Adjuvant radiochemotherapy in the elderly affected by glioblastoma: single-institution experience and literature review

Fiorentino, Alba; Chiumento, C.; Caivano, Rocchina; Cozzolino, M.; Pedicini, P.; Fusco, Vincenzo

doi:10.1007/s11547-012-0906-7

Cited by 10 publications

(5 citation statements)

References 32 publications

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“…Malignant glioma is the most common form of brain cancer ( 1 ). Patients with malignant glioma are typically treated with a combination of surgery, chemotherapy and radiation therapy ( 1 – 4 ); however, the median survival time is only 12–15 months ( 2 ). Therefore, an improved understanding of the molecular mechanisms underlying glioma pathogenesis is essential in order to identify novel molecular targets for the treatment of glioma.…”

Section: Introductionmentioning

confidence: 99%

PCDH8 inhibits glioma cell proliferation by negatively regulating the AKT/GSK3β/β-catenin signaling pathway

Zong¹,

Hui²,

Yu³

et al. 2017

Oncology Letters

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Protocadherin-8 (PCDH8), a member of the protocadherin superfamily of proteins, is frequently lost in numerous types of cancer. However, the role that PCDH8 serves in human glioma, and the molecular mechanisms underlying this, remain unclear. Data from the present study demonstrated that the expression levels of PCDH8 mRNA and protein were significantly decreased in human glioma tissue compared with normal brain tissue. This suggested that PCDH8 is associated with the development of glioma. Thus, the role of PCDH8 in glioma cell proliferation was investigated by silencing and overexpressing PCDH8 in U251 glioma cells. Overexpression of PCDH8 significantly inhibited glioma cell proliferation, while silencing of PCDH8 using small interfering RNA promoted glioma cell proliferation. Restoration of PCDH8 decreased phosphorylated (p)-Rac-α serine/threonine-protein kinase (AKT) [Threonine (T)308/Serine (S)473] and p-glycogen synthase kinase-3β (p-GSK3β) (S9) protein expression, thereby reducing the level of β-catenin when compared with the control. By contrast, silencing of PCDH8 increased levels of p-AKT (T308/S473) and p-GSK3β (S9), thereby increasing the level of β-catenin. In conclusion, the results of the present study suggested that PCDH8 suppressed glioma cell proliferation, and that the loss of PCDH8 may stimulate the proto-oncogene Wnt/β-catenin signaling pathway and therefore promote glioma cell proliferation.

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Section: Introductionmentioning

confidence: 99%

PCDH8 inhibits glioma cell proliferation by negatively regulating the AKT/GSK3β/β-catenin signaling pathway

Zong¹,

Hui²,

Yu³

et al. 2017

Oncology Letters

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“…Malignant glioma is the most lethal tumor in the central nervous system and has much higher proliferative capacity . Despite advances in surgery and adjuvant therapy, the median survival of patients has changed little over recent decades . Therefore, it is important to elucidate the mechanisms of glioma development and to find key molecular targets for the development of effective therapies.…”

Section: Introductionmentioning

confidence: 99%

Lower expression of Nrdp1 in human glioma contributes tumor progression by reducing apoptosis

Shi

Wang

et al. 2014

IUBMB Life

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Ubiquitin ligase Nrdp1 (neuregulin receptor degradation protein 1) plays important roles in multiple physiological process because it can ubiquitinate various substrates such as ErbB3, BRUCE, MyD88, C/EBPb, and Parkin, and so forth. In addition to the physiological function, it was also found to be involved in tumor progression. It has been shown that loss of Nrdp1 enhances breast cancer cell growth. Up to now, the role of Nrdp1 in glioma has not been elucidated. Here, we reported that Nrdp1 as well as cleaved caspase 3 was lower expressed in human glioma tissues comparing with the nontumorous. And then we found that the expression of Nrdp1 and cleaved caspase 3 was increased in the treatment of Temozolomide (TMZ), a drug for glioma chemotherapy. Further investigation indicated that transient transfection of Nrdp1 significantly promoted cell apoptosis by aggravating the degradation of BRUCE and activation of caspase 3. In addition, overexpression of Nrdp1 augmented TMZ induced apoptosis by evaluating the degradation of BRUCE and the activation of caspase 3, while silencing of Nrdp1 reduced the sensitivity to the TMZ by inhibiting the degradation of BRUCE and the activation of caspase 3 in human glioma cells. These observations show that Nrdp1 is a pro-apoptotic protein in human glioma and lower expression of Nrdp1 in human glioma may promote tumor progression by reducing apoptosis, suggesting that Nrdp1 may be an important regulator in the development of human glioma. V C 2014 IUBMB Life, 66(10): [704][705][706][707][708][709][710] 2014

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“…Recently, gliomas have received more attention due to the unsatisfactory 5-year survival rates and median survival times of glioma patients [1][2][3][4][5]. However, current comprehensive treatments, comprising surgery, radiotherapy, and chemotherapy, have not achieved the desired therapeutic effects [2,3].…”

Section: Introductionmentioning

confidence: 99%

PART1 and hsa-miR-429-Mediated SHCBP1 Expression Is an Independent Predictor of Poor Prognosis in Glioma Patients

Xuan¹,

Jin²,

Wang³

et al. 2020

BioMed Research International

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Gliomas are the most common primary brain tumors. Because of their high degree of malignancy, patient survival rates are unsatisfactory. Therefore, exploring glioma biomarkers will play a key role in early diagnosis, guiding treatment, and monitoring the prognosis of gliomas. We found two lncRNAs, six miRNAs, and nine mRNAs that were differentially expressed by analyzing genomic data of glioma patients. The diagnostic value of mRNA expression levels in gliomas was determined by receiver operating characteristic (ROC) curve analysis. Among the nine mRNAs, the area under the ROC curve values of only CEP55 and SHCBP1 were >0.7, specifically 0.834 and 0.816, respectively. Additionally, CEP55 and SHCBP1 were highly expressed in glioma specimens and showed increased expression according to the glioma grade, and outcomes of high expression patients were poor. CEP55 was enriched in the cell cycle, DNA replication, mismatch repair, and P53 signaling pathway. SHCBP1 was enriched in the cell cycle, DNA replication, ECM receptor interaction, and P53 signaling pathway. Age, grade, IDH status, chromosome 19/20 cogain, and SHCBP1 were independent factors for prognosis. Our findings suggest the PART1-hsa-miR-429-SHCBP1 regulatory network plays an important role in gliomas.

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Adjuvant radiochemotherapy in the elderly affected by glioblastoma: single-institution experience and literature review

Abstract: Our data suggest that RCT with TMZ seems to produce a better outcome with a mild toxicity profile in elderly patients affected by GBM.

Cited by 10 publications

References 32 publications

PCDH8 inhibits glioma cell proliferation by negatively regulating the AKT/GSK3β/β-catenin signaling pathway

PCDH8 inhibits glioma cell proliferation by negatively regulating the AKT/GSK3β/β-catenin signaling pathway

Lower expression of Nrdp1 in human glioma contributes tumor progression by reducing apoptosis

PART1 and hsa-miR-429-Mediated SHCBP1 Expression Is an Independent Predictor of Poor Prognosis in Glioma Patients

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