Anti-Cancer Drugs最新文献

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Treatment of RET/ALK comutated advanced lung large cell neuroendocrine carcinoma: a case report and literature review. RET/ALK治疗晚期肺大细胞神经内分泌癌1例并文献复习。
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-07-01 Epub Date: 2025-05-07 DOI: 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":2.2,"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}
引用次数: 0
Reply to: Association between nilotinib-induced hyperbilirubinemia and UGT1A1 polymorphisms in a chronic myeloid leukemia patient. 回复:尼洛替尼诱导的高胆红素血症与慢性髓系白血病患者UGT1A1多态性之间的关系。
IF 1.8 4区 医学
Anti-Cancer Drugs Pub Date : 2025-07-01 Epub Date: 2025-05-07 DOI: 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}
引用次数: 0
Occult epidermal growth factor receptor-mutant lung adenocarcinoma complicated by prostatic metastasis: a case report. 隐性表皮生长因子受体突变型肺腺癌合并前列腺转移1例。
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-07-01 Epub Date: 2025-02-28 DOI: 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":2.2,"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}
引用次数: 0
Metformin-induced E6/E7 inhibition prevents HPV-positive cancer progression through p53 reactivation. 二甲双胍诱导的E6/E7抑制通过p53再激活阻止hpv阳性癌症进展。
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-07-01 Epub Date: 2025-05-07 DOI: 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":2.2,"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}
引用次数: 0
The tetravalent, bispecific properties of FS118, an anti-LAG-3/PD-L1 antibody, mediate LAG-3 shedding from CD4 + and CD8 + tumor-infiltrating lymphocytes. FS118是一种抗LAG-3/PD-L1抗体,具有四价双特异性,可介导LAG-3从CD4+和CD8+肿瘤浸润淋巴细胞中脱落。
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-07-01 Epub Date: 2025-03-03 DOI: 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":2.2,"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}
引用次数: 0
GZ17-6.02 interacts with carboplatin and etoposide to kill neuroblastoma cells. GZ17-6.02与卡铂和依托泊苷相互作用杀死神经母细胞瘤细胞。
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-07-01 Epub Date: 2025-05-07 DOI: 10.1097/CAD.0000000000001708
Michael R Booth, Laurence Booth, Jane L Roberts, Cameron West, Paul Dent
{"title":"GZ17-6.02 interacts with carboplatin and etoposide to kill neuroblastoma cells.","authors":"Michael R Booth, Laurence Booth, Jane L Roberts, Cameron West, Paul Dent","doi":"10.1097/CAD.0000000000001708","DOIUrl":"10.1097/CAD.0000000000001708","url":null,"abstract":"<p><p>The biology of GZ17-6.02 alone and more so in combination with either of the standard-of-care agents etoposide or carboplatin killed MYCN overexpressing neuroblastoma (NB) cells is unknown. The methods involved in this study are in-cell immunoblotting, trypan blue exclusion, plasmid and siRNA transfection, assessment of autophagy using a plasmid expressing LC3-GFP-RFP. GZ17-6.02 (602) comprises, by mass, a ratio of curcumin (1.0), harmine (1.3), and isovanillin (7.7). In tumors dosed with 602, the ratio becomes curcumin (1.0), harmine (16), and isovanillin (6.1) (602NR). GZ17-6.02 activated ATM, AMPK, ULK1, ATG13, and PERK and inactivated ERBB1, ERBB2, ERBB3, ERBB4, AKT, mTORC1, mTORC2, SRC, NFκB, YAP, and eIF2α. 602 enhanced autophagosome formation and autophagic flux that was amplified when it was combined with etoposide or carboplatin. Compared with 602, 602NR caused significantly greater autophagosome formation that was also amplified when in combination with chemotherapy and which was reduced ~40% by knockdown of ATM or AMPKα and abolished by knockdown of Beclin1 or ATG5. Knockdown of ATM or AMPKα significantly reduced tumor cell death caused by 602 of 602NR, whereas endoplasmic reticulum stress (eIF2α) and macroautophagy (Beclin1, ATG5) were more effective at maintaining tumor cell survival. Combined knockdown of Beclin1 and the death receptor CD95 almost abolished the antitumor actions of 602 and 602NR. 602, and more so 602NR, kills MYCN NB cells and interacts with standard-of-care chemotherapeutics to cause further killing via autophagy and death receptor signaling.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"478-488"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603576","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}
引用次数: 0
Effect of adjuvant chemotherapy with toad venom injection in the treatment of intermediate and advanced colon cancer and its effect on cellular immunity, PTEN, and PI3k. 蟾蜍毒注射液辅助化疗治疗中晚期结肠癌的疗效及对细胞免疫、PTEN、PI3k的影响
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-07-01 Epub Date: 2025-02-18 DOI: 10.1097/CAD.0000000000001706
Haijun Ding, Xuedian Tang, Wenjun Tang
{"title":"Effect of adjuvant chemotherapy with toad venom injection in the treatment of intermediate and advanced colon cancer and its effect on cellular immunity, PTEN, and PI3k.","authors":"Haijun Ding, Xuedian Tang, Wenjun Tang","doi":"10.1097/CAD.0000000000001706","DOIUrl":"10.1097/CAD.0000000000001706","url":null,"abstract":"<p><p>The objective of this study is to explore the effect of adjuvant chemotherapy with toad venom injection in patients with intermediate and advanced colon cancer, in order to provide new reference drugs for clinical treatment. Prospectively, 148 patients with mid-stage to late-stage colon cancer in our hospital from January 2021 to May 2023 were selected for the study and randomly divided into two groups of 74 cases each. The control group was treated with FOLFOX4 chemotherapy, and the observation group was treated with four consecutive chemotherapy cycles based on the control group combined with toad venom injection. The treatment effects, adverse reactions, quality of life improvement rate, prognosis and cellular immune indexes [natural killer (NK) cells, CD4 + /CD8 + , CD4 + , CD3 + ], phosphatase tensin gene ( PTEN ), phosphatidylinositol-3-kinase (PI3k), and serine threonine protein kinase (pAKT) protein expression before and after treatment were counted in the two groups. The total effective rate of treatment in the observation group was 58.11% (43/74) after four cycles of chemotherapy, which was higher than that in the control group of 41.89% (31/74) ( P  < 0.05). After two cycles of chemotherapy and four cycles of chemotherapy, PTEN , CD4 + /CD8 + , CD4 + , CD3 + , and NK cells in peripheral blood were higher in the observation group than in the control group, and PI3k and pAKT were lower than in the control group ( P  < 0.05). There was no statistically significant difference in the rate of adverse reactions in the observation group compared with the control group ( P  > 0.05); the improvement rate of quality of life in the observation group was better than that in the control group after four chemotherapy cycles of treatment ( P  < 0.05); the survival rate was 75.00% (54/72) in the observation group compared with 54.29% (38/70) in the control group at 1-year follow-up. Toad venom injection adjuvant chemotherapy is effective in treating patients with intermediate and advanced colon cancer, which can upregulate PTEN level, inhibit PI3k and AKT expression, and improve immune function and quality of life of patients, thus improving prognosis.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"495-500"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439841","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}
引用次数: 0
Long-term survival of an ALK fusion lung adenocarcinoma patient with high mutation burden and microsatellite instability high: a case report. 高突变负担和高微卫星不稳定性的ALK融合肺腺癌患者的长期生存:1例报告。
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-06-01 Epub Date: 2025-02-06 DOI: 10.1097/CAD.0000000000001693
Yanrong Guo, Jinfang Zhai, Yanli Yang, Qin Wei, Shengshu Li, Rujie Huo, Guoping Tong, Enwei Xu, Yan Chen, Songyan Han, Deyi Chen
{"title":"Long-term survival of an ALK fusion lung adenocarcinoma patient with high mutation burden and microsatellite instability high: a case report.","authors":"Yanrong Guo, Jinfang Zhai, Yanli Yang, Qin Wei, Shengshu Li, Rujie Huo, Guoping Tong, Enwei Xu, Yan Chen, Songyan Han, Deyi Chen","doi":"10.1097/CAD.0000000000001693","DOIUrl":"10.1097/CAD.0000000000001693","url":null,"abstract":"<p><p>Immune checkpoint blockage (ICB) therapy has shown minimal effectiveness in anaplastic lymphoma kinase (ALK)-positive nonsmall cell lung cancer (NSCLC) regardless of Programmed death-ligand 1 expression. ALK fusion accompanied by mismatch repair deficiency or microsatellite instability-high (MMRd/MSI-H) and high tumor mutation burden (TMB-H) are extremely rare in NSCLC, and the efficacy of ALK inhibitors or ICB-based therapies is unclear. Here, we report the case of a 60-year-old female patient with metastatic lung adenocarcinoma accompanied by EML4-ALK fusion, TMB-H, MMRd/MSI-H, and pathogenic mutations in TP53, MLH1, and STK11. The patient experienced progression on initial iruplinalkib and subsequent alectinib therapy within 5 months. After the failure of third-line therapy with cisplatin-pemetrexed combined with bevacizumab, she received sintilimab plus anlotinib which led to a progression-free survival of 6.5 months. She received sintilimab combined with albumin-paclitaxel plus carboplatin and achieved partial response after 6 months. She developed adverse events after one cycle of sintilimab plus albumin-paclitaxel treatment. Then she was continued with sintilimab plus anlotinib as a maintenance therapy due to intolerance to chemotherapy. After progression on ICB-based therapy, the patient was treated with lorlatinib and still under follow-up with overall survival of more than 3 years. Our findings highlight the therapeutic potential of ICB-based regimens in patients with MSI-H and ALK-rearranged NSCLC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"427-431"},"PeriodicalIF":2.2,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254273","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}
引用次数: 0
Comparative efficacy of cetuximab combined with FOLFOX or CAPEOX in first-line treatment of RAS/BRAF wild-type metastatic colorectal cancer: a multicenter case-control study. 西妥昔单抗联合FOLFOX或CAPEOX一线治疗RAS/BRAF野生型转移性结直肠癌的比较疗效:一项多中心病例对照研究
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-06-01 Epub Date: 2025-02-04 DOI: 10.1097/CAD.0000000000001697
Chang Xu, Jing Ren, Changqing Liu, Yi Gai, Xiangyu Cheng, Yusheng Wang, Guangyu Wang
{"title":"Comparative efficacy of cetuximab combined with FOLFOX or CAPEOX in first-line treatment of RAS/BRAF wild-type metastatic colorectal cancer: a multicenter case-control study.","authors":"Chang Xu, Jing Ren, Changqing Liu, Yi Gai, Xiangyu Cheng, Yusheng Wang, Guangyu Wang","doi":"10.1097/CAD.0000000000001697","DOIUrl":"10.1097/CAD.0000000000001697","url":null,"abstract":"<p><p>FOLFOX combined with cetuximab is a recommended first-line treatment regimen for RAS/BRAF wild-type metastatic colorectal cancer (mCRC). CAPEOX combined with cetuximab differs from the FOLFOX regimen by using oral capecitabine instead of continuous infusion of fluorouracil, offering greater convenience and cost-effectiveness with higher patient acceptance. However, the comparative efficacy of these two regimens remains debatable, necessitating further evidence to explore any differences in their efficacy. This study collected medical records of mCRC patients who were treated with CAPEOX or FOLFOX combined with cetuximab from 1 October 2021 to 16 October 2023 at Harbin Medical University Cancer Hospital and the First Hospital of Shanxi Medical University. Eligible patients were selected based on inclusion criteria and followed up through the hospital's follow-up system and telephone interviews. Kaplan-Meier survival analysis and Cox proportional hazards regression analysis were used to assess patients' progression-free survival (PFS) and overall survival (OS). A total of 71 eligible patients were enrolled in this study; 43 patients received CAPEOX combined with cetuximab (Group A, n  = 43), and 28 patients received FOLFOX combined with cetuximab (Group B, n  = 28). The two groups achieved similar median PFS (mPFS) and median OS (mOS), with mPFS of 18 months and 12 months, respectively ( P  = 0.23), and mOS of 33 months and 20 months, respectively ( P  = 0.21), with no statistically significant differences. The results of this study demonstrated that CAPEOX combined with cetuximab is an equally viable option for first-line treatment of RAS/BRAF wild-type mCRC as FOLFOX combined with cetuximab.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"383-393"},"PeriodicalIF":2.2,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188094","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}
引用次数: 0
A phase II study of anlotinib as first-line maintenance therapy for advanced ovarian cancer. anlotinib作为晚期卵巢癌一线维持治疗的II期研究。
IF 2.2 4区 医学
Anti-Cancer Drugs Pub Date : 2025-06-01 Epub Date: 2025-01-29 DOI: 10.1097/CAD.0000000000001698
Siyuan Li, Yanqin Zhang, Rong Yang, Qingfan Yang, Shuangyan Han, Dan Li, Zhenhua Zhang, Qinglian Wen
{"title":"A phase II study of anlotinib as first-line maintenance therapy for advanced ovarian cancer.","authors":"Siyuan Li, Yanqin Zhang, Rong Yang, Qingfan Yang, Shuangyan Han, Dan Li, Zhenhua Zhang, Qinglian Wen","doi":"10.1097/CAD.0000000000001698","DOIUrl":"10.1097/CAD.0000000000001698","url":null,"abstract":"<p><p>Anlotinib, a tyrosine kinase inhibitor, has shown encouraging antitumor activity in platinum-resistant/refractory ovarian cancer. The efficacy of anlotinib as maintenance therapy in advanced ovarian cancer remains unclear. Therefore, we designed this study to evaluate the efficacy and safety of anlotinib maintenance therapy following first-line treatment with paclitaxel and platinum-based chemotherapy in advanced ovarian cancer. In this single-arm, phase II clinical trial, patients with newly diagnosed advanced ovarian cancer were received anlotinib monotherapy as maintenance therapy once after a response to platinum-based chemotherapy until tumor progression or intolerable toxicity. The primary endpoint was progression-free survival. From April 2020 to June 2021, 24 patients were enrolled in this study. The median follow-up was 40.17 months (interquartile range, 32.40-47.93 months). Of 21 patients with efficacy value, the median progression-free survival and median overall survival were 15.8 months (95% confidence interval, 6.8-24.8 months) and 43.8 months (95% confidence interval, 25.45-62.15 months). The quality-adjusted progression-free survival was 14.4 months and there were no observed treatment-related deaths or serious treatment-emergent adverse events, demonstrating the safety of anlotinib in maintenance therapy. Anlotinib shows significant potential as a first-line maintenance therapy for advanced ovarian cancer, extending survival and providing a reliable treatment option.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"394-400"},"PeriodicalIF":2.2,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143057708","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}
引用次数: 0
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