Zofia Piotrowska, MD, MHS, a medical oncologist at Massachusetts General Hospital and an instructor at Harvard Medical School, discusses treatment strategies for EGFR-mutant non—small cell lung cancer (NSCLC).

The randomized phase III FLAURA trial, which compared osimertinib (Tagrisso) with erlotinib (Tarceva) and gefitinib (Iressa), showed that osimertinib improved progression-free survival and overall survival compared with the first-generation EGFR drugs in patients with metastatic EGFR-mutant NSCLC. The FLAURA trial establishes osimertinib as a standard of care for newly diagnosed EGFR-mutant patients with NSCLC, according to Piotrowska.

Aside from monotherapy, some combination treatments have potential to become a standard of care, including the combination of EGFR inhibitors with VEGF-targeted therapies or with chemotherapy, says Piotrowska. Both of these strategies have shown promise when combined with first-generation EGFR inhibitors, according to Piotrowska, and upcoming trials will look at combinations with osimertinib.

Piotrowska says it is important to identify EGFR-mutant patients early because, even if they have high PD-L1 expression, EGFR inhibitors are the standard treatment. There is risk to starting immunotherapy prior to receiving the results of the EGFR test, because immunotherapy is not an effective treatment for patients with this molecular driver. Additionally, the risks of an EGFR inhibitor can be increased if started after immunotherapy. Therefore, the results of the EGFR test must be received before starting treatment to give EGFR-mutant patients the appropriate TKI, concludes Piotrowska.

"We performed comprehensive testing of NAPRT at the gene expression level, the methylation level, and the protein level, and found that approximately 30% to 40% of patients also have loss of NAPRT expression. [Based on this, we think that NAPRT expression] could be a viable biomarker for [the efficacy of NAMPT inhibitors] going forward."

Juan Vasquez, MD, an assistant professor of Pediatrics (Hematology/ Oncology) and the associate program director of the Pediatrics Hematology/Oncology Fellowship at Yale School of Medicine, discussed research elucidating the potential predictive utility of NAPRT expression due to tumor-specific promoter CpG island methylation for successful responses to NAMPT inhibition in a subset of patients with pediatric rhabdomyosarcoma.

In a preclinical study, Vasquez and colleagues evaluated the role of NAPRT expression as a potential biomarker of sensitivity to NAMPT inhibitors. Approximately 50% of rhabdomyosarcoma models demonstrated loss of NAPRT expression, which conferred marked sensitivity to NAMPT inhibition, Vasquez began. In vitro, NAPRT-deficient cells exhibited profound cell death upon treatment with NAMPT inhibitors at nanomolar concentrations, whereas NAPRT-expressing cells were resistant, he detailed. Notably, the cytotoxic effect of NAMPT inhibitors in NAPRT-expressing models was reversed with the addition of nicotinic acid, suggesting the salvage pathway mediated by NAPRT functionally protects against NAD+ depletion, Vasquez explained.

This mechanistic relationship was validated in vivo using rhabdomyosarcoma mouse models, Vasquez continued. NAPRT-deficient tumors responded robustly to NAMPT inhibition, whereas co-administration of dietary nicotinic acid reversed this therapeutic effect in NAPRT-expressing models, he reported. These findings supported the hypothesis that NAPRT loss renders rhabdomyosarcoma cells dependent on the NAMPT-mediated salvage pathway for NAD+ synthesis, creating a selective vulnerability to NAMPT inhibition, he said.

To assess the clinical relevance of this biomarker, Vasquez and colleagues partnered with the Children’s Oncology Group to access tumor specimens from 109 pediatric patients with rhabdomyosarcoma previously enrolled on cooperative group trials. Comprehensive profiling of these samples—including gene expression, promoter methylation, and protein analysis—revealed that approximately 30% to 40% of tumors lacked NAPRT expression, Vasquez shared. These data suggest that NAPRT loss may be a clinically relevant biomarker to identify patients who are most likely to benefit from NAMPT-targeted therapies and inform the design of future biomarker-driven clinical trials in pediatric rhabdomyosarcoma, he concluded.

“This is a study we’ve been conducting for 7 years. It’s the only study of its kind. We have gone to [approximately] 150 sites in the United States, and we’ve [suggested to hematologists]: If you’re seeing a patient who has cytopenias and in whom you suspect a diagnosis of MDS, enroll them to this study. We received, through the generosity of patients, samples of their bone marrow, clinical data, and quality-of-life data.”

Mikkael A. Sekeres, MD, a professor of medicine and chief of the Division of Hematology in the Leukemia Section at the University of Miami Health System and Sylvester Comprehensive Cancer Center, discussed the design of a study investigating the association between smoking intensity, genetic mutations, and disease progression in patients with myelodysplastic syndrome (MDS). 

Sekeres explained that he and coinvestigators carried out a unique prospective cohort study to assess the relationship between smoking intensity/duration and the quantity/types of genetic mutations detected in patients diagnosed with MDS starting in June 2016. This study was led by Sangeetha Venugopal, MD, MS, of Sylvester Comprehensive Cancer Center. The investigators used prospective data from patients across approximately 150 sites in the United States who were enrolled in the National Heart, Lung, and Blood Institute MDS Natural History Study, Sekeres described. Hematologists were asked to consider enrollment to this study for patients with cytopenias and suspected MDS, he explained. Bone marrow samples, clinical data, and quality-of-life data were collected from 1898 enrolled patients, who were also followed over time, according to Sekeres.

Univariate analyses revealed that the total number of mutations was comparable between smokers and nonsmokers, including within specific disease categories, such as idiopathic cytopenia of undetermined significance, clonal cytopenia of undetermined significance, MDS, MDS/myeloproliferative neoplasm overlap syndrome, and acute myeloid leukemia. Nonetheless, the overall prevalence of mutations was higher in smokers than in nonsmokers, particularly for mutations in gene pathways for chromatin modification (smokers, 15% vs nonsmokers, 11%; P < .01) and RNA splicing (26% vs 19%; P < .001), as well as mutation in individual genes like ASXL1 (12% vs 8%; P < .01), SF3B1 (9% vs 6%; P < .05), U2AF1 (6% vs 3%; P < .05), and ZRSR2 (2% vs 1%; P < .05). Furthermore, multivariable regression models showed that after adjusting for sex, age, and disease group, the average number of mutations was significantly higher among smokers (2.0) vs nonsmokers (1.4; P = .04).

First-Line Maintenance Lurbinectedin

Plus Atezolizumab in ES-SCLC | Image

Credit: © catalin – stock.adobe.com

Frontline maintenance treatment with lurbinectedin (Zepzelca) plus atezolizumab (Tecentriq) improved progression-free survival (PFS) and overall survival (OS) vs atezolizumab alone in patients with extensive-stage small cell lung cancer (ES-SCLC), according to primary results from the phase 3 IMforte trial (NCT05091567) presented at the 2025 ASCO Annual Meeting.1

The median PFS with the doublet (n = 242) was 5.4 months (95% CI, 4.2-5.8) by independent review facility (IRF) assessment vs 2.1 months (95% CI, 1.6-2.7) with the monotherapy (n = 241), translating to a 46% reduction in the risk of disease progression or death (HR, 0.54; 95% CI, 0.43-0.67; 2-sided P < .0001). The 6-month IRF-PFS rates in the respective arms were 41.2% and 18.7%; at 12 months, these rates were 20.5% and 12.0%.

A clinically meaningful OS benefit was also observed with the addition of lurbinectedin to atezolizumab vs atezolizumab alone, at a median of 13.2 months (95% CI, 11.9-16.4) vs 10.6 months (95% CI, 9.5-12.2), respectively (HR, 0.73; 95% CI, 0.57-0.95; 2-sided P = .0174). The 12-month OS rate with the doublet was 56.3% vs 44.1% with the monotherapy.

“IMforte is the first phase 3 study to show PFS and OS improvement with first-line maintenance treatment for ES-SCLC, highlighting the potential of lurbinectedin plus atezolizumab to become a new standard of care [SOC] for first-line maintenance therapy in patients with this aggressive and difficult-to-treat disease,” Luis Paz-Ares, MD, PhD, of Hospital Universitario 12 de Octubre, H12O-CNIO Lung Cancer Unit, Universidad Complutense and Ciberonc, in Madrid, Spain, said in a press briefing ahead of the meeting.

Underscoring the Unmet Need

SCLC represents approximately 15% of all lung cancer cases, and 70% of these cases are extensive-stage disease, according to Paz-Ares. For these patients, SOC treatment is comprised of induction etoposide, platinum, and an immune checkpoint inhibitor (ICI) in the form of atezolizumab or durvalumab (Imfinzi), followed by maintenance treatment with the same ICI. Although patients respond to induction, many will experience early disease progression and poor survival. Earlier phase trials have shown that when lurbinectedin is paired with ICIs, it is active with favorable tolerability.2-4

Shining a Light on IMforte: Eligibility, Treatment, End Points

The global, open-label, randomized, phase 3 trial enrolled patients with ES-SCLC who had not previously received systemic treatment, who did not have central nervous system metastases, and who have an ECOG performance status of 0 or 1 (n = 660). They received induction treatment with atezolizumab plus carboplatin and etoposide for 4 cycles every 3 weeks.

Patients were screened again and those with an ongoing complete response/partial response or stable disease after induction treatment and an ECOG performance status of 0 or 1 went on to receive maintenance treatment (n = 483). These patients were randomly assigned 1:1 to receive 1200 mg of intravenous atezolizumab every 3 weeks with or without 3.2 mg/m2 of lurbinectedin. Treatment continued until disease progression or intolerable toxicity.

Notably, no crossover was allowed. Patients were stratified by performance status (0 vs 1), lactate dehydrogenase (≤ upper limit of normal [ULN] vs > ULN), liver metastases at baseline induction (yes vs no), and receipt of prophylactic cranial irradiation (yes vs no).

The trial’s primary end points were IRF-PFS and OS, and secondary end points comprised investigator-assessed PFS, objective response rate, duration of response, and safety. Efficacy was evaluated from randomization into the maintenance phase of the design. Investigators assessed safety from day 1 of cycle 1 of treatment.

Additional Efficacy Revelations

Investigator-assessed PFS aligned with what was reported with regard to IRF assessment. The median PFS with lurbinectedin plus atezolizumab was 5.4 months vs 2.7 months with atezolizumab monotherapy (stratified HR, 0.55; 95% CI, 0.45-0.68).

Safety Spotlight

All-cause adverse effects (AEs) were reported in 97.1% of those on the combination arm vs 80.8% of those on the monotherapy arm, with 38.0% and 22.1% of these respective effects being grade 3 or 4. Treatment-related grade 3 or 4 AEs were experienced by more patients in the investigative arm vs those in the control arm, at 25.6% vs 5.8%, respectively.

Twelve patients who received the doublet experienced grade 5 AEs vs 6 patients who received the monotherapy; they were treatment related for 2 patients in the investigative arm and 1 patient in the control arm. More serious AEs occurred with the doublet vs the monotherapy (31.0% vs 17.1%).

AEs led to dose interruption or modification of any drug for 38.0% of those in the investigative arm vs 13.8% of those in the control arm; they led to discontinuation of any drug for 6.2% and 3.3% of patients, respectively.

“The safety profile of lurbinectedin plus atezolizumab was manageable, with mostly low-grade AEs and low treatment discontinuation rates,” Paz-Ares said. “No clinically meaningful increase in immune-related AEs was observed [with the addition of lurbinectedin],” he noted.

The most common AEs experienced by at least 10% of those in the lurbinectedin/atezolizumab and atezolizumab-alone arms were nausea (36.4% vs 4.2%), anemia (31.8% vs 6.7%), fatigue (20.2% vs 7.9%), decreased appetite (16.9% vs 6.7%), decreased platelet count (15.3% vs 2.9%), diarrhea (14.0% vs 7.5%), vomiting (13.6% vs 2.5%), asthenia (12.8% vs 6.3%), thrombocytopenia (12.8% vs 1.7%), decreased neutrophil count (12.8% vs 1.3%), constipation (12.0% vs 6.3%), and neutropenia (10.7% vs 1.7%).

“You see a clear increase for those patients treated with lurbinectedin/atezolizumab, particularly AEs related to the lurbinectedin—nausea, vomiting, diarrhea, asthenia, and also some more myelosuppression,” Paz-Ares noted. “Concerning myelosuppression, that was one of the main concerns, we have seen febrile neutropenia only in 1.7% of cases.”

He added that grade 3 or 4 infections and infestations occurred in 6.6% of those who received the doublet vs 5.0% of those who were given the monotherapy.

Topline Takeaway

“I think it’s important to note that at least in the US, lurbinectedin is FDA approved in the second-line setting, and so, with the results of this study, we would anticipate that it would be moved into the first-line maintenance setting—so, moving it into an earlier line before there is progression on the first-line therapy,” Julie R. Gralow, MD, chief medical officer and executive vice president of ASCO, commented. “The study is important because both PFS and OS were increased. But I would point out, while this is a next step, PFS is still quite low in both arms, and we need to work on additional ways of advancing this even further. So, it is a small next step; it is extending the time that the tumor doesn’t progress and the amount of time that the patients are living, but we need to do more research in ES-SCLC, as well.”

Disclosures: Paz-Ares listed no disclosures.

References

1. Paz-Ares L, Borghaei H, Liu SV, et al. Lurbinectedin (lurbi) + atezolizumab (atezo) as first-line (1L) maintenance treatment (tx) in patients (pts) with extensive-stage small cell lung cancer (ES-SCLC): primary results of the phase 3 IMforte trial. Presented at: 2025 ASCO Annual Meeting; May 30-June 3, 2025; Chicago, IL. Abstract 8006.
2. Calles A, Navarro A, Doger de Speville Uribe BG, et al. Lurbinectedin plus pembrolizumab in relapsed SCLC: the phase I/II LUPAR study. J Thorac Oncol. Published online February 10, 2025. doi:10.1016/j.jtho.2025.02.005
3. Aix SP, 2SMALL (NCT04253145) phase I part: lurbinectedine (LUR) in combination with atezolizumab (ATZ) for second line extensive stage small cell lung cancer (ES-SCLC) patients (pts). J Immunother Cancer. 2021;9. doi:10.1136/jitc-2021-SITC2021.464
4. Aix SP, Navarro A, Garcia MEO, et al. Safety and efficacy of lurbinectedin plus atezolizumab as second-line treatment for advanced small-cell lung cancer: results of the 2SMALL phase 1/2 study (NCT04253145). Presented at: 2025 ASCO Annual Meeting; May 30-June 3, 2025; Chicago, IL. Abstract 8013.

"The most pressing question we have right now is the use of CAR T-cell therapy for patients at their first relapse. I don’t believe there is uniformity in opinion in terms of what to do because some [clinicians] still want to see more data and to better understand the risk of certain toxicities, particularly the long-term toxicities."

Rafael Fonseca, MD, director for Innovation and Transformational Relationships, at Mayo Clinic, discussed factors that he considers when selecting a treatment for patients with relapsed/refractory multiple myeloma.

In prior years, understanding the entire possible sequence of therapy was a focus with respect to treatment selection, but now the priority has become selecting the best treatment possible, Fonseca began. This is partially due to the benefit of treatment and duration of response decreasing with each subsequent line of therapy, he continued.

Additionally, with each line of therapy that is given, there is a portion of patients who do not go on to receive more treatment, Fonseca noted. This is frequently due to disease progression, death, or treatment toxicity, he said. Therefore, although reserving certain therapies for later seems logical, this rate of attrition must be factored into treatment selection decisions, he said.

Fonseca noted that a major question that remains is the role of CAR T-cell therapies for patients at their first relapse. In April 2024, the FDA expanded the approval of ciltacabtagene autoleucel (cilta-cel; Carvykti) to include patients with relapsed/refractory multiple myeloma who received at least 1 prior line of therapy, including a proteasome inhibitor and an immunomodulatory agent, and are refractory to lenalidomide (Revlimid). The regulatory decision made the agent the first BCMA-targeted therapy approved for the treatment of patients with multiple myeloma as early as first relapse. Data from the phase 3 CARTITUDE-4 study (NCT04181827), which supported the approval, demonstrated that patients who received cilta-cel experienced a 59% reduction in the risk of disease progression or death compared with standard-of-care treatments.

Some investigators are still waiting for additional data and want to better understand the potential toxicities of CAR T-cell agents in the first-relapse setting, Fonseca said. However, the benefit of these therapies in this setting, particularly in terms of progression-free survival and patient quality of life, are notable, he concluded.

Image Credit: © catalin – stock.adobe.com

Health Canada has approved osimertinib (Tagrisso) with conditions for the treatment of patients with locally advanced, unresectable stage III non–small cell lung cancer (NSCLC) whose tumors harbor EGFR exon 19 deletions or exon 21 L858R substitution mutations—either alone or with other EGFR mutations—and who did not experience disease progression during or after platinum-based chemoradiation.1 Of note, a validated test is necessary to determine EGFR mutation–positive status before a patient receives osimertinib.

The conditional approval of osimertinib was supported by data from the phase 3 LAURA trial (NCT03521154). Findings published in The New England Journal of Medicine revealed that osimertinib reduced the risk of disease progression or death by 84% vs placebo (HR, 0.16; 95% CI, 0.10-0.24; P < .001).2 The median progression-free survival (PFS) was 39.1 months compared with 5.6 months in the osimertinib and placebo arms, respectively, per blinded independent central review (BICR). Furthermore, the 12-month PFS rate was 74% (95% CI, 65%-80%) vs 22% (95% CI, 13%-32%) in the osimertinib and placebo arms, respectively. At 36 months, the overall survival (OS) rates were 84% (95% CI, 75%-89%) vs 74% (95% CI, 57%-85%) in the respective arms (HR, 0.81; 95% CI, 0.42-1.56; P = .53).

“With this approval, we’re now able to offer people living with stage III, EGFR-mutated NSCLC an oral targeted therapy,” Paul Wheatley-Price, MBChB, BSc, MD, associate professor of medicine at the University of Ottawa and medical oncologist at the Ottawa Hospital in Canada, stated in a news release.1 “The LAURA trial demonstrated that with [osimertinib], patients were able to live, on average, for more than 3 years without disease progression, which is an impressive result in this patient population.”

In September 2024, the FDA approved osimertinib for the treatment of adult patients with locally advanced, unresectable stage III NSCLC who have not experienced disease progression during or after concurrent or sequential platinum-based chemoradiation therapy and harbor EGFR exon 19 deletions or exon 21 L858R mutations, as detected by an FDA-approved test.3 The regulatory decision was also based on data from the LAURA trial.

Regarding safety, the incidence of grade 3 or higher adverse effects (AEs) was 35% vs 12% in the osimertinib and placebo arms, respectively.2 Specifically, radiation pneumonitis was reported in 48% and 38%, respectively, of which the majority were grade 1 or 2. No new safety signals emerged. Additionally, the discontinuation rate for osimertinib due to AEs was 8.4%.1 The most common any-grade AEs occurring in at least 10% of patients included diarrhea (35.7%), rash (35.7%), paronychia (23.1%), dry skin (17.5%), stomatitis (15.4%), and pruritus (12.6%). The most common grade 3 or higher AEs caused by treatment were diarrhea (2.1%), radiation pneumonitis (2.1%), and interstitial lung disease (1.4%).

“With the approval of [osimertinib], we have a new approach of managing unresectable stage III NSCLC with EGFR mutations,” Nathalie Daaboul, MD, associate professor at the Centre intégré de cancérologie de la Montérégie at the University of Sherbrooke in Canada, stated in the news release. “The LAURA trial results reinforce the potential benefits of [osimertinib] after chemoradiation, offering hope for extended PFS and improved outcomes, which is good news for patients.”

The double-blind, placebo-controlled study enrolled patients 18 years of age or older with histologically documented NSCLC and predominantly nonsquamous pathology with locally advanced, unresectable stage III disease.4 Patients were randomly assigned to receive oral osimertinib at 80 mg or 40 mg, or placebo at the same dose levels. The primary end point was PFS by BICR; secondary end points included OS, objective response rate (ORR), duration of response, and disease control rate.

“We’re pleased to see that Health Canada has recognized the efficacy of [osimertinib] demonstrated in the LAURA study,” Shem Singh, executive director of Lung Cancer Canada, stated in the press release.1 “The ability for people with lung cancer to have more time living life without their cancer progressing is so important for their quality of life and that of their family, and this new treatment option will be welcome news for those with stage III EGFR-mutated NSCLC.”

References

1. Tagrisso approved (with conditions) in Canada for patients with unresectable, stage III EGFR-mutated non–small cell lung cancer (NSCLC). News release. BioSpace. May 21, 2025. Accessed May 22, 2025. https://www.biospace.com/press-releases/tagrisso-approved-with-conditions-in-canada-for-patients-with-unresectable-stage-iii-egfr-mutated-non-small-cell-lung-cancer-nsclc
2. Lu S, Kato T, Dong X, et al. Osimertinib after chemoradiotherapy in stage III EGFR-Mutated NSCLC. N Engl J Med. 2024;391(7):585-597. doi:10.1056/NEJMoa2402614
3. FDA approves osimertinib for locally advanced, unresectable (stage III) non–small cell lung cancer following chemoradiation therapy. FDA. September 25, 2024. Accessed May 22, 2025. https://www.fda.gov/drugs/resources-information-approved-drugs/fda-approves-osimertinib-locally-advanced-unresectable-stage-iii-non-small-cell-lung-cancer
4. A global study to assess the effects of osimertinib following chemoradiation in patients with stage III unresectable non–small cell lung cancer (LAURA). ClinicalTrials.gov. Updated April 3, 2025. Accessed May 22, 2025. https://clinicaltrials.gov/study/NCT03521154

Breast Cancer | Image Credit:

© Sebastian Kaulitzki – stock.adobe.com

The FDA has granted breakthrough device designation to the EnVisio X1 In-Body Spatial Intelligence System—a next-generation localization platform— for the real-time, non-imaging detection, localization, and surgical navigation of the SmartClip soft tissue marker, tracked surgical instruments, and other compatible tools used for the surgical excision of soft tissue in patients with cancer and other diseases.1

The goal of the device is to enhance surgical precision, minimize positive margins, and reduce the need for re-excisions to improve outcomes for patients undergoing soft tissue excisions in the thoracic and abdominal cavities. EnVisio X1 provides surgeons with real-time, intraoperative localization of the SmartClip and precise positioning and tracking of surgical instruments in relation to the SmartClip and other navigational reference points.

The device is currently not available for commercial sale or clinical use in the United States.

“Receiving breakthrough device designation for EnVisio X1 is a pivotal milestone, not only for Elucent [Medical] but for the future of surgical care,” Jason Pesterfield, chief executive officer of Elucent Medical, stated in a news release. “This recognition reinforces the urgency and potential of our technology to transform the current standard of care by empowering surgeons with real-time localization and surgical navigation tools. Our goal is to redefine what’s possible in minimally invasive surgery—helping patients receive more precise, less invasive interventions that can truly change lives.”

EnVisio X1 is designed to be integrated into current surgical workflows. The SmartClip is a smart fiducial marker placed percutaneously or bronchoscopically that can be permanently implanted to allow for increased flexibility with the logistics of surgery. The SmartClip also has no minimum distance requirements, which could also improve the bracketing solution and allow for surgical approaches to start from any angle.2

When a patient undergoes surgery, the surgical stapler includes the EnVisio SmartSensor X, which tracks the location of the SmartClip and the stapler via real-time 3D guidance to aid in resection and margin control.1 EnVisio X1 is immune to interference from traditional surgical instruments, hematoma, air, or dense tissue, allowing for the device to maintain performance across various tissue types and malignancies.2 The system also provides a spatial field five times greater in depth compared with traditional localization methods.

The device was invented at the University of Wisconsin–Madison and developed by Elucent Medical with the goal of improving the efficiency of efficacy of surgery and decreasing patient stress.3 With current procedures, a small metal clip is left behind during biopsy to mark the location of a tumor, and during surgery, a radiologist will replace a hook wire through the skin to the biopsy clip to guide surgeons to the lesion.

With EnVisio X1, the SmartClip replaces the conventional metal clip, and it can be placed during the biopsy or at any time leading up to surgery. The SmartClip emits a high frequency signal when activated; by providing a continuous, real-time 3D image of the smart clip, surgeons can pick the safest, least disfiguring path to the tumor. Up to 3 SmartClips can be used for multiple targets or to bracket a single target.

In August 2024, Elucent Medical announced that it had partnered with Froedtert and the Medical College of Wisconsin health network to use its advanced in-body spatial intelligence systems for patients with breast cancer undergoing surgery.4

The breakthrough device designation from the FDA is intended to expedite patient access to innovative technologies that could provide improved treatment or diagnosis for life-threatening or irreversibly debilitating conditions.1 The designation opens the door for priority review and active collaboration with device developers to accelerate the path to approval and commercialization.

References

1. Elucent Medical receives FDA breakthrough device designation for EnVisio X1 In-Body Spatial Intelligence™ System. News release. Elucent Medical. May 15, 2025. Accessed May 22, 2025. https://www.globenewswire.com/news-release/2025/05/15/3082333/0/en/Elucent-Medical-Receives-FDA-Breakthrough-Device-Designation-for-EnVisio-X1-In-Body-Spatial-Intelligence-System.html
2. Technology. Elucent Medical. Accessed May 22, 2025. https://elucent.com/technology/
3. 75 years later, UW-Madison inventors aim to replace old-style breast-surgery marker. News release. University of Wisconsin–Madision. January 3, 2020. Accessed May 22, 2025. https://engineering.wisc.edu/news/75-years-later-uw-madison-inventors-aim-replace-old-style-breast-surgery-marker/
4. Elucent Medical announces Froedtert & the Medical College of Wisconsin health network to provide new breast cancer surgical technology. News release. Elucent Medical. August 9, 2024. Accessed May 22, 2025.