Anti-Cancer Drugs最新文献

{"title":"Isovanillin regulates gastric cancer cells apoptosis and metastasis by targeting ROS-mediated MAPK and PI3K signaling pathways.","authors":"Jing-Jing Wen, Xiao-Yu Jin, Ying-Hua Luo, Nan Wu, Yan-Jun Tang, Yan-Zhi Liu, Zhe Liu, Cheng-Hao Jin","doi":"10.1097/CAD.0000000000001808","DOIUrl":"10.1097/CAD.0000000000001808","url":null,"abstract":"<p><p>Isovanillin, a natural coumarin compound, exhibits biological functions; however, its anti-gastric cancer process is not well understood. This research examined the pathway underlying isovanillin's effects on gastric cancer cells. Cell viability assays demonstrated that isovanillin effectively reduced the viability of various gastric cancer cell lines. Network pharmacological analysis identified 41 key targets implicated in isovanillin's anti-gastric cancer activity, highlighting the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), mitogen-activated protein kinase (MAPK), and reactive oxygen species (ROS) pathways as critical components. Apoptosis assays revealed that isovanillin promoted apoptosis by upregulating the manifestation of p-p38 and p-JNK and suppressing p-ERK and p-STAT3. Cellular cycle examination revealed that isovanillin triggered G2/M stage block via the suppression of p-PI3K, p-AKT, cell cycle regulators 1/2 (CDK1/2), and cyclin B1, and the increase of cell cycle inhibitor 1A (p21) and cell cycle inhibitor 1B (p27). Cell metastasis assays showed that isovanillin suppressed the migration of MKN-45 cells through diminishing the concentrations of p-PI3K, p-AKT, N-cadherin, matrix metalloproteinase-2, as well as matrix metalloproteinase-9, while increasing E-cadherin expression. Furthermore, isovanillin exerted its anti-gastric cancer effects by promoting ROS accumulation, thereby modulating associated signaling pathways. The ROS scavenger N-acetyl- l -cysteine reversed isovanillin-induced protein expression changes. In conclusion, isovanillin induces apoptosis, G2/M phase arrest, and inhibits MKN-45 cell migration by mediating ROS to regulate the MAPK and PI3K signaling pathways.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"488-499"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145987666","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":"Acquired FGFR2 mutation leads resistance to pemigatinib in a patient with FGFR2-driven Borrmann type IV gastric cancer.","authors":"Qiong Sun, Sicheng Du, Jing Meng, Weiwei Shi","doi":"10.1097/CAD.0000000000001807","DOIUrl":"10.1097/CAD.0000000000001807","url":null,"abstract":"<p><p>Scirrhous gastric cancer (SGC), including the Borrmann type IV subtype, is characterized by a desmoplastic stroma, rapid progression, and a poor prognosis with limited effective treatment options. While fibroblast growth factor receptor 2 (FGFR2) alterations are recognized therapeutic targets in some cancers, their clinical application in gastric cancer, particularly in SGC, remains underexplored. We present the case of a 47-year-old female with advanced, chemotherapy-refractory Borrmann type IV gastric cancer harboring FGFR2 rearrangement and amplification. Treatment with the selective FGFR1-3 inhibitor pemigatinib elicited a marked clinical and serological response; however, disease progression ensued after 3 months. Comprehensive genomic profiling revealed an acquired FGFR2 N549K mutation, a recognized on-target resistance mechanism. Subsequent administration of the irreversible FGFR1-4 inhibitor futibatinib was associated with a declining trend in tumor biomarkers, indicating preliminary antitumor activity against the resistant clone. This case underscores the clinical activity of FGFR inhibition in FGFR2-altered SGC and exemplifies the emergence of kinase domain mutations as a principal resistance pathway. It further suggests that irreversible FGFR inhibitors may represent a rational therapeutic strategy upon progression on prior FGFR-directed therapy, warranting further clinical investigation in this molecularly defined patient subset.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"522-526"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017276","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":"Dauricine induces ferroptosis in neuroblastoma by inhibiting methyltransferase-like 1-mediated N7-methylguanosine methylation of solute carrier family 3 member 2.","authors":"Liping Tang, Na Huang, Tianyun Li, Lifen Ren","doi":"10.1097/CAD.0000000000001809","DOIUrl":"10.1097/CAD.0000000000001809","url":null,"abstract":"<p><p>Neuroblastoma is one of the most common extracranial solid tumors in children, characterized by high heterogeneity, aggressive biological behavior, and poor clinical prognosis. Ferroptosis, a form of programmed cell death driven by iron accumulation and lipid peroxidation, has been reported to be closely associated with neuroblastoma progression. Dauricine (Dau), a bisbenzylisoquinoline alkaloid extracted from traditional Chinese medicine, has demonstrated antitumor activity, but its role in regulating ferroptosis in neuroblastoma remains unclear. Cell viability, apoptosis, invasion, stemness, and angiogenesis were evaluated using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, terminal deoxynucleotidyl transferase dUTP nick end labeling, transwell, sphere formation, and tube formation assays, respectively. Ferroptosis-related indicators were detected using corresponding commercial kits. The methyltransferase-like 1 (METTL1)-mediated N7-methylguanosine (m7G) methylation of solute carrier family 3 member 2 (SLC3A2) was examined through methylated RNA immunoprecipitation. RNA immunoprecipitation and RNA pull-down assays were conducted to confirm the interaction between METTL1 and SLC3A2 mRNA. Real-time quantitative PCR and western blotting were utilized to assess mRNA and protein expression, respectively. Molecular docking was performed to evaluate the potential binding interaction between Dau and METTL1. A xenograft tumor model was used for in vivo validation. The results showed that Dau inhibited neuroblastoma cell progression and promoted ferroptosis, while overexpression of SLC3A2 countered these effects. METTL1 mediated the m7G methylation of SLC3A2. Overexpression of SLC3A2 reversed the inhibition of neuroblastoma cell progression and the promotion of ferroptosis caused by METTL1 knockdown. Dau suppressed METTL1 expression, thus inhibiting neuroblastoma cell progression and promoting ferroptosis. Additionally, Dau reduced tumor growth in vivo. Together, Dau enhanced ferroptosis and impeded neuroblastoma development by suppressing METTL1-mediated m7G methylation of SLC3A2, suggesting a novel therapeutic strategy for neuroblastoma.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"500-511"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145987652","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":"SENP3-mediated deSUMOylation stabilizes programmed death-ligand 1 to promote immune evasion in hepatocellular carcinoma.","authors":"Bin Zhang, Jianbo Zheng, Yingan Zhao, Zehao Yu, Siming Zheng","doi":"10.1097/CAD.0000000000001785","DOIUrl":"10.1097/CAD.0000000000001785","url":null,"abstract":"<p><p>Despite the clinical benefits of immune checkpoint blockade in hepatocellular carcinoma (HCC), therapeutic efficacy remains limited due to persistent immune evasion. SENP3, a SUMO2/3-specific protease sensitive to redox regulation, has emerged as a critical regulator of protein homeostasis and immune modulation. This study investigates how SENP3 regulates programmed death-ligand 1 (PD-L1) stability through SUMOylation to facilitate immune escape in HCC. We performed comprehensive molecular and functional analyses in HCC cell lines using SENP3 manipulation strategies. PD-L1 expression and SUMOylation status were evaluated by Western blotting and Ni-NTA pulldown assays. Protein interactions were examined through coimmunoprecipitation. Functional immune assays included T cell cytotoxicity measurements using coculture systems, colony formation assays to quantify tumor cell survival, cytokine profiling by ELISA, and granzyme B (GzmB) expression analysis in CD8⁺ T cells via flow cytometry. Clinical samples and experimental models demonstrated significant SENP3 overexpression in HCC. SENP3 knockdown reduced PD-L1 abundance while enhancing T cell-mediated tumor killing, pro-inflammatory cytokine secretion, and cytotoxic GzmB expression in CD8⁺ T cells. Mechanistic studies revealed that SENP3 directly interacts with PD-L1 and catalyzes its deSUMOylation, thereby extending PD-L1 protein half-life. Importantly, SENP3 overexpression rescued the immunostimulatory effects of PD-L1 knockdown, confirming the specificity of this regulatory pathway. Our findings establish SENP3 as a novel posttranslational regulator of PD-L1 that promotes immune evasion in HCC through direct deSUMOylation and stabilization of PD-L1 protein. Therapeutic targeting of SENP3 may overcome resistance to immune checkpoint inhibitors in HCC by restoring antitumor immunity.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"471-481"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760054","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":"Efficacy and safety of fulvestrant combined with abemaciclib in patients with hormone receptor-positive advanced breast cancer.","authors":"Lei Su, Yunyi Du, Jingyu Yao, Mina Wang, Guangjun Zhang, Li Luo, Chunmei Yao, Jun Zhao","doi":"10.1097/CAD.0000000000001806","DOIUrl":"10.1097/CAD.0000000000001806","url":null,"abstract":"<p><p>This study evaluated the efficacy and safety of fulvestrant combined with abemaciclib in patients with hormone receptor-positive advanced breast cancer and compared the outcomes with those reported in the MONARCH 2 trial. Forty-six patients with hormone receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer received fulvestrant 500 mg administered intramuscularly (days 1, 15, and 28, then every 28 days) combined with abemaciclib 150 mg taken orally twice daily until disease progression or unacceptable toxicity. The primary endpoint was progression-free survival (PFS). Secondary endpoints included objective response rate (ORR), disease control rate (DCR), and safety. All 46 patients were evaluable for efficacy. No complete response was observed; 21 patients (45.7%) achieved partial response, 8 (17.4%) had stable disease, and 17 (37.0%) experienced progressive disease (PD). The ORR was 45.7%, and the DCR was 63.0%. Median PFS was 19.1 months (95% confidence interval: 16.0-NR). Compared with the MONARCH 2 trial, ORR was slightly higher (45.7% vs. 35.2%), whereas the DCR was lower (63.0% vs. 83.0%), accompanied by a markedly higher PD rate (37.0% vs. 9.0%, P  < 0.001). The most frequently reported adverse events were leukopenia (30.4%), nausea/vomiting (47.8%), and fatigue (32.6%), consistent with findings from MONARCH 2, with no new safety signals identified. Fulvestrant combined with abemaciclib demonstrated antineoplastic activity and a manageable safety profile in patients with hormone receptor-positive advanced breast cancer. Relative to the MONARCH 2 trial, this real-world cohort exhibited a higher ORR but a lower DCR, potentially reflecting differences in prior treatments and baseline characteristics. Additional large-scale, multicenter studies are warranted to validate these findings.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"482-487"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931904","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":"Anlotinib inhibits glioma cell proliferation, migration, and invasion by suppressing c-MET/AKT/mTOR signaling and altering autophagy-associated protein expression.","authors":"Chunmiao Bao, Xibang Liu","doi":"10.1097/CAD.0000000000001844","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001844","url":null,"abstract":"<p><p>Glioma remains difficult to treat because malignant cells show rapid proliferation, diffuse invasion, and frequent recurrence. This study investigated the direct antitumor effects of anlotinib in human glioma cells and examined whether these effects were associated with hepatocyte growth factor receptor/protein kinase B/mechanistic target of rapamycin (c-MET/AKT/mTOR) signaling, apoptosis-associated responses, mesenchymal-transition-related proteins, and autophagy-associated proteins. U87 and U251 cells were treated with anlotinib in vitro. Cell viability was assessed using Cell Counting Kit-8 assays, migration and invasion were evaluated using wound-healing and Transwell assays, Hoechst 33342 staining was used for qualitative assessment of apoptosis-associated nuclear morphology; and protein expression was analyzed by western blotting. Anlotinib reduced cell viability in a concentration-dependent manner, with estimated 24 h IC50 values of 68.00 μM for U87 cells and 45.53 μM for U251 cells. At lower concentrations, anlotinib reduced wound closure and Transwell invasion, decreased Vimentin, N-cadherin, and β-catenin expression, increased B-cell lymphoma 2 (BCL-2)-associated X protein, decreased BCL-2, altered poly(ADP-ribose) polymerase/caspase-9 expression, reduced total c-MET expression, and decreased AKT/mTOR phosphorylation. Analysis of autophagy-associated proteins showed an increased LC3-II/LC3-I and time-dependent p62 changes. Anlotinib may suppress malignant glioma-cell phenotypes in vitro. These phenotypic changes were associated with alterations in c-MET/AKT/mTOR pathway proteins, apoptosis-associated responses, mesenchymal-transition-related proteins, and autophagy-associated protein expression.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148878996","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":"Prophylactic tramadol for oxaliplatin-induced peripheral vascular pain: a single-arm retrospective study.","authors":"Fumitaka Kawaguchi, Takafumi Tsuneki, Michiko Kobayashi, Motohiko Sano","doi":"10.1097/CAD.0000000000001842","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001842","url":null,"abstract":"<p><p>Oxaliplatin-induced peripheral vascular pain (OIVP) often requires central venous port placement. Conventional preventive strategies have limited efficacy, and the use of some effective analgesics is restricted. This single-center retrospective study evaluated the efficacy and safety of prophylactic tramadol. Electronic medical records of patients who received oxaliplatin-based chemotherapy via a peripheral intravenous line and experienced vascular pain [numerical rating scale (NRS) score ≥ 4] were reviewed. Patients who received prophylactic tramadol in a subsequent cycle were included (n = 23). The primary endpoint was the response rate (≥30% reduction in the NRS score from baseline). The secondary endpoint was the change in NRS score compared with the baseline score in the previous cycle. The response rate was 73.9% [95% confidence interval (CI): 51.6-89.8%]. The median NRS score for OIVP decreased significantly from 7.0 at baseline to 3.0 following tramadol administration (P < 0.0001). Administration greater than or equal to 60 min before infusion was associated with a higher response rate (88.9%; 95% CI: 51.8-99.7%) than administration at 30 min (64.3%; 95% CI: 35.1-87.2%), although this difference was not statistically significant (P = 0.208). Adverse events were mild, with grade 2 nausea reported in two (8.7%; 95% CI: 1.1-28.0%) patients. This exploratory study suggested that prophylactic tramadol was associated with a reduction in pain severity in OIVP, with a favorable safety profile. Thus, tramadol may be a promising and accessible prophylactic option, particularly when access to controlled analgesics is limited.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148856934","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":"Estrogen-related receptor α promotes breast cancer cell migration and invasion by activating transforming growth factor β signaling.","authors":"Monica Prusty, Kartik Muduli, Jagannath Pradhan, Archana Priyadarshini Samal, Joytirmay Tripathy, K Sony Reddy, Selvakumar Elangovan","doi":"10.1097/CAD.0000000000001840","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001840","url":null,"abstract":"<p><p>Breast cancer is a major cause of cancer-related mortality among women, and many patients eventually experience recurrence and progression to metastasis, despite advances in treatment. Estrogen-related receptor α (ERRα), an orphan nuclear receptor, is frequently overexpressed in aggressive breast cancer subtypes and is associated with poor prognosis and an increased risk of recurrence. This study aimed to investigate the role of transforming growth factor β (TGFβ) signaling in ERRα-mediated epithelial-mesenchymal transition (EMT), migration, and invasion in breast cancer cells. ERRα expression was modulated in breast cancer cells using XCT790-mediated inhibition, shRNA-mediated knockdown, and overexpression. Cell viability, clonogenicity, migration, invasion, EMT marker expression, and matrix metalloproteinase (MMP) activity were evaluated. TGFβ1 secretion and Smad signaling were also evaluated. XCT790-mediated inhibition or shRNA-mediated silencing of ERRα significantly reduced cell viability, migration, invasion, and MMP secretion in breast cancer cell lines, whereas ERRα overexpression upregulated migration, invasion, and MMP levels. ERRα suppression also upregulated the epithelial marker ZO-1 and downregulated mesenchymal markers, such as vimentin and β-catenin. This effect was associated with a significant decrease in TGFβ secretion, downregulation of TGFβ-mediated Smad signaling, and reduced expression of its downstream target ANGPTL4. These findings indicate that ERRα promotes EMT, migration, and invasion in breast cancer by upregulating TGFβ secretion and its signaling, underscoring its potential as a therapeutic target.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148856896","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":"MLN4924 suppresses pancreatic cancer progression and enhances chemosensitivity to gemcitabine by targeting the PTGS2/EGFR-PI3K/Akt/mTOR signaling axis.","authors":"Min Wang, Yu Mou, Ji-Yin Qiu, Xiao-Feng He, Can Tang, Hai-Tao Zhu","doi":"10.1097/CAD.0000000000001838","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001838","url":null,"abstract":"<p><p>Pancreatic cancer is a highly lethal digestive malignancy characterized by insidious onset and rapid progression. Approximately 80% of patients are diagnosed at an advanced stage with metastasis, missing the opportunity for radical surgery, and chemotherapy remains the main palliative treatment. Its incidence is rising annually, highlighting the urgent need for novel therapeutic strategies. MLN4924 (Pevonedistat), a first-in-class NEDD8-activating enzyme inhibitor, exhibits promising antitumor activity in various cancers, yet its role and mechanism in pancreatic cancer remain largely undefined. Potential hub targets of MLN4924 in pancreatic cancer were screened using Swiss Target-Prediction and Gene-Cards databases. Western blot was used to detect the expression of hub genes and the activity of the prostaglandin G/H synthase 2 (PTGS2)-epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3K)/RAC-gamma serine/threonine-protein kinase (Akt)/serine/threonine-protein kinase (mTOR) axis following MLN4924 intervention. CCK-8, EdU, and wound-healing assays were performed to evaluate cell proliferation and migration after MLN4924 treatment. Furthermore, PTGS2 knockdown via siRNA transfection was applied to verify its effects on EGFR-PI3K/Akt/mTOR pathway activity, malignant phenotypes, and gemcitabine sensitivity in pancreatic cancer cells. We identified four hub genes (CASP3, PTGS2, MMP9, and MAPK8) of MLN4924 in pancreatic cancer. We validated that MLN4924 suppressed proliferation and migration of pancreatic cancer cells, downregulated hub gene expression, and inhibited the PTGS2-mediated PI3K/AKT/mTOR signaling pathway. Furthermore, siRNA-mediated silencing of PTGS2 phenocopied the inhibitory effects of MLN4924 on cell proliferation. Notably, both MLN4924 and PTGS2 knockdown significantly enhanced the chemosensitivity of pancreatic cancer cells to gemcitabine. Collectively, our results demonstrate that MLN4924 exerts antitumor effects in pancreatic cancer by targeting the PTGS2-EGFR-PI3K/AKT/mTOR axis, providing a mechanistic rationale for its clinical application in pancreatic cancer therapy.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757757","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":"Capecitabine-induced pneumonitis: a rare case report and literature review.","authors":"Mustafa A Tunç, Ali K Güren, Burak Paçaci, Firat Akagündüz, Erkam Kocaaslan, Ahmet Demirel, Yeşim Ağyol, Pinar Erel, Nazim C Demircan, Selver Işik, Abdussamed Çelebi, Ezgi Çoban, Osman Köstek, İbrahim V Bayoğlu, Murat Sari","doi":"10.1097/CAD.0000000000001839","DOIUrl":"https://doi.org/10.1097/CAD.0000000000001839","url":null,"abstract":"<p><p>Capecitabine is an oral fluoropyrimidine prodrug widely used in the treatment of various malignancies, including colorectal cancer. While it is generally well-tolerated, rare and life-threatening toxicities can occur. Pneumonitis is an exceedingly rare complication associated with capecitabine monotherapy. A 36-year-old male with pT3N0 (stage IIA) colon adenocarcinoma underwent curative resection and was started on adjuvant capecitabine monotherapy. During the second cycle, the patient developed a cough and exertional dyspnea. Symptoms progressed during the third cycle, leading to hospitalization. Imaging revealed diffuse ground-glass opacities, and pulmonary function tests showed a severely reduced diffusion capacity of the lung for carbon monoxide (38% of predicted). Dihydropyrimidine dehydrogenase deficiency was ruled out. Based on clinical and radiological findings, a diagnosis of capecitabine-induced pneumonitis was made. Capecitabine was discontinued, and intravenous methylprednisolone (1 mg/kg) was initiated. The patient showed rapid symptomatic improvement and was discharged with a tapered steroid regimen. Follow-up imaging at 1 month showed complete resolution of pulmonary opacities. The patient remains in remission at a 3-year follow-up. Although capecitabine-induced pneumonitis is remarkably rare, it carries a risk of significant morbidity. Clinicians should maintain a high index of suspicion for drug-induced pulmonary toxicity in patients presenting with new respiratory symptoms during capecitabine therapy, as early recognition and treatment are crucial for recovery.</p>","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148856963","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}