Growth Hormone - Science topic

Hi,

Here are a few references which could be of help to you:

Hashiguchi Y, Molina PE, Fan J, Lang CH, Abumrad NN. Central opiate modulation of growth hormone and insulin-like growth factor-I. Brain Res Bull. 1996;40(2):99-104. doi: 10.1016/0361-9230(96)00045-7. PMID: 8724426.

Barb CR, Kraeling RR, Rampacek GB. Opioid modulation of FSH, growth hormone and prolactin secretion in the prepuberal gilt. J Endocrinol. 1992 Apr;133(1):13-9. doi: 10.1677/joe.0.1330013. PMID: 1517702.

Guido M, Romualdi D, Mancini A, Lattanzi F, Villa P, Barini A, Lanzone A, De Marinis L. Effect of the opioid blockade on the feeding-induced growth hormone response to growth hormone-releasing hormone in women with polycystic ovary syndrome. Fertil Steril. 2002 Nov;78(5):994-1000. doi: 10.1016/s0015-0282(02)04201-2. PMID: 12413983.

Stop using UREA as source of nitrogen and replace with other source with is cool to the dates

Rivera JD. et al 2022. Determination of gibberellic acid and abscisic acid in (Zea mays L.) (ICA-V305) seeds germinated using dynamic sonication assisted solvent extraction and maceration. MethodsX, 9.

https://doi.org/10.1016/j.mex.2022.101821.

Would you have preferred plants to produce their own growth hormones? Plants are soil-growing biological systems and soil microorganisms make or mar the soil for plants of diverse kinds. Planks obtain the most essential nutrients from their environment (soil) by simply sourcing for them just like every other life form. It is important to note that microbes that synthesize plant growth hormones do not set out to do so to help plants. The compound very frequently is, first and foremost, of physiological and/or ecological value to the producing microbe. Microbes are not that generous you know.

A method for the quantitative determination of gibberellic acid in fermentation media, using descending paper chromatography in butylacetate-water.

Also check..

I just realized that 1 Dalton = 1g/mol. Therefore, to convert the nM wouldn't I have to multiply the nM by 22000g/mol x 1L/10^3mL to get ng/mL?

Why did you say multiply by 3?

The Tropic hormones are the ones that influence the activities of other endocrine glands and are contrasted with non-tropic hormones which directly stimulate the tissue. For example, mammotropin (prolactin) is tropic but cortisol or vasopressin is non-tropic. The other definition that may confuse with tropic is trophic. Trophic hormones have specific growth stimulatory effects (hyperplastic or hypertrophic) on their target tissues. We mean the hormones which end with -tropin is classified as Tropic hormones and have tropic effects. If one hormone stimulates any aspects of growth in one tissue, classifies as trophic hormones. So somatotropin is a tropic and trophic hormone but IGF-1 is only a trophic hormone.

Yes, the main factor may be growth regulator as example and explant type, media type, sugar concentration or medium concentration as secondary factor.

Dear Waleid,

In this case, you need a shuttle vector which contain an origin of replication (2U) and a selectable marker (e.g, antibiotic resistance) for E.coli transformation, beside; the components for replication in yeast which include an origin of replication (e.g, pUC) and a selectable marker such as URA3: a gene that encodes an enzyme for uracil synthesis. A typical vector would be pEYA vector which is suitable for both E. coli and S. cerevisiae.

Best wishes

Please go through the following RG links and PDF attachment.

There animal studies, some showing a increase in growth hormone or the related IGF-1, others show a decrease, so its hard to know what it will do in people, it might be biphasic, dose dependent. Here the abstracts I found:

Am J Vet Res. 2014 Aug;75(8):752-9. doi: 10.2460/ajvr.75.8.752.

Modulation of growth and immunity by dietary supplementation with resveratrol in young chickens receiving conventional vaccinations.

Zhang C1, Tian Y, Yan F, Kang X, Han R, Sun G, Zhang H.

Author information

Abstract

OBJECTIVE:

To determine the effects of resveratrol (RES) on growth and immune status in chickens receiving conventional vaccinations.

ANIMALS:

Two hundred forty 1-day-old layer chickens.

PROCEDURES:

Chickens received conventional vaccinations throughout the study and were randomly assigned to 1 of 4 treatments in 6 replicate pens/treatment. Treatments included 1 control group (basal diet) and 3 experimental groups fed the basal diet plus 200, 400, and 800 mg of RES/kg of diet. At 40 days of age, 1 bird/pen was randomly selected to have blood and tissues collected to determine serum immunity indices; mRNA relative expression of proinflammatory cytokines in splenocytes; mRNA relative expression of nuclear transcription factor-κB, growth hormone receptor, and insulin-like growth factor-1 in hepatocytes; cell proliferation; and apoptosis.

RESULTS:

Average daily gain, antibody titers against Newcastle disease virus and avian influenza viruses H5 and H9, and insulin-like growth factor-1 expression were quadratically increased with increasing RES concentration. In hepatocytes, growth hormone receptor gene mRNA relative expression was quadratically increased and nuclear transcription factor-κB gene mRNA relative expression was linearly decreased with increasing RES concentration. In splenocytes, nterleukin-1β and tumor necrosis factor-α mRNA relative expression was linearly decreased with increasing RES concentration. Resveratrol supplementation delayed cell proliferation and reduced apoptosis in immunocytes. With increasing RES concentration, proliferation index and relative weight of the thymus, ratio of CD4+ to CD8+ cells, and CD4+ cell count were quadratically increased, and IgM concentration was linearly increased.

CONCLUSIONS AND CLINICAL RELEVANCE:

Dietary resveratrol supplementation improved growth, protected immunocytes against antigen-induced apoptosis, and upregulated immune response in chickens that received conventional vaccinations.

PMID:

25061707

DOI:

10.2460/ajvr.75.8.752

[Indexed for MEDLINE]

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Select item 24570423 2.

Poult Sci. 2014 Jan;93(1):54-62. doi: 10.3382/ps.2013-03423.

Resveratrol induces antioxidant and heat shock protein mRNA expression in response to heat stress in black-boned chickens.

Liu LL1, He JH, Xie HB, Yang YS, Li JC, Zou Y.

Author information

Abstract

This study investigated the effects of dietary resveratrol at 0, 200, 400, or 600 mg/kg of diet on the performance, immune organ growth index, serum parameters, and expression levels of heat shock protein (Hsp) 27, Hsp70, and Hsp90 mRNA in the bursa of Fabricius, thymus, and spleen of 42-d-old female black-boned chickens exposed to heat stress at 37 ± 2°C for 15 d. The results showed that heat stress reduced daily feed intake and BW gain; decreased serum glutathione (GSH), growth hormone, and insulin-like growth factor-1 levels; and inhibited GSH peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities compared with birds subjected to thermo-neutral circumstances. Chickens that were fed diets supplemented with resveratrol exhibited a linear increase in feed intake and BW gain (P < 0.001); serum GSH, growth hormone, and insulin-like growth factor-1 levels (P ≤ 0.01); and GSH-Px, SOD, and CAT activities (P < 0.001) compared with chickens that were fed diets without resveratrol during heat stress. In contrast, serum malonaldehyde concentrations were decreased (P < 0.001) in the chickens fed a resveratrol-supplemented diet. Heat stress also reduced (P < 0.05) the growth index of the bursa of Fabricus and spleen; however, it had no effect on the growth index of the thymus. The growth index of the bursa of Fabricius and spleen increased (P < 0.05) upon heat stress and coincided with an increase in supplemental resveratrol levels. The expression of Hsp27, Hsp70, and Hsp90 mRNA in the bursa of Fabricius and spleen were increased (P < 0.01), but those of Hsp27 and Hsp90 mRNA in thymus were decreased (P < 0.01) under heat stress compared with no heat stress. Resveratrol attenuated the heat stress-induced overexpression of Hsp27, Hsp70, and Hsp90 mRNA in the bursa of Fabricius and spleen and increased the low expression of Hsp27 and Hsp90 mRNA in thymus upon heat stress. The results suggest that supplemental resveratrol improves growth performance and reduces oxidative stress in heat-stressed black-boned chickens by increasing serum growth hormone concentrations and modulating the expression of heat shock genes in organs of the immune system.

KEYWORDS:

antioxidant response; black-boned chicken; heat shock protein; heat stress; resveratrol

PMID:

24570423

DOI:

10.3382/ps.2013-03423

[Indexed for MEDLINE]

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FASEB J. 2013 Apr;27(4):1561-71. doi: 10.1096/fj.12-220129. Epub 2013 Jan 4.

Sirt1 inhibits the transcription factor CREB to regulate pituitary growth hormone synthesis.

Monteserin-Garcia J1, Al-Massadi O, Seoane LM, Alvarez CV, Shan B, Stalla J, Paez-Pereda M, Casanueva FF, Stalla GK, Theodoropoulou M.

Author information

Abstract

Growth hormone (GH) is a major anabolic hormone and the primary regulator of organism growth. Its transcription is triggered by GH-releasing hormone (GHRH) through the transcription factor cAMP response element-binding protein (CREB) and by caloric intake. In contrast, the deacetylase Sirt1 is activated by caloric restriction. Therefore, the present study investigates how Sirt1 affects CREB function and GH synthesis. Sirt1 pharmacological activation with resveratrol (IC₅₀=87 μM) suppressed GHRH-induced GH secretion from rat anterior pituitary cells in vivo and in vitro, while vehicle controls showed no effect. Resveratrol's effects were abolished after knocking down Sirt1 with RNA interference, but not in control scrambled siRNA-transfected rat somatotrophs, confirming the Sirt1 specificity. Sirt1 activation and overexpression suppressed forskolin-induced CREB-Ser(133) phosphorylation, but no effect was seen with vehicle and empty plasmid controls. The deacetylase-dead mutant Sirt1 retained CREB-Ser(133) phosphorylation by keeping protein phosphatase protein phosphatase 1 activity low. Sirt1 activation suppressed glycogen synthase kinase 3 β acetylation, and a mutation on the GSK3β-Lys(205) residue mimicking a hypoacetylated form revealed increased activity. In summary, this is a novel mechanism through which Sirt1 intercepts the cAMP pathway by suppressing CREB transcriptional activation, resulting in decreased GH synthesis.

PMID:

23292070

DOI:

10.1096/fj.12-220129

[Indexed for MEDLINE]

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Carcinogenesis. 2007 Sep;28(9):1946-53. Epub 2007 Aug 3.

Resveratrol suppresses prostate cancer progression in transgenic mice.

Harper CE1, Patel BB, Wang J, Arabshahi A, Eltoum IA, Lamartiniere CA.

Author information

Abstract

Resveratrol, a natural polyphenolic phytochemical, has been reported to act as an antioxidant and provide anticancer activities. We hypothesized that resveratrol would exert a chemopreventive effect against prostate cancer via regulation of sex steroid receptor and growth factor signaling pathways. In the current study, Transgenic Adenocarcinoma Mouse Prostate males were fed resveratrol (625 mg resveratrol per kg AIN-76A diet) or phytoestrogen-free, control diet (AIN-76A) starting at 5 weeks of age. Mechanisms of action and histopathology studies were conducted at 12 and 28 weeks of age, respectively. Resveratrol in the diet significantly reduced the incidence of poorly differentiated prostatic adenocarcinoma by 7.7-fold. In the dorsolateral prostate, resveratrol significantly inhibited cell proliferation, increased androgen receptor, estrogen receptor-beta, and insulin-like growth factor-1 receptor, and significantly decreased insulin-like growth factor (IGF)-1 and phospho-extracellular regulating kinase 1 (phospho-ERK 1). In the ventral prostate, resveratrol significantly reduced cell proliferation and phospho-ERKs 1 and 2, but did not significantly alter insulin-like growth factor-1 receptor and IGF-1. Serum total testosterone, free testosterone, estradiol, dihydrotestosterone and sex hormone-binding globulin (SHBG) concentrations and Simian Virus-40 large T antigen expression in the prostate were not altered in resveratrol-treated mice. Total resveratrol concentration in the blood serum of 12-week-old mice treated for 3 weeks with 625 mg resveratrol per kg diet was 52 +/- 18 nM. The decrease in cell proliferation and the potent growth factor, IGF-1, the down-regulation of downstream effectors, phospho-ERKs 1 and 2 and the increase in the putative tumor suppressor, estrogen receptor-beta, provide a biochemical basis for resveratrol suppressing prostate cancer development.

PMID:

17675339

DOI:

10.1093/carcin/bgm144

[Indexed for MEDLINE]

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Nutr Metab (Lond). 2010 May 10;7:40. doi: 10.1186/1743-7075-7-40.

Subchronic exposure to phytoestrogens alone and in combination with diethylstilbestrol - pituitary tumor induction in Fischer 344 rats.

Jeng YJ1, Kochukov M, Nauduri D, Kaphalia BS, Watson CS.

Author information

Abstract

BACKGROUND:

Subchronic administration of the potent pharmaceutical estrogen diethylstilbestrol (DES) to female Fischer 344 (F344) rats induces growth of large, hemorrhagic pituitaries that progress to tumors. Phytoestrogens (dietary plant estrogens) are hypothesized to be potential tumor inhibitors in tissues prone to estrogen-induced cancers, and have been suggested as "safer" estrogen replacements. However, it is unknown if they might themselves establish or exacerbate the growth of estrogen-responsive cancers, such as in pituitary.

METHODS:

We implanted rats with silastic capsules containing 5 mg of four different phytoestrogens - either coumestrol, daidzein, genistein, or trans-resveratrol, in the presence or absence of DES. We examined pituitary and other organ weights, blood levels of prolactin (PRL) and growth hormone (GH), body weights, and pituitary tissue histology.

RESULTS:

Blood level measurements of the administered phytoestrogens confirmed successful exposure of the animals to high levels of these compounds. By themselves, no phytoestrogen increased pituitary weights or serum PRL levels after 10 weeks of treatment. DES, genistein, and resveratrol increased GH levels during this time. Phytoestrogens neither changed any wet organ weight (uterus, ovary, cervix, liver, and kidney) after 10 weeks of treatment, nor reversed the adverse effects of DES on pituitaries, GH and PRL levels, or body weight gain after 8 weeks of co-treatment. However, they did reverse the DES-induced weight increase on the ovary and cervix. Morphometric examination of pituitaries revealed that treatment with DES, either alone or in combination with phytoestrogens, caused gross structural changes that included decreases in tissue cell density, increases in vascularity, and multiple hemorrhagic areas. DES, especially in combination with phytoestrogens, caused the development of larger and more heterogeneous nuclear sizes in pituitary.

CONCLUSIONS:

High levels of phytoestrogens by themselves did not cause pituitary precancerous growth or change weights of other estrogen-sensitive organs, though when combined with DES, they counteracted the growth effects of DES on reproductive organs. In the pituitary, phytoestrogens did not reverse the effects of DES, but they did increase the sizes and size heterogeneity of nuclei. Therefore, phytoestrogens may oppose some but not all estrogen-responsive tissue abnormalities caused by DES overstimulation, and appear to exacerbate DES-induced nuclear changes.

PMID:

20459739

PMCID:

PMC2881934

DOI:

10.1186/1743-7075-7-40

Free PMC Article

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Thanks Yuan

Your answer is a straight one - increased exercise will increase GH levels and increase muscle mass (assuming you are not consuming excess calories that need to be converted to fat) but GH will also decrease fat deposition. It changes body composition. Look at transgenic pigs with extra GH - lean with virtually no fat. Look at cattle with GH administration - fat stores are preferentially tapped for energy and milk production. Sprague-Dawley rats (fed a moderately high fat diet diverge into 2 populations - obese and obesity resistant. The resistant (i.e. lean) rats have a higher GH production than the obese rats (this is before the diet was fed). So GH was actually protective in this model against obesity. There is lots out there. I had an NIH grant 20 years ago looking at this.

ELISA is the best and safe technique for T3 and T4 determination.

So that it has no effect on bowel motility

From the bottom of my heart - thank-you!!!!

Does the endocrinologist community know about all of this? I feel as though they might not and it seems very important.

I am very grateful for this information and your work.

Sincerely,

Julie

this question is beyond difficult and not amenable to short bytes of reply.

however, the short answer, ethically, if success is the criterion, is a simple NO!

here are 2 of dozens of papers on the subject:

Acta Paediatr. 2001 Jan;90(1):69-73.

Growth hormone in short children: beyond medicine?

Bolt LL(1), Mul D.

Author information:

(1)Department of Medical Ethics, Faculty of Medicine and Health Care, Erasmus

University Rotterdam, The Netherlands.

Comment in

Acta Paediatr. 2001 Jan;90(1):5-6.

The indications for growth hormone (GH) treatment in non-GH-deficient short

children are in debate, with some arguing that this treatment does not belong

solely in the medical domain. We describe three different approaches to the

issue, and argue that neither a disease-oriented nor client-oriented approach is

sufficient. Both lead to withdrawal of medical interventions or to an undesirable

application.CONCLUSION: An approach focusing on suffering as an indication for

treatment of short stature is the most appropriate. The challenge is to develop

proper tools by which to evaluate suffering and the efficacy of GH treatment in

these children in order to relieve or prevent suffering.

PMID: 11227337 [Indexed for MEDLINE]

---------------------

Soc Sci Med. 2015 Apr;131:305-12. doi: 10.1016/j.socscimed.2014.10.015. Epub 2014

Oct 7.

Growth hormone, enhancement and the pharmaceuticalisation of short stature.

Morrison M(1).

Author information:

(1)Centre for Health, Law & Emerging Technologies (HeLEX), Nuffield Department of

Population Health, University of Oxford, Room 120, Rosemary Rue Building, Old

Road Campus, Headington, OX3 7LF Oxford, Oxon, UK. Electronic address:

michael.morrison@dph.ox.ac.uk.

This paper takes the biological drug human Growth Hormone (hGH) as a case study

to investigate processes of pharmaceuticalisation and medicalisation in

configuring childhood short stature as a site for pharmaceutical intervention.

Human growth hormone is considered to have legitimate applications in treating

childhood growth hormone deficiency and short stature associated with other

recognised conditions. It is also regarded by bioethicists and others as a form

of human biomedical enhancement when applied to children with idiopathic or

'normal' short stature. The purpose of this study is not to evaluate whether

treatment of idiopathic short stature is enhancement or not, but to evaluate how

some applications of hGH in treating short stature have come to be accepted and

stabilised as legitimate 'therapies' while others remain contested as

'enhancements'. A comparative, historical approach is employed, drawing on

approaches from medical sociology and Science and Technology Studies (STS) to set

out a socio-technical history of hGH in the US and UK. Through this history the

relative influence and interplay of drivers of pharmaceuticalisation, including

industry marketing and networks of drug distribution, and processes of

medicalisation will be employed to address this question and simultaneously query

the value of enhancement as a sociological concept.

Copyright © 2014 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.socscimed.2014.10.015

PMID: 25455477 [Indexed for MEDLINE]

obviously there is a marked difference but again it depends on alot of exogenous and endogenous factors

Thank you for the follow-up Lea. I did understand you realizing it not being the normal competitive assay, I should have expanded my thought on that. Adding the labeled antigen in a separate step, if it displaces the standard/sample antigen, is competition just the same. Separating the competition into more of a "displacement" scenario could be different depending upon which antigen gets access to the antibody first.

Anyways, it's good to know that modifying wash steps has that impact. Best wishes with the sensitivity end. I've often pondered methods to stop the signal at the low end of the std curve from overwhelming the detection system, essentially blocking the ability to see differences between 80-100%

Dear Muhammad,

In plant physiologie generally is accepted the expérience with living plants;

and plant growth hormones - proteines - were also study in not dry plants.

Best regards,

MTT

Thank you so much!

Please check

1. Christopher J. Romero, Elyse Pine-Twaddell, Daniela. Sima, Ryan S. Miller, Ling He, Fredric Wondisford, and Sally Radovick .Insulin-Like Growth Factor 1 Mediates Negative Feedback to Somatotroph GH Expression via POU1F1/CREB Binding ProteinInteractions. Molecular and Cellular Biology. 2012 .32 ( 21); p. 4258–4269.

2. S. Harvey Extrapituitary growth hormone. Endocr (2010) 38:335–359

3. Sofiya Milman, Derek M. Huffman, and Nir Barzila.The Somatotropic Axis in Human Aging:Framework for the Current State of Knowledge and Future Research. Cell Metabolism 23, June 14, 2016; 980-989.

GH is a fasting hormone become active during sleeping that is why we recommend children sleep early, the the peak of this hormone during sleep is from 12 am to 4 am, also become active during exercise that needs source of energy (glucose). I n malnourished children it was recommended to give them growth GH next to a balanced diet to help lean body mass.

This link of article is very useful

In the most general sense: "human growth hormone, by some cooperative mechanism, produces a conformational change in [membrane proteins (upon interaction with them)]" Sonenberg (1971) PNAS 68:1051-1055.

Lots of methods freely available to you. All it takes is a few minutes (at most) of an Internet search and then the time to read the methods. It's called "research"; it takes some effort and it is not free.

According to pharmacopoeia standard tests, the comparability of production scaled of DS with the standard required  providing the same protein concentration and same buffer. Personally speaking, as per  CQAs you already mentioned (RP, SE, HCD, HCP, ...) that have met the acceptance ranges don't be worried about the color. maybe  related to the buffer components. Try to use the fresh raw materials.

I worked on TC of Himalayan Yew.

Try to read the book of Richard Arteca entitled "Plant Growth Substances: Principles and Application". You will learn more concepts and methods about this topic.

Hi Alan,

Amino Acids are precursors or activators of phytohormones and growth substances. As Methionine is the precursor of ethylene and of growth factors such as spermine and spermidine, which are synsthesized from 5 – Adenosyl Methionine

Tryptophan is precursor for Auxin synthesis.The application of amino acids for foliar use is based on its requirement by plants in general or at critical stages of growth and development. Plants absorb Amino Acids through Stomas and distributes itself in the synthesis of building blocks or as precursor to the respective hormone according to the plant need and acclimatization to environment....

Thank you.

I am assuming you want to make an inject-able form.  Check purity, and indotoxin levels.   I am not sure what indotoxin level will not cause shock it is low. Once you have pure protein.  You generally need to polish your protein on a Q matrix to remove indotoxins.  Tangential flow filtration into sterile PBS, sterile filter.  Everything should be done in a clean room, with proper monitoring, under aseptic conditions.  Everything cleaned with 1 M NaOH for a minimum of 30 minuets.  If you can not a hood will work.  I would be very careful if you are thinking about putting this in anyone.

at present, liposome, nanocapsules are widely used for delivery of growth hormones and peptides.....only thing you have to keep in mind is the polymers used  for the delivery.

PVA and PAA are mostly used ..you can search for preparation of nanocapsules OR liposomes using these polymers.....

Good Luck

You can please refer to the links below to obtain certain valuable informations:-

1. http://link.springer.com/article/10.1023%2FA%3A1005334104110

2. http://www.nature.com/nbt/journal/v3/n2/abs/nbt0285-151.html

3. http://www.google.co.in/patents/US3265579

To my knowledge, several sugar transporter gene mutation and sugar metabolism (such as for some phophatase) mutatiosn will cause this watery endopserm, which could be explained by the block of the conversion of soluble sugar to polysaccharides like amylose and amylopectin. I've never heard about if or how 2,4-D affect rice grouting.

The salmon GH gene was cloned from coho salmon already in 1985 (Sekine et al Proc. Nati. Acad. Sci. USA Vol. 82, pp. 4306-4310, July 1985) and since, the GH sequences of the two salmonid GHs have been cloned in several salmonid species. The easiest way for you to find these sentences is through GeneBank.

The GH gene is primarily expressed in the pituitary gland, so that's the tissue you want to work with, not blood or brain.

I attach two publications from my group where GH expression has been studied in Atlantic salmon, during sexual maturation and smoltification, respectively, but there are a lot of other published papers studying GH gene expression in various other salmonid species.

wow..., interesting question,  agree with Ezzat's suggestion if you think that steroids boosted up muscle development...but it may be worth to see the steroid residues just like a simple common steroid tests for body builder, perhaps?

Instead of Chlorocholine Chloride as a plant growth hormone we can not use choline chloride because choline chloride containd OH group . bur CCC contains Cl group instead of OH wtich is easily polarized  reacts easily with the cellular components of the plant cell regulating growth(size).

Insulin stimulates the type I receptor, and our work, we used a conc. of 50 ng/mL to effect the insulin receptor, but not trigger the IGF receptor.

Thank you...

I want to know this cross talk in breast cancer cells (epithelial cells).

Don't grow them on MS medium.  It is totally unsuitable.  If you look at the literature you will see that most use Q&L or DKW or some special media for Prunus species.  Always start "at the library" and use Google Scholar before you grow a plant.

Dear Babak, I think answer of your question is yes.

There are many published papers which reveal association between excess GH (e.g. Acromegaly) and cancer and indeed it is consider as a risk factor for cancers.

Increase of thyroid cancer risk in Acromegaly:

Pituitary. 2014 Aug;17(4):299-306. doi: 10.1007/s11102-013-0501-5.

Increased thyroid cancer risk in acromegaly.

Dagdelen S1, Cinar N, Erbas T.

Increased CRC(Colorectal cancer) risk in Acromegaly:

Best Pract Res Clin Endocrinol Metab. 2008 Aug;22(4):639-57. doi: 10.1016/j.beem.2008.08.011.

Acromegaly, growth hormone and cancer risk.

Renehan AG1, Brennan BM.

Increase of Brain tumor risk in acromegaly:

Cancer Causes Control. 2002 Jun;13(5):395-400.

Acromegaly and cancer risk: a cohort study in Sweden and Denmark.

Baris D1, Gridley G, Ron E, Weiderpass E, Mellemkjaer L, Ekbom A, Olsen JH, Baron JA, Fraumeni JF Jr.

and http://www.medscape.com/viewarticle/522728

Clin Endocrinol (Oxf). 2006 Feb;64(2):115-21.

Does growth hormone cause cancer?

Jenkins PJ1, Mukherjee A, Shalet SM.

The ability of GH, via its mediator peptide IGF-1, to influence regulation of cellular growth has been the focus of much interest in recent years. In this review, we will explore the association between GH and cancer. Available experimental data support the suggestion that GH/IGF-1 status may influence neoplastic tissue growth. Extensive epidemiological data exist that also support a link between GH/IGF-1 status and cancer risk. Epidemiological studies of patients with acromegaly indicate an increased risk of colorectal cancer,

best

mehdi

You can also try DMSO, use for control as well

Hi, a review of cytokinin methods is listed here:

Megestrol acetate?