintenance of differentiated NB cells in culture is independent of the trophic activity of GDNF, but depends on TRKA signaling, thereby reenacting the differentiation of normal sympathoadrenal (SA) progenitor cells.

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Section: Discussionmentioning

confidence: 75%

The RET and TRKA pathways collaborate to regulate neuroblastoma differentiation

Peterson

Bogenmann

2004

Oncogene

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“…With little experimental data, this rationale prompted an early clinical trial in children with metastatic neuroblastoma where NGF was given to promote tumor cell maturation and retard malignant growth; disappointingly, the clinical course was not affected (98).…”

Section: Other Differentiating Agents Nerve Growth Factormentioning

confidence: 99%

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Abemayor¹,

Sidell²

1989

Environ Health Perspect

143

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Neuroblastoma is a childhood solid tumor composed of primitive cells derived from precursors of the autonomic nervous system. This neoplasm has the highest rate of spontaneous regression of all cancer types and has been noted to undergo spontaneous and chemically induced differentiation into elements resembling mature nervous tissue. As such, neuroblastoma has been a prime model system for the study of neuronal differentiation and the process of cancer cell maturation. In this paper we review those agents that have been described to induce the differentiation of neuroblastoma, with an emphasis on the effects and possible mechanisms of action of a group of related compounds, the retinoids. With this model system and the availability of subclones that are both responsive and resistant to chemically induced differentiation, fundamental questions regarding the mechanisms and processes underlying cell maturation have become more amenable to in vitro study.

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“…Some neuroblastoma cells are known to form processes in response to NGF,3,4 and a therapeutic trial of NGF administration to patients with widespread metastases has been attempted. 17 The trial was unsuccessful, but no prior attempt had been made to determine whether the patients' tumor cells responded to NGF in vitro.…”

Section: Discussionmentioning

confidence: 99%

Nerve growth factor may function as a survival factor for human neuroblastoma cells in culture

Tischler

Slayton

Costopoulos

et al. 1984

Cancer

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Cells from two human neuroblastomas were found to exhibit a marked dependency on nerve growth factor (NGF) for survival in primary cultures. Cells from both tumors also responded to NGF by forming processes, but survival was not necessarily associated with process outgrowth. Lines of replicating cells could not be obtained from either tumor. NGF‐dependent survival has not previously been reported as a characteristic of NGF‐responsive human neuroblastoma cells in primary cultures or in cultures of established cell lines. Our findings suggest that tumors which require NGF for survival might constitute a biologically distinctive subset of neuroblastomas, or that NGF might function as a survival factor for some human neuroblastomas only in suboptimal or deleterious environments.

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The administration of the nerve growth factor to children with widespread neuroblastoma

Cited by 16 publications

References 10 publications

The RET and TRKA pathways collaborate to regulate neuroblastoma differentiation

The RET and TRKA pathways collaborate to regulate neuroblastoma differentiation

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Nerve growth factor may function as a survival factor for human neuroblastoma cells in culture

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