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Is there any evidence about a relation of cancer development and the use of steroids?
- Thread starter elmerpr
- Start date
solidspine
New member
There are no studies and there is no evidence of the use of gear and cancer or any other disease.
Zero, Nada, nothing,
Zero, Nada, nothing,
macrophage69alpha
New member
anything that increases growth can have carcenogenic effects. Though unaware of any links between testosterone and stomach cancer. so its unlikely that there is a connection
tamoxifen and oral AAS have been linked to non metatstatic liver tumors. That usually recede with cessation of use.
tamoxifen and oral AAS have been linked to non metatstatic liver tumors. That usually recede with cessation of use.
N
niv
Guest
macrophage69alpha said:
so you're sayin that nolva is as bad as oral aas??
M
Mr.X
Guest
I saw something a long time ago that linked anadrol to cancer (direct?). Overall, if you abuse anything, you're going to cause your body harm. It could be aspirin, GH or steroids...
macrophage69alpha
New member
niv said:
hard to say, it may actually be worse. though better or worse likely depends on usage and time duration as well as individual variations. Most studies indicate that issues occur with longer term usage.
things that help with tamoxifen toxicity, taurine, green tea and ppar-alpha agonists (sesapure, fibrates,etc..).
1: Carcinogenesis. 2006 Aug;27(8):1713-20. Epub 2006 Apr 22. Links
Effect of long-term tamoxifen exposure on genotoxic and epigenetic changes in rat liver: implications for tamoxifen-induced hepatocarcinogenesis.Tryndyak VP, Muskhelishvili L, Kovalchuk O, Rodriguez-Juarez R, Montgomery B, Churchwell MI, Ross SA, Beland FA, Pogribny IP.
Division of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Tamoxifen is a non-steroidal anti-estrogen used for the treatment of breast cancer and, more recently, as a chemopreventive agent in healthy women at high risk of developing breast cancer. On the other hand, tamoxifen is a potent hepatocarcinogen in rats, with both tumor-initiating and tumor-promoting properties. There is substantial evidence that hepatic tumors in rats are initiated as a result of formation of tamoxifen-DNA adducts; however, events subsequent to DNA adduct formation are not clear. Recently, it has been demonstrated that genotoxic carcinogens, in addition to exerting genotoxic effects, often cause epigenetic alterations. In the current study, we investigated whether or not the mechanism of tamoxifen-induced hepatocarcinogenesis includes both genotoxic and epigenetic components. Female Fisher 344 rats were fed a 420 p.p.m. tamoxifen diet for 6, 12, 18 or 24 weeks. Hepatic tamoxifen-DNA adduct levels, as assessed by high-performance liquid chromatography and electrospray tandem mass spectrometry, were 580 adducts/10(8) nt at 6 weeks, and increased to approximately 1700 adducts/10(8) nt by 18 weeks. Global liver DNA hypomethylation, as determined by an HpaII-based cytosine extension assay, was increased at all time points, with the maximum increase (approximately 200%) occurring at 6 weeks. Protein expressions of maintenance (DNMT1) DNA methyltransferase and de novo DNA methyltransferases DNMT3a and DNMT3b were decreased at all time points. Likewise, trimethylation of histone H4 lysine 20 was significantly decreased at all time points. In contrast, non-target tissues (i.e. mammary gland, pancreas and spleen) did not show any changes in global DNA methylation or DNA methyltransferase activity. These data indicate the importance of genotoxic and epigenetic alterations in the etiology of tamoxifen-induced hepatocarcinogenesis.
1: Clin Chim Acta. 2006 Aug;370(1-2):129-36. Epub 2006 Feb 23. Links
Attenuation of tamoxifen-induced hepatotoxicity by taurine in mice.Tabassum H, Rehman H, Banerjee BD, Raisuddin S, Parvez S.
Immunotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110 062, India.
BACKGROUND: One of the most attractive approaches to disease prevention involves the use of natural antioxidants to protect tissue against toxic injury. We investigated the modulatory effects of exogenously administered taurine on the toxicity of the anticancer drug tamoxifen with special reference to protection against disruption of drug metabolizing and antioxidant enzymes in Swiss albino mice. METHODS: Male Swiss albino mice were divided into 4 groups. The extent of lipid peroxidation was evaluated in terms of thiobarbituric acid reactive substances formed. The following assays were performed in the hepatic tissue (a) antioxidant enzymes such as superoxide dismutase and catalase, (b) cytochrome P450 content, (c) glutathione-metabolizing enzymes such as glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose 6-phosphate dehydrogenase, and (d) low molecular weight antioxidants (reduced glutathione, ascorbic acid) and protein carbonyl content. RESULTS: Tamoxifen induced lipid peroxidation, protein carbonyl content and inhibited the enzymes of antioxidant defense system. It was also observed that the activities of antioxidant enzymes and glutathione-metabolizing enzymes were considerably stabilized in mice pretreated with taurine. CONCLUSION: Taurine protects the integrity of the hepatic tissue by stabilizing the reactive oxygen species mediated lipid peroxidation and protein carbonyl formation. Additionally taurine may prove to be efficacious as an antioxidant in tamoxifen-induced hepatotoxicity.
1: Toxicology. 2006 Aug 15;225(2-3):109-18. Epub 2006 May 20. Links
Catechin prevents tamoxifen-induced oxidative stress and biochemical perturbations in mice.Parvez S, Tabassum H, Rehman H, Banerjee BD, Athar M, Raisuddin S.
Immunotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), New Delhi 110062, India. [email protected]
Natural antioxidants like catechin are now known to have a modulatory role on physiological functions and biotransformation reactions involved in the detoxification process, thereby affording protection from toxic metabolic actions of xenobiotics. Reactive oxygen intermediates have been demonstrated to play an etiological role in anticancer drug-induced toxicity. This study was performed to explore the modulatory and protective effect of catechin on the toxicity of an anticancer drug, tamoxifen (TAM) with special reference to protection against disruption of glutathione metabolizing and antioxidant enzymes. TAM treatment resulted in a significant increase in the lipid peroxidation (LPO), H(2)O(2) generation and protein carbonyl (PC) contents in the liver and kidney as compared to controls while catechin+TAM-treated group showed significant decrease in LPO levels, H(2)O(2) generation and PC contents in liver and kidney when compared with TAM-treated group. Non-enzymatic antioxidants like reduced glutathione (GSH) and low molecular antioxidants like ascorbic acid (AsA) also showed normalcy due to exogenous catechin administration. Catechin pre-treatment showed restoration in the level of cytochrome P450 (CYP) content and in the activities of glutathione metabolizing enzymes, viz., glutathione-S-transferase (GST), glutathione reductase (GR) and glutathione peroxidase (GPx) and other antioxidant enzymes such as, glucose-6-phosphate dehydrogenase (G6-PD), catalase (CAT) and superoxide dismutase (SOD) in both liver and kidney when compared to TAM-treated animals. The results of the study show that catechin supplementation might be helpful in abrogation of TAM toxicity during chemotherapy. Additionally, it makes it a prophylactic and preventive agent of anticancer drug-induced oxidative stress.
N
niv
Guest
macrophage69alpha said:
oh..
macrophage69alpha said:
I wouldnt say anything that increases growth can be carcinogenic.....there is nothing about several AAS that do not cause the mutations needed to make a cell line malignant. Do malignant cells produce excess groth factors, receptors, cytoplasmic signaling factors, transcription factors.....yes, but in these cases, the genes controling them have been mutated, or tumor supressor genes (p53, RB, BRCA1 ect) have been mutated. It takes a number of mutations to cause cancer. Drugs like anadrol and most likely tamoxofen cause liver cell damage and strain when they are metabolized, this over time can lead to cancer....like how alcohol can over time.....the damage accumulates.
As for prostate cancer.....anadrogens do not cause it, they make it grow faster because of the over expression of androgen receptors (similar to testicle or breast with the HER-1 and 2 receptors, ER and PR positive).
Dont worry, AAS did not cause stomach cancer, it cant, not that type of chemical.
Whats his prognosis if i may ask? Stage? Marker level? Are they resecting?
Intrinsic mutations
i) Cell must be able to leave G1 by itself. It is no longer dependent on external signals from the body to induce its growth. This can occur due to a mutation in a type 1 oncogene, i.e. endothelial growth factor receptor (EGFR) or H-Ras.
ii) Cells must be able to lose their checkpoints, so they can’t be stopped during points of the cell cycle. They must avoid tumor suppressor genes like p53 and retinoblastoma protein which would recognize the cancerous cell and stop its division.
iii) The cell must be able to evade apoptosis, negating any signals that would lead to its death. This can also be due to loss of tumor suppressor genes like p53. p53 is required in any cancer cell for chemotherapy to work. Chemotherapy induces p53 to signal apoptosis. This is a big problem for chemotherapy resistant tumors because then chemotherapy is only harmful to normal cells with no advantage. Example: BCL-2 is an oncogene in B-cell lymphoma that induces a survival phenotype. Since it doesn’t induce growth of the cancerous cells B-cell lymphoma is a slow growing cancer due to the eventual build up of these eternal B-cells.
iv) 90% of cancer cells turn on telomerase which induces resynthesis the ends of chromosomes prevent fraying or loss of DNA. This basically causes the cell to evade aging.
Extrinsic mutations
v) The newly formed tumor must be able to create new blood vessels to feed its mass (angiogenesis). Once a tumor gets to be about 2mm in size the cells in the middle of the tumor don’t have enough oxygen or glucose and they start undergoing metabolic stress and become hypoxic. This hypoxia response synthesizes vascular endothelial growth factor (VEGF) to induce blood vessels to grow towards the starving cells. Once this occurs it’s considered the kiss of death because of (vi).
vi) Tissue invasion/metastasis. Once the blood vessels are formed these same tumors secrete matrix metalloproteinase and enzymes that degrade the basement membrane of the vessels. This initiates the motility and invasion of the tumor into other parts of the body. Once the cancer cells are in the circulation it’s not immediate trouble. 99% of the time they die off. Unfortunately that 1% where they live they can grow into a secondary tumor by invading a different tissue (let’s say liver), dedifferentiating into that tissue (into a liver cell) like it was a stem cell, and then undergoing more mutations (if it wants to, it may not, a cancer cell is much like a woman and Bobby Brown in that it has prerogatives).
7) Evading immune response. there’s a burgeoning field of study that’s looking at the ability of the body to label these cancerous cells as weird things you don’t want. Basically a cancerous cell should be putting out signals that this is one weirdo cell and should be gotten rid of, but it doesn’t so your body doesn’t recognize it as really really wrong. If it did, it would initiate an immune response like it was a foreign body. So there’s the idea of immunotherapy for cancer. There’s study into activate your own immunes system (lymphocytes and dendritic cells) to kill off tumors down to the individual cellular level. Also there are a number of monoclonal antibodies being made to treat cancers due to the variety of unhealthy signals most tumors secrete. Example is the angiogenesis signal (v) that leads to new blood vessels to help the tumor grow.
People who take AAS are most concerned with Intrinsic factor 1. Sure AAS doesnt lead to an actual mutation(unless possible liver cancer that I wont get into right now) so the idea is the same. You are basically just supplying an excessive signal. For examplem activation of a proto-oncogene generally leads to a gain of function, this can be quantitative or qualitative. Quantitative just increases the number of unaltered products via increased gene expression, expression no regulated in response to normal signals and decreased degradation of proteins. But qualitative just produces a modified product via either point mutations, deletions etc. So to just summarize AAS just keep the signal on, so if there is a screw up the tumor will likely grow faster, just like certain cancers are IGF dependant like i believe melanoma is. That was a lot more info then what you asked though....
i) Cell must be able to leave G1 by itself. It is no longer dependent on external signals from the body to induce its growth. This can occur due to a mutation in a type 1 oncogene, i.e. endothelial growth factor receptor (EGFR) or H-Ras.
ii) Cells must be able to lose their checkpoints, so they can’t be stopped during points of the cell cycle. They must avoid tumor suppressor genes like p53 and retinoblastoma protein which would recognize the cancerous cell and stop its division.
iii) The cell must be able to evade apoptosis, negating any signals that would lead to its death. This can also be due to loss of tumor suppressor genes like p53. p53 is required in any cancer cell for chemotherapy to work. Chemotherapy induces p53 to signal apoptosis. This is a big problem for chemotherapy resistant tumors because then chemotherapy is only harmful to normal cells with no advantage. Example: BCL-2 is an oncogene in B-cell lymphoma that induces a survival phenotype. Since it doesn’t induce growth of the cancerous cells B-cell lymphoma is a slow growing cancer due to the eventual build up of these eternal B-cells.
iv) 90% of cancer cells turn on telomerase which induces resynthesis the ends of chromosomes prevent fraying or loss of DNA. This basically causes the cell to evade aging.
Extrinsic mutations
v) The newly formed tumor must be able to create new blood vessels to feed its mass (angiogenesis). Once a tumor gets to be about 2mm in size the cells in the middle of the tumor don’t have enough oxygen or glucose and they start undergoing metabolic stress and become hypoxic. This hypoxia response synthesizes vascular endothelial growth factor (VEGF) to induce blood vessels to grow towards the starving cells. Once this occurs it’s considered the kiss of death because of (vi).
vi) Tissue invasion/metastasis. Once the blood vessels are formed these same tumors secrete matrix metalloproteinase and enzymes that degrade the basement membrane of the vessels. This initiates the motility and invasion of the tumor into other parts of the body. Once the cancer cells are in the circulation it’s not immediate trouble. 99% of the time they die off. Unfortunately that 1% where they live they can grow into a secondary tumor by invading a different tissue (let’s say liver), dedifferentiating into that tissue (into a liver cell) like it was a stem cell, and then undergoing more mutations (if it wants to, it may not, a cancer cell is much like a woman and Bobby Brown in that it has prerogatives).
7) Evading immune response. there’s a burgeoning field of study that’s looking at the ability of the body to label these cancerous cells as weird things you don’t want. Basically a cancerous cell should be putting out signals that this is one weirdo cell and should be gotten rid of, but it doesn’t so your body doesn’t recognize it as really really wrong. If it did, it would initiate an immune response like it was a foreign body. So there’s the idea of immunotherapy for cancer. There’s study into activate your own immunes system (lymphocytes and dendritic cells) to kill off tumors down to the individual cellular level. Also there are a number of monoclonal antibodies being made to treat cancers due to the variety of unhealthy signals most tumors secrete. Example is the angiogenesis signal (v) that leads to new blood vessels to help the tumor grow.
People who take AAS are most concerned with Intrinsic factor 1. Sure AAS doesnt lead to an actual mutation(unless possible liver cancer that I wont get into right now) so the idea is the same. You are basically just supplying an excessive signal. For examplem activation of a proto-oncogene generally leads to a gain of function, this can be quantitative or qualitative. Quantitative just increases the number of unaltered products via increased gene expression, expression no regulated in response to normal signals and decreased degradation of proteins. But qualitative just produces a modified product via either point mutations, deletions etc. So to just summarize AAS just keep the signal on, so if there is a screw up the tumor will likely grow faster, just like certain cancers are IGF dependant like i believe melanoma is. That was a lot more info then what you asked though....
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