Just a portion of the title is already paradoxical, according to mainstream medical dogma. Namely, how can an estrogen antagonist treat triple-negative breast cancer that is supposedly fully immune to any hormonal effects!? Well, maybe the whole idea of hormonal “receptors” as the only mechanism through which hormones exert their effects on cells is rather obsolete/incorrect and requires prompt updating. That is, there is really no such thing as “triple-negative” breast cancer, which was already suggested by another study I posted about in 2021, showing that a strong androgen such as DHT can treat such hormone-insensitive breast tumors. However, the good news does not end there. The study also discovered that the estrogen antagonist is effective against a multitude of other cancer types, which had long been considered non-endocrine tumors. In other words, virtually all major cancer types responsible for the majority of cancer deaths worldwide ARE in fact endocrine cancers and are driven primarily by estrogen signalling. Conversely, administering an estrogen antagonist (in this case ERX-11) may be a viable treatment for most cancers. Rather than using exotic and untested molecules such as ERX-11, interventions such as aspirin, progesterone, vitamins A/E/D/K, tetracycline antibiotics, etc are all viable anti-estrogenic interventions (especially when used in combination) and have the potential to treat 90%+ of the cancer types afflicting humans globally.
“…The Vadlamudi lab studies breast and ovarian cancer progression, including in therapy resistance, with a goal to developing small-molecule inhibitors for therapy-resistant cancers. In 2017, he and his colleagues identified a compound called ERX-11 that targets the estrogen receptor (ER), a protein that drives the vast majority of breast cancers. From a screen of chemical analogs of ERX-11, the researchers identified that a compound called ERX-41 not only killed ER-positive cancers in petri dishes, but also readily killed triple-negative breast cancers (TNBCs), including more than 20 distinct TNBC cell lines. TNBC is a cancer subtype lacking receptors for estrogen, progesterone and human epidermal growth factor 2, and for which there is a paucity of targeted treatments. The researchers expanded these studies to show ERX-41 had activity against a large number of human tumors grown from several of these cell lines in mouse models. In addition, ERX-41 was potent against patient-derived xenografts, as well, causing shrinkage of these human tumors grown in mouse models without affecting normal breast cells or causing any discernible toxicity in these animals. “The safety profile and high therapeutic index of this compound is particularly notable and bodes well for clinical translation,” Dr. Vadlamudi said. Other experiments showed that in addition to ER-positive breast cancers and TNBC, ERX-41 is also effective against other cancer types with elevated endoplasmic reticulum stress, including pancreatic, glioblastoma and ovarian cancers, which all have few effective treatments. The endoplasmic reticulum is a structure in many cell types that performs assorted functions, including manufacture of proteins.”