Transcript
ReachMD Announcer:
You’re listening to Project Oncology on ReachMD. This medical industry feature, titled “Treating ER+/HER2− ESR1m mBC: New EMERALD Subgroup Analyses in CCR,” is developed and sponsored by Stemline Inc. US Medical Affairs. This activity is intended for United States healthcare professionals only.
The US Medical Affairs department of Stemline Inc. is the sole author and copyright owner of this presentation and has paid ReachMD to host this presentation. Stemline is solely responsible for all written and oral content within this presentation.
Dr. Jhaveri has received compensation from the Menarini Stemline US Medical Affairs Department to prepare and present the following information and is speaking on behalf of herself with input from Menarini Stemline.
Here’s your host, Dr. Jennifer Caudle.
Dr. Caudle:
This is Project Oncology on ReachMD, and I’m your host, Dr. Jennifer Caudle. And today, we’ll be discussing a recent publication in Clinical Cancer Research featuring post hoc analyses from the EMERALD trial. The article is titled, “Elacestrant in ER+, HER2− Metastatic Breast Cancer with ESR1-Mutated Tumors: Subgroup Analyses from the Phase III EMERALD Trial by Prior Duration of Endocrine Therapy plus CDK4/6 Inhibitor and in Clinical Subgroups.” Joining me in this conversation is Dr. Komal Jhaveri.
She’s a breast medical oncologist and early drug development specialist at Memorial Sloan Kettering Cancer Center in New York. Dr. Jhaveri is a consultant for Stemline Therapeutics, Inc.
Dr. Jhaveri, welcome to the program.
Dr. Jhaveri:
It’s great to be here today.
Dr. Caudle:
Before we jump into our discussion, let’s review the approved indication for elacestrant.
ReachMD Announcer:
INDICATION
Elacestrant is indicated for the treatment of postmenopausal women or adult men with estrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-negative, ESR1-mutated advanced or metastatic breast cancer with disease progression following at least one line of endocrine therapy.
Please stay tuned to the whole program to hear Important Safety Information.
Dr. Caudle:
Let’s start with some background. Dr. Jhaveri, what are some key challenges in managing patients who progress during first-line therapy for ER-positive/HER2-negative metastatic breast cancer?
Dr. Jhaveri:
Thank you. Such an important question and a really good place to start. For patients with ER-positive/HER2-negative metastatic breast cancer, first-line treatment with endocrine therapy and a CDK4/6 inhibitor is initially highly effective.1–5
However, tumors can then develop resistance to standard-of-care endocrine therapy and patients develop progression of their disease.6–11
And as a result, these tumors can be challenging to treat with standard-of-care options with monotherapy drugs like aromatase inhibitors or fulvestrant.1,12–16 The median progression-free survival with fulvestrant monotherapy after progression on a CDK4/6 inhibitor therapy with endocrine therapy is about two to three months.16,17
One of the main drivers of resistance in this setting are ESR1 mutations.11,18 Unlike intrinsic mutations such as PIK3CA, ESR1 mutations are acquired and may develop during treatment for metastatic disease under the selective pressure of endocrine therapy, namely aromatase inhibitors, which is why they’re rarely detected in early-stage breast cancer.9–11,18,19 ESR1 mutations increase with each disease progression and are found in up to 50 percent of patients after first-line therapy.11,20–24
They are not only associated with endocrine therapy resistance and disease progression, but also with visceral metastases and a worse prognosis.25-29
And this is why managing patients after progression on first-line treatment requires a more targeted approach. This is where therapies like elacestrant have made a difference. Elacestrant is the first oral selective estrogen receptor degrader, or SERD, to show improved efficacy over endocrine monotherapy in the randomized Phase III EMERALD trial, particularly in patients harboring ESR1 mutations.16
Now because these ESR1 mutations predominantly arise in the metastatic disease setting during first-line therapy, and there’s now an approved ESR1-targeting therapeutic, multiple clinical guidelines recommend testing for the emergence of these ESR1 mutations at every disease progression after first-line therapy in the metastatic setting. Recommendations in ESR1 mutation testing are included in guidelines such as The National Comprehensive Cancer Network®, or NCCN, American Society of Clinical Oncology, or ASCO guidelines, and European Society of Medical Oncology, or ESMO guidelines.18,19,30–32
The preferred testing method uses circulating tumor DNA, or what you would call a ctDNA, which is minimally invasive and more sensitive in detecting these ESR1 mutations than a tissue biopsy.19,30–32 Primary archived breast cancer tissue isn’t reliable for detecting ESR1 mutations because these mutations are acquired during endocrine therapy treatment and may not be present in primary tissue samples.30
Dr. Caudle:
With that background in mind, Dr. Jhaveri, let’s turn to the EMERALD trial, which led to the approval of elacestrant. Can you walk us through its design and the key findings on efficacy and safety?
Dr. Jhaveri:
Of course. The phase III EMERALD trial included men and postmenopausal women with ER-positive/HER2-negative advanced or metastatic breast cancer. All participants had previously progressed on the standard-of-care first-line treatment with a CDK4/6 inhibitor plus endocrine therapy.17
Now these patients were randomized to receive either single-agent elacestrant or a standard-of-care endocrine therapy of the investigator’s choice, which included an aromatase inhibitor or fulvestrant. The primary endpoint was progression-free survival, including in patients whose tumors harbored ESR1 mutations.17
In terms of efficacy, for patients with ESR1-mutated tumors, the median progression-free survival was 3.8 months with elacestrant compared to 1.9 months with standard-of-care endocrine therapy. This was statistically significant and represented a hazard ratio of 0.55 with a 95 percent confidence interval of 0.39 to 0.77, demonstrating a 45 percent reduction in the risk of disease progression or death with elacestrant monotherapy.17
In the intention-to-treat population, there was also a statistically significant improvement in progression-free survival; however, these results were primarily attributable to patients in the ESR1-mutated subgroup.16
Most adverse reactions experienced by patients in EMERALD were grade one or two in severity.17
Now looking at the safety of elacestrant, serious adverse reactions occurred in 12 percent of patients who received elacestrant, with musculoskeletal pain reported in 1.7 percent and nausea in 1.3 percent. Fatal adverse events occurred in 1.7 percent of patients in the elacestrant group.17 These most common adverse reactions, seen in at least 10 percent of patients, did include musculoskeletal pain, nausea, fatigue, vomiting, decreased appetite, diarrhea, headache, constipation, abdominal pain, hot flush, and dyspepsia.
Nausea occurred in 35 percent of patients who received elacestrant across all grades, but most cases were mild to moderate.17 Nausea was observed in 19 percent of patients in the standard-of-care arm. Vomiting was 19 percent in the elacestrant arm versus nine percent in the standard-of-care arm. There were no reports of grade four nausea or vomiting on elacestrant.33
Antiemetic use was low across treatment arms: eight percent with elacestrant, and 3.7 percent with fulvestrant, and 10.3 percent with aromatase inhibitors. Taking elacestrant with food may further help reduce nausea, and antiemetics can be used as needed.33
Treatment discontinuations due to adverse reactions were six percent, with dose reductions at three percent and dose interruptions at 15 percent. And the discontinuation rate specifically due to nausea was low at 1.3 percent. The discontinuation rate for musculoskeletal pain was 1.7 percent.17
And so overall, the EMERALD trial showed that elacestrant demonstrated a statistically significant and clinically meaningful improvement in progression-free survival in patients with ESR1-mutated metastatic breast cancer compared to standard-of-care endocrine therapy, but was also generally well-tolerated with manageable safety profile.33
Dr. Caudle:
Now, the EMERALD trial generated a lot of follow-up research. So what questions did these post hoc exploratory analyses aim to answer?
Dr. Jhaveri:
So the post hoc analyses sought to better define treatment selection in subgroups of patients with ESR1-mutated tumors. By evaluating factors like prior treatment duration with endocrine therapy plus a CDK4/6 inhibitor, tumor metastatic sites, and common coexisting mutations or molecular expressions, the analyses explored how these variables may influence elacestrant efficacy. These subgroup analyses aimed to help identify ESR1-mutated tumors that may remain endocrine-sensitive despite acquired resistance to prior endocrine therapy, offering insights that can help inform treatment decisions.33
However, keep in mind that the results of these post hoc analyses were observational in nature and should be interpreted with caution, as there was no prespecified statistical procedure controlling for type one error.33
Now, the first subgroup analysis looked at progression-free survival in patients with tumors harboring detectable ESR1 mutations based on the duration of prior endocrine therapy plus CDK4/6 inhibitors in the advanced or metastatic setting. Patients were grouped by whether they’d had greater than or equal to six months, 12 months, or 18 months of prior therapy. This helped illustrate how the duration of prior treatment with an endocrine therapy, which is often linked to an increased risk of resistance and ESR1 mutations, could impact progression-free survival outcomes with elacestrant compared to standard-of-care endocrine therapy.33
The results showed that a longer duration of prior endocrine therapy plus a CDK4/6 inhibitor was associated with an improvement in progression-free survival with elacestrant compared to standard-of-care endocrine therapy in patients with tumors harboring detectable ESR1 mutations. Patients who’d had at least 12 months of prior endocrine therapy plus a CDK4/6 inhibitor represented about 70 percent of the trial population. And in this population, the median progression-free survival was 8.6 months with elacestrant compared to 1.9 months with standard-of-care endocrine therapy.33
These exploratory findings suggested that in patients with ESR1-mutated tumors, a longer duration of endocrine therapy with CDK4/6 inhibitor treatment may indicate that tumors remain sensitive to some forms of endocrine therapy, such as elacestrant, despite progression on standard-of-care endocrine treatment.33
Dr. Caudle:
And were there any other subgroup analyses we should be aware of?
Dr. Jhaveri:
Yes. So as I mentioned earlier, another post hoc analysis of the EMERALD trial examined subgroups with clinically relevant tumor characteristics, such as metastatic sites and additional mutations. This analysis was conducted in patients with ESR1-mutated tumors who had received at least 12 months of prior endocrine therapy plus a CDK4/6 inhibitor.33
As with other post hoc analyses, these findings were observational and should be interpreted cautiously, as no prespecified statistical procedure controlled for type one error.
This analysis focused on clinically-relevant subgroups, including patients with33:
- Bone metastases,
- Liver and/or lung metastases,
- Three or more metastatic sites versus fewer than three,
- Co-occurring PIK3CA or TP53 mutations,
- HER2-low tumor expression,
And ESR1 mutation variants, including D538G and Y537S/N mutations.
The findings showed that patients with ESR1-mutated tumors who received at least one year of prior endocrine therapy plus CDK4/6 inhibitor had a longer progression-free survival with elacestrant compared to those patients who received standard-of-care endocrine therapy across all clinically relevant subgroups, regardless of metastatic site location or number, coexisting PIK3CA or TP53 gene mutations, HER2-low expression, or ESR1 mutation variant.33
Among patients with bone metastases, the median progression-free survival was 9.1 months with elacestrant compared to 1.9 months with standard-of-care endocrine treatment. Similarly, patients with liver and/or lung metastases had a median progression-free survival of 7.3 months with elacestrant compared to 1.9 months with standard-of-care endocrine therapy.33
When comparing the number of metastatic sites, patients with fewer than three had a median progression-free survival of nine months with elacestrant compared to 1.9 months with standard-of-care, while those with three or more had an even longer median progression-free survival of 10.8 months, compared to just 1.8 months with standard-of-care endocrine therapy.33
The subgroup analyses suggest that elacestrant may be an option for patients with ESR1-mutated, endocrine-sensitive tumors regardless of metastatic site location or number. Even among patients with coexisting mutations, including PIK3CA and TP53, elacestrant demonstrated prolonged median progression-free survival compared to standard-of-care therapy. Patients with coexisting PIK3CA and ESR1 mutations had a median progression-free survival of 5.5 months compared to 1.9 months with standard-of-care endocrine therapy.33
Patients with coexisting TP53 and ESR1 mutations had a median progression free survival of 8.6 months compared to 1.9 months with standard-of-care endocrine therapy.33
However, it should be noted that elacestrant is not indicated for mutations like PIK3CA or TP53.17
These results highlight a potential benefit with elacestrant in patients with tumors harboring coexisting ESR1 and PIK3CA mutations, suggesting that in this subgroup, disease progression after endocrine therapy plus a CDK4/6 inhibitor may still be driven by estrogen receptors.33
And finally, prolonged median progression-free survival results also extended to HER2-low expression and different ESR1 mutations. The benefit observed with elacestrant compared to standard-of-care endocrine therapy wasn’t impacted by the presence of these commonly occurring mutations or molecular expressions.33
While these analyses were exploratory and hypothesis-generating, they suggested that certain tumors with poor prognostic factors may retain endocrine sensitivity to elacestrant. So identifying these characteristics could help guide our selection of patients who are most likely to benefit from elacestrant as a next-line option.33
Dr. Caudle:
For those of you who are just tuning in, you’re listening to Project Oncology on ReachMD. I’m your host, Dr. Jennifer Caudle, and Dr. Komal Jhaveri and I are discussing a subgroup analysis from the EMERALD trial, published in Clinical Cancer Research. The trial examined elacestrant for ER-positive/HER2-negative ESR1-mutated metastatic breast cancer after progression on endocrine therapy plus CDK4/6 inhibitor.
So Dr. Jhaveri, as we keep exploring the latest data on elacestrant, can you share the updated safety findings from the EMERALD trial?
Dr. Jhaveri:
The analysis showed that safety data for patients with ESR1-mutated tumors by prior endocrine therapy plus CDK4/6 inhibitor duration or clinical and biomarker subgroups were consistent with the safety profile in the overall population. 33
Dr. Caudle:
And as we near the end of our program, Dr. Jhaveri, how could these results help inform treatment strategies moving forward?
Dr. Jhaveri:
Well, clinicians often face uncertainty about the right second-line treatment sequencing after progression on first-line CDK4/6 inhibitors and endocrine therapy. Ideally, in the absence of visceral crisis, we aim to exhaust all endocrine therapy options per clinical guidelines.16,33
In the EMERALD trial, we saw that elacestrant nearly doubled median progression-free survival compared to standard-of-care endocrine therapy—3.8 months compared to 1.9 months—with a manageable safety profile.16 In a post hoc analysis of patients with ESR1 mutations and at least 12 months of prior endocrine therapy plus CDK4/6 inhibitors, elacestrant showed a median progression-free survival of 8.6 months versus 1.91 months.33
These findings suggest that for patients with ESR1-mutated tumors that remain endocrine sensitive, elacestrant may support sequencing in the second-line setting before other targeted therapies or drug combinations and may delay chemotherapy, including antibody-drug conjugates. It’s also important to note that these exploratory analyses in patients with ESR1-mutated tumors who received at least one year of prior endocrine therapy with CDK4/6 inhibitor in the metastatic setting showed consistent benefit with elacestrant compared with standard-of-care endocrine therapy across all clinically relevant subgroups of patients with poor prognostic factors, such as co-mutations or visceral metastases. For example, patients with liver and/or lung metastases saw consistent efficacy with elacestrant.33
Lastly, these results support current guidelines recommending routine testing for ESR1 mutations using ctDNA at each progression to guide treatment decisions.33 I’m looking forward to more data on tailored treatment strategies to optimize care for these patients.
Dr. Caudle:
Well, given those potential impacts, let’s hear some Important Safety Information on elacestrant.
ReachMD Announcer:
IMPORTANT SAFETY INFORMATION
Warnings and Precautions
- Dyslipidemia: Elacestrant may cause hypercholesterolemia and hypertriglyceridemia. Monitor lipid profile prior to starting treatment and periodically thereafter.
- Embryo-Fetal Toxicity: Elacestrant can cause fetal harm. Advise of the potential risk to a fetus and to use effective contraception.
Adverse Reactions
- The most common (≥10%) adverse reactions, including laboratory abnormalities, of elacestrant were musculoskeletal pain, nausea, increased cholesterol, increased AST, increased triglycerides, fatigue, decreased hemoglobin, vomiting, increased ALT, decreased sodium, increased creatinine, decreased appetite, diarrhea, headache, constipation, abdominal pain, hot flush, and dyspepsia.
Drug Interactions
- Concomitant use with strong and moderate CYP3A4 inducers and/or inhibitors: Avoid concomitant use with elacestrant.
Use in Specific Populations
- Lactation: Advise not to breastfeed.
- Hepatic Impairment: Avoid use in patients with severe hepatic impairment (Child-Pugh C). Reduce the dosage for patients with moderate hepatic impairment (Child-Pugh B).
Dr. Caudle:
And as that brings us to the end of our program, I’d like to thank my guest, Dr. Komal Jhaveri, for helping us better understand these analyses of elacestrant in patients with metastatic or advanced ER-positive/HER2-negative breast cancer. Dr. Jhaveri, it was great speaking with you today.
Dr. Jhaveri:
Thank you so much for having me, it was a pleasure.
Announcer Close
This medical industry feature was sponsored by Stemline Inc., US Medical Affairs. Copyright 2025 Stemline Inc., a Menarini Group company. All rights reserved.
If you missed any part of this discussion or to find others in this series, visit Project Oncology on ReachMD.com, where you can Be Part of the Knowledge.
References:
- Burstein HJ, Somerfield MR, Barton DL, et al. Endocrine treatment and targeted therapy for hormone receptor–positive, human epidermal growth factor receptor 2–negative metastatic breast cancer: ASCO Guideline update. J Clin Oncol. 2021;39(35):3959-3977. doi:10.1200/JCO.21.01392
- Palbociclib. Package Insert. Pfizer; 2024.
- Ribociclib. Package Insert. Novartis Pharmaceuticals Corporation; 2024.
- Abemaciclib. Package Insert. Lilly USA; 2024.
- Hortobagyi GN, Stemmer SM, Burris HA, et al. Updated results from MONALEESA-2, a phase III trial of first-line ribociclib plus letrozole versus placebo plus letrozole in hormone receptor-positive, HER2-negative advanced breast cancer. Ann Oncol. 2018;29(7):1541-1547. doi:10.1093/annonc/mdy155
- Gennari A, André F, Barrios CH, et al. ESMO Clinical Practice Guideline for the diagnosis, staging and treatment of patients with metastatic breast cancer. Ann Oncol. 2021;32(12):1475-1495. doi:10.1016/j.annonc.2021.09.019
- Rasha F, Sharma M, Pruitt K. Mechanisms of endocrine therapy resistance in breast cancer. Mol Cell Endocrinol. 2021;532:111322. doi:10.1016/j.mce.2021.111322
- Patel R, Klein P, Tiersten A, Sparano JA. An emerging generation of endocrine therapies in breast cancer: a clinical perspective. NPJ Breast Cancer. 2023;9(1):20. doi:10.1038/s41523-023-00523-4
- Rani A, Stebbing J, Giamas G, Murphy J. Endocrine resistance in hormone receptor positive breast cancer–from mechanism to therapy. Front Endocrinol (Lausanne). 2019;10. doi:10.3389/fendo.2019.00245
- Xu X, Pan X, Wang T, et al. Intrinsic and acquired resistance to CDK4/6 inhibitors and potential overcoming strategies. Acta Pharmacol Sin. 2021;42(2):171-178. doi:10.1038/s41401-020-0416-4
- Brett JO, Spring LM, Bardia A, Wander SA. ESR1 mutation as an emerging clinical biomarker in metastatic hormone receptor-positive breast cancer. Breast Cancer Res. 2021;23(1):85. doi:10.1186/s13058-021-01462-3
- Lindeman GJ, Fernando TM, Bowen R, et al. VERONICA: randomized phase II study of fulvestrant and venetoclax in ER-positive metastatic breast cancer post-CDK4/6 inhibitors – efficacy, safety, and biomarker results. Clin Cancer Res. 2022;28(15):3256-3267.
- Osborne CK, Schiff R. Mechanisms of endocrine resistance in breast cancer. Annu Rev Med. 2011;62(1):233-247. doi:10.1146/annurev-med-070909-182917
- Burstein HJ. Systemic therapy for estrogen receptor–positive, HER2-negative breast cancer. New Engl J Med. 2020;383(26):2557-2570.
- Zhao M, Hanson KA, Zhang Y, Zhou A, Cha-Silva AS. Place in therapy of cyclin-dependent kinase 4/6 inhibitors in breast cancer: a targeted literature review. Target Oncol. 2023;18(3):327-358. doi:10.1007/s11523-023-00957-7
- Bidard FC, Kaklamani VG, Neven P, et al. Elacestrant (oral selective estrogen receptor degrader) versus standard endocrine therapy for estrogen receptor–positive, human epidermal growth factor receptor 2–negative advanced breast cancer: results from the randomized phase III EMERALD trial. J Clin Oncol. 2022;40(28):3246-3256. doi:10.1200/JCO.22.00338
- Elacestrant. Package Insert. Stemline Therapeutics; 2023.
- Toy W, Shen Y, Won H, et al. ESR1 ligand-binding domain mutations in hormone-resistant breast cancer. Nat Genet. 2013;45(12):1439-1445. doi:10.1038/ng.2822
- Burstein HJ, DeMichele A, Somerfield MR, Henry NL. Testing for ESR1 mutations to guide therapy for hormone receptor–positive, human epidermal growth factor receptor 2–negative metastatic breast cancer: ASCO Guideline Rapid Recommendation update. J Clin Onc. 2023;41(18):3423-3425.
- Bidard FC, Hardy-Bessard AC, Dalenc F, et al. Switch to fulvestrant and palbociclib versus no switch in advanced breast cancer with rising ESR1 mutation during aromatase inhibitor and palbociclib therapy (PADA-1): a randomised, open-label, multicentre, phase 3 trial. Lancet Oncol. 2022;23(11):1367-1377. doi:10.1016/S1470-2045(22)00555-1
- Santiago Novello RG, Lobo M, Silveira Vilbert M, Sanches SM, Cesca MG. Abstract 220P - Oral selective estrogen receptor degraders for metastatic hormone receptor-positive, HER2 negative breast cancer according to ESR1 mutation: a systematic review and meta-analysis of randomized control trials. ESMO Open. 2023; 8(1 Suppl 4):25. doi:10.1016/j.esmoop.2023.101409.
- Jhaveri K, Jeselsohn R, Ma CX, et al. Imlunestrant with or without everolimus or alpelisib, in ER+, HER2- advanced breast cancer(aBC): results from the phase Ia/b EMBER study. Ann Oncol. 2023;34(Supplement 2):S338-S339.
- Lin NU, Borges VF, Patel MR, et al. Updated results from the phase I/II study of OP-1250, an oral complete estrogen receptor(ER) antagonist(CERAN) and selective ER degrader(SERD) in patients(pts) with advanced or metastatic ER-positive, HER2-negative breast cancer. Ann Oncol. 2023;34(Supplemental 2):S338.
- Bhave MA, Quintanilha JCF, Tukachinsky H, et al. Comprehensive genomic profiling of ESR1, PIK3CA, AKT1, and PTEN in HR(+)HER2(−) metastatic breast cancer: prevalence along treatment course and predictive value for endocrine therapy resistance in real-world practice. Breast Cancer Res Treat. 2024;207(3):599-609. doi:10.1007/s10549-024-07376-w
- Clatot F, Perdrix A, Beaussire L, et al. Risk of early progression according to circulating ESR1 mutation, CA-15.3 and cfDNA increases under first-line anti-aromatase treatment in metastatic breast cancer. Breast Cancer Res. 2020;22(1):56. doi:10.1186/s13058-020-01290-x
- Chandarlapaty S, Chen D, He W, et al. Prevalence of ESR1 mutations in cell-free DNA and outcomes in metastatic breast cancer. JAMA Oncol. 2016;2(10):1310. doi:10.1001/jamaoncol.2016.1279
- Turner NC, Swift C, Kilburn L, et al. ESR1 mutations and overall survival on fulvestrant versus exemestane in advanced hormone receptor–positive breast cancer: a combined analysis of the phase III SoFEA and EFECT Trials. Clin Cancer Res. 2020;26(19):5172-5177. doi:10.1158/1078-0432.CCR-20-0224
- Zundelevich A, Dadiani M, Kahana-Edwin S, et al. ESR1 mutations are frequent in newly diagnosed metastatic and loco-regional recurrence of endocrine-treated breast cancer and carry worse prognosis. Breast Cancer Res. 2020;22(1):16. doi:10.1186/s13058-020-1246-5
- Gerratana L, Fanotto V, Bonotto M, et al. Pattern of metastasis and outcome in patients with breast cancer. Clin Exp Metastasis. 2015;32(2):125-133. doi:10.1007/s10585-015-9697-2
Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Breast Cancer V.2.2025. © National Comprehensive Cancer Network, Inc. 2025. All rights reserved. Accessed March 11, 2025. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way.
- Mosele MF, Westphalen CB, Stenzinger A, et al. Recommendations for the use of next-generation sequencing (NGS) for patients with advanced cancer in 2024: a report from the ESMO Precision Medicine Working Group. Ann Oncol. 2024;35(7):588-606. doi:10.1016/j.annonc.2024.04.005
- Pascual J, Attard G, Bidard FC, et al. ESMO recommendations on the use of circulating tumour DNA assays for patients with cancer: a report from the ESMO Precision Medicine Working Group. Ann Oncol. 2022;33(8):750-768. doi:10.1016/j.annonc.2022.05.520
- Bardia A, Cortés J, Bidard FC, et al. Elacestrant in ER+, HER2− metastatic breast cancer with ESR1 -mutated tumors: subgroup analyses from the phase III EMERALD trial by prior duration of endocrine therapy plus CDK4/6 inhibitor and in clinical subgroups. Clin Cancer Res. 2024;30(19):4299-4309. doi:10.1158/1078-0432.CCR-24-1073
MED-05232 / Copyright 2025. Stemline Therapeutics, Inc. All rights reserved. April 2025
