Growth hormone plays critical role in breast cancer: promotes angiogenesis, stimulated mTOR, promotes chemoresistance, promotes breast stem activity, promotes metastasis via increase in epithelial to mesenchymal transition...
Four studies have reported that the probability of GHD (peak GH criteria ranging from < 2.3 to < 5 μg/liter) in patients with three to four PHDs ranges from 91% to 100%
95% accuracy by the presence of either three or more PHDs or a serum IGF-I concentration less than 84 μg/lite
adult GHD could be predicted with 95% accuracy by the presence of either three or four PHDs or a serum IGF-I concentration less than 84 μg/liter
Hypopituitary adults with GHD have been reported to have normal serum IGF-I levels in 37–70% of patients in various studies (5, 9, 18, 21, 22). This is owing in part to the fact that multiple factors regulate serum IGF-I concentrations including nutritional status; hepatic and renal function; and circulating concentrations of thyroid hormone, androgens, and estrogens
changes in concentrations of IGF-binding proteins (IGFBPs) influence the total concentration of IGF-I in plasma
Among patients with an IGF-I sd score above −1 in the present study, 46% had a peak GH less than 2.5 μg/liter and 67% had a peak GH less than 5 μg/liter.
In summary, adult GHD can be predicted with 95% accuracy by the presence of either three or four PHDs or a serum IGF-I concentration less than 84 μg/liter
We propose that adult patients with three or four PHDs (three or four of the following deficiencies: TSH, ACTH, gonadotropins [LH and/or FSH], and AVP [central diabetes insipidus]) do not require a GH stimulation test to make the diagnosis of adult GHD
Insulin Tolerance Test is the gold standard for HGH diagnosis, but this an unpopular test do to long list of side effects. This study finds a 95% accuracy for IGF-1 less than 84 with 3 or more coexisting pituitary hormone deficiencies.
Thought GH in those with Prader-Willi Syndrome did not see an improvement in lipid and glucose metabolism, lean body mass increased and fat mass decreased.
of the approximately 108 cannabinoids produced by C. sativa, Δ9-tetrahydrocannabinol (thc) is the most relevant because of its high potency and abundance in plant preparations
Tetrahydrocannabinol exerts a wide variety of biologic effects by mimicking endogenous substances—the endocannabinoids anandamide3 and 2-arachidonoylglycerol4,5—that engage specific cell-surface cannabinoid receptors
the cb2 receptor was initially described to be present in the immune system6, but was more recently shown to also be expressed in cells from other origins
transient receptor potential cation channel subfamily V, member 1
orphan G protein–coupled receptor 55
Most of the effects produced by cannabinoids in the nervous system and in non-neural tissues rely on cb1 receptor activation
two major cannabinoid-specific receptors—cb1 and cb2
cardiovascular tone, energy metabolism, immunity, and reproduction
cannabinoids are well known to exert palliative effects in cancer patients
best-established use is the inhibition of chemotherapy-induced nausea and vomiting
thc and other cannabinoids exhibit antitumour effects in a wide array of animal models of cancer
cannabinoid receptors and their endogenous ligands are both generally upregulated in tumour tissue compared with non-tumour tissue
cb2 promotes her2 (human epidermal growth factor receptor 2) pro-oncogenic signalling in breast cancer
pharmacologic activation of cannabinoid receptors decreases tumour growth
endocannabinoid signalling can also have a tumour-suppressive role
pharmacologic stimulation of cb receptors is, in most cases, antitumourigenic. Nonetheless, a few reports have proposed a tumour-promoting effect of cannabinoids
most prevalent effect is the induction of cancer cell death by apoptosis and the inhibition of cancer cell proliferation
impair tumour angiogenesis and block invasion and metastasis
thc and other cannabinoids induce the apoptotic death of glioma cells by cb1- and cb2-dependent stimulation
Autophagy is primarily a cytoprotective mechanism, although its activation can also lead to cell death
autophagy is important for cannabinoid antineoplastic activity
autophagy is upstream of apoptosis in the mechanism of cannabinoid-induced cell death
the effect of cannabinoids in hormone- dependent tumours might rely, at least in part, on the ability to interfere with the activation of growth factor receptors
glioma cells), pharmacologic blockade of either cb1 or cb2 prevents cannabinoid-induced cell death with similar efficacy
other types of cancer cells (pancreatic48, breast24, or hepatic43 carcinoma cells, for example), antagonists of cb2 but not of cb1 inhibit cannabinoid antitumour actions
thc promotes cancer cell death in a cb1- or cb2-dependent manner (or both) at lower concentrations
cannabidiol (cbd), a phytocannabinoid with a low affinity for cannabinoid receptors15, and other marijuana-derived cannabinoids57 have also been proposed to promote the apoptotic death of cancer cells acting independently of the cb1 and cb2 receptors
In cancer cells, cannabinoids block the activation of the vascular endothelial growth factor (vegf) pathway, an inducer of angiogenesi
In vascular endothelial cells, cannabinoid receptor activation inhibits proliferation and migration, and induces apoptosis
cb1 or cb2 receptor agonists (or both) reduce the formation of distant tumour masses in animal models of both induced and spontaneous metastasis, and inhibit adhesion, migration, and invasiveness of glioma64, breast65,66, lung67,68, and cervical68 cancer cells in culture
the ceramide/p8–regulated pathway plays a general role in the antitumour activity of cannabinoids targeting cb1 and cb2
cbd, by acting independently of the cb1 and cb2 receptors, produces a remarkable anti-tumour effect—including reduction of invasiveness and metastasis
cannabinoids can also enhance immune system–mediated tumour surveillance in some contexts
ability of thc to reduce inflammation75,76, an effect that might prevent certain types of cancer
recent observations suggest that the combined administration of cannabinoids with other anticancer drugs acts synergistically to reduce tumour growth
combined administration of gemcitabine (the benchmark agent for the treatment of pancreatic cancer) and various cannabinoid agonists synergistically reduced the viability of pancreatic cancer cells
Other reports indicated that anandamide and HU-210 might also enhance the anticancer activity of paclitaxel89 and 5-fluorouracil90 respectively
Combined administration of thc and cbd enhances the anticancer activity of thc and reduces the dose of thc needed to induce its tumour growth-inhibiting activity
Preclinical animal models have yielded data indicating that systemic (oral or intraperitoneal) administration of cannabinoids effectively decreases tumour growth
Combinations of cannabinoids with classical chemotherapeutic drugs such as the alkylating agent temozolomide (the benchmark agent for the management of glioblastoma80,84) have been shown to produce a strong anticancer action in animal models
pharmacologic inhibition of egfr, erk83, or akt enhances the cell-death-promoting action of thc in glioma cultures (unpublished observations by the authors), which suggests that targeting egfr and the akt and erk pathways could enhance the antitumour effect of cannabinoids
Good review of the mixed pathway of hormones in cancer development--prostate. Estrogens, through estrogen receptors, promote prostate cancer development and growth.
Endurance training increases GH more than resistance and sprints/short interval training. This increase in GH, though seen in all age groups, decreased in older aged men.