The descriptive epidemiology of craniopharyngioma

Bunin, Greta R.; Surawicz, Tanya; Witman, Philip A.; Preston‐Martin, Susan; Davis, Faith G.; Bruner, Janet M.

doi:10.3171/jns.1998.89.4.0547

Cited by 603 publications

(203 citation statements)

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“…The age distribution of craniopharyngioma [5, 8, 32] has two peak incidences; the first in childhood between the ages of 5–15 years old and the second in adult life between the ages of 50–70 years old (fig. 2b).…”

Section: Resultsmentioning

confidence: 99%

“…There are two hypotheses: the first relates to the development of the adenohypophysis during embryogenesis, which is consistent with pediatric tumor development; the second proposes that residual squamous epithelium from the adenohypophysis undergoes metaplasia, which explains the adult tumors [32]. …”

Section: Resultsmentioning

confidence: 99%

“…The overall incidence of craniopharyngioma, as determined by Bunin et al[ 32], calculates to a rate of 1.3 per million person years.…”

Section: Resultsmentioning

confidence: 99%

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Craniopharyngiomas in Children

2007

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Background: The modern era of pediatric craniopharyngioma treatment includes multiple modalities including microsurgical resection, irradiation, brachytherapy or chemotherapy. No clear consensus as to the best therapeutic approach has yet been established. The aim of this study was to describe the techniques and strategies for the treatment of pediatric craniopharyngiomas in light of a literature review with particular attention to the incidence of adverse postoperative effects. Methods: Twenty-seven pediatric patients (median age 9.0 years) who were surgically treated for craniopharyngiomas were evaluated. We reviewed the recent literature for clinical features of craniopharyngiomas in children, including the present cases. Results: The overall rate of radiographically complete resection of our cases was 92.6%. In the literature we reviewed, the rate of gross total resection was 33–91% (average 57.8%). According to the literature, recurrence rates range from zero to 52.8% (average 16.1%) in the gross total resection group, 51.1% in the subtotal resection without radiation therapy group, and 33.5% in the subtotal resection with radiation therapy group. In six of our most recent cases, for whom we have complete outcome analysis, radiographically complete resection is 100% with only one recurrence so far over 4 years. Conclusions: For patients in whom early postoperative MRI reveals complete craniopharyngioma removal, a very low rate of recurrence is anticipated. In the authors’ experience, radiographically total excision of even large craniopharyngiomas can be safely achieved by one or a combination of several advanced microsurgical techniques, sometimes by a staged strategy. Major morbidities can be avoided, although moderate morbidities occur and require management.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Craniopharyngiomas in Children

2007

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“…Based on the annual incidence of CO-CP (0.4/million person-years) (36), the present cohort is thus representative for the entire population of CO-CP patients. However, as we included survivors, we cannot exclude that non-survivors may have exhibited a somewhat different demographic profile from our study cohort.…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic involvement and insufficient sex steroid supplementation are associated with low bone mineral density in women with childhood onset craniopharyngioma

Holmer

Popović²,

Ekman³

et al. 2011

European Journal of Endocrinology

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Context: Data on bone mineral density (BMD) are lacking in adults with childhood onset (CO)-craniopharyngioma (CP) with hypothalamic damage from the tumor. In patients with CO GH deficiency, BMD increases during GH treatment. Objective: The aims were to evaluate BMD in adults with CO-CPs on complete hormone replacement, including long-term GH and to evaluate the impact of hypothalamic damage on these measures. Design and participants: BMD (dual-energy X-ray absorptiometry), markers of bone turn over, physical activity and calcium intake were assessed in 39 CO-CP adults (20 women), with a median age of 28 (17-57) years, in comparison with matched population controls. Results: Late puberty induction was recorded in both genders, but reduced androgen levels in females only. Only CP women had lower BMD (PZ0.03) at L2-L4, and reduced Z-scores at femoral neck (PZ0.004) and L2-L4 (PZ0.004). Both genders had increased serum leptin levels (PZ0.001), which significantly correlated negatively with BMD at L2-L4 (PZ0.003; rZK0.5) and 45% of CP women had Z-score levels %K2.0 S.D. Furthermore, 75% of those with a Z-score %K2.0 S.D. had hypothalamic involvement by the tumor. Calcium intake (PZ0.008) and physical activity (PZ0.007) levels were reduced in CP men only. Levels of ostecalcin and crossLaps were increased in CP men only. Conclusions: Despite continuous GH therapy, low BMD was recorded in CO-CP females. Insufficient estrogen and androgen supplementation during adolescence was the main cause, but hypothalamic involvement with consequent leptin resistance was also strongly associated with low BMD in both genders.

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“…Adamantinomatous CPs (ACPs) represent the most common non-neuroepithelial intracranial lesions in children, and they contribute to 1.5-11.6% of all paediatric CNS tumours (Bunin et al 1998). There is a well-described bimodal age distribution in incidence, with peaks occurring between the ages of 5 and 14 (childhood-onset ACP) and between ages 65 and 74 (adult-onset ACP) (Bunin et al 1998, Nielsen et al 2011. ACPs are the archetypal suprasellar tumour for causing neuroendocrine disruption and dysfunction, not just from tumour pressure and invasive effects but also from treatments targeted to this area.…”

Section: Introductionmentioning

confidence: 99%

60 YEARS OF NEUROENDOCRINOLOGY: Biology of human craniopharyngioma: lessons from mouse models

Martinez-Barbera¹

2015

Journal of Endocrinology

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Adamantinomatous craniopharyngiomas (ACP) are clinically relevant tumours that are associated with high morbidity, poor quality of life and occasional mortality. Human and mouse studies have provided important insights into the biology of these aggressive tumours, and we are starting to understand why, how and when these tumours develop in humans. Mutations in b-catenin that result in the over-activation of the WNT/b-catenin signalling pathway are critical drivers of most, perhaps of all, human ACPs. Mouse studies have shown that only pituitary embryonic precursors or adult stem cells are able to generate tumours when targeted with oncogenic b-catenin, which suggests that the cell context is critical in order for mutant b-catenin to exert its oncogenic effect. Interestingly, mutant stem cells do not generate the bulk of the tumour cells; instead, they induce tumours in a paracrine manner. Combining basic studies in mice and humans will provide further insights into the biology of these neoplasms and will reveal pathogenic pathways that could be targeted with specific inhibitors for the benefit of patients. These benign tumours may additionally represent a unique model for investigating the early steps that lead to oncogenesis.

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The descriptive epidemiology of craniopharyngioma

Abstract: Craniopharyngioma is a rare brain tumor of uncertain behavior that occurs at a rate of 1.3 per million person years. Approximately 338 cases of this disease are expected to occur annually in the United States, with 96 occurring in children from 0 to 14 years of age.

Cited by 603 publications

References 10 publications

Craniopharyngiomas in Children

Craniopharyngiomas in Children

Hypothalamic involvement and insufficient sex steroid supplementation are associated with low bone mineral density in women with childhood onset craniopharyngioma

60 YEARS OF NEUROENDOCRINOLOGY: Biology of human craniopharyngioma: lessons from mouse models

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