Growth hormone and tumour recurrence.

Ogilvy-Stuart, Amanda; Ryder, W. David J.; Gattamaneni, H. R.; Clayton, Peter E.; Shalet, Stephen M

doi:10.1136/bmj.304.6842.1601

Cited by 116 publications

(39 citation statements)

References 10 publications

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“…Additional characteristics of the included studies are shown in Table 1. As shown in table, seven of the selected studies obtained seven or more scores, which indicated that the study quality was relatively higher [5][6][7][14][15][16][17][18][19][20][21][22]; whereas, other studies with relatively lesser scores were considered of lower quality [23][24][25].…”

Section: Resultsmentioning

confidence: 99%

“…Results have confirmed that GHRT in children decreased the risk of tumor recurrence/progression (RR 0.44, 95 % CI 0.34-0.54). No sufficient evidence from the studies indicated that GH promoted the progression of intracranial tumors [14,16,25]. Ergun-Longmire et al performed a retrospective study with 361 survivors treated with GH, and confirmed that these survivors were easier to trap in second neoplasms (RR 3.21) [3,16].…”

Section: Discussionmentioning

confidence: 99%

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Growth hormone therapy and risk of recurrence/progression in intracranial tumors: a meta-analysis

Shen

Sun

et al. 2015

Neurol Sci

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Growth hormone deficiency is common in intracranial tumors, which is usually treated with surgery and radiotherapy. A number of previous studies have investigated the relationship between the growth hormone replacement therapy (GHRT) and risk of tumor recurrence/ progression; however, the evidence remains controversial. We conducted a meta-analysis of published studies to estimate the potential relation between GHRT and intracranial tumors recurrence/progression. Three comprehensive databases, PUBMED, EMBASE, and Cochrane Library, were researched with no limitations, covering all published studies till the end of July, 2014. Reference lists from identified studies were also screened for additional database. The summary relative risks (RR) and 95 % confidence intervals (CI) were calculated by fixed-effects models for estimation. Fifteen eligible studies, involving more than 2232 cases and 3606 controls, were included in our meta-analysis. The results indicated that intracranial tumors recurrence/progression was not associated with GHRT (RR 0.48, 95 % CI 0.39-0.56), and for children, the pooled RR was 0.44 and 95 % CI was 0.34-0.54. In subgroup analysis, risks of recurrence/progression were decreased for craniopharyngioma, medulloblastoma, astrocytoma, glioma, but not for pituitary adenomas, and non-functioning pituitary adenoma (NFPA), ependymoma.Results from our analysis indicate that GHRT decreases the risk of recurrence/progression in children with intracranial tumors, craniopharyngioma, medulloblastoma, astrocytoma, or glioma. However, GHRT for pituitary adenomas, NFPA, and ependymoma was not associated with the recurrence/progression of the tumors. GH replacement seems safe from the aspect of risk of tumor progression.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Growth hormone therapy and risk of recurrence/progression in intracranial tumors: a meta-analysis

Shen

Sun

et al. 2015

Neurol Sci

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“…However, epidemiological studies that suggest a correlation between the mean IGF-I level and the risk of developing malignant tumours have alerted both the public and the medical experts (7,8,12). Furthermore, individual anecdotal reports related the relapse of an intracranial tumour to GH treatment (4,13). In contrast to acromegaly, where IGF-I levels are unequivocally elevated and the rate of colonic neoplasms is increased, in GH-deficient patients, the substitution therapy aims at augmentation of hormone levels and normalization of IGF-I.…”

Section: Discussionmentioning

confidence: 99%

“…While the advantage of this expensive treatment for metabolism, body composition and psychosocial well-being has been shown convincingly in a number of publications, relevant concern has been raised as to the safety of such a substitution therapy. Large epidemiological observational studies revealed higher mean IGF-I levels in patients who developed prostate, breast and colonic cancer, in comparison with normal controls (4)(5)(6)(7)(8). However, all of these IGF-I levels were still within normal limits.…”

Section: Introductionmentioning

confidence: 99%

Influence of GH substitution therapy in deficient adults on the recurrence rate of hormonally inactive pituitary adenomas: a case–control study

Buchfelder

Kann²,

Wüster³

et al. 2007

European Journal of Endocrinology

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Objective: Several studies documented metabolic and psychological benefits of GH substitution in deficient adults, most of them suffering from benign pituitary adenomas. Since GH substitution is considered to promote tumour regrowth, adequate treatment is performed with some reservation. Therefore, we aimed to elucidate the effect of GH replacement therapy on tumour recurrence following surgery. Methods: In patients with hormonally inactive pituitary adenomas undergoing tumour surgery, a retrospective case-control study was performed. Pre-and postoperative magnetic resonance (MR) images of GH-treated and untreated patients were matched for best fit by two independent observers. The treated patients were retrieved from the surveillance programme of the German KIMS database and the untreated from the database of the Department of Neurosurgery, University of Erlangen. A total of 55 matched pairs were followed for at least 5 years. Tumour recurrence and progression rates were determined according to the postoperative MR. Results: There were 16 tumour progressions in the treatment group and 12 in the control group. Statistical analysis revealed no significant increase in either recurrence (PZ0.317) or progression (PZ0.617) within the follow-up period of 5 years when GH was adequately replaced. Conclusions: This study provides further observational data of substitution therapy in GH-deficient adults with pituitary adenomas. Comparing long-term surgical results, we found no evidence that GH substitution should be withheld in deficient patients. Even residual tumour does not constitute a contraindication to GH replacement. However, since pituitary tumours are slow growing, an observational period of 5 years may not have been long enough to verify any absolute influence on recurrence potential. 157 149-156 European Journal of Endocrinology

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“…Estrov et al [5] reported rhGH could increase the risk of human leukemia and solid tumor at a high concentration. Ogiliy-Stuart et al [15] thought rhGH was associated with the increasing risk for tumor, especially for colonic cancer, when it was used at a high concentration in patients with tumor. Akaza et al [16] found rhGH promoted carcinogenesis of chemically induced rat urinary bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

In vitroeffects of recombinant human growth hormone on growth of human gastric cancer cell line BGC823 cells

Chen¹,

Liang²,

Gan³

et al. 2004

WJG

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AIM:To study the effects of recombinant human growth hormone (rhGH) on growth of human gastric cancer cell line in vitro. METHODS:Experiment was divided into control group, rhGH group, oxaliplatin (L-OHP) group and rhGH+L-OHP group. Cell inhibitory rate, cell cycle, cell proliferation index (PI) and DNA inhibitory rate of human gastric cancer line BGC823, at different concentrations of rhGH treatment were studied by cell culture, MTT assay and flow cytometry. RESULTS:The distinctly accelerated effects of rhGH on multiplication of BGC823 cell line were not found in vitro. There was no statistical significance between rhGH group and control group, or between rhGH+L-OHP group and L-OHP group (P>0.05). The cell growth curve did not rise. Cell inhibitory rate and cells arrested in G 0 -G 1 phase were obviously increased. Meanwhile, cells in S phase and PI were distinctly decreased and DNA inhibitory rate was obviously increased in rhGH+L-OHP group in comparison with control group and rhGH group, respectively (P<0.01). Cell inhibitory rate showed an increasing trend and PI showed a decreasing trend in rhGH+L-OHP group compared with L-OHP group. CONCLUSION:In vitro rhGH does not accelerate the multiplication of human gastric cancer cells. It may increase the therapeutic efficacy when it is used in combination with anticancer drugs.

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Growth hormone and tumour recurrence.

Cited by 116 publications

References 10 publications

Growth hormone therapy and risk of recurrence/progression in intracranial tumors: a meta-analysis

Growth hormone therapy and risk of recurrence/progression in intracranial tumors: a meta-analysis

Influence of GH substitution therapy in deficient adults on the recurrence rate of hormonally inactive pituitary adenomas: a case–control study

In vitroeffects of recombinant human growth hormone on growth of human gastric cancer cell line BGC823 cells

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