Why anti‑estrogen therapy fails in ovarian cancer, and how to make it work
Mutant p53 proteins bind estrogen receptors and block estrogen signaling, driving resistance to anti‑estrogen therapy in ovarian cancer; silencing mutant p53 or using p53‑restoring drugs such as rezatapopt can resensitize tumors to hormone therapy, offering a promising combination treatment strategy.
Anti‑estrogen therapy often fails in high‑grade serous ovarian cancer because mutant p53, present in 96% of cases, disrupts estrogen receptor signaling and drives resistance. Silencing mutant p53 or using drugs like rezatapopt to restore p53 function can resensitize tumors to hormone therapy, suggesting a promising combination treatment strategy.
High‑grade serous ovarian cancer has a high relapse rate and limited effective therapies; understanding the mechanisms of endocrine resistance can improve treatment options and patient outcomes.
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