Anti-Cancer Drugs最新文献

{"title":"Interferon regulatory factor 4 drives M2 macrophage polarization in lung adenocarcinoma via the absent in melanoma 2-mediated phosphoinositide 3-kinase/protein kinase B signaling pathway.","authors":"Xiaoyun Zou, Qing Ji, Zhongzheng Wen, Limei Lei, Xuan Chen, Wen Hu","doi":"10.1097/CAD.0000000000001795","DOIUrl":"10.1097/CAD.0000000000001795","url":null,"abstract":"<p><p>Tumor-associated macrophages, predominant immunosuppressive components within the tumor microenvironment, critically regulate lung adenocarcinoma (LUAD) progression; however, their molecular regulatory mechanisms remain incompletely characterized. The Cancer Genome Atlas database analysis revealed absent in melanoma 2 (AIM2) expression in LUAD. The correlation between AIM2 expression and M2 macrophage infiltration levels was further evaluated. Putative transcriptional regulators upstream of AIM2 were predicted through bioinformatics screening, with JASPAR employed to identify potential binding sites between candidate factors and the AIM2 promoter. These predictions were experimentally validated using dual-luciferase reporter assays. Furthermore, we established a LUAD cell-macrophage coculture system. We performed flow cytometric analysis of macrophage surface CD206 expression, quantitative PCR quantification of mRNA levels, ELISA quantification of cytokine secretion profiles, and Western blot detection of proteins. Bioinformatics analysis revealed that AIM2 was highly expressed in LUAD tumor tissues and positively correlated with the marker genes of M2 macrophages. Overexpression of AIM2 in LUAD cells promoted the expression of CD206 on the macrophage surface, upregulated the mRNA expression levels of M2 macrophage marker genes such as CD163 , ARG1 , and MRC1 , and enhanced the secretion of transforming growth factor-beta and interleukin-10 . These results indicated an increased level of macrophage polarization towards the M2 phenotype, and inhibiting the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway reversed the above phenomenon. Furthermore, the interferon regulatory factor 4 (IRF4) promoted the transcription of AIM2. IRF4 knockdown in LUAD cells suppressed M2 macrophage polarization, but simultaneous overexpression of AIM2 restored it to baseline levels. IRF4 drives M2 macrophage polarization in LUAD via the AIM2-mediated PI3K/AKT signaling pathway.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"343-351"},"PeriodicalIF":2.2,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145817463","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}

{"title":"The novel integrin-linked kinase inhibitor nilotinib suppresses cancer progression by promoting ubiquitylation of autoimmune regulator in oesophageal squamous cell carcinoma.","authors":"Xiaoli Ma, Yu Wei, LeiYu Cao, Yan Gao, Chengcheng Qu, Kalima Muhetaer, Li Zhang","doi":"10.1097/CAD.0000000000001828","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001828","url":null,"abstract":"<p><p>Integrin-linked kinase (ILK) is a key oncogenic driver in oesophageal squamous cell carcinoma (ESCC). This study evaluated the antitumour effects of the novel ILK inhibitor Nilotinib and explored its downstream mechanisms. In vitro, TE-1 and KYSE150 cells were assessed using Cell Counting Kit-8, lactate dehydrogenase release, colony formation, 5-ehynyl-2 ' -deoxyuridine incorporation, flow cytometry, Transwell assays, and Western blotting to confirm ILK targeting and determine functional changes. Electron microscopy and fluorescent probes with flow cytometry were used to analyse mitochondrial alterations. In vivo, a nude mouse subcutaneous xenograft model was established to examine tumour growth after peritumoural Nilotinib administration; hematoxylin and eosin staining assessed tissue changes, and immunohistochemistry measured Ki67 and cleaved-caspase 3 expression. ILK overexpression alleviated Nilotinib-induced cytotoxicity, restored proliferation, increased proliferating cell nuclear antigen (PCNA) and Ki67, and reduced cleaved-caspase 3 and cleaved poly(ADP-ribose) polymerase (PARP), supporting ILK as a primary target. Nilotinib dose-dependently inhibited proliferation, invasion, and metastasis while promoting apoptosis, accompanied by downregulation of PCNA, Ki67, [matrix metalloproteinase 2 (MMP2), MMP9, and COX2] and upregulation of cleaved-caspase 3 and cleaved-PARP. In xenografts, Nilotinib significantly reduced tumour size and weight, decreased Ki67, and increased cleaved-caspase 3.RNA sequencing identified autoimmune regulator (AIRE) as a markedly downregulated molecule following Nilotinib treatment. Cycloheximide chase assays indicated accelerated AIRE protein degradation, while MG132 partially rescued AIRE levels, implicating proteasome-dependent degradation. Overall, Nilotinib suppresses ESCC progression by inhibiting ILK and destabilising AIRE, suggesting its potential as a targeted therapy for ILK-positive ESCC.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809809","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}

{"title":"Temozolomide-based therapy may remodel the tumor microenvironment and enhance immunotherapy sensitivity in advanced leiomyosarcoma.","authors":"Huijing Tan, Zhuo Li, Jianguo Zhou, Susheng Shi, Liming Jiang, Lijie Zuo, Aijiang Su, Huike Wang, Yuting Sun, Wenjuan Xuan, Yihebali Chi","doi":"10.1097/CAD.0000000000001826","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001826","url":null,"abstract":"<p><p>Leiomyosarcoma (LMS) is characterized by inherent resistance to immune checkpoint blockade, with no conclusive evidence supporting the efficacy of programmed death-1 (PD-1)/programmed death-ligand 1 inhibitor, and it is generally classified as a nonimmunogenic sarcoma subtype. This study analyzed the therapeutic efficacy of temozolomide (TEM)-based regimens in patients with advanced LMS and evaluated pathological changes after TEM treatment to explore the potential role of immunotherapies and the mechanisms that could enhance immunotherapy sensitivity after TEM treatment. This retrospective review included patients with advanced LMS treated at the Cancer Hospital, Chinese Academy of Medical Sciences, and Peking Union Medical College. All patients initiated TEM-based treatments between September 2018 and December 2024. We evaluated patients with advanced LMS and available pathological data before and after TEM-based therapy and those who received subsequent immunotherapy. In total, 47 patients received anthracycline combined with TEM, and 18 patients received gemcitabine combined with TEM. Overall median progression-free survival (mPFS) was 10.0 months, whereas median overall survival (mOS) was 31.0 months. Among six patients who received subsequent PD-1-based immunotherapy after TEM-containing regimens, mPFS and mOS were 13.0 and 45.0 months, respectively. O6-methylguanine DNA methyltransferase negativity tended to be associated with improved survival. Post-TEM biopsies revealed dynamic changes in mismatch repair gene expression, tertiary lymphoid structure counts, and the combined positive score. TEM-based regimens are effective for advanced LMS. Furthermore, pathological changes observed after TEM treatment suggest potential modulation of the tumor microenvironment, supporting further investigation into the integration of immunotherapies in this setting.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809740","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}

{"title":"Response of undifferentiated and dedifferentiated endometrial cancer to pembrolizumab: a case report.","authors":"Peter G Rose, Johanna Kelley, Aaron Petty, Robert Soslow","doi":"10.1097/CAD.0000000000001824","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001824","url":null,"abstract":"<p><p>To report our experience with pembrolizumab in undifferentiated and dedifferentiated endometrial cancer. We performed an institutional review board-approved, retrospective study of computerized pharmacy records to identify all patients with undifferentiated and dedifferentiated endometrial carcinomas treated with pembrolizumab. Eleven patients who received pembrolizumab were identified with the following stages: International Federation of Gynecology and Obstetrics stages IC (1), IIC (2), IIIB (2), IIIC2 (2), and IVB (4). One hundred and forty cycles of pembrolizumab were administered. Ten of the 11 patients were mismatch repair (MMR)-deficient. Eight of the patients received pembrolizumab in combination with chemotherapy. Three partial and two complete responses were seen. Both complete responses were seen when pembrolizumab was given with chemotherapy. Four patients were treated in the adjuvant setting with pembrolizumab had no measurable disease and were not evaluable for response but remain disease-free. Two treatment-emergent adverse effects were noted: colitis and hepatitis. Because of the very high rate of MMR deficiency in undifferentiated and dedifferentiated endometrial carcinomas, incorporation of immunotherapy to chemotherapy should strongly be considered in patients with this histologic type in advanced and early-stage disease.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809719","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}

{"title":"Synergistic antitumor effect between Olaparib and Chidamide by regulation of MYBL2 in lung cancer.","authors":"Lila Zhu, Zhi Ji, Xia Wang, Jiaqi Xin, Lijun Ma, Runshi Zhang, Ting Deng, Yi Ba, Rui Liu","doi":"10.1097/CAD.0000000000001783","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001783","url":null,"abstract":"<p><strong>Abstract: </strong>Recently, various basic research and clinical studies have revealed the further potential of poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitor Olaparib and histone deacetylase inhibitor Chidamide in lung cancer. However, no research available was found to report whether there is a synergistic effect of Olaparib in combination with Chidamide. This research was conducted to investigate whether there is a synergistic effect between the two drugs and the underlying mechanism in lung cancer cell lines. Here, we treat lung cancer cell lines with Olaparib with or without Chidamide in vivo and in vitro. Based on that, we found that there were synergistic effects between Olaparib and Chidamide. Combined use of them cooperatively downregulated the expression of MYBL2, which was responsible for the downregulation of BRCA1, a main member of DNA damage repair. Simultaneously, Olaparib-induced inhibition of PARP expression leads to the 'synthetic lethality' of cells. On the other hand, MYBL2 may regulate the expression of cycle protein dependent kinase 1, causing G2M cell cycle arrest. Consequently, the combination of Olaparib and Chidamide synergistically induces cell apoptosis through synthetic lethality and cell cycle arrest to exert an antitumor effect.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809807","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}

{"title":"Remarkable efficacy of ivonescimab-based second-line therapy in advanced lung adenocarcinoma resistant to chemoimmunotherapy: a case report.","authors":"Xuan Wang, Kunning Yang, Ping Yin","doi":"10.1097/CAD.0000000000001825","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001825","url":null,"abstract":"<p><p>PD-1/PD-L1 inhibitors combined with chemotherapy are the current standard first-line treatment for advanced lung adenocarcinoma (LUAD). However, chemotherapy typically becomes the main therapeutic approach for subsequent treatment once the development of resistance to this initial chemoimmunotherapy, and there are limited effective treatment options available. This case report describes a 41-year-old male patient with stage IVA LUAD (PD-L1 tumor proportion score: 5%, next-generation sequencing: no mutation) who achieved a partial response (PR) with first-line camrelizumab plus pemetrexed and carboplatin, but later experienced disease progression. Upon switching to second-line therapy with ivonescimab (an anti-PD-1/vascular endothelial growth factor-A bispecific antibody) combined with docetaxel, the patient achieved a significant clinical and radiographic response, again evaluated as PR, which was sustained over 12 treatment cycles. Up to now, the progression-free survival (PFS) is more than 12 months, which is significantly longer than the 9-month PFS achieved by the first-line treatment. The regimen was well-tolerated, with only grade 1 adverse events. This case highlights the potential of ivonescimab-based therapy as an effective and manageable second-line option for patients with advanced LUAD who have progressed on prior immune checkpoint inhibitor therapy, even with low PD-L1 expression.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809796","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}

{"title":"Prochlorperazine inhibits the proliferation of hepatocellular carcinoma cells by promoting phosphorylation of β-catenin.","authors":"Yongjie Liang, Xiao Wang, Ruifeng Tian, Xi Wang, Xin Zhang, Juan Wan, Lu Wan, Xiaojing Zhang, Yi Ding","doi":"10.1097/CAD.0000000000001822","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001822","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the most prevalent form of primary liver cancer and ranks as the third leading cause of cancer-related fatalities worldwide. Recently, prochlorperazine (PCZ), a synthetic antipsychotic medication, has gained attention for its potential anticancer properties. However, the specific mechanisms underlying its anticancer effects remain unclear. In this study, we have identified that PCZ effectively inhibits the proliferation of HCC cells and diminishes the number and size of HCC foci in the mouse model. Subsequent studies have revealed that PCZ can directly bind to β-catenin and enhance the phosphorylation level of β-catenin. This, in turn, inhibits the Wnt signaling pathway, thereby exerting its anticancer effects. This novel finding sheds light on the potential molecular mechanisms of PCZ as a therapeutic strategy for HCC. In summary, our study provides fresh insights into the utility of PCZ as a therapeutic option for HCC and elucidates its molecular mechanisms.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809688","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}

{"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":"https://doi.org/10.1097/CAD.0000000000001823","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-07","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}

{"title":"Locoregional and symptomatic response to neoadjuvant dual HER2 blockade with chemotherapy in HER2-positive breast cancer: a pilot study.","authors":"Gurjeet Singh Chowdhary, Ankush Nayyar, Sridharan Vasudevan, Kamalpreet Kaur","doi":"10.1097/CAD.0000000000001780","DOIUrl":"10.1097/CAD.0000000000001780","url":null,"abstract":"<p><p>Dual HER2 blockade with trastuzumab and pertuzumab in combination with chemotherapy has improved pathological complete response (pCR) rates in HER2-positive breast cancer in randomized trials. However, real-world pilot data on locoregional and symptomatic outcomes in patients receiving this regimen before surgery are limited. This was a prospective pilot study including 20 patients with HER2-positive breast cancer treated with neoadjuvant trastuzumab, pertuzumab, and chemotherapy. Patients were assessed clinically and radiologically at baseline and following completion of neoadjuvant therapy. Primary endpoints were locoregional response (tumor shrinkage, nodal downstaging, and operability) and symptomatic improvement (pain, heaviness, and nipple/skin changes). All patients subsequently underwent definitive surgery. Median age was 46 years (range 32-65). Most patients presented with locally advanced disease, and 70% had palpable axillary nodes. Following neoadjuvant therapy, the overall clinical response rate was 85%, with 25% achieving complete clinical response and 60% partial response. Median tumor reduction was approximately 50%. Nodal downstaging was seen in 60%, with complete nodal response in 30%. Symptomatic improvement was reported in 80% for pain, 70% for heaviness, and 60% for skin/nipple changes. All patients proceeded to surgery, and pCR was achieved in 25%. The regimen was well tolerated, with no major cardiac events or treatment-related mortality. Neoadjuvant dual HER2 blockade with chemotherapy is feasible in HER2-positive breast cancer, achieving high clinical response rates, meaningful symptomatic improvement, and acceptable safety in this pilot study. These findings provide early single-center, prospective pilot evidence supporting dual HER2-targeted neoadjuvant therapy, with implications for operability and patient-centered outcomes. Larger multicentre studies are needed to validate these results.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"265-271"},"PeriodicalIF":2.2,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145429954","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}

{"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":"https://doi.org/10.1097/CAD.0000000000001820","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-04-01","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}