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Falsodex (anti-estrogen and anti-progestin)
- Thread starter LT3
- Start date
macrophage69alpha
New member
LT3 said:
the effects that you are describing are going to be very similar. basically because of E deprivation (either by blocking or inhibition of aromatase).
see here
Br J Cancer. 2006 Mar 14; [Epub ahead of print] Related Articles, Links
Proliferation, steroid receptors and clinical/pathological response in breast cancer treated with letrozole.
Miller WR, White S, Dixon JM, Murray J, Renshaw L, Anderson TJ.
1The Edinburgh Breast Unit, Western General Hospital, Edinburgh EH4 2XU, UK.
Sixty-three postmenopausal women with large primary breast cancers were treated with neoadjuvant letrozole (2.5 mg daily) for 3 months. Tumour samples were taken at diagnosis and after 10-14 days and 3 months treatment. Immunohistochemical staining for Ki67, oestrogen receptor (ER) and progesterone receptor (PgR) was performed and related to clinical (ClinR) and pathological responses (PathR) after 3 months treatment. ClinR was observed in 48 of 63 cases (76.2%) and PathR in 47 of 62 (75.8%). Pretreatment Ki67 scores were similar in responders (R) and non-responders (NR). Highly significant Ki67 decreases occurred in all tumour subgroups at 10-14 days (P<0.005). A significant difference in Ki67 scores at 10-14 days (P<0.007) was found between PathR and PathNR but not between ClinR and ClinNR. At 3 months, decreases from pretreatment Ki67 scores were highly significant in all tumour subgroups irrespective of response status. However, whereas Ki67 scores were significantly different between pathological R and NR (P=0.009), the corresponding comparison of ClinR status was not. Significant decreases between 10-14 days and 3 months were found only in ClinR and PathR (P=0.02 and 0.045, respectively). Treatment significantly reduced PgR expression at 14 days and 3 months (both P<0.0001), but the level of changes was not different between response status groups. In summary, letrozole produces rapid and profound decreases in expression of Ki67 and PgR but changes do not always correlate with clinical and pathological responses.British Journal of Cancer advance online publication, 14 March 2006; doi:10.1038/sj.bjc.6603001 www.bjcancer.com.
though not arguing that its not effective, just that you will see similar effects to likley rather severe oestrogen suppression (though hard to say since dosing for AAS users has not really been even experimentally addressed)
Curr Top Med Chem. 2006;6(3):195-216. Related Articles, Links
Estrogen receptors as therapeutic targets in breast cancer.
Ariazi EA, Ariazi JL, Cordera F, Jordan VC.
Fox Chase Cancer Center, Philadelphia, PA 19111-2497 USA. [email protected].
The estrogen receptor alpha (ERalpha) has proven to be the single most important target in breast cancer over the last 30 years. The use of the selective ER modulator (SERM) tamoxifen for the treatment and prevention of breast cancer has changed therapeutics. The SERM raloxifene, approved for the treatment of osteoporosis, lacks tamoxifen's increased risk for endometrial cancer and is being evaluated for the prevention of breast cancer. Other SERMs approved or under development for use against breast cancer or osteoporosis include toremifene, GW5638, GW7604 (the active metabolite of GW5638), idoxifene, lasofoxifene, arzoxifene, bazedoxifene, EM-800 and acolbifene (the active metabolite of EM-800). Aromatase inhibitors (AIs) have recently proven to be more efficacious than tamoxifen as first-line therapy, efficacious for second-line therapy (e.g. against tamoxifen-resistant disease), and useful for extended adjuvant therapy after tamoxifen. The AIs include the non-steroidal agents letrozole and anastrole, and the steroidal agent exemestane. The pure antiestrogen fulvestrant has proven to be just as effective as AIs. Other pure antiestrogens, ZK-703, ZK-253, RU 58668 and TAS-108 show great promise. The development of resistance to endocrine therapy remains a clinically important problem, and laboratory models based on human breast cancer cells grown as tumors in immune-compromised mice have led to important insights into this problem. Progesterone receptor-negative status of ER-positive breast cancers may reflect altered growth factor receptor signaling, and helps to explain why this subclass of tumors exhibits lower response rates to tamoxifen compared to cancers typed progesterone receptor-positive. Crosstalk among plasma membrane-localized ER, growth factor receptor signaling, and nuclear-localized ER provide further insights into antihormonal-resistant breast cancer.
macrophage69alpha
New member
LT3 said:
YES.... EXCEPT in cases where you have a promiscuous ligand. For instance like a progestin that binds to the ER. though aspect of many AAS has not been explored (so it would just be a guess which ones did-- IF ANY)
there are also probably other limited cases, perhaps with ultra, ultra high doses where you have receptor cross reactivity, where it might be quite different.
macrophage69alpha
New member
LT3 said:
in truth, completely unknown.
likely yes, but for the above reason (promiscuos ligand) faslodex might be better. though if better, likely only slightly.
as a point of reference the ER binding of MENT 7alpha-methyl-19-nortestosterone is 1/200 of estradiol.
macrophage69alpha
New member
LT3 said:
hey,
searching and discussion are how new methods and ideas are found.
and there may be benefits to it when used with progestins (its just not clear how much- from the MENT not much, but other progestins may have much higher binding potentials)
