Cancer

Grimberg, Adda

doi:10.1007/0-387-26274-1_13

Cited by 3 publications

(3 citation statements)

References 193 publications

(138 reference statements)

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“…Elevated IGF‐1 levels do not necessarily translate into increased cancer risk. However, multiple large case‐control studies showed a positive association between high concentrations of circulating IGF‐1 and increased risk for different types of cancer (Grimberg, ). It is noteworthy that GH receptors were identified in plexiform neurofibromas of NF1, and it was suggested that GH might influence their development (Cunha, Barboza, & Fonseca, .).…”

Section: Discussionmentioning

confidence: 99%

Growth hormone excess in children with neurofibromatosis type‐1 and optic glioma

Cambiaso

Galassi

Palmiero

et al. 2017

American J of Med Genetics Pt A

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In children with neurofibromatosis type 1 (NF1) and optic pathways glioma (OPG), growth hormone (GH) excess has been rarely reported and mainly associated to central precocious puberty. The aim of our study is to evaluate the prevalence of GH excess, the association with central precocious puberty, the relation with tumor site and the evolution over time in a large cohort of children with NF1 and OPG. Sixty-four NF1 children with OPG were evaluated. Patients with stature and/or height velocity >2 SD for age were studied for GH secretion. Seven out of 64 children (10.9%) with NF1 and optic pathways glioma showed GH excess, isolated in 5 cases and associated to central precocious puberty in 2. All the children with GH excess had a tumor involving the chiasma. Children with GH excess underwent medical treatment with lanreotide and a minimum clinical/biochemical follow up of 2 years is reported. The present study demonstrates that GH excess should be considered as a relative frequent endocrine manifestation in NF1 patients, similarly to central precocious puberty. Therefore, these patients should undergo frequent accurate auxologic evaluations. On the other hand, an increase in height velocity in children with NF1, even despite normal ophthalmological exams, can suggest the presence of OPG and therefore represents an indication to perform brain MRI.

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Section: Discussionmentioning

confidence: 99%

Growth hormone excess in children with neurofibromatosis type‐1 and optic glioma

Cambiaso

Galassi

Palmiero

et al. 2017

American J of Med Genetics Pt A

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“…Although current evidence does not support a causal role of IGF in cancer, epidemiologic studies of cancer risk factors, in vivo tumor models and in vitro experiments on altered cellular signaling all suggest that IGF signaling can contribute to cancer progression and aggressiveness. 36,37 IGF/IGF1R signaling proceeds through the receptor tyrosine kinase pathway and the phosphoinositide 3 kinase (PI3-K)/Akt pathway, both of which are commonly altered in the neoplastic process. 38 Cross-talk and coordination between the p53 and IGF-I-Akt-TOR pathways have been proposed as means of integrating growth factor signaling, changes in nutrient levels and stress signals into regulation of cell growth, mitogenesis and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence shows that IGFBP-3 can induce apoptosis in an IGF-independent fashion and suggests IGFBP-3 can serve a protective role against cancer. 12,37 Whether the IGF-independent activities of IGFBP-2 are also cancer protective remain unclear, as very little is known about them. IGF-independent activities of IGFBP-2 have been suggested by its interactions with α5β1-integrin, 40 its cytosolic uptake, 41 and its nuclear translocation.…”

Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor binding protein-2 is a novel mediator of p53 inhibition of insulin-like growth factor signaling

Grimberg

Coleman²,

Shi³

et al. 2006

Cancer Biology & Therapy

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Risk of Neoplasia in Pediatric Patients Receiving Growth Hormone Therapy—A Report From the Pediatric Endocrine Society Drug and Therapeutics Committee

Raman

Grimberg

Waguespack³

et al. 2015

The Journal of Clinical Endocrinology & Metabolism

102

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In children without known risk factors for malignancy, GH therapy can be safely administered without concerns about an increased risk for neoplasia. GH use in children with medical diagnoses predisposing them to the development of malignancies should be critically analyzed on an individual basis, and if chosen, appropriate surveillance for malignancies should be undertaken. GH can be used to treat GH-deficient childhood cancer survivors who are in remission with the understanding that GH therapy may increase their risk for second neoplasms.

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Cancer

Cited by 3 publications

References 193 publications

Growth hormone excess in children with neurofibromatosis type‐1 and optic glioma

Growth hormone excess in children with neurofibromatosis type‐1 and optic glioma

Insulin-like growth factor binding protein-2 is a novel mediator of p53 inhibition of insulin-like growth factor signaling

Risk of Neoplasia in Pediatric Patients Receiving Growth Hormone Therapy—A Report From the Pediatric Endocrine Society Drug and Therapeutics Committee

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