Growth hormone treatment and risk of recurrence or progression of brain tumors in children: a review

Bogarin, Roberto; Steinbok, Paul

doi:10.1007/s00381-008-0790-6

Cited by 15 publications

(7 citation statements)

References 25 publications

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“…15,16 These results suggest that our study has reflected clinical doses, and patients on GHRT are exposed to possible risk of CP re-growth. Our findings are not supported by clinical observations that GHRT is irrelevant to tumor recurrence 17,18 ; however, both these studies are retrospective, with limited numbers of patients included. Karavitaki et al, 18 enrolled 41 patients and the p value was 0.06, showing a tendency that GHRT may be an independent predictor of recurrence.…”

Section: Discussioncontrasting

confidence: 69%

Craniopharyngioma cell growth is promoted by growth hormone (GH) and is inhibited by tamoxifen: Involvement of growth hormone receptor (GHR) and IGF-1 receptor (IGF-1R)

You

Liu

et al. 2013

Journal of Clinical Neuroscience

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Section: Discussioncontrasting

confidence: 69%

Craniopharyngioma cell growth is promoted by growth hormone (GH) and is inhibited by tamoxifen: Involvement of growth hormone receptor (GHR) and IGF-1 receptor (IGF-1R)

You

Liu

et al. 2013

Journal of Clinical Neuroscience

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“…Each of these physical traumas can lead to inadequate GH production from the hypothalamus or the pituitary gland. Tumors may also cause insufficient secretion of one or more hormones and lead to GHD (Bogarin and Steinbok 2009;Stein et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Leptin expression and leptin receptor gene polymorphisms in growth hormone deficiency patients

Chen

et al. 2011

Hum Genet

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Growth hormone deficiency (GHD) patients have lower weight, height, bone age, insulin-like growth factor 1 (IGF-1) levels, GH levels, fat metabolism and skeletal growth. The association of leptin with GHD characteristics and the effect of gene variants of leptin on GHD are unknown. Our aim was to examine the association of circulating leptin levels and common genetic variants in leptin (LEP) and leptin receptor (LEPR) genes with anthropometric measures, circulating hormone concentrations and GHD. A case control study of 125 GHD cases and 159 control subjects were characterized for bone age, body mass index (BMI), height, weight, leptin, IGF-1, GH and their genotype at the leptin promoter G-2548A, and LEPR variants, K109R and Q223R, at Chung Shan Medical University Hospital. Leptin levels were significantly associated with lower bone age, weight and BMI in GHD patients. Leptin levels were also significantly associated with reduced IGF-1 levels in girls but not boys in both groups. The frequency of LEPR223 [A/G or A/A] genotype was significantly higher than the LEPR223 G/G genotype in the GHD group. The LEPR223 [A/G or A/A] genotype was significantly associated with increased weight and BMI in the control group, but not in the GHD group. In conclusion, the GHD group carried a significantly higher frequency of the LEPR [G/A or A/A] genotype and of the A allele (LEPR223R). The LEPR223R polymorphism affected weight and BMI in control, but not in GHD patients, suggesting that the effect of LEPR223 [A/G or A/A] genotype was counteracted by other factor(s) in GHD patients.

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“…For growth hormone, although GH receptors are well demonstrated in some craniopharyngiomas,[89] many authors continue to think GH is safe,[10111213] and craniopharyngiomas volume increase and recurrence are related to the quality of surgery excision and to the natural outcome where male gender, early onset, and cranial hypertension are the most important predictive factors of tumor progression and recurrence. [14] Others, less optimistic, think GH should be indicated only if the craniopharyngioma is stable for at least 1 year after surgery, and growth retardation is clinically evident as some children continue to grow despite a lack of GH response to different stimulation tests.…”

Section: Discussionmentioning

confidence: 99%

Volume increase in craniopharyngiomas under growth hormone and/or sex hormones substitution: Role of tumors receptors or mere coincidence?

et al. 2013

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Craniopharyngiomas are rare embryonic tumors with low grade of malignancy that arise in supra-or intra-sellar areas with severe ophthalmological, neurological, and endocrine damages. Among pituitary deficits, somatotroph and gonadotroph deficiencies are the most challenging because of potential increased risk of tumor growth and recurrence. While data exist to suggest that growth hormone (GH) treatment is safe, very little is known about sex hormones replacement on tumor growth. Our aim was to report 3 craniopharyngiomas with tumor increase under GH and/or estrogen (E2) therapy. The three patients, aged 21, 22, and 23, were studied for severe short stature related to calcified (n = 1) or apparently stable (for more than 2 years) craniopharyngiomas with somatotroph and gonadotroph deficiencies. After 4 months to 1 year GH (n = 2) and/or E2 replacement (n = 3), there was an increase in craniopharyngiomas’ size with signs of intracranial hypertension in two cases. In our three craniopharyngiomas that were either totally calcified or stable before substitution, the tumor increase seemed to be the result of GH and/or E2 substitution. But, as spontaneous evolution of these tumors is unpredictable, we could not exclude a mere coincidence.

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Growth hormone treatment and risk of recurrence or progression of brain tumors in children: a review

Cited by 15 publications

References 25 publications

Craniopharyngioma cell growth is promoted by growth hormone (GH) and is inhibited by tamoxifen: Involvement of growth hormone receptor (GHR) and IGF-1 receptor (IGF-1R)

Craniopharyngioma cell growth is promoted by growth hormone (GH) and is inhibited by tamoxifen: Involvement of growth hormone receptor (GHR) and IGF-1 receptor (IGF-1R)

Leptin expression and leptin receptor gene polymorphisms in growth hormone deficiency patients

Volume increase in craniopharyngiomas under growth hormone and/or sex hormones substitution: Role of tumors receptors or mere coincidence?

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