Correlation between Histological Grade, MIB-1, p53, and Recurrence in 69 Completely Resected Primary Intracranial Meningiomas with a 6 Year Mean Follow-up

Lanzafame, Salvatore; Torrisi, Antonietta; Barbagallo, Giuseppe; Emmanuele, Carmela; Alberio, Nicola; Albanese, Vincenzo

doi:10.1016/s0344-0338(00)80050-3

Cited by 61 publications

(43 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There was increased expression of p53 protein in atypical ( Figure 1h) and anaplastic meningioma (Figure 1i) compared to negligible p53 expression in benign meningiomas (Figure 1g). Overexpression of p53 protein in meningiomas was associated with increased MIB-1 labeling index and with recurrence in some studies, 24,25 and aggressive histology 26 in others.…”

Section: Discussionmentioning

confidence: 92%

Methylation of p14 gene in meningiomas and its correlation to the p53 expression and mutation

2004

View full text Add to dashboard Cite

We have previously reported the statistically significant correlation of immunohistochemical expression of MIB-1 and p53 proteins among benign, atypical, and anaplastic meningiomas and p53 protein expression was high in atypical and anaplastic meningiomas. In the present study, we analyzed 22 cases of meningiomas for mutation of p53 gene in its spectrum of exon 5 to 8 using automated genetic analyzer. We did not find any mutation of p53 in any of these cases, thus suggesting the p53 protein expression is wild type. We analyzed 72 cases of meningiomas for determining the methylation status of p14 ARF gene and the immunohistochemical expression of MDM2 protein to explain p53 protein expression in these meningiomas. We found methylation of p14 ARF gene in five of 58 cases of benign meningiomas (8.6%), two of 10 cases of atypical meningiomas (20%), and two of four cases of anaplastic meningiomas (50%). In absence of p53 gene mutation, the high percentage of p14 ARF gene methylation in high-grade meningioma may have been responsible for accumulation of wild-type p53 protein. In addition, we also found the loss of MDM2 protein in high-grade meningiomas. These deregulations of p14-MDM2-p53 pathway may contribute to the malignant progression of meningioma.

show abstract

Section: Discussionmentioning

confidence: 92%

Methylation of p14 gene in meningiomas and its correlation to the p53 expression and mutation

2004

View full text Add to dashboard Cite

show abstract

“…Mib1 is the usually applied clone of the Ki-67 antibody which is widely used as a proliferative marker in the routine diagnostic work-up. The Mib1 LI shows a strong correlation with tumour growths, relapse/recurrence, length of disease free survival in various tumours [2,3,34] including meningioma [18,19].…”

Section: Introductionmentioning

confidence: 99%

Assessment of candidate immunohistochemical prognostic markers of meningioma recurrence

Csonka¹,

Murnyák²,

Szepesi³

et al. 2016

View full text Add to dashboard Cite

show abstract

“…2,3,7,14,29 Although the criteria clarification has benefited the evaluation of meningiomas by making interobserver and intrainstitutional comparisons more valid, 13,20,22,24,27 the change has required most institutions to adopt new and substantially different criteria for the grading of meningiomas. 11 In the years following the WHO reclassification, many institutions began to record different rates of atypical meningiomas than they had in the past.…”

mentioning

confidence: 99%

Hitting a moving target: evolution of a treatment paradigm for atypical meningiomas amid changing diagnostic criteria

Pearson¹,

Markert²,

Fisher³

et al. 2008

FOC

183

View full text Add to dashboard Cite

Object The World Health Organization (WHO) reclassified atypical meningiomas in 2000, creating a more clear and broadly accepted definition. In this paper, the authors evaluated the pathological and clinical transition period for atypical meningiomas according to the implementation of the new WHO grading system at their institution. Methods A total of 471 meningiomas occurring in 440 patients between 1994 and 2006 were retrospectively reviewed to determine changes in diagnostic rates, postoperative treatment trends, and early outcomes. Results Between 1994 and 2000, the incidence of the atypical meningiomas ranged from 0 to 3/year, or 4.4% of the meningiomas detected during the entire period. After 2002, the annual percentage of atypical meningiomas rose over a 2-year period, leveling off at between 32.7 and 35.5% between 2004 and 2006. The authors also found a recent trend toward increased use of adjuvant radiation therapy for incompletely resected atypical meningiomas. Prior to 2003, 18.7% were treated with this therapy; after 2003, 34.4% of lesions received this treatment. Incompletely resected tumors were treated with some form of radiation 76% of the time. In cases of complete resection, most patients were not given adjuvant therapy but were expectantly managed by close monitoring using serial imaging and by receiving immediate treatment for tumor recurrence. The overall recurrence rate for expectantly managed tumors was 9% over 28.2 months, and 75% of recurrences responded to delayed radiation therapy. Conclusions The authors documented a significant change in the proportion of meningiomas designated as atypical during a transition period from 2002 to 2004, and propose a conservative strategy for the use of radiation therapy in atypical meningiomas.

show abstract

Correlation between Histological Grade, MIB-1, p53, and Recurrence in 69 Completely Resected Primary Intracranial Meningiomas with a 6 Year Mean Follow-up

Cited by 61 publications

References 14 publications

Methylation of p14 gene in meningiomas and its correlation to the p53 expression and mutation

Methylation of p14 gene in meningiomas and its correlation to the p53 expression and mutation

Assessment of candidate immunohistochemical prognostic markers of meningioma recurrence

Hitting a moving target: evolution of a treatment paradigm for atypical meningiomas amid changing diagnostic criteria

Contact Info

Product

Resources

About