Targeted Oncology最新文献

{"title":"The Impact of Uncommon HRR Alterations as Predictors of Efficacy of PARP Inhibitors in Metastatic Castration-Resistant Prostate Cancer: A Meta-Analysis of Randomized Controlled Trials.","authors":"Giada Pinterpe, Fortuna Migliaccio, Chiara Ciccarese, Romina Rose Pedone, Rachele Belletto, Pierluigi Russo, Angelo Totaro, Luca Tagliaferri, Chiara Sighinolfi, Luigi Formisano, Rossana Berardi, Bernardo Rocco, Giampaolo Tortora, Roberto Iacovelli","doi":"10.1007/s11523-025-01141-9","DOIUrl":"10.1007/s11523-025-01141-9","url":null,"abstract":"<p><strong>Background: </strong>Metastatic castration-resistant prostate cancer (mCRPC) patients with BRCA1/2 mutations show significant responses to poly-ADP ribose polymerase inhibitors (PARPi), while the efficacy of these agents in patients with homologous recombination repair (HRR) gene alterations other than BRCA remains unclear.</p><p><strong>Objective: </strong>This meta-analysis aimed at assessing the efficacy of PARPi in mCRPC harboring alterations in four rare HRR genes (i.e. CDK12, PALB2, ATM, and CHEK2).</p><p><strong>Patients and methods: </strong>Five randomised phase III trials (PROfound, PROpel, MAGNITUDE, TALAPRO-2, TRITON3) were selected through searching the Medline/PubMed, Cochrane Library, and ASCO Meeting abstracts. Data extraction followed the PRISMA statement. The primary endpoints, radiographic progression-free survival (rPFS) and overall survival (OS) with the relative 95% CI, were calculated using fixed- or random-effects methods, depending on the studies' heterogeneity. RevMan software for meta-analysis (v.5.2.3) was used.</p><p><strong>Results: </strong>PARPi significantly improved rPFS in mCRPC patients with CDK12 alterations (hazard ratio (HR) = 0.65; p = 0.02) without OS benefit. In patients with ATM, CHEK2, or PALB2 alterations, no significant benefit was observed in rPFS or OS. Due to the low incidence of these rare mutations, we grouped them into gene panels, revealing a significant rPFS advantage when CDK12+PALB2 (HR = 0.63; p = 0.009) were combined, and a similar benefit when including CHEK2 in the gene panel (HR = 0.69; p = 0.01).</p><p><strong>Conclusion: </strong>CDK12 alterations could be considered as a predictive biomarker of rPFS benefit with PARPi. A gene panel grouping CDK12 and PALB2 with or without CHEK2 mutations could also enable prediction of rPFS benefit with PARPi.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"405-418"},"PeriodicalIF":4.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144011576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Second-Line Treatment Options for Patients with Metastatic Triple-Negative Breast Cancer: A Review of the Clinical Evidence.","authors":"José Ángel García-Saenz, Álvaro Rodríguez-Lescure, Josefina Cruz, Joan Albanell, Emilio Alba, Antonio Llombart","doi":"10.1007/s11523-024-01125-1","DOIUrl":"10.1007/s11523-024-01125-1","url":null,"abstract":"<p><p>Metastatic triple-negative breast cancer has a poor prognosis and poses significant therapeutic challenges. Until recently, limited therapeutic options have been available for patients with advanced disease after failure of first-line chemotherapy. The aim of this review is to assess the current evidence supporting second-line treatment options in patients with metastatic triple-negative breast cancer. Evidence was reviewed from controlled clinical trials in which eribulin, vinorelbine, capecitabine, gemcitabine, gemcitabine plus carboplatin, fam-trastuzumab-deruxtecan, sacituzumab govitecan, olaparib, and talazoparib were used in the second-line treatment for metastatic breast cancer, either as study drugs or as comparators. The benefit of treatment was evaluated using the European Society for Medical Oncology-Magnitude of Clinical Benefit Scale. Based on the evidence review, sacituzumab govitecan was identified as the preferred second-line treatment option for patients with metastatic triple-negative breast cancer, supported by clinical evidence and consensus across international clinical guidelines. Olaparib and talazoparib are of use in patients with human epidermal growth factor receptor 2-negative metastatic breast cancer and germline BRCA1/2 mutations. Exploratory data for fam-trastuzumab-deruxtecan suggest a survival benefit in human epidermal growth factor receptor 2-low, hormone-receptor-negative patients, but further solid evidence is required. Other chemotherapies with lower European Society for Medical Oncology-Magnitude of Clinical Benefit Scale scores may continue to be useful in highly selected patients.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"191-213"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The User's Guide to Amivantamab.","authors":"Danielle Brazel, Janellen Smith, Sai-Hong Ignatius Ou, Misako Nagasaka","doi":"10.1007/s11523-025-01128-6","DOIUrl":"10.1007/s11523-025-01128-6","url":null,"abstract":"<p><p>Targeted therapies have revolutionized treatment of non-small-cell lung cancer (NSCLC); however, epidermal growth factor receptor (EGFR) exon20ins mutations are resistant to tyrosine kinase inhibitors. Amivantamab utilizes multiple mechanisms of action to bypass the altered binding site conformation and recruits immune cells for anti-cancer activity. Amivantamab is approved in the frontline setting of EGFR exon20ins-mutated NSCLC in combination with carboplatin plus pemetrexed. Single-agent amivantamab is approved in second line or later for EGFR exon20ins. Furthermore, amivantamab with lazertinib for first line as well as amivantamab in combination with carboplatin and pemetrexed for second line after osimertinib have both been approved in the treatment of NSCLC harboring EGFR-sensitizing mutations. Now with multiple indications, we must learn how to manage the unique side effects of amivantamab to maximize treatment benefit for the patients. Side effects of amivantamab can be associated with inhibition of the EGFR and/or mesenchymal epithelial transcription factor (MET) signaling pathways. This work reviews the mechanism of action, pharmacology, clinical trial data, and covers management of toxicities. This guide is designed as a practical reference tool for clinicians, pharmacists, and basic science researchers.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"235-245"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143190709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leveraging the Immunomodulatory Potential of Ibrutinib for Improved Outcomes of T Cell-Mediated Therapies of B Cell Malignancies: A Narrative Review.","authors":"David B Miklos, Peter A Riedell, Alex Bokun, Julio C Chavez, Stephen J Schuster","doi":"10.1007/s11523-025-01133-9","DOIUrl":"10.1007/s11523-025-01133-9","url":null,"abstract":"<p><p>Standard treatment options for B cell malignancies include immunochemotherapies and/or targeted therapies, which often provide temporary disease remission. However, many patients do not achieve complete remission with these treatments, develop resistance, and eventually experience disease relapse. New immunomodulatory treatments, such as T cell-based therapies, show promise in treating various types of blood cancers, including B cell malignancies. However, their effectiveness is often limited by the immunosuppressive tumor microenvironment and altered function of patient-derived T cells. Ibrutinib, a Bruton tyrosine kinase inhibitor, has been shown to restore immune balance and function in patients with chronic lymphocytic leukemia. Ibrutinib is being studied as adjuvant or combinatorial therapy with chimeric antigen receptor (CAR) T cells or T cell-engaging bispecific antibodies for the treatment of B cell malignancies. Current evidence suggests that ibrutinib could be beneficial when used before, during, or after CAR T cell administration, potentially providing higher complete response rates and reduced toxicity. In conclusion, existing evidence strongly supports the combined use of ibrutinib and T cell therapies. However, additional clinical trials are needed to further validate the effectiveness of this treatment strategy in patients with various B cell malignancies.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"217-234"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143543480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Development of ATM Inhibitors in Cancer Therapy.","authors":"Elizabeth A Ampolini, Judit Jimenez-Sainz, David T Long","doi":"10.1007/s11523-025-01136-6","DOIUrl":"10.1007/s11523-025-01136-6","url":null,"abstract":"<p><p>The ataxia-telangiectasia mutated (ATM) protein kinase plays a critical role in activating the cellular response to DNA double-strand breaks and promoting homology-directed repair. ATM is frequently mutated in cancer, contributing to an accumulation of DNA damage that drives genomic instability. To exploit cancer cells' inherent vulnerability to DNA damage, various small molecule inhibitors have been developed that target ATM. ATM inhibitors have shown great versatility in preclinical studies and increasing use in the clinic. Here, we review the development of ATM inhibitors and their role in cancer therapy. We describe their limitations and the advances that have led to increases in both the number and diversity of active clinical trials targeting ATM. We also discuss ATM's role in personalized medicine and the current challenges to more widespread use of ATM inhibitors in the clinic.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"281-297"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933189/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Second-Line Treatment Options for Patients with Metastatic Triple-Negative Breast Cancer: A Review of the Clinical Evidence.","authors":"José Ángel García-Saenz, Álvaro Rodríguez-Lescure, Josefina Cruz, Joan Albanell, Emilio Alba, Antonio Llombart","doi":"10.1007/s11523-025-01138-4","DOIUrl":"10.1007/s11523-025-01138-4","url":null,"abstract":"","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"215"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential Disease Behavior of Immune-Mediated Colitis Among Different Types of Immune Checkpoint Inhibition.","authors":"Malek Shatila, Farzin Eshaghi, Carolina Colli Cruz, Antonio Pizuorno Machado, Antony Mathew, Dan Zhao, Bilal A Siddiqui, Anusha Shirwaikar Thomas, Suresh T Chari, Yinghong Wang","doi":"10.1007/s11523-025-01135-7","DOIUrl":"10.1007/s11523-025-01135-7","url":null,"abstract":"<p><strong>Background: </strong>Immune-checkpoint inhibitors (ICIs) enhance the immune response against cancer but can cause immune-related adverse events, with immune-mediated colitis (IMC) being among the most common.</p><p><strong>Objective: </strong>We investigated variations in gastrointestinal disease behavior and outcomes among patients receiving different ICI regimens.</p><p><strong>Methods: </strong>This retrospective chart review included patients who received ICIs and developed IMC. Groups were categorized by their last ICI regimen before IMC onset into either programmed cell death protein-1/ligand-1 monotherapy or cytotoxic T-lymphocyte antigen 4 (CTLA-4) monotherapy/combination immunotherapy. Demographic and IMC-related clinical information was collected.</p><p><strong>Results: </strong>There were 414 patients included in this study: 169 treated with programmed cell death protein-1/ligand-1 monotherapy and 245 treated with CTLA-4 mono/combination therapy. Patients treated with CTLA-4 therapy had an earlier onset of IMC (median 46 days vs 123 days, p < 0.001). They were more likely to present with fever (p = 0.02), abdominal pain (p = 0.049), or hematochezia (p < 0.001). They also had more severe colitis with 47.3% of patients in the CTLA-4 group presenting with grade ≥3 colitis versus 20.2% in the programmed cell death protein-1/ligand-1 group (p < 0.05). On endoscopy, CTLA-4 mono/combination therapy was associated with increased ulcerative findings (24.4 vs 8.4%, p = 0.002). On histology, the programmed cell death protein-1/ligand-1 group was more likely to have microscopic colitis (13.9 vs 5.8%, p < 0.045).</p><p><strong>Conclusions: </strong>This study provides insight into the effect of ICI type on IMC disease course. Cytotoxic T-lymphocyte antigen 4 inhibition leads to an earlier and more severe IMC onset with distinct endoscopic and histologic features. Further research is needed to refine treatment algorithms and identify the mechanisms underlying the variability in IMC presentation among different ICI regimens.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"339-347"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose Optimization of Elranatamab to Mitigate the Risk of Cytokine Release Syndrome in Patients with Multiple Myeloma.","authors":"Mohamed Elmeliegy, Andrea Viqueira, Erik Vandendries, Anne Hickman, Umberto Conte, Donald Irby, Jennifer Hibma, Hoi-Kei Lon, Joseph Piscitelli, Pooneh Soltantabar, Athanasia Skoura, Sibo Jiang, Diane Wang","doi":"10.1007/s11523-025-01134-8","DOIUrl":"10.1007/s11523-025-01134-8","url":null,"abstract":"<p><strong>Background: </strong>Elranatamab is a BCMA-CD3 bispecific antibody approved for the treatment of relapsed or refractory multiple myeloma. Cytokine release syndrome is one of the most common adverse events associated with bispecific antibodies.</p><p><strong>Objective: </strong>We aimed to determine the optimal elranatamab dosing regimen for mitigating cytokine release syndrome.</p><p><strong>Patients and methods: </strong>Safety, pharmacokinetics, and exposure-response were analyzed across four clinical studies (MagnetisMM-1, MagnetisMM-2, MagnetisMM-3, and MagnetisMM-9). Different priming regimens evaluated across these studies included a one-step-up dose priming regimen of 44 mg with or without premedication, a two-step-up dose priming regimen of 12 mg on day 1 and 32 mg on day 4 with premedication, and a two-step-up dose priming regimen of 4 mg on day 1 and 20 mg on day 4 with premedication.</p><p><strong>Results: </strong>The maximum elranatamab serum concentration on day 1 was positively associated with any-grade and grade ≥ 2 cytokine release syndrome. A slower time to maximum serum concentration and a lower dose-normalized maximum serum concentration were observed with subcutaneous versus intravenous administration, supporting subcutaneous dosing to help mitigate cytokine release syndrome.</p><p><strong>Conclusions: </strong>Based on the incidence, severity, and predictable profile of cytokine release syndrome, the 12/32-mg priming-dose regimen with premedication was determined to be the optimal regimen before the first full dose of 76 mg on day 8.</p><p><strong>Clinical trial registration: </strong>ClinicalTrials.gov identifiers: NCT03269136, NCT04798586, NCT04649359, and NCT05014412.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"349-359"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143503728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumour Mutational Burden and Immune Checkpoint Inhibitor Response in Non-small Cell Lung Cancer: A Continuous Modelling Approach.","authors":"Michael J Sorich, Arkady T Manning-Bennett, Lee X Li, Adel Shahnam, Ganessan Kichenadasse, Christos S Karapetis, Ahmad Y Abuhelwa, Ross A McKinnon, Andrew Rowland, Ashley M Hopkins","doi":"10.1007/s11523-024-01124-2","DOIUrl":"10.1007/s11523-024-01124-2","url":null,"abstract":"<p><strong>Background: </strong>Tumour mutational burden (TMB) is an established biomarker for patients treated with immune checkpoint inhibitors (ICIs). The optimal TMB cut-off is uncertain. It is also uncertain whether there is a sharp TMB threshold or a more graduated change in clinical outcomes as TMB increases.</p><p><strong>Objective: </strong>We aimed to determine the relationship between TMB and ICI treatment outcomes using alternative statistical approaches in patients with non-small cell lung cancer.</p><p><strong>Methods: </strong>Tumour mutational burden was evaluated as a prognostic and predictive biomarker in advanced non-small cell lung cancer utilising data from two real-world cohorts of ICI use (n = 968) and three randomised controlled trials evaluating ICIs (n = 1588). The non-linear relationship between continuous TMB and response/survival/efficacy outcomes was evaluated using statistical methods that do not require specifying a TMB cut-off.</p><p><strong>Results: </strong>Median TMB for all cohorts was seven mutations/megabase, excluding MYSTIC, where the median was 13 mutations/megabase. Progressively higher TMB was significantly associated with a progressively higher objective response rate and progression-free survival in ICI-treated patients in Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets [MSK-IMPACT] (objective response rate: p < 0.001, progression-free survival: p < 0.001), Strata Clinical Molecular Database [SCMD] (progression-free survival: p = 0.023) and OAK/POPLAR (objective response rate: p = 0.017, progression-free survival: p < 0.001) This relationship was not apparent for patients treated with chemotherapy. There was no obvious TMB threshold for ICI response. The relationship between TMB and overall survival was more complex and heterogeneous.</p><p><strong>Conclusions: </strong>Using a single cut-off to analyse a continuous biomarker may hide important information. Methods that provide more nuance to the underlying relationship between TMB and outcomes enable readers to judge for themselves the value and limitations of TMB cut-offs proposed for clinical practice.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"361-369"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142955431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Compassionate Access to Brigatinib for Patients with Non-small-cell Lung Cancer Harboring a ROS1 Rearrangement: Results from the BRIGAROS Study.","authors":"Jean Mourlanette, Gaelle Rousseau-Bussac, Siham Mallah, Florian Guisier, Gerard Zalcman, Rémi Veillon, Clarisse Audigier-Valette, Magali Roa, Isabelle Nicolle, Helene Doubre, Nicolas Cloarec, Régine Lamy, Hugues Morel, Hubert Curcio, Aurélie Lagrange, Roland Schott, Marielle Sabatini, Anne Claire Toffart, Julian Pinsolle, Jaafar Bennouna, Christos Chouaid, Julien Mazieres","doi":"10.1007/s11523-025-01131-x","DOIUrl":"10.1007/s11523-025-01131-x","url":null,"abstract":"<p><strong>Background: </strong>ROS1 chromosomic rearrangement is a rare oncogenic driver, and patients with this rearrangement benefit from specific targeted treatments in the first-line setting. However, therapeutic options are limited in pretreated patients. Brigatinib is a validated drug for ALK rearrangements, and also has an in vitro activity against ROS1. In vivo efficacy is also suggested in some clinical series.</p><p><strong>Objective: </strong>We aimed to specifically study brigatinib in patients with pretreated advanced non-small-cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>We retrospectively collected data from 20 centers in France. Brigatinib was delivered through a compassionate use program in France between 2018 and 2020. The primary endpoint was progression-free survival. Secondary endpoints were the objective response rate, overall survival, and tolerance.</p><p><strong>Results: </strong>Twenty-five patients treated with brigatinib were included in our study. All patients were pretreated, and all of them previously received crizotinib. Median progression-free survival was 3.8 months (95% confidence interval 2.8-7.1). The objective response rate was 32%, with a disease control rate of 48%. Three patients had a prolonged response of more than 18 months at the end of data collection. We did not identify factors predictive of prolonged response. There were no grade 4 or 5 toxicities.</p><p><strong>Conclusion: </strong>Brigatinib may represent an interesting therapeutic option for patients who have progressed after standard treatments.</p>","PeriodicalId":22195,"journal":{"name":"Targeted Oncology","volume":" ","pages":"311-317"},"PeriodicalIF":4.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11933156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143626040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}