Anti-Cancer Drugs最新文献

Prochlorperazine inhibits the proliferation of hepatocellular carcinoma cells by promoting phosphorylation of β-catenin. 丙氯哌嗪通过促进β-连环蛋白的磷酸化抑制肝癌细胞的增殖。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-10-07 DOI: 10.1097/CAD.0000000000001822

Yongjie Liang, Xiao Wang, Ruifeng Tian, Xi Wang, Xin Zhang, Juan Wan, Lu Wan, Xiaojing Zhang, Yi Ding

引用次数: 0

Publishing with Anti-Cancer Drugs: what authors should know. 出版与抗癌药物：作者应该知道什么。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-10-07 DOI: 10.1097/CAD.0000000000001849

Sergio Huerta

引用次数: 0

Successful treatment of hairy cell leukemia with TP53 abnormality using cladribine combined with low-dose rituximab: a case report and literature review. 克拉德里滨联合小剂量利妥昔单抗治疗TP53异常毛细胞白血病1例并文献复习

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-10-07 DOI: 10.1097/CAD.0000000000001823

Zixin Chen, Lin Chen

{"title":"Successful treatment of hairy cell leukemia with TP53 abnormality using cladribine combined with low-dose rituximab: a case report and literature review.","authors":"Zixin Chen, Lin Chen","doi":"10.1097/CAD.0000000000001823","DOIUrl":"10.1097/CAD.0000000000001823","url":null,"abstract":"Hairy cell leukemia (HCL) is a rare mature B-cell malignancy characterized by the BRAF V600E mutation. TP53 abnormalities in HCL are associated with poor response to standard therapies and a higher risk of relapse. We report an elderly male patient diagnosed with classical HCL (BRAF V600E-positive) who also presented with a TP53 deletion detected by fluorescence in situ hybridization (FISH) and bone marrow fibrosis. The patient was treated with one cycle of cladribine combined with low-dose rituximab (100 mg). The treatment was well tolerated. At the 7-month follow up, the patient achieved complete molecular remission, characterized by normalized blood counts, recovery of bone marrow morphology, disappearance of the TP53 deletion by FISH, negative minimal residual disease by flow cytometry, and reversal of bone marrow fibrosis from MF-2 to MF-0. This case suggests that the combination of cladribine and low-dose rituximab may be an effective therapeutic strategy for classical HCL with TP53 abnormality, enabling deep molecular response and reversal of associated bone marrow fibrosis. Further prospective studies are warranted to validate these findings.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"638-642"},"PeriodicalIF":2.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760097","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

Hyperthermia combined with intraperitoneal perfusion of drugs improves malignant ascites caused by gastrointestinal tumors by reshaping the tumor immune microenvironment. 热疗联合药物腹腔灌注通过重塑肿瘤免疫微环境改善胃肠道肿瘤所致恶性腹水。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-10-07 DOI: 10.1097/CAD.0000000000001820

Yongjian Zhang, Baomei Wang, Junhua Zhang, Shuxiang Han, Yuetian Xu, Yunxiao Wang, Jingjing Yan, Wenling Wang

{"title":"Hyperthermia combined with intraperitoneal perfusion of drugs improves malignant ascites caused by gastrointestinal tumors by reshaping the tumor immune microenvironment.","authors":"Yongjian Zhang, Baomei Wang, Junhua Zhang, Shuxiang Han, Yuetian Xu, Yunxiao Wang, Jingjing Yan, Wenling Wang","doi":"10.1097/CAD.0000000000001820","DOIUrl":"10.1097/CAD.0000000000001820","url":null,"abstract":"Malignant ascites treatment remains challenging. Hyperthermia is a promising adjunct to intraperitoneal therapies, but its mechanisms are unclear. We aimed to investigate whether combining hyperthermia with endostatin and cisplatin alleviates malignant ascites by reprogramming immune microenvironment. A total of 28 patients with malignant ascites were enrolled and divided into three groups: untreated, recombinant human endostatin plus cisplatin, and hyperthermia combined with recombinant human endostatin and cisplatin. Ascites volume was monitored by B-ultrasound. VEGF, IL-10, and IFN-γ levels in ascitic fluid were measured via ELISA. Immune cell proportions and macrophage polarization were analyzed by flow cytometry. A murine malignant ascites model was established. Mice were treated according to same therapeutic groupings. Tumor burden was assessed via in vivo fluorescence imaging, ascites volume measurement, body weight changes, and survival analysis. Cytokine levels and macrophage polarization in murine ascites were also evaluated. Hyperthermia combined with endostatin and cisplatin reduced ascites volume and modulated ascitic microenvironment in patients with malignant ascites. Triple therapy of hyperthermia, endostatin, and cisplatin functioned dually to eliminate pro-tumoral leukocytes in ascites and reprogram macrophages into M1 phenotypes. Hyperthermia synergized with endostatin and cisplatin to suppress malignant ascites progression, mitigate systemic toxicity, and extend survival in mice. Triple therapy modulated ascitic microenvironment and promoted macrophage M1 polarization in a murine malignant ascites model. Macrophage ablation abolished therapeutic efficacy of triple therapy in malignant ascites mice. The combined strategy of hyperthermia, endostatin, and cisplatin suppresses malignant ascites in gastrointestinal cancer through inducing M1 macrophage polarization.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"597-607"},"PeriodicalIF":2.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809432","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

Tertiary lymphoid structure transcriptomic signatures show limited and cohort-dependent value for predicting axillary nodal involvement in oestrogen receptor-positive luminal breast cancer. 在雌激素受体阳性的腔内乳腺癌中，三级淋巴结构转录组特征在预测腋窝淋巴结累及方面显示有限的和依赖队列的价值。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-07-28 DOI: 10.1097/CAD.0000000000001836

Tao Wang, Yi Zhang, Xinhua Yang, Peng Qi

{"title":"Tertiary lymphoid structure transcriptomic signatures show limited and cohort-dependent value for predicting axillary nodal involvement in oestrogen receptor-positive luminal breast cancer.","authors":"Tao Wang, Yi Zhang, Xinhua Yang, Peng Qi","doi":"10.1097/CAD.0000000000001836","DOIUrl":"10.1097/CAD.0000000000001836","url":null,"abstract":"Tertiary lymphoid structures (TLS) are associated with prognosis in solid tumours. Their value for predicting axillary nodal involvement in oestrogen receptor-positive luminal breast cancer remains uncertain. Three published TLS signatures were scored by single-sample gene set enrichment analysis in oestrogen receptor-positive luminal tumours. The Cancer Genome Atlas Breast Invasive Carcinoma cohort (TCGA-BRCA) included 632 cases, of which 379 met strict consensus. METABRIC included 1086 cases, of which 663 met strict consensus. Logistic models adjusted for age and pathological tumour stage. Strict consensus, majority vote, and continuous scores were compared. Performance assessment included bootstrapped changes in area under the receiver-operating-characteristic curve, Brier scores, calibration, and decision-curve analysis. Survival was evaluated in METABRIC and explored in TCGA-BRCA. Strict-consensus TLS status was not associated with nodal positivity in TCGA-BRCA (adjusted odds ratio: 0.95, 95% confidence interval: 0.62-1.45, P = 0.822). METABRIC was similar (odds ratio: 0.76, 95% confidence interval: 0.55-1.06, P = 0.105). Full-cohort METABRIC analyses detected small majority-vote and continuous-score associations, absent in TCGA-BRCA. Across specifications, bootstrapped changes in area under the receiver-operating-characteristic curve ranged from 0.0002 to 0.0089, with minimal Brier-score improvement and no stable decision-curve benefit. In METABRIC, the univariable overall survival association attenuated after age adjustment (hazard ratio: 1.33-1.10). TCGA-BRCA survival analyses were nonsignificant. TLS transcriptomic signals showed small, cohort-dependent associations with nodal status but no reproducible or clinically meaningful incremental predictive value. These data do not support replacing sentinel lymph node biopsy with a TLS signature in oestrogen receptor-positive luminal breast cancer.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"608-619"},"PeriodicalIF":2.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652886","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

Prolonged multimodal disease control with trifluridine/tipiracil plus bevacizumab in KRAS-mutant metastatic rectal cancer: a case report. 在kras突变的转移性直肠癌中，trifluridine/tipiracil + bevacizumab的长期多模式疾病控制：1例报告。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-06-16 DOI: 10.1097/CAD.0000000000001833

Onur Alkan, Ahmet Başgöze, İsmail Nazli

引用次数: 0

Case report: successful use of repotrectinib in a ROS1 fusion-positive lung adenocarcinoma patient with severe renal insufficiency and prior tyrosine kinase inhibitor treatment failure. 病例报告：成功使用repotrectinib治疗ROS1融合阳性肺腺癌患者严重肾功能不全和既往酪氨酸激酶抑制剂治疗失败。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-10-07 DOI: 10.1097/CAD.0000000000001818

Zhengjie Liang, Hao Li

{"title":"Case report: successful use of repotrectinib in a ROS1 fusion-positive lung adenocarcinoma patient with severe renal insufficiency and prior tyrosine kinase inhibitor treatment failure.","authors":"Zhengjie Liang, Hao Li","doi":"10.1097/CAD.0000000000001818","DOIUrl":"10.1097/CAD.0000000000001818","url":null,"abstract":"During sequential targeted therapy for ROS1 fusion-positive non-small cell lung cancer, some patients may develop severe renal insufficiency due to drug-related adverse events, resulting in limited subsequent treatment options with uncertain efficacy. We report a case of a 69-year-old female patient with advanced lung adenocarcinoma harboring an SDC4-ROS1 fusion mutation. Imaging revealed multiple nodules and masses in both lungs, enlarged mediastinal lymph nodes, and bilateral pleural effusion. The patient received treatment with crizotinib and entrectinib successively. During this period, the patient experienced renal hemorrhage and developed renal cysts and renal atrophy. Laboratory findings revealed persistently elevated serum creatinine levels and a significant decline in estimated glomerular filtration rate. She ultimately developed severe renal insufficiency, concurrent with tumor progression. Repotrectinib therapy was initiated based on tumor progression and renal function status under close monitoring, and an objective response occurred in this patient. Moreover, the serum creatinine levels decreased and remained relatively stable, indicating improved renal function. No new severe drug-related adverse events were observed. This case suggests that in patients with ROS1 fusion-positive nonsmall cell lung cancer who have experienced prior ROS1-tyrosine kinase inhibitor treatment failure and concomitant severe renal insufficiency, repotrectinib may represent a potential and tolerable treatment option when fully assessing clinical risks and ensuring close monitoring.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"629-633"},"PeriodicalIF":2.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147571676","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

Akt inhibitor-IV in estrogen receptor-positive breast cancer cells: cytotoxic, apoptotic, transcriptional, and in-silico comparison with tamoxifen. Akt抑制剂- iv在雌激素受体阳性乳腺癌细胞中的作用：与他莫昔芬的细胞毒性、凋亡、转录和芯片比较

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-11-01 Epub Date: 2026-10-07 DOI: 10.1097/CAD.0000000000001834

Ahmet Karakuş, Orhan Erdoğan

{"title":"Akt inhibitor-IV in estrogen receptor-positive breast cancer cells: cytotoxic, apoptotic, transcriptional, and in-silico comparison with tamoxifen.","authors":"Ahmet Karakuş, Orhan Erdoğan","doi":"10.1097/CAD.0000000000001834","DOIUrl":"10.1097/CAD.0000000000001834","url":null,"abstract":"Dysregulation of the phosphoinositide 3-kinase/protein kinase B (AKT)/mechanistic target of rapamycin pathway is a hallmark of breast cancer, making AKT a focus of therapeutic interest. AKT inhibitor-IV is a benzimidazolium compound that inhibits AKT phosphorylation, but its activity and binding mechanism in breast cancer cells have not been characterized in detail. We compared AKT inhibitor-IV with tamoxifen in MCF-7 cells. Cell viability after 24-h treatment was measured by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay (AKT inhibitor-IV: 0.1-5 μM; tamoxifen: 5-50 μM); apoptotic death was quantified by nucleosome ELISA; and AKT1 , BCL-2 , BAX , and CASP3 mRNA levels were measured by quantitative real-time PCR. Both compounds were docked into the ATP-binding pockets of 3-phosphoinositide-dependent protein kinase-1 (PDK1) (PDB 1H1W) and AKT1 (PDB 3MVH) using AutoDock Vina v1.2.6. AKT inhibitor-IV reduced viability with an IC50 of 1.1 μM, compared with 5.2 μM for tamoxifen, and induced 5.9-fold apoptosis enrichment versus 3.65-fold for tamoxifen. AKT inhibitor-IV downregulated AKT1 (0.32-fold) and BCL-2 (0.55-fold) and upregulated BAX (5.97-fold) and CASP3 (6.43-fold) mRNA; tamoxifen showed qualitatively similar but quantitatively weaker transcriptional changes. Docking returned affinities of -9.91 kcal/mol for PDK1 and -9.66 kcal/mol for AKT1 , with AKT inhibitor-IV contacting catalytic-core residues of both kinases. AKT inhibitor-IV was more potent than tamoxifen in this in-vitro setting and warrants further preclinical evaluation. Because MCF-7 cells carry the CASP3 exon 3 deletion and lack functional caspase-3 protein, the observed CASP3 mRNA upregulation reflects transcriptional reprogramming rather than restored executioner activity. The modest docking difference requires biochemical confirmation before any PDK1-versus- AKT1 selectivity claim can be established.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"620-628"},"PeriodicalIF":2.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366620","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

Primary resistant disease is clinically heterogeneous in metastatic renal cell carcinoma treated with nivolumab plus ipilimumab. 原发性耐药疾病在临床上是异质性的，在转移性肾细胞癌中，纳伏单抗加伊匹单抗治疗。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-10-06 DOI: 10.1097/CAD.0000000000001847

Noriyuki Abe, Ryuma Tanaka, Yuya Sekine, Masanao Shinohara, Shin Kobayashi, Naoki Fujita, Satoshi Sato, Tomonori Habuchi, Shingo Hatakeyama, Kazuyuki Numakura

{"title":"Primary resistant disease is clinically heterogeneous in metastatic renal cell carcinoma treated with nivolumab plus ipilimumab.","authors":"Noriyuki Abe, Ryuma Tanaka, Yuya Sekine, Masanao Shinohara, Shin Kobayashi, Naoki Fujita, Satoshi Sato, Tomonori Habuchi, Shingo Hatakeyama, Kazuyuki Numakura","doi":"10.1097/CAD.0000000000001847","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001847","url":null,"abstract":"The study aimed to characterize clinical heterogeneity among patients with primary resistant disease (PRD) after first-line nivolumab plus ipilimumab (NIVO+IPI) for metastatic renal cell carcinoma (mRCC) and to explore clinical factors associated with death within 1 year among patients with PRD. We retrospectively analyzed 151 patients with mRCC who received first-line NIVO+IPI at four institutions in Japan between May 2018 and January 2025. PRD was defined as disease progression occurring within 3 months after treatment initiation, based on radiographic and clinical assessment, or death from any cause within the same period. For exploratory analyses, primary resistant disease with early mortality (PRD-EM) was defined as death within 1 year among patients with PRD. Survival was estimated by the Kaplan-Meier method. Because the PRD subgroup was small and several variables had sparse cell counts, associations with PRD-EM were assessed using Firth penalized logistic regression. PRD occurred in 31 of 151 patients (20.5%). Median overall survival was 3.9 months [95% confidence interval (CI) = 1.8-13.6] in patients with PRD and 46.7 months (95% CI = 38.8-62.8) in those without PRD (log-rank P < 0.001). Among patients with PRD, 20 of 31 (64.5%) met the exploratory PRD-EM definition. In the parsimonious two-variable Firth model, baseline C-reactive protein (CRP) ≥2 mg/dL [adjusted odds ratio (OR) = 7.95; 95% CI = 1.32-68.18; P = 0.023] and lymph node involvement (adjusted OR = 11.65; 95% CI = 1.78-142.82; P = 0.009) were associated with PRD-EM. PRD after first-line NIVO+IPI was associated with heterogeneous clinical outcomes. Elevated baseline CRP and lymph node involvement were associated with PRD-EM in an exploratory analysis. The PRD-EM classification and these associations require validation in larger independent cohorts before they can be used for clinical decision-making.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102748","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

Macrophage-associated epithelial-mesenchymal transition in human breast cancer: contextualizing innate immune sensing programs. 人乳腺癌中巨噬细胞相关的上皮-间质转化：先天免疫感知程序的背景。

IF 2 4区医学

Anti-Cancer Drugs Pub Date : 2026-10-05 DOI: 10.1097/CAD.0000000000001848

Steven Lehrer, Peter Rheinstein

{"title":"Macrophage-associated epithelial-mesenchymal transition in human breast cancer: contextualizing innate immune sensing programs.","authors":"Steven Lehrer, Peter Rheinstein","doi":"10.1097/CAD.0000000000001848","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001848","url":null,"abstract":"To determine whether innate immune-sensing activity is associated with epithelial-mesenchymal transition (EMT) and related tumor-aggressiveness programs in human breast cancer. We analyzed RNA sequencing and clinical data from The Cancer Genome Atlas breast cancer cohort (n = 1087). Gene expression-based signatures were constructed for innate immune sensing, interferon signaling, CD8 T cells, macrophages, EMT, invasion, and metastasis. Associations were evaluated using Pearson correlation, Cox proportional hazards models, and multivariable linear regression, including adjustment for PAM50 molecular subtype and immune cell signatures. Innate immune-sensing signatures were strongly correlated with interferon signaling (r = 0.73) and macrophage-associated signatures (r = 0.77), indicating a coordinated inflammatory program. Innate immune sensing was moderately associated with EMT (r = 0.48), invasion (r = 0.45), and metastasis-related transcriptional programs (r = 0.48). In multivariable models, innate immune sensing remained associated with EMT after adjustment for molecular subtype and immune cell signatures (β = 0.17, P < 0.001), while macrophage signatures were the dominant predictors (β = 0.51, P < 2 × 10-16) and CD8 signatures were inversely associated (β = -0.14, P < 0.001). No association with overall survival was observed. Innate immune-sensing signatures are associated with macrophage-driven EMT programs in breast cancer, consistent with activation of inflammatory pathways within the tumor microenvironment.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102724","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