cyclin-d1 has been researched along with Neuroectodermal-Tumors--Primitive--Peripheral* in 2 studies
2 other study(ies) available for cyclin-d1 and Neuroectodermal-Tumors--Primitive--Peripheral
| Article | Year |
|---|---|
Diagnostic utility of cyclin D1 in the diagnosis of small round blue cell tumors in children and adolescents.
Small round blue cell tumors (SRBCTs) of children and adolescents are often diagnostically challenging lesions. With the increasing diagnostic approach based on small biopsies, there is the need of specific immunomarkers that can help in the differential diagnosis among the different tumor histotypes to assure the patient a correct diagnosis for proper treatment. Based on our recent studies showing cyclin D1 overexpression in both Ewing sarcoma/primitive peripheral neuroectodermal tumor (EWS/pPNET) and peripheral neuroblastic tumors (neuroblastoma and ganglioneuroblastoma), we immunohistochemically assessed cyclin D1 immunoreactivity in 128 cases of SRBCTs in children and adolescents to establish its potential utility in the differential diagnosis. All cases of EWS/pPNET and the undifferentiated/poorly differentiated neuroblastomatous component of all peripheral neuroblastic tumors exhibited strong and diffuse nuclear staining (>50% of neoplastic cells) for cyclin D1. In contrast, this marker was absent from rhabdomyosarcoma (regardless of subtype) and lymphoblastic lymphoma (either B- or T-cell precursors), whereas it was only focally detected (<5% of neoplastic cells) in some cases of Wilms tumor (blastemal component) and desmoplastic small round cell tumor. Our findings suggest that cyclin D1 can be exploitable as a diagnostic adjunct to conventional markers in confirming the diagnosis of EWS/pPNET or neuroblastoma/ganglioneuroblastoma. Its use in routine practice may also be helpful for those cases of SRBCT with undifferentiated morphology that are difficult to diagnose after application of the conventional markers. Topics: Adolescent; Biomarkers, Tumor; Biopsy; Bone Neoplasms; Cell Differentiation; Child; Child, Preschool; Cyclin D1; Desmoplastic Small Round Cell Tumor; Diagnosis, Differential; Female; Ganglioneuroblastoma; Humans; Immunohistochemistry; Infant; Kidney Neoplasms; Male; Neuroblastoma; Neuroectodermal Tumors, Primitive, Peripheral; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Predictive Value of Tests; Retrospective Studies; Rhabdomyosarcoma; Sarcoma, Ewing; Wilms Tumor; Young Adult | 2017 |
The iron chelator, deferasirox, as a novel strategy for cancer treatment: oral activity against human lung tumor xenografts and molecular mechanism of action.
Deferasirox is an orally effective iron (Fe) chelator currently used for the treatment of iron-overload disease and has been implemented as an alternative to the gold standard chelator, desferrioxamine (DFO). Earlier studies demonstrated that DFO exhibits anticancer activity due to its ability to deplete cancer cells of iron. In this investigation, we examined the in vitro and in vivo activity of deferasirox against cells from human solid tumors. To date, there have been no studies to investigate the effect of deferasirox on these types of tumors in vivo. Deferasirox demonstrated similar activity at inhibiting proliferation of DMS-53 lung carcinoma and SK-N-MC neuroepithelioma cell lines compared with DFO. Furthermore, deferasirox was generally similar or slightly more effective than DFO at mobilizing cellular (59)Fe and inhibiting iron uptake from human transferrin depending on the cell type. However, deferasirox potently inhibited DMS-53 xenograft growth in nude mice when given by oral gavage, with no marked alterations in normal tissue histology. To understand the antitumor activity of deferasirox, we investigated its effect on the expression of molecules that play key roles in metastasis, cell cycle control, and apoptosis. We demonstrated that deferasirox increased expression of the metastasis suppressor protein N-myc downstream-regulated gene 1 and upregulated the cyclin-dependent kinase inhibitor p21(CIP1/WAF1) while decreasing cyclin D1 levels. Moreover, this agent increased the expression of apoptosis markers, including cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase 1. Collectively, we demonstrate that deferasirox is an orally effective antitumor agent against solid tumors. Topics: Administration, Oral; Animals; Antigens, CD; Antineoplastic Agents; Apoptosis; Benzoates; Cell Cycle; Cell Line, Tumor; Copper; Cyclin D1; Cyclin-Dependent Kinase Inhibitor p21; Deferasirox; Female; Humans; Iron; Iron Chelating Agents; Lung Neoplasms; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Metastasis; Neoplasm Transplantation; Neuroectodermal Tumors, Primitive, Peripheral; Protein Serine-Threonine Kinases; Receptors, Transferrin; Small Cell Lung Carcinoma; Transplantation, Heterologous; Triazoles; Zinc | 2013 |