Hormone receptor-positive breast cancer is the most common form of the disease, accounting for roughly 70 percent of all breast cancer cases worldwide. These tumors depend on estrogen receptor signaling to grow, which is why the backbone of treatment for metastatic disease combines endocrine therapy, typically an aromatase inhibitor that deprives tumors of estrogen, with a cyclin-dependent kinase 4 and 6 inhibitor, a targeted drug that halts cancer cell division. Although this combination has transformed outcomes for many patients, resistance almost inevitably develops, and once the disease progresses, subsequent therapies tend to be less effective and harder to tolerate. Understanding the molecular seeds of that resistance has become one of the most urgent questions in breast cancer medicine.

One of the most important mechanisms of resistance involves the ESR1 gene itself, which encodes the estrogen receptor alpha protein, the principal molecular target of endocrine therapy. Activating mutations in ESR1 are rare at the time of metastatic diagnosis, but they emerge under the selective pressure of aromatase inhibitor treatment, appearing in roughly 40 percent of patients with recurrent disease who have been previously exposed to endocrine therapy. These mutations lock the estrogen receptor into a permanently active state, allowing cancer cells to proliferate even when estrogen is pharmacologically depleted. Crucially, previous research has shown that ESR1 mutations can be detected in circulating tumor DNA, fragments of tumor genetic material drifting in the bloodstream, a median of approximately six months before radiographic progression becomes apparent.

That lead time matters because two landmark clinical trials have demonstrated that acting on it can change patient outcomes. In the phase 3 PADA-1 study, French investigators showed that switching from an aromatase inhibitor to the selective estrogen receptor degrader fulvestrant, while continuing the CDK4/6 inhibitor palbociclib, upon detection of a rising ESR1 mutation in blood significantly improved progression-free survival, reducing the risk of progression by 39 percent. More recently, the phase 3 SERENA-6 trial demonstrated that switching to camizestrant, a next-generation oral selective estrogen receptor degrader, while maintaining a CDK4/6 inhibitor produced a statistically significant and clinically meaningful benefit in an interim analysis. Together, these trials suggest that ESR1 mutation emergence is not merely a biological curiosity but a genuine clinical decision point.

Yet clinical trials are conducted under idealized conditions, with protocol-mandated serial blood testing and standardized treatment algorithms. What actually happens in ordinary oncology practices across the United States, and what the emergence of ESR1 mutations means for patients treated there, has remained far less certain. To address this gap, a research team led by investigators from Emory University, AstraZeneca, and Flatiron Health conducted a retrospective cohort study of patients diagnosed with ER-positive, HER2-negative metastatic breast cancer between January 2018 and June 2024. The database draws deidentified records from both community and academic oncology practices, offering a portrait of care that closely resembles the average patient experience rather than the rarefied environment of a major cancer center.

The scale of the analysis was substantial. Of 8,581 eligible patients, 7,772, or 91 percent, initiated first-line therapy. Among these, only 17 percent had their tumors tested for ESR1 mutations during first-line treatment, revealing that systematic monitoring for this resistance mechanism is far from routine. The median age of patients was 63 years, about 63 percent were White, 75 percent received care in community rather than academic settings, and the median time from the start of first-line therapy to the first ESR1 test was 7.4 months. Treatment patterns were strikingly similar regardless of mutation status: the combination of an aromatase inhibitor with a CDK4/6 inhibitor was the most common first-line regimen overall, used in 55 percent of all tested patients, 58 percent of those with mutations, and 54 percent of those without.

The clinical consequences of mutation detection, however, were anything but similar. To avoid statistical biases that can distort retrospective analyses, the researchers anchored all outcome measurements to the time of the first ESR1 test rather than the start of therapy, and they used propensity score matching to balance the two groups on key covariates including liver metastases, estrogen receptor expression level, age, duration of prior aromatase inhibitor therapy, and menopausal status. After matching, patients with an ESR1 mutation detected at their first test had a median real-world progression-free survival of just 7.7 months, compared with 13.6 months for those without a detected mutation, a hazard ratio of 0.68. Overall survival told the same story: median overall survival was 32.2 months in the mutation group versus a median that had not yet been reached in the non-mutation group, with a hazard ratio of 0.58, corresponding to a substantially elevated risk of death.

The mutation also reshaped the trajectory of care. A dramatically higher share of patients with detected ESR1 mutations, 84 percent compared with 52 percent, went on to receive second-line therapy during follow-up, and those who did were more likely to receive a CDK4/6 inhibitor combined with fulvestrant, or the oral selective estrogen receptor degrader elacestrant, a drug specifically approved for ESR1-mutated disease. In the unmatched analysis, 23 percent of patients with mutations initiated second-line therapy versus 9 percent of those without. These patterns are consistent with the interpretation that ESR1 mutation emergence marks a biologically aggressive, endocrine-resistant phase of disease that shortens the time clinicians must change course, while also reflecting a growing awareness among oncologists that this mutation calls for mutation-directed treatments.

The study’s authors were careful to acknowledge its limitations. Only a minority of patients were tested at all, and the reasons for testing were unknown, meaning the tested population may not represent all patients with metastatic disease. Testing in routine practice often occurs as part of broader genomic panels searching for actionable alterations in genes such as BRCA1, BRCA2, PIK3CA, AKT1, and PTEN, rather than as longitudinal ESR1 monitoring, and the mix of tissue-based and blood-based assays from different commercial vendors introduces variability in sensitivity that could have caused misclassification. Additionally, real-world progression, defined by clinician documentation rather than standardized RECIST imaging criteria, may not perfectly align with trial endpoints, and residual confounding cannot be excluded despite careful matching. Only about 14 percent of all first-line patients could be included in the survival analyses, raising questions about generalizability.

Even with these caveats, the real-world progression-free survival of 7.7 months following mutation detection closely mirrors the 9.2 months observed in the control arm of SERENA-6, where patients with emerging mutations remained on their original aromatase inhibitor and CDK4/6 inhibitor combination. That convergence between randomized trial data and observational practice is striking: it suggests that patients whose ESR1 mutations are detected but left unaddressed fare just as poorly in the community as they did in trial control arms, while trial patients whose therapy was switched fared better. The message for oncology is becoming difficult to ignore. ESR1 mutation emergence defines a clinically vulnerable, pre-progression window of roughly six to nine months, and the tools to exploit that window, liquid biopsy monitoring and next-generation estrogen receptor degraders, now exist. The remaining challenge, the study’s authors conclude, is figuring out how to weave systematic ESR1 surveillance and timely treatment modification into the everyday fabric of cancer care, so that the warning sign carried in a patient’s bloodstream is never missed.

Subject of Research: Real-world treatment patterns and outcomes of emerging ESR1-mutated ER-positive metastatic breast cancer in the United States.

Article Title: Real-world treatment patterns and clinical outcomes in patients with emerging estrogen receptor 1 (ESR1)-mutated ER+ metastatic breast cancer in the U.S., 2018-2024

Article References: Meisel, J. L., Chen, C., Kris, A., Ru, M., Pham, T., & Roose, J. (2026). Real-world treatment patterns and clinical outcomes in patients with emerging estrogen receptor 1 (ESR1)-mutated ER+ metastatic breast cancer in the U.S., 2018-2024. Breast Cancer Research and Treatment, 219(2), Article 9. https://doi.org/10.1007/s10549-026-08061-w

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DOI: 10.1007/s10549-026-08061-w

Keywords: ESR1 mutations, metastatic breast cancer, endocrine resistance, ER-positive HER2-negative, circulating tumor DNA, CDK4/6 inhibitors, aromatase inhibitors, selective estrogen receptor degraders, real-world evidence, progression-free survival, SERENA-6, PADA-1

Since its inception in 1977 with a modest group of 50 attendees, SABCS has evolved into a cornerstone event uniting a diverse cohort of oncologists, researchers, nurses, and patient advocates committed to innovation in breast cancer research and clinical care. The symposium’s continual growth mirrors the escalating global urgency to address breast cancer’s multifaceted challenges through collaborative scientific endeavors. Its hosting by UT Health San Antonio’s Mays Cancer Center, in partnership with the American Association for Cancer Research (AACR), highlights the integration of cutting-edge research with clinical practice.

The 2025 symposium showcased groundbreaking studies that are reshaping the breast cancer therapeutic landscape. Among these was the presentation on giredestrant, an oral selective estrogen receptor degrader, which demonstrated a statistically significant extension in progression-free survival compared to standard endocrine therapies in early-stage hormone receptor-positive breast cancer. This development emphasizes the maturation of targeted hormone treatments that balance efficacy with improved patient tolerability.

Parallel to advancements in hormone receptor-positive malignancies, SABCS 2025 illuminated progress in treating the notoriously challenging HER2-positive subgroup. Data supporting the addition of tucatinib, a highly selective HER2 tyrosine kinase inhibitor, to existing regimens showed a noteworthy improvement in delaying disease progression. Remarkably, this regimen achieved these clinical benefits while reducing reliance on cytotoxic chemotherapy, thereby potentially mitigating long-term adverse effects and enhancing patients’ quality of life.

Innovative immunotherapeutic approaches also took center stage at the symposium, particularly concerning triple-negative breast cancer (TNBC), a subtype characterized by poor prognosis and limited targeted treatment options. Early-phase trials of a novel vaccine strategy elicited immune responses in 74% of participants, an encouraging signal that harnessing the immune system could pave a viable path toward both treatment and prevention strategies for aggressive breast cancers. These findings catalyze a paradigm shift from conventional therapies to immune-based modalities.

Integral to the symposium’s discourse was the emphasis on the heterogeneity of patient populations, highlighting research that elucidates the unique biological and psychosocial needs of younger breast cancer patients. This segment of attendees underscored the pressing need for personalized treatment regimens that account for the long-term survivorship issues and fertility preservation, factors critically relevant for this demographic. Additionally, lifestyle considerations such as obesity and nutrition emerged as modifiable risk factors that directly influence cancer incidence and treatment responsiveness, steering public health strategies toward integrative oncology.

SABCS 2025 also featured compelling investigations into the pharmacodynamics and therapeutic implications of GLP-1 receptor agonists—commonly prescribed for weight management—in the context of breast cancer care. Presented by fellows from UT Health San Antonio, these studies examined how these agents may affect tumor microenvironment, treatment efficacy, and adverse effect profiles, foreshadowing a nuanced intersection between metabolic therapies and oncologic outcomes.

The symposium’s role extends beyond scientific exchange to act as a powerful catalyst for local and global economic development. The influx of delegates during the four-day event generated over $22.8 million in direct expenditure within San Antonio, catalyzing revenue streams for hotels, dining establishments, and transportation services, while simultaneously supporting thousands of jobs. This economic influx reinforces the symposium’s stature as a vital contributor to the city’s robust $21.5 billion tourism industry and broader economic ecosystem.

Leaders of the Mays Cancer Center eloquently captured the symbiosis between research excellence and community impact during SABCS. Dr. Virginia Kaklamani, co-chair of SABCS, and Dr. Lei Zheng, executive director of the Mays Cancer Center, articulated how the symposium embodies the institution’s commitment to innovative translational research—moving discoveries swiftly from bench to bedside—and reinforces San Antonio’s identity as a global hub for cancer research.

The synthesis of groundbreaking discoveries presented at SABCS precipitates tangible improvements in clinical practice, elucidating the symposium’s role as a fulcrum of innovation that directly benefits patient populations worldwide. Margaret Foti, CEO of AACR, emphasized the gathering’s consistent ability to convene the foremost minds in breast cancer research, fostering a collaborative environment that accelerates the development of novel therapeutic and preventive modalities.

Looking ahead to the 49th annual symposium scheduled for December 8–11, 2026, expectations remain high for continued scientific breakthroughs and interdisciplinary collaboration. As breast cancer remains a leading cause of cancer morbidity and mortality globally, events such as SABCS are indispensable for disseminating knowledge, shaping clinical guidelines, and inspiring the next generation of oncology researchers and clinicians.

UT Health San Antonio’s stewardship of SABCS, alongside AACR’s partnership, exemplifies a model framework for orchestrating events that merge scientific rigor, patient-centered care evolution, and substantial socioeconomic contributions. The Mays Cancer Center’s alignment with MD Anderson Cancer Center further enhances access to advanced therapeutic options, empowering both research innovation and community health outcomes in South Texas and beyond.

In sum, the 2025 San Antonio Breast Cancer Symposium not only catalyzed pivotal advancements across multiple domains of breast cancer research but also demonstrated the intrinsic value of such scientific congregations in fostering global health innovation and fortifying local economies. This confluence of scientific excellence and regional impact positions SABCS as a unique and invaluable institution in the global fight against breast cancer.

Subject of Research: Breast cancer research, including targeted therapies, immunotherapy, and translational science.

Article Title: Groundbreaking Advances at the 2025 San Antonio Breast Cancer Symposium Propel Global Oncology Forward

News Publication Date: March 31, 2026

Web References: https://sabcs.org, https://cancer.uthscsa.edu/, https://uthscsa.edu

Keywords: Breast cancer, oncology, cancer research, clinical research, translational research, drug development, hormone therapy, HER2-positive breast cancer, immunotherapy, triple-negative breast cancer, GLP-1 receptor agonists, breast cancer vaccine

The estrogen receptor has long been recognized as a critical driver of breast cancer proliferation in ER+ tumors. Conventional therapies primarily rely on endocrine treatment strategies that either block the receptor’s activity or reduce estrogen production. However, resistance mechanisms frequently emerge, rendering these treatments less effective over time and leading to disease progression. The new therapeutic paradigm investigated in this phase 1 trial focuses not merely on inhibiting the receptor but on actively degrading it, thereby offering the potential to overcome resistance and achieve more sustained tumor suppression.

At the core of this study lies a class of compounds known as selective estrogen receptor degraders (SERDs). These molecules operate by binding to the estrogen receptor and promoting its degradation via the ubiquitin-proteasome system, effectively eliminating the receptor from cancer cells. This process halts the aberrant signaling cascade that fuels tumor growth. While previous generations of SERDs have shown clinical promise, issues such as suboptimal bioavailability and adverse side effects have limited their widespread use. The investigational drug assessed in this trial represents a significant refinement, demonstrating improved pharmacokinetics and tolerability.

The phase 1 trial enrolled patients with advanced or metastatic ER+/HER2– breast cancer who had exhausted standard treatment options. The primary objectives were to evaluate the safety, tolerability, pharmacokinetics, and preliminary efficacy of the novel ER degrader. Patients received escalating doses of the compound, monitored closely for adverse effects, and underwent comprehensive biomarker analyses to elucidate the drug’s mechanism of action and impact on tumor biology.

Encouragingly, the investigational agent exhibited a favorable safety profile, with most adverse events being mild to moderate and manageable. Importantly, no dose-limiting toxicities emerged during the study, allowing for the identification of an optimal dosing regimen. Pharmacokinetic data revealed that the drug achieved therapeutic plasma concentrations rapidly and maintained them with once-daily oral administration, a noteworthy advantage over previous SERDs requiring more complex dosing strategies.

Preliminary efficacy signals were equally promising, with several patients exhibiting partial responses or stable disease lasting multiple months. These early tumor responses, observed even in heavily pretreated populations, underscore the potential of ER degradation as a viable strategy to circumvent resistance to classical endocrine therapies. Moreover, biomarker assessments confirmed robust downregulation of estrogen receptor expression and suppression of downstream signaling pathways, validating the intended mechanism of therapeutic action.

The implications of these findings resonate strongly within the oncology community. By advancing beyond receptor blockade to receptor elimination, this therapy could redefine the clinical management of ER+ breast cancer, particularly for patients with metastatic disease who face limited options. Although this phase 1 study primarily addresses safety and early efficacy, its results lay the groundwork for larger, randomized trials to establish definitive clinical benefit and elucidate long-term outcomes.

One of the notable scientific achievements of this trial is the integration of cutting-edge molecular diagnostic techniques. High-throughput sequencing, circulating tumor DNA analysis, and advanced imaging modalities were employed to monitor treatment response in real-time and identify molecular correlates of efficacy and resistance. These comprehensive datasets enrich our understanding of tumor heterogeneity and adaptive mechanisms, potentially guiding personalized treatment strategies in the future.

Furthermore, the study’s design exemplifies the growing trend toward precision oncology, wherein therapies are tailored based on individual tumor biology rather than a one-size-fits-all approach. The selective degradation of estrogen receptors targets a fundamental vulnerability specific to ER+ cancers, sparing non-tumor tissues and minimizing systemic toxicity, thereby enhancing the therapeutic window.

The successful implementation of selective ER degradation also stimulates a broader reevaluation of receptor-targeted therapies across cancer types. By harnessing the cell’s own protein degradation machinery, similar strategies could be adapted to target other oncogenic receptors that have historically been challenging to inhibit effectively. This trial thus serves as a proof-of-concept not only for breast cancer treatment but as a beacon for drug development in oncology at large.

While the current findings generate significant optimism, several questions remain to be addressed. The durability of clinical responses, optimal sequencing with other therapeutic modalities, and potential resistance pathways to ER degraders warrant comprehensive investigation. Additionally, identifying predictive biomarkers to select patients most likely to benefit will be crucial for maximizing clinical impact.

Collaboration among academic institutions, pharmaceutical industry partners, and regulatory agencies will be vital to accelerate the development and approval of this promising therapeutic class. The speed and rigor with which this early-phase trial was conducted exemplify the collaborative spirit essential to translating bench science into transformative clinical solutions.

In summary, the phase 1 trial led by Hamilton, Layman, Cosgrove, and colleagues represents a milestone in breast cancer research by demonstrating the feasibility, safety, and preliminary efficacy of ER degradation in advanced ER+/HER2– breast cancer. This novel approach could ultimately reshape treatment paradigms, offering hope to patients confronted with aggressive disease and limited therapeutic options. As the oncology field eagerly anticipates forthcoming phase 2 and 3 studies, the potential to improve survival and quality of life for millions of patients worldwide shines brighter than ever.

The journey from conceptual innovation to clinical application continues, propelled by relentless scientific inquiry and patient-centered research. Selective estrogen receptor degradation stands poised to become an integral weapon in the arsenal against breast cancer, transforming outcomes and exemplifying the power of targeted molecular therapy.

Subject of Research:
Advanced or metastatic estrogen receptor-positive (ER+)/human epidermal growth factor receptor 2-negative (HER2–) breast cancer treatment through selective estrogen receptor degradation.

Article Title:
ER degradation for ER⁺/HER2– advanced or metastatic breast cancer: a phase 1 trial.

Article References:
Hamilton, E., Layman, R.M., Cosgrove, D. et al. ER degradation for ER⁺/HER2– advanced or metastatic breast cancer: a phase 1 trial. Nat Commun (2025). https://doi.org/10.1038/s41467-025-67485-y

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Hormone receptor-positive breast cancers constitute a substantial fraction of breast cancer cases worldwide, often treated initially with endocrine therapies aimed at suppressing estrogen receptor signaling. However, resistance to these therapies frequently arises, leading to disease progression. Fulvestrant, a selective estrogen receptor degrader, has established itself as an essential component in endocrine therapy regimens, particularly in advanced settings. Yet, the development of resistance mechanisms remains a formidable barrier to long-term control. This clinical trial explores the addition of capivasertib—a potent, selective pan-AKT kinase inhibitor—to disrupt intracellular signaling pathways downstream of the phosphoinositide 3-kinase (PI3K)/AKT/mTOR axis, which is often implicated in therapeutic resistance and tumor survival.

The CAPItello-291 trial enrolls a broad patient population characterized by HR-positive and HER2-negative advanced breast cancer, focusing on those with disease progression following prior endocrine therapy. By combining capivasertib with fulvestrant, the study hypothesizes a synergistic effect whereby the blockade of estrogen receptor signaling is reinforced by concurrent inhibition of the AKT-mediated proliferation pathways—a multifaceted assault designed to circumvent the adaptive resistance that typically undermines monotherapy efficacy. This combined regimen represents a targeted therapeutic strategy, harnessing molecular insights into tumor biology to optimize clinical response.

In the context of pharmacodynamics, capivasertib functions by selectively inhibiting AKT, a serine/threonine kinase that acts as a central node transducing survival and growth signals from receptor tyrosine kinases. Dysregulation of the PI3K/AKT/mTOR pathway is frequently observed in breast cancer, and aberrant activation contributes to oncogenesis, cell proliferation, and survival, especially in the context of endocrine resistance. By interfering with AKT activity, capivasertib impairs downstream signaling cascades, potentially sensitizing cancer cells to endocrine agents like fulvestrant.

The Chinese cohort within CAPItello-291 presents an essential opportunity to investigate population-specific pharmacogenomics and drug response profiles. Differences in genetic polymorphisms, tumor mutational landscapes, and pharmacokinetics can influence therapeutic efficacy and safety. Validating the combination therapy’s effectiveness and tolerability in this demographic broadens the universal applicability of treatment recommendations and addresses disparities in clinical outcomes.

Efficacy endpoints in the trial include progression-free survival (PFS), overall response rate (ORR), and clinical benefit rate (CBR), with safety profiles meticulously documented. Preliminary analysis reveals that capivasertib plus fulvestrant significantly extends PFS compared to fulvestrant alone, indicating improved disease control. Encouragingly, the combination exhibits a manageable safety profile, with adverse events consistent with known effects of AKT inhibition and endocrine therapy, such as hyperglycemia, rash, and gastrointestinal symptoms.

From a mechanistic viewpoint, the rationale for targeting the PI3K/AKT/mTOR pathway lies in its critical role in mediating resistance to hormone therapies. Tumor cells frequently activate compensatory survival pathways upon estrogen receptor blockade, with AKT emerging as a central player facilitating cellular adaptation. The dual blockade strategy effectively disrupts the resilience of cancer cells, preventing them from circumventing therapy-induced stress. These molecular insights pave the way for combination regimens becoming standard care in managing resistant breast cancer phenotypes.

Moreover, the integration of biomarker analyses within the trial enhances understanding of patient subgroups most likely to benefit from this therapeutic approach. Genomic alterations such as PIK3CA mutations, PTEN loss, or AKT amplification may serve as predictive markers, allowing for patient stratification and personalized treatment planning. The study’s findings encourage further development of companion diagnostics to optimize patient selection and improve clinical outcomes.

Importantly, the CAPItello-291 findings scoop into an evolving narrative where combination therapies are tailored based on tumor biology rather than histology alone. This paradigm advances precision oncology, shifting away from the one-size-fits-all approach to a more individualized strategy that exploits vulnerabilities within cancer’s molecular circuitry. As a result, patients gain access to more effective treatments with the potential for longer-term remission and improved quality of life.

The trial also underscores the challenges and complexities in translating promising preclinical results into clinical practice. Managing adverse effects requires careful dose optimization and patient monitoring, emphasizing the need for multidisciplinary care involving oncologists, nurses, and supportive care teams. Education on potential side effects and proactive management strategies are critical to maximizing adherence and therapeutic success.

In parallel, the study highlights the critical role of international collaboration in cancer research. By extending trials into diverse populations, researchers can capture variations in disease biology and treatment response, which ultimately refine global treatment guidelines. This inclusive approach ensures that advances in medicine benefit broad patient populations, avoiding regional inequities in outcomes.

The publication of CAPItello-291’s extended data in Nature Communications marks a pivotal contribution to breast cancer literature. It fuels optimism for new therapeutic combinations that may delay or prevent resistance, extending survival in a disease that remains a leading cause of cancer morbidity and mortality among women globally. The knowledge generated propels ongoing drug development pipelines that aim to exploit the vulnerabilities of HR-positive/HER2-negative breast cancer cells.

Furthermore, integrating molecularly targeted agents like capivasertib aligns with the broader oncology movement toward combination regimens that address complex resistance mechanisms. This multifactorial assault strategy differs fundamentally from traditional chemotherapies by sparing normal tissues and focusing therapies precisely on tumor-driven pathways. As such, the therapeutic index improves, offering enhanced efficacy with reduced toxicity.

The extended Chinese cohort findings also provide actionable insights for regulatory bodies considering approval of new drug combinations. They demonstrate robust evidence of clinical benefit within a previously underrepresented population, bolstering confidence in treatment scalability. Regulatory endorsement may facilitate access to these novel therapies, ensuring that patients in various geographic regions can benefit from advances emanating from international research consortia.

Looking ahead, future studies may explore combining capivasertib and fulvestrant with other targeted agents such as CDK4/6 inhibitors or emerging immunotherapies. The evolving understanding of tumor microenvironment and immune modulation opens avenues for integrated treatment approaches that further potentiate anti-tumor responses. The ongoing evolution of therapeutic strategies exemplifies the dynamic nature of breast cancer research.

In conclusion, the CAPItello-291 phase 3 study’s extension to the Chinese cohort affirms the promise of capivasertib combined with fulvestrant as a potent therapeutic duo in HR-positive/HER2-negative advanced breast cancer. By merging molecular targeting with endocrine therapy, this approach addresses the critical clinical challenge of treatment resistance, heralding a new era of precision medicine. These findings set a new benchmark for combination regimens and reinforce the imperative for continued investment in personalized cancer therapies, ultimately improving outcomes for millions of patients worldwide.

Subject of Research: Capivasertib plus fulvestrant treatment efficacy in HR-positive/HER2-negative advanced breast cancer

Article Title: Capivasertib plus fulvestrant in patients with HR-positive/HER2-negative advanced breast cancer: phase 3 CAPItello-291 study extended Chinese cohort

Article References:
Hu, X., Zhang, Q., Sun, T. et al. Capivasertib plus fulvestrant in patients with HR-positive/HER2-negative advanced breast cancer: phase 3 CAPItello-291 study extended Chinese cohort. Nat Commun 16, 4324 (2025). https://doi.org/10.1038/s41467-025-59210-6

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