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1.
Pediatr Blood Cancer ; 70(7): e30331, 2023 07.
Artículo en Inglés | MEDLINE | ID: mdl-37066594

RESUMEN

There is no clear consensus on the most effective treatment for relapsed/refractory high-risk neuroblastoma (NB). We retrospectively assessed seven NB patients with relapsed/refractory disease who received high-dose carboplatin-irinotecan-temozolomide (HD-CIT). Five of seven patients showed favorable therapeutic response (complete remission or partial remission). Regarding toxicity, the cytopenia period tended to prolong when more than three cycles were repeated, but nonhematological toxicities were controllable with general supportive care. Due to its antitumor efficacy and well-tolerated nonhematologic toxicity, HD-CIT is a promising salvage chemotherapy for relapsed/refractory NB. However, it is important to pay attention to the exacerbation of hematological toxicity when repeating the regimen.


Asunto(s)
Neuroblastoma , Humanos , Carboplatino , Irinotecán , Temozolomida , Estudios Retrospectivos , Protocolos de Quimioterapia Combinada Antineoplásica , Terapia Recuperativa , Recurrencia Local de Neoplasia
2.
Cancer Sci ; 112(11): 4617-4626, 2021 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-34464480

RESUMEN

Neuroblastoma, the most common extracranial solid tumor of childhood, is thought to arise from neural crest-derived immature cells. The prognosis of patients with high-risk or recurrent/refractory neuroblastoma remains quite poor despite intensive multimodality therapy; therefore, novel therapeutic interventions are required. We examined the expression of a cell adhesion molecule CD146 (melanoma cell adhesion molecule [MCAM]) by neuroblastoma cell lines and in clinical samples and investigated the anti-tumor effects of CD146-targeting treatment for neuroblastoma cells both in vitro and in vivo. CD146 is expressed by 4 cell lines and by most of primary tumors at any stage. Short hairpin RNA-mediated knockdown of CD146, or treatment with an anti-CD146 polyclonal antibody, effectively inhibited growth of neuroblastoma cells both in vitro and in vivo, principally due to increased apoptosis via the focal adhesion kinase and/or nuclear factor-kappa B signaling pathway. Furthermore, the anti-CD146 polyclonal antibody markedly inhibited tumor growth in immunodeficient mice inoculated with primary neuroblastoma cells. In conclusion, CD146 represents a promising therapeutic target for neuroblastoma.


Asunto(s)
Anticuerpos/uso terapéutico , Antígeno CD146/antagonistas & inhibidores , Terapia Molecular Dirigida/métodos , Neuroblastoma/terapia , ARN Interferente Pequeño/uso terapéutico , Animales , Apoptosis , Antígeno CD146/metabolismo , Línea Celular Tumoral , Supervivencia Celular , Quinasa 1 de Adhesión Focal/metabolismo , Proteína-Tirosina Quinasas de Adhesión Focal/metabolismo , Técnicas de Silenciamiento del Gen , Xenoinjertos , Humanos , Ratones , FN-kappa B/metabolismo , Recurrencia Local de Neoplasia , Trasplante de Neoplasias , Neuroblastoma/metabolismo , Neuroblastoma/patología , Pronóstico , Transducción de Señal , Esferoides Celulares , Transducción Genética/métodos
3.
Pediatr Blood Cancer ; 65(2)2018 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-28921816

RESUMEN

BACKGROUND: Donor cell leukemia (DCL) occurs after allogeneic hematopoietic stem cell transplantation. Several mechanisms, including occult leukemic/preleukemic subclones in the donor graft and germline predisposition to leukemia, are proposed to be associated with DCL's molecular pathogenesis. We report a comprehensive genetic analysis of a patient with KMT2A-rearranged DCL after allogeneic bone marrow transplantation for refractory cytopenia of childhood. PROCEDURE: We performed a whole-exome sequencing of the recipient's peripheral blood before transplant and the donor's peripheral blood and the recipient's bone marrow at the time of DCL diagnosis. RNA sequencing was also performed to detect fusion genes in DCL blasts. RESULTS: There were no germline mutations that were associated with a predisposition to leukemia in the recipient and donor. Furthermore, there were no detectable somatic alterations except KMT2A-MLLT10 and other related gene fusions in DCL. KMT2A-MLLT10 was not detectable in the donor's bone marrow. CONCLUSION: We propose a novel pattern of the molecular pathogenesis of DCL solely involving a genetic mutation acquired after transplant with no identifiable genetic factor related to the donor and recipient.


Asunto(s)
Crisis Blástica/genética , Trasplante de Médula Ósea , Reordenamiento Génico , N-Metiltransferasa de Histona-Lisina/genética , Leucemia/genética , Proteína de la Leucemia Mieloide-Linfoide/genética , Pancitopenia/terapia , Donantes de Tejidos , Aloinjertos , Preescolar , Femenino , Humanos , Lactante , Masculino , Pancitopenia/genética , Factores de Transcripción/genética
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