Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-03-04DOI: 10.1097/CAD.0000000000001712
Chao Zhu, Peng Xu, Lantao Li, Hongmei Wei
{"title":"Response to PARP inhibitor in EGFR-tyrosine kinase inhibitor-resistant metastatic lung adenocarcinoma with germline PALB2 mutation.","authors":"Chao Zhu, Peng Xu, Lantao Li, Hongmei Wei","doi":"10.1097/CAD.0000000000001712","DOIUrl":"10.1097/CAD.0000000000001712","url":null,"abstract":"<p><p>Tumors with homologous recombination deficiency (HRD) can benefit from treatment with poly ADP-ribose polymerase inhibitors (PARPi). However, the methods for identifying HRD vary and are controversial. Several DNA repair genes in the homologous recombination repair pathway may be linked to PARPi susceptibility, and studies are underway to identify biomarkers that can predict the response to PARPi. We present a case of EGFR-tyrosine kinase inhibitor-resistant metastatic lung adenocarcinoma with a germline PALB2 mutation that was treated with fluzoparib (an orally administered PARPi). The treatment achieved surprising results and lasted for more than 4.5 months. Our study provided evidence that metastatic lung adenocarcinoma with germline PALB2 could benefit from PARPi, which improves patient outcomes.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"518-520"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-03-10DOI: 10.1097/CAD.0000000000001713
Meiling Weng, Xiaoping Zhu
{"title":"Thrombospondin-2 induces M2 macrophage polarization through fatty acid metabolism to drive lung adenocarcinoma proliferation.","authors":"Meiling Weng, Xiaoping Zhu","doi":"10.1097/CAD.0000000000001713","DOIUrl":"10.1097/CAD.0000000000001713","url":null,"abstract":"<p><p>Tumor-associated macrophages play a critical role in regulating the progression of lung adenocarcinoma (LUAD). Platelet-derived protein thrombospondin-2 (THBS2) has been identified as a tumor marker and is known to be overexpressed in LUAD. However, the specific role of THBS2 in M2 macrophage polarization within LUAD remains unclear. We conducted bioinformatics analyses to assess the clinical significance of THBS2 expression in LUAD, which was subsequently validated using quantitative PCR. We examined the relationship between THBS2 expression and M2 macrophage infiltration. A coculture system of LUAD cells and M0 macrophages was established to investigate the influence of THBS2 on macrophage infiltration and polarization through immunofluorescence and ELISA. We explored the impact of THBS2 on fatty acid metabolism (FAM) using oil red O staining and relevant kits and elucidated the role of THBS2 in regulating M2 macrophage polarization and LUAD proliferation through cell counting kit-8 (CCK-8) and colony formation assays. Western blot was employed to assess expression changes of Bax and Bcl-2. THBS2 was highly expressed in LUAD and was associated with poor prognosis in patients. In-vitro experiments demonstrated that silencing THBS2 significantly inhibited macrophage infiltration and polarization. THBS2 primarily activated FAM pathways, inducing M2 macrophage polarization and promoting LUAD cell proliferation. THBS2 enhanced LUAD proliferation by regulating FAM to induce M2 macrophage polarization. These findings provide a theoretical basis for targeting THBS2 as a novel therapeutic strategy in LUAD.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"459-467"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143575681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-03-21DOI: 10.1097/CAD.0000000000001716
Liangshan Da, Ziting Qu, Yiyin Zhang, Jie Da, Kangsheng Gu
{"title":"Correlative analysis of immune-related thyroid dysfunction and prognosis in patients with advanced esophageal squamous cell carcinoma.","authors":"Liangshan Da, Ziting Qu, Yiyin Zhang, Jie Da, Kangsheng Gu","doi":"10.1097/CAD.0000000000001716","DOIUrl":"10.1097/CAD.0000000000001716","url":null,"abstract":"<p><p>To explore the clinical characteristics of immune-related thyroid dysfunction (TD) and its correlation with prognosis. By collecting the clinical data of 116 patients with advanced esophageal squamous cell carcinoma (ESCC) who received programmed death receptor-1 (PD-1) inhibitor treatment, we analyzed the clinical characteristics of immune-related TD and its influencing factors and compared the prognostic differences among patients in different groups. Immune-related TD occurred in 45 (38.8%) patients after PD-1 inhibitor treatment, and the median time to its occurrence was 11.3 weeks. The toxicity of immune-related TD was grade 1 or grade 2 and only required symptomatic treatment. Female patients, as well as those with an Eastern Cooperative Oncology Group Performance Status less than equal to 1, no lymph node metastasis, no history of drinking, and high baseline thyroid-stimulating hormone levels, were likely to develop immune-related TD. Compared with the patients in the group without immune-related TD [TD(-)], the median progression-free survival (mPFS) and median overall survival (mOS) of the patients in the immune-related TD [TD(+)] group were significantly prolonged (mPFS: 12.6 vs. 6.5 months, P = 0.001; mOS: 20.2 vs. 11.2 months, P < 0.001). Further subgroup analysis showed that compared with the patients in the group without immune-related overt TD (Overt_TD), the patients in the Overt_TD group had a longer PFS (mPFS: 12.4 vs. 7.3 months, P = 0.015) and OS (mOS: 20.2 vs. 12.2 months, P = 0.001). The 60-, 90-, and 120-day landmark analysis further confirmed that immune-related TD was significantly associated with the improvement of PFS and OS. Multivariate Cox regression analysis indicated that immune-related TD was an independent prognostic factor for PFS ( P = 0.015) and OS ( P = 0.004). Immune-related TD is a very common immune-related adverse event. It is safe and manageable and has potential prognostic value for patients with advanced ESCC treated with PD-1 inhibitors.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"501-508"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-02-14DOI: 10.1097/CAD.0000000000001707
Xianhuai Jin, Yaping Quan, Jiao Liu, Yong Hu, Hao Li
{"title":"Transformation from acquired EGFR 19del/C797S to EGFR 19del/T790M in an advanced non-small cell lung cancer patient: a case report and literature review.","authors":"Xianhuai Jin, Yaping Quan, Jiao Liu, Yong Hu, Hao Li","doi":"10.1097/CAD.0000000000001707","DOIUrl":"10.1097/CAD.0000000000001707","url":null,"abstract":"<p><p>Third-generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are the first-line treatment of choice for patients with EGFR-mutant advanced non-small cell lung cancer (NSCLC). However, patients treated with these inhibitors eventually develop resistance. One of the most common mechanisms is the emergence of the EGFR C797S mutation. Whether first-generation EGFR inhibitors (e.g. icotinib or gefitinib) can sustainably control EGFR-sensitive mutations/C797S NSCLC following third-generation EGFR inhibitor treatment remains insufficiently reported. Our case report discusses a female patient with advanced lung adenocarcinoma carrying an EGFR exon 19 E746_A750delELREA mutation who received almonertinib as first-line treatment and developed C797S resistance during therapy. The patient was subsequently treated with a double dose of icotinib for 8 months until disease progression occurred, along with the development of an EGFR exon 20 T790M point mutation and TP53 mutation. This case provides clinical evidence suggesting that first-generation EGFR-TKIs may be an effective treatment strategy for patients with acquired EGFR 19del/C797S resistance following EGFR TKI therapy.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"513-517"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12061377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-04-10DOI: 10.1097/CAD.0000000000001703
Emad Tashkandi
{"title":"Impact of obesity on cancer therapy outcomes: a multicenter cohort study of 30-day mortality and morbidity.","authors":"Emad Tashkandi","doi":"10.1097/CAD.0000000000001703","DOIUrl":"10.1097/CAD.0000000000001703","url":null,"abstract":"<p><p>Obesity is a substantial concern in oncology, influencing cancer characteristics and treatment outcomes. This study investigated whether obesity contributes to increased 30-day mortality and morbidity in patients receiving anticancer therapy. In this multicenter retrospective cohort study, patients with cancer were categorized as either normal weight or obese and analyzed based on demographics, cancer types, treatment modalities, and 30-day posttreatment mortality and morbidity rates. Statistical comparisons were performed to determine associations between obesity, treatment type, and clinical outcomes. Among 1635 patients, 46.6% ( n = 760) were of normal weight and 53.4% ( n = 875) were obese. Obesity was more prevalent among female patients, while 60.4% of male patients were of normal weight ( P = 0.001). Substantial associations have been found between obesity and specific cancers, including colorectal cancer, lymphoma, head and neck cancer, and sarcoma. Chemotherapy was more frequently administered to patients with obesity (62.5%, P = 0.001), while hormonal therapy was predominantly administered to patients with normal weight (81.8%). Patients with normal weight exhibited a higher 30-day mortality rate (74.5%, P = 0.05), although morbidity rates did not differ substantially between the weight groups. Obesity is associated with specific cancer types and influences treatment selection, but it does not independently increase the incidence of short-term treatment complications. These findings suggest that the effect of obesity is more prominent in terms of cancer type and treatment choice than in predicting short-term morbidity. Further studies are warranted to elucidate the long-term effects of obesity on cancer outcomes.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"36 6","pages":"489-494"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12061370/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-05-07DOI: 10.1097/CAD.0000000000001715
Ying Luo, De Li, Qi Yang, Youyou Dong, Weijun Chen
{"title":"Treatment of RET/ALK comutated advanced lung large cell neuroendocrine carcinoma: a case report and literature review.","authors":"Ying Luo, De Li, Qi Yang, Youyou Dong, Weijun Chen","doi":"10.1097/CAD.0000000000001715","DOIUrl":"10.1097/CAD.0000000000001715","url":null,"abstract":"<p><p>The prognosis of advanced lung large-cell neuroendocrine carcinoma is poor, and the efficacy of targeted therapy is still being explored. A case of RET fusion mutation combined with ALK rearrangement positive advanced lung complex large cell neuroendocrine carcinoma was reported. The patient developed intrapulmonary and bone metastases 8 months after chemotherapy after lung cancer surgery, RET fusion mutations were detected by genetic testing, and intracranial progression occurred 1 year after pilatinib was applied. The comutation of RET and ALK was detected by genetic testing, and the pulmonary progression occurred 2 months after the application of aletinib, after being treated with pilatinib and aletinib, he progressed again in 9 months. We point out that large cell neuroendocrine carcinoma complex patients with RET gene mutation can benefit from targeted therapy, and when drug resistance is accompanied by ALK comutation, the patient can benefit from the treatment of the aletinib combined with pilatinib targeted therapy and the side effect is slight. At the same time, we further explore the resistance mechanism of targeted therapy in lung cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"509-512"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-02-28DOI: 10.1097/CAD.0000000000001710
Fan Yang, Xing Zhao, Hua Xie, Yajie Zhu, Yi Wang, Jin Zhou
{"title":"Occult epidermal growth factor receptor-mutant lung adenocarcinoma complicated by prostatic metastasis: a case report.","authors":"Fan Yang, Xing Zhao, Hua Xie, Yajie Zhu, Yi Wang, Jin Zhou","doi":"10.1097/CAD.0000000000001710","DOIUrl":"10.1097/CAD.0000000000001710","url":null,"abstract":"<p><p>Herein, we report a case of occult epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma complicated by prostatic metastasis. A 75-year-old male with >30 years of smoking history presented with lower back pain as the initial symptom. Respiratory symptoms, including cough and sputum production, were absent. PET-computed tomography revealed the presence of bone and prostatic metastases, without any lung abnormalities. Biopsies of the space-occupying bone and metastatic lesions suggested that the metastases originated from primary lung adenocarcinoma. Genetic testing indicated EGFR 21L858R(+). The patient had an abnormal serum carcinoembryonic antigen level but a normal prostate-specific antigen level. Following a multidisciplinary discussion, a diagnosis of occult primary lung adenocarcinoma complicated by bone and prostatic metastases (TxN0M1b, Stage IVB) was considered. Following targeted therapy with oral osimertinib, the patient achieved a partial response, with alleviation of pain symptoms alleviated and normalization of carcinoembryonic antigen levels. In the absence of tissue biopsy, such cases can often be misdiagnosed as prostate cancer complicated by multiple bone metastases. Hence, the present case highlights the importance of comprehensive diagnostic testing, including tissue biopsy, to accurately identify the underlying cause of metastatic disease.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"521-524"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12061367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-05-07DOI: 10.1097/CAD.0000000000001711
Ruiyang Zhang, Feifei Hou, Jianguo Gan, Lishen Zhang, Dan Yang, Fan Yang, Xiaoqiang Xia, Qianming Chen, Ce Bian, Xiaodong Feng
{"title":"Metformin-induced E6/E7 inhibition prevents HPV-positive cancer progression through p53 reactivation.","authors":"Ruiyang Zhang, Feifei Hou, Jianguo Gan, Lishen Zhang, Dan Yang, Fan Yang, Xiaoqiang Xia, Qianming Chen, Ce Bian, Xiaodong Feng","doi":"10.1097/CAD.0000000000001711","DOIUrl":"10.1097/CAD.0000000000001711","url":null,"abstract":"<p><p>The human papillomavirus (HPV) is implicated in multiple lethal cancers, although it is more sensitive to certain therapies than HPV-negative cancers. Therefore, the development of more targeted therapeutic strategies is imperative. The HPV oncogenes E6/E7 are ideal targets for HPV-positive cancer, but there are no clinical strategies that have been proven to effectively target E6/E7. Notably, metformin significantly inhibits E6/E7 expression; however, the underlying mechanism and therapeutic potential remain unclear, limiting its clinical translation. Cell Counting Kit-8, ethynyl-2'-deoxyuridine, and terminal-deoxynucleotidyl transferase-mediated Nick end labeling assays were conducted to evaluate the effects of metformin on cell viability, proliferation, and apoptosis. Quantitative real-time PCR, western blotting, and immunofluorescence assays were performed to determine changes in E6/E7 and p53 expression levels following metformin treatment. Patient-derived organoids and in-vivo xenograft models were constructed to evaluate the anticancer activity of metformin against HPV-positive cancer. Our research demonstrated enhanced sensitivity of HPV-positive cancer cells to metformin. Mechanistic studies have revealed that metformin exerts anticancer effects by inhibiting E6/E7 expression, which is associated with p53 reactivation. Furthermore, we substantiated the anticancer potential of metformin in HPV-positive patient-derived organoids and in-vivo tumor models. Our study focused on the mechanism underlying the enhanced responsiveness of HPV-positive cancer to metformin, highlighting the clinical potential of metformin as a targeted therapeutic strategy for HPV-positive cancer.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"468-477"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143655883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-05-07DOI: 10.1097/CAD.0000000000001709
Daniele Cattaneo, Alessandra Iurlo
{"title":"Reply to: Association between nilotinib-induced hyperbilirubinemia and UGT1A1 polymorphisms in a chronic myeloid leukemia patient.","authors":"Daniele Cattaneo, Alessandra Iurlo","doi":"10.1097/CAD.0000000000001709","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001709","url":null,"abstract":"","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"36 6","pages":"525"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anti-Cancer DrugsPub Date : 2025-07-01Epub Date: 2025-03-03DOI: 10.1097/CAD.0000000000001705
Claire S Reader, Wenjia Liao, Beatrice J Potter-Landua, Christel Séguy Veyssier, Claire J Seal, Neil Brewis, Michelle Morrow
{"title":"The tetravalent, bispecific properties of FS118, an anti-LAG-3/PD-L1 antibody, mediate LAG-3 shedding from CD4 + and CD8 + tumor-infiltrating lymphocytes.","authors":"Claire S Reader, Wenjia Liao, Beatrice J Potter-Landua, Christel Séguy Veyssier, Claire J Seal, Neil Brewis, Michelle Morrow","doi":"10.1097/CAD.0000000000001705","DOIUrl":"10.1097/CAD.0000000000001705","url":null,"abstract":"<p><p>Tumor-infiltrating lymphocytes (TILs) often have upregulated expression of immune checkpoint receptors, such as programmed cell death 1 (PD-1) and lymphocyte-activation gene 3 (LAG-3). Patients treated with antibodies targeting PD-1 or its ligand (PD-L1) can develop resistance or relapse, with LAG-3 upregulation on T cells being one possible mechanism. FS118 is a tetravalent, bispecific antibody comprising a full-length IgG 1 anti-PD-L1 antibody with bivalent LAG-3-binding capability in the fragment crystallizable region. Here we demonstrate how the structure of FS118 is important for its function. We generated variants of FS118 and tested their ability to mediate LAG-3 shedding using staphylococcal enterotoxin B assays, antigen recall assays, and soluble LAG-3 ELISAs. Mediated by metalloproteases ADAM10 and ADAM17, FS118 induced shedding of LAG-3 from the surface of both CD4 + and CD8 + T cells. We also determined the effect of surrogate antibodies on immune cell LAG-3 expression and proliferation in syngeneic mouse models. In vivo , the bivalent LAG-3 binding sites of a mouse surrogate of FS118 and their location in the fragment crystallizable region were important for eliciting maximal reduction in LAG-3 levels on the surface of TILs, as variants with a single LAG-3 binding site in the fragment crystallizable region, or with reversed orientation of the LAG-3 and PD-L1 binding sites, were less efficient at inducing shedding. We also show that PD-L1, not PD-1, binding drives the LAG-3 reduction on TILs. We hypothesize that the LAG-3 bivalency in the fragment crystallizable region of FS118 allows LAG-3 clustering, which optimizes cleavage by ADAM10/ADAM17 and thus shedding.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"447-458"},"PeriodicalIF":1.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12061380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}