Polyploidy in atypical grade II choroid plexus papilloma of the posterior fossa

Brassesco, María Sol; Valera, Elvis Terci; Neder, Luciano; Castro‐Gamero, Angel Mauricio; Arruda, Darlene; Machado, Hélio Rubens; Sakamoto-Hojo, Elza T.; Tone, Luíz Gonzaga

doi:10.1111/j.1440-1789.2008.00949.x

Cited by 26 publications

(19 citation statements)

References 23 publications

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“…The primary culture was derived from the biopsy specimens of glioblastoma patients under a protocol approved by the institutional review board at the University Hospital of the School of Medicine of Ribeirão Preto, SP, Brazil. Cultures were obtained according to Brassesco et al (2009) and maintained at low passage numbers (p2-p5) under standard culture conditions. Drugs ZM447439 (ZM) was obtained from Tocris Cookson Inc. (Ellisville, MO).…”

Section: Cell Lines and Primary Culturementioning

confidence: 99%

Inhibition of Aurora kinases enhances chemosensitivity to temozolomide and causes radiosensitization in glioblastoma cells

Borges

Castro‐Gamero

Moreno

et al. 2011

J Cancer Res Clin Oncol

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Section: Cell Lines and Primary Culturementioning

confidence: 99%

Inhibition of Aurora kinases enhances chemosensitivity to temozolomide and causes radiosensitization in glioblastoma cells

Borges

Castro‐Gamero

Moreno

et al. 2011

J Cancer Res Clin Oncol

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“…Cytogenetic preparations from fresh tumor sample were obtained as previously described [9]. However, the subsequent analysis by GTG-banding was hampered by the poor chromosome morphology.…”

Section: Pathologists From Both Institutions Lastly Agreed With the Dmentioning

confidence: 99%

Pitfalls in the differential diagnosis of renal tumor in an adolescent

Valera

Brassesco

Cortez

et al. 2009

Pediatric Blood & Cancer

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The differential diagnosis of renal tumors, particularly in adolescents, may be challenging. We describe an 11‐year‐old female with a primary intra‐renal mass. Initial differential diagnoses included primitive neuroectodermal tumor (PNET), desmoplastic small round cell tumor (DSRCT), and Wilms Tumor (WT). Extensive pathologic and molecular analysis on initial and relapsed tumor samples confirmed WT. The EWS‐WT1 and EWS‐FLI1 rearrangements, distinctive of DSRCT and PNET were negative. The differential diagnosis on monophasic blastemal WT may be complex. Primary renal DSRCT and PNET have been rarely described. Nevertheless, molecular confirmation for these rare conditions may be necessary in selected cases. Pediatr Blood Cancer 2010;54:319–321. © 2009 Wiley‐Liss, Inc.

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“…Primary tumor cultures were derived from the tissue samples using the method described by Brassesco et al [18]. Human GBM cell line U87 (maintained in SYSUCC) were obtained from American Type Culture Collection.…”

Section: Methodsmentioning

confidence: 99%

MiR-181b sensitizes glioma cells to teniposide by targeting MDM2

et al. 2014

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BackgroundAlthough the incidence of glioma is relatively low, it is the most malignant tumor of the central nervous system. The prognosis of high-grade glioma patient is very poor due to the difficulties in complete resection and resistance to radio-/chemotherapy. Therefore, it is worth investigating the molecular mechanisms involved in glioma drug resistance. MicroRNAs have been found to play important roles in tumor progression and drug resistance. Our previous work showed that miR-181b is involved in the regulation of temozolomide resistance. In the current study, we investigated whether miR-181b also plays a role in antagonizing the effect of teniposide.MethodsMiR-181b expression was measured in 90 glioma patient tissues and its relationship to prognosis of these patients was analyzed. Cell sensitivity to teniposide was tested in 48 primary cultured glioma samples. Then miR-181b stably overexpressed U87 cells were generated. The candidate genes of miR-181b from our previous study were reanalyzed, and the interaction between miR-181b and target gene MDM2 was confirmed by dual luciferase assay. Cell sensitivity to teniposide was detected on miR-181b over expressed and MDM2 down regulated cells.ResultsOur data confirmed the low expression levels of miR-181b in high-grade glioma tissues, which is related to teniposide resistance in primary cultured glioma cells. Overexpression of miR-181b increased glioma cell sensitivity to teniposide. Through target gene prediction, we found that MDM2 is a candidate target of miR-181b. MDM2 knockdown mimicked the sensitization effect of miR-181b. Further study revealed that miR-181b binds to the 3’-UTR region of MDM2 leading to the decrease in MDM2 levels and subsequent increase in teniposide sensitivity. Partial restoration of MDM2 attenuated the sensitivity enhancement by miR-181b.ConclusionsMiR-181b is an important positive regulator on glioma cell sensitivity to teniposide. It confers glioma cell sensitivity to teniposide through binding to the 3’-UTR region of MDM2 leading to its reduced expression. Our findings not only reveal the novel mechanism involved in teniposide resistance, but also shed light on the optimization of glioma treatment in the future.

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Polyploidy in atypical grade II choroid plexus papilloma of the posterior fossa

Cited by 26 publications

References 23 publications

Inhibition of Aurora kinases enhances chemosensitivity to temozolomide and causes radiosensitization in glioblastoma cells

Inhibition of Aurora kinases enhances chemosensitivity to temozolomide and causes radiosensitization in glioblastoma cells

Pitfalls in the differential diagnosis of renal tumor in an adolescent

MiR-181b sensitizes glioma cells to teniposide by targeting MDM2

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