Pituitary derived and peripherally produced growth hormone (GH) is a crucial mediator of longitudinal growth, organ development, metabolic regulation with tissue specific, sex specific, and age-dependent effects. GH and its cognate receptor (GHR) are expressed in several forms of cancer and have been validated as an anti-cancer target through a large body of in vitro, in vivo and epidemiological analyses. However, the underlying molecular mechanisms of GH action in cancer prognosis and therapeutic response had been sparse until recently. This review assimilates the critical details of GH-GHR mediated therapy resistance across different cancer types, distilling the therapeutic implications based on our current understanding of these effects.

/pdf/the-effects-of-growth-hormone-on-therapy-resistance-in-19yohlg18h.pdf

The effects of growth hormone on therapy resistance in cancer.

https://febs.onlinelibrary.wiley.com/doi/pdf/10.1002/2211-5463.12816

Growth hormone receptor promotes breast cancer progression via the BRAF/MEK/ERK signaling pathway.

Sorafenib is approved for treatment of advanced hepatocellular carcinoma (HCC) by the Drug Administration. However, the efficacy of sorafenib has become very limited because most tumors have developed resistance to this drug. In this study, we found that sorafenib stimulated GHR expression in HCC cell lines. Thus, GHR might be linked to sorafenib resistance. To verify this hypothesis, we researched the roles of GHR knockdown and sorafenib combination in cell viability, apoptosis, cycle, and migration. The results showed that GHR blockage enhanced sorafenib blocking of cell cycle progression, leading to inhibition of this drug on HCC cell viability, and the improved promoting ability of sorafenib on cell apoptosis. In addition, it was found that GHR knockdown enhanced sorafenib inhibition of cell migration. The synergistic antitumor effects of sorafenib and GHR knockdown combination may be attributed to inhibition of PI3K/AKT/ERK1/2 signaling pathway. In conclusion, the findings suggest that GHR knockdown enhances the sensitivity of HCC cells to sorafenib. and the inactivation of PI3K/AKT/ERK1/2 signaling pathway may be the underlying mechanisms. This highlights the absence of GHR as a promising way to enhance sorafenib efficacy in HCC.

https://paperchase-aging.s3-us-west-1.amazonaws.com/pdf/5f3fc34aee918f00072c181a.pdf

GHR knockdown enhances the sensitivity of HCC cells to sorafenib.

This is a narrative review of literature introducing somatostatin receptors (SSTRs) as part of understanding the somatotroph cells since they are positive in normal cells but also in tumoral cells as seen in somatotropinoma, a growth hormone (GH)-producing neoplasia, which causes acromegaly. They are five subtypes of SSTRs (1 to 5), which are immunohistochemically positive in different proportions in somatotropinomas. SSTR types 2 and 5 are most frequent in GH-secreting adenomas and they are both targeted by medical therapy with somatostatin analogues (SSTAs) like first generation Octreotide and Lanreotide (mainly targeting SSTR2) and second generation Pasireotide (with highest affinity for SSTR5), thus heterogeneous SSTRs configuration into the tumor explains different pattern of response to treatment and it might predict it once the SSTRs immunostaining is performed. Monoclonal antibodies are used for immunohistochemical detection of SSTRs; currently, a lack of standardization is presented, and scoring systems, such as Volante, H-score or human epidermal growth factor receptor 2 (HER2)-score, are applied. Immunoreactive markers like SSTRs are the U-turn in clinical practice regarding somatotropinomas since the configuration of subtypes 2 and 5 explains the responsiveness to medical therapy like SSTA. Further achievement of disease control is imperiously necessary because acromegaly has an increased rate of morbidity and mortality.

/pdf/somatostatin-receptors-in-normal-and-acromegalic-somatotroph-2vapmda3vd.pdf

Somatostatin receptors in normal and acromegalic somatotroph cells: the U-turn of the clinician to immunohistochemistry report - a review.

I am pleased to introduce Translational Biomedicine (IPTB) Translational Biomedicine is an international open access*, peer-reviewed academic journal with Journal Impact Factor 1.12. The Journal publishes original science-based research that advances communication between the scientific discovery and health improvement. I am pleased to announce that, all issues of volume 10 were published online well within the time and the print issues were also brought out and dispatched within 30 days of publishing the issue online during the year of 2019.

/pdf/editorial-note-for-translational-biomedicine-2ulznxmvoy.pdf

Editorial Note for Translational Biomedicine

Background: The interaction between pituitary hormones (Growth Hormone-Prolactin), ovarian hormones (Estradiol) and growth factors forms the basis of the mechanisms underlying the growth of tumors of the breast. The literature contains reports of the increased expression of the mitogenic GH (Growth Hormone)/IGF1 (Insulin-Like Growth Factor) axis in tumor tissues compared to healthy tissues, with a directly proportional dose-dependent relationship between GH/IGF1, proliferative index and invasive ability in numerous types of tumors.
Methods and Findings: We carried out this experimental research on the mitogenic role of GH and consequently on the rationale of the anticancer use of its inhibition. The levels of expression of several genes, GH and GHR, were evaluated in 39 cases of breast cancer, divided according to different risk levels on the basis of immunohistochemical and histological tests with nuclear grade.
Conclusion: Research showed that breast cancers with a high and intermediate risk of recurrence are characterized by over-expression of GH and of its receptor (GHR). The expression was limited in cases with a low risk. The overexpression of GH-GHR in breast cancer with a ratio proportional to the level of aggressiveness is a rationale that can encourage a therapeutic intervention with inhibition of the mitogenic GH-IGF1-PRL axis and estrogen.

/pdf/over-expression-of-gh-ghr-in-breast-cancer-and-3fqq4huaw8.pdf

Over-Expression of GH/GHR in Breast Cancer and Oncosuppressor Role of Somatostatin as a Physiological Inhibitor

Background: Breast cancer is still the leading cause of death in women worldwide.
Study question: Our purpose is to improve survival, objective response and quality of life with a non-toxic biological therapy.
Study design: The DBM (Di Bella Method) with MLT (Melatonin), Retinoids, solubilized in vitamin E, D3, and C, Folates, proteoglycans and calcium, has a differentiating, cytostatic, anti-angiogenic, immune-modulating, factorially synergic effect, simultaneously reinforcing the functions which physiology considers to be essential for life. With Somatostatin/Octreotide, prolactin and estrogen inhibitors, DBM has an antiproliferative, antiangiogenic and antimetastatic effect. These molecules govern negatively pituitary secretions like GH-PRL, whose mitogenic properties are enhanced by the combination of ovarian hormones such as estrogen. The negative regulation of GH extends to IGF-1, EGF (Epidermal Growth Factor), VEGF (Vascular Endothelial Growth Factor), and GHdependent growth factors. The DBM (Di Bella Method) uses minimal metronomic apoptotic, non-cytotoxic and non-mutagenic doses of cyclophosphamide. The tolerability of which is enhanced by MLT and by the vitamins included in the DBM. We report a retrospective observational study with 5-year follow-up, carried out on 297 patients affected by breast cancer and treated with the Di Bella Method biological therapy.
Results and conclusion: complete and stable objective responses without cytolytic chemotherapy, in some cases even without surgery or radiotherapy, with a generalized improvement in quality of life and no significant and/or prolonged toxicity. The most important 5-year survival rate was 69.4% at stage IV cancer versus 26.3% reported by the National Cancer Institute.

/pdf/the-synergism-of-somatostatin-melatonin-vitamins-prolactin-3wubjl167q.pdf

The Synergism of Somatostatin, Melatonin, Vitamins Prolactin and Estrogen Inhibitors Increased Survival, Objective Response and Performance Status In 297 Cases of Breast Cancer

The interaction between pituitary hormones, GH - PRL, and Growth Factors, GF, plays a fundamental role in the physiological and neoplastic mechanisms of growth, the latter using these factors to a much greater extent compared to the former, with a direct dose-dependent effect on the speed of local or metastatic expansion. In hormone-dependent tumours, the respective male and female sex hormones interact with GH - PRL - GF to sustain the expansion of the tumour. We carried out a review of the literature on the relationship between the expression of GH and GHR in tumour tissues compared to healthy tissues, and on the correlation between this expression and tumour aggressiveness. An over-expression of GH and GHR in tumours was a constant finding. In more than a thousand cases published in various clinical, observational, retrospective studies investigating cervico-facial tumours, lymphoproliferative diseases, breast cancer, prostate cancer, non-small-cell lung cancer, neuroblastomas, oesophageal cancer, glioblastomas, and sarcomas, we constantly found an improvement in objective response, quality of life and survival, compared to conventional oncological protocols, by inhibiting GH and correlated GF using somatostatin.

The over-expression of GH/GHR in tumour tissues with respect to healthy ones confirms its oncogenic role and the consequent oncosuppressor role of its physiological inhibitor, somatostatin: a review of the literature.

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Papers

Over-Expression of GH/GHR in Breast Cancer and Oncosuppressor Role of Somatostatin as a Physiological Inhibitor

The Synergism of Somatostatin, Melatonin, Vitamins Prolactin and Estrogen Inhibitors Increased Survival, Objective Response and Performance Status In 297 Cases of Breast Cancer

The over-expression of GH/GHR in tumour tissues with respect to healthy ones confirms its oncogenic role and the consequent oncosuppressor role of its physiological inhibitor, somatostatin: a review of the literature.