We are analyzing https://link.springer.com/article/10.1007/s10555-022-10066-y.

Title:
The race to develop oral SERDs and other novel estrogen receptor inhibitors: recent clinical trial results and impact on treatment options | Cancer and Metastasis Reviews
Description:
Hormonal therapy plays a vital part in the treatment of estrogen receptor–positive (ER +) breast cancer. ER can be activated in a ligand-dependent and independent manner. Currently available ER-targeting agents include selective estrogen receptor modulators (SERMs), selective estrogen receptor degraders (SERDs), and aromatase inhibitors (AIs). Estrogen receptor mutation (ESR1 mutation) is one of the common mechanisms by which breast cancer becomes resistant to additional therapies from SERMs or AIs. These tumors remain sensitive to SERDs such as fulvestrant. Fulvestrant is limited in clinical utilization by its intramuscular formulation and once-monthly injection in large volumes. Oral SERDs are being rapidly developed to replace fulvestrant with the potential of higher efficacy and lower toxicities. Elacestrant is the first oral SERD that went through a randomized phase III trial showing increased efficacy, especially in tumors bearing ESR1 mutation, and good tolerability. Two other oral SERDs recently failed to achieve the primary endpoints of longer progression-free survival (PFS). They targeted tumors previously treated with several lines of prior therapies untested for ESR1 mutation. Initial clinical trial data demonstrated that tumors without the ESR1 mutation are less likely to benefit from the SERDs and may still respond to SERMs or AIs, including tumors previously exposed to hormonal therapy. Testing for ESR1 mutation in ongoing clinical trials and in hormonal therapy for breast cancer is highly recommended. Novel protein degradation technologies such as proteolysis-targeting chimera (PROTACS), molecular glue degrader (MGD), and lysosome-targeting chimeras (LYTACS) may result in more efficient ER degradation, while ribonuclease-targeting chimeras (RIBOTAC) and small interfering RNA (siRNA) may inhibit the production of ER protein.
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Keywords {🔍}

cancer, breast, article, estrogen, google, scholar, receptor, oral, clinical, therapy, fulvestrant, patients, serds, cas, phase, protein, trial, esr, degradation, study, treatment, advanced, mutation, endocrine, journal, research, target, selective, trials, inhibitors, ais, serd, metastatic, oncology, efficacy, elacestrant, palbociclib, degrader, tamoxifen, cdk, versus, protac, tumors, iii, amcenestrant, giredestrant, pfs, proteins, receptorpositive, randomized,

Topics {✒️}

er + /her2 − unresectable loco-regional recurrent er + /her2 − unresectable loco-regional advanced recruits 2ʹ-5ʹ-linked tetra-adenylate hormone-receptor-positive locally advanced er + /her2-negative locally advanced estrogen-receptor positive endocrine-resistant er + /her2 − early breast cancer shou-ching tang exhibits anti-tumor activity er/pr-positive mbc involve early-stage breast cancer erbb2-negative breast cancer her2 − advanced breast cancer gov/archive/csr/1975_2011/ esr-bearing breast cancers er + /her2 − locally advanced er+/her2- locally advanced article download pdf human bag-1/rap46 protein nucleic acid–based tool er + metastatic breast cancer metastatic er + breast cancer hr + metastatic breast cancer nuclear-initiated steroid signaling endocrine-resistant breast cancer growth factor receptors nucleic acid–based agents membrane-initiated steroid signaling lysosome-targeting chimeras evolve enhances protein–protein interactions prevent er + breast cancers ligand-dependent transcription factors selective estrogen modulators open-label multicenter study preferentially inhibits proliferation suppress er + breast cancer catalytic subunit α molecular therapy-nucleic acids targeting egfr/her2/her3 selective estrogen receptor inhibiting er + breast cancer estrogen receptor isoforms/variants anti-her2 therapy tumors expressing wild-type treatment-related adverse events hormone receptor–positive hormone receptor-positive hormone-receptor positive effectively target membrane-bound regulate cell growth

Questions {❓}

Are estrogen receptors cytoplasmic or nuclear?

Schema {🗺️}

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         description:Hormonal therapy plays a vital part in the treatment of estrogen receptor–positive (ER +) breast cancer. ER can be activated in a ligand-dependent and independent manner. Currently available ER-targeting agents include selective estrogen receptor modulators (SERMs), selective estrogen receptor degraders (SERDs), and aromatase inhibitors (AIs). Estrogen receptor mutation (ESR1 mutation) is one of the common mechanisms by which breast cancer becomes resistant to additional therapies from SERMs or AIs. These tumors remain sensitive to SERDs such as fulvestrant. Fulvestrant is limited in clinical utilization by its intramuscular formulation and once-monthly injection in large volumes. Oral SERDs are being rapidly developed to replace fulvestrant with the potential of higher efficacy and lower toxicities. Elacestrant is the first oral SERD that went through a randomized phase III trial showing increased efficacy, especially in tumors bearing ESR1 mutation, and good tolerability. Two other oral SERDs recently failed to achieve the primary endpoints of longer progression-free survival (PFS). They targeted tumors previously treated with several lines of prior therapies untested for ESR1 mutation. Initial clinical trial data demonstrated that tumors without the ESR1 mutation are less likely to benefit from the SERDs and may still respond to SERMs or AIs, including tumors previously exposed to hormonal therapy. Testing for ESR1 mutation in ongoing clinical trials and in hormonal therapy for breast cancer is highly recommended. Novel protein degradation technologies such as proteolysis-targeting chimera (PROTACS), molecular glue degrader (MGD), and lysosome-targeting chimeras (LYTACS) may result in more efficient ER degradation, while ribonuclease-targeting chimeras (RIBOTAC) and small interfering RNA (siRNA) may inhibit the production of ER protein.
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      description:Hormonal therapy plays a vital part in the treatment of estrogen receptor–positive (ER +) breast cancer. ER can be activated in a ligand-dependent and independent manner. Currently available ER-targeting agents include selective estrogen receptor modulators (SERMs), selective estrogen receptor degraders (SERDs), and aromatase inhibitors (AIs). Estrogen receptor mutation (ESR1 mutation) is one of the common mechanisms by which breast cancer becomes resistant to additional therapies from SERMs or AIs. These tumors remain sensitive to SERDs such as fulvestrant. Fulvestrant is limited in clinical utilization by its intramuscular formulation and once-monthly injection in large volumes. Oral SERDs are being rapidly developed to replace fulvestrant with the potential of higher efficacy and lower toxicities. Elacestrant is the first oral SERD that went through a randomized phase III trial showing increased efficacy, especially in tumors bearing ESR1 mutation, and good tolerability. Two other oral SERDs recently failed to achieve the primary endpoints of longer progression-free survival (PFS). They targeted tumors previously treated with several lines of prior therapies untested for ESR1 mutation. Initial clinical trial data demonstrated that tumors without the ESR1 mutation are less likely to benefit from the SERDs and may still respond to SERMs or AIs, including tumors previously exposed to hormonal therapy. Testing for ESR1 mutation in ongoing clinical trials and in hormonal therapy for breast cancer is highly recommended. Novel protein degradation technologies such as proteolysis-targeting chimera (PROTACS), molecular glue degrader (MGD), and lysosome-targeting chimeras (LYTACS) may result in more efficient ER degradation, while ribonuclease-targeting chimeras (RIBOTAC) and small interfering RNA (siRNA) may inhibit the production of ER protein.
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      dateModified:2022-10-14T00:00:00Z
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         Selective estrogen receptor degraders
         Clinical trials
         Protein degradation
         Oral SERDs
         PROTC
         LYTAC
         RIBOTAC
         Aptamers
         Cancer Research
         Oncology
         Biomedicine
         general
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