Oncology Letters最新文献

{"title":"Long-term survival with tocilizumab treatment for tislelizumab-related pneumonitis in a patient with non-small cell lung cancer: A case report.","authors":"Lan Yu, Qing-Ming Guo, Li Liu, Yu Wang, Fei Chen, Xiao-Tao Zhang","doi":"10.3892/ol.2026.15699","DOIUrl":"10.3892/ol.2026.15699","url":null,"abstract":"<p><p>Tislelizumab, an immune checkpoint inhibitor (ICI) that is approved for the treatment of non-small cell lung cancer (NSCLC), has shown superior overall and progression-free survival benefits compared with chemotherapy in clinical trials. However, like other ICIs, tislelizumab administration may lead to a series of immune-related adverse events (irAEs), including checkpoint inhibitor pneumonitis. Corticosteroids are recommended as the first-line treatment for the management of irAEs. However, biological immunomodulatory agents, such as infliximab and tocilizumab, are often needed in patients with steroid-refractory or steroid-resistant irAEs. The present study reports the case of a patient with NSCLC and tislelizumab-related pneumonitis, who showed complete resolution of symptoms and clear computed tomography imaging after tocilizumab treatment, and achieved a long-term survival period of >5 years. In the current patient, the involvement of interleukin-6 (IL-6) in corticosteroid-refractory pneumonitis was demonstrated by elevated serum IL-6 levels, and subsequent treatment with the IL-6 receptor inhibitor tocilizumab achieved complete resolution and long-term survival. The present case suggests that IL-6 may be involved in the pathogenesis of irAEs and that tocilizumab may be an effective option for treating steroid-refractory or steroid-resistant irAEs.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"344"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13288791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318319","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}

{"title":"Long survival of PD-L1-positive mediastinal sarcomatoid carcinoma after immunotherapy and anti-angiogenic target therapy: A case report.","authors":"Shuling Wu, Danping Wang, Qiong Fu, Yingying Ding","doi":"10.3892/ol.2026.15690","DOIUrl":"10.3892/ol.2026.15690","url":null,"abstract":"<p><p>Mediastinal sarcomatoid carcinoma (SC) is rare and is often associated with poor survival outcomes. At present, there have been no investigations into the use of immunotherapy and anti-angiogenic target therapy to treat mediastinal SC. In the present study, a 74-year-old woman with mediastinal SC who achieved long-term survival was described. Immunohistochemistry of tumor specimens showed high expression of programmed cell death ligand 1 (PD-L1) and a combined positive score of 80. The patient initially received two cycles of chemotherapy and one cycle of radiotherapy combined with anlotinib; subsequent evaluation confirmed stable disease. After which, the patient received two cycles of immunotherapy with durvalumab, and received continued administration with anlotinib; follow-up evaluation revealed a partial response. Immunotherapy was halted due to severe adverse effects, but treatment with anlotinib has remained ongoing. At present, the patient remains alive with no evidence of disease progression, achieving a progression-free survival of >42 months. The present case report highlights the potential of immunotherapy combined with anti-angiogenic targeted therapy in treating PD-L1-positive mediastinal SC, despite the life-threatening adverse reactions, offering a viable treatment option for similar clinical cases.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"335"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295875","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}

{"title":"Vanishing liver metastases in pancreatic cancer: A case report.","authors":"Evangelia Florou, Paul Ross, Parthi Srinivasan, Andreas Prachalias","doi":"10.3892/ol.2026.15691","DOIUrl":"10.3892/ol.2026.15691","url":null,"abstract":"<p><p>Metastatic pancreatic cancer carries a poor prognosis, with palliative chemotherapy offering limited survival benefit and conversion to resectability considered rare. The present study reports the case of a 60-year-old woman with pancreatic adenocarcinoma and extensive liver metastases treated with palliative FOLFIRINOX, achieving complete radiological disappearance of hepatic disease and sustained control of the primary tumour. After a treatment pause and subsequent reinitiation of chemotherapy for local progression, the liver metastases remained absent. At 32 months post-diagnosis, the patient underwent pancreatic resection with negative margins and remains alive and free from hepatic recurrence 84 months from diagnosis. This case highlights that select patients may achieve long-term survival through individualized, multimodal treatment strategies.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"336"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295618","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}

{"title":"Construction and validation of a predictive model of pathological complete response combined with MRI and tumor indicators for HER2-positive breast cancer after neoadjuvant targeted therapy.","authors":"Keying Zhu, Zeying Li, Jiaqian Liao, Changan Wang, Rong Guo, Yiyin Tang, Shaoqiang Zhou, Yingying Ding, Dedian Chen, Jiankui Wang, Jianyun Nie, Sheng Huang","doi":"10.3892/ol.2026.15693","DOIUrl":"10.3892/ol.2026.15693","url":null,"abstract":"<p><p>Accurate models for predicting pathological complete response (pCR) after neoadjuvant therapy (NAT) are increasingly needed in patients with human epidermal growth factor receptor 2 (HER2)-positive breast cancer (BC). In the present study, a nomogram was developed to estimate the probability of achieving a pCR in this population. Clinical data were retrospectively and prospectively collected from patients with HER2-positive BC at three time points: Before NAT, after the first cycle of neoadjuvant targeted therapy and after the completion of NAT before surgery. Logistic regression analysis was performed to identify independent predictors of pCR, and these variables were used to construct a predictive model and corresponding nomogram. Model performance was evaluated using calibration curves, decision curve analysis, receiver operating characteristic (ROC) curves and the area under the ROC curve (AUC), with retrospective data and prospective data used for internal and external validations, respectively. Logistic regression analysis of the retrospective cohort identified eight predictors associated with pCR, which were incorporated into a concise nomogram. Internal validation demonstrated good calibration and strong predictive performance, with an AUC value of 0.886 (P<0.001), sensitivity of 0.822 and specificity of 0.818. External validation further confirmed the excellent discriminatory ability of the model, yielding an AUC value of 0.961 (P<0.001), sensitivity of 1.000 and specificity was 0.875. Overall, this nomogram, which integrates multiple clinically relevant factors, may serve as a useful tool for predicting post-NAT pCR in patients with HER2-positive BC and may support more precise treatment decision-making in clinical practice.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"339"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295932","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}

{"title":"Spatiotemporal heterogeneity in non-small cell lung cancer: A paradigm shift from characterization to dynamic management (Review).","authors":"Li Cao, Wei Zhang","doi":"10.3892/ol.2026.15697","DOIUrl":"10.3892/ol.2026.15697","url":null,"abstract":"<p><p>Treatment of non-small cell lung cancer (NSCLC) has entered the era of precision medicine, characterized by targeted therapies and immunotherapies. However, tumor heterogeneity across spatial and temporal dimensions remains a central cause of therapeutic failure and acquired resistance. Spatial heterogeneity manifests as clonal diversity within a single tumor and between metastatic lesions, while temporal heterogeneity reflects the dynamic evolution of clonal populations under therapeutic pressure. It has proved difficult for traditional static diagnostic and therapeutic models to comprehensively capture this complexity. Advances in technologies such as single-cell sequencing, spatial transcriptomics and liquid biopsy now allow the spatiotemporal evolutionary patterns of NSCLC to be deciphered with unprecedented resolution. Based on these developments, the present review proposed that clinical management strategies need to shift from a static classification paradigm towards a new paradigm of dynamic monitoring and intervention. Emerging strategies are systematically discussed, including evolutionary trap therapy, niche intervention and adaptive therapy, which aim to achieve long-term control of disease progression by steering tumor evolutionary paths, remodeling the tumor microenvironment or leveraging competitive suppression mechanisms. Despite ongoing challenges at the technical, biological and clinical translation levels, a dynamic management framework integrating multi-omics data and intelligent algorithms represents promise for transforming NSCLC into a chronic, controllable disease.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"342"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13288788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148318337","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}

{"title":"Comprehensive bioinformatics analysis of NCAPH expression and its clinical importance in endometrial cancer.","authors":"Yuxiu Huang, Kang Kang, Qian Zhuo, Qianqian Ma, Yujie Xue, Yaning Zhu, Mingde Huang","doi":"10.3892/ol.2026.15696","DOIUrl":"10.3892/ol.2026.15696","url":null,"abstract":"<p><p>Emerging evidence has implicated non-SMC condensin I complex subunit H (NCAPH) as a key regulator of mitosis and driver of tumorigenesis. However, its expression profiling and clinical relevance in endometrial cancer (EC) remain inadequately characterized. The present study aimed to systematically investigate the expression profiling, mutational landscape, co-expression networks and prognostic importance of NCAPH in EC through integrated bioinformatics approaches. NCAPH expression was evaluated in pan-cancer and EC cohorts derived from The Cancer Genome Atlas and Genotype Tissue Expression databases. Mutational analysis was performed using the 'maftools' package in R software. Genes co-expressed with NCAPH (with a significance threshold of P<0.05) were subjected to functional enrichment analysis using Metascape. Single-sample Gene Set Enrichment Analysis (ssGSEA) was used to evaluate the correlation between gene expression and pathway scores. The Tumor Immune Estimation Resource database was utilized to explore the correlation between NCAPH expression and the abundance of tumor-infiltrating immune cells in EC. The prognostic importance of NCAPH was assessed by Kaplan-Meier survival analysis and receiver operating characteristic curve analysis. Immunohistochemistry and western blotting was performed to validate NCAPH protein expression in clinical specimens. Results indicated that NCAPH mRNA and protein expression were significantly elevated in EC compared with normal endometrium. In addition, NCAPH expression was found to be positively correlated with advanced International Federation of Gynecology and Obstetrics stage, advanced age, TP53 mutation and aggressive histological subtypes. Somatic mutations of NCAPH occurred in 4.92% of EC cases, with missense mutations being the predominant type (79.3%). Functional enrichment analysis indicated that NCAPH-associated genes were involved in 'cell cycle', 'DNA replication' and 'oocyte meiosis'. ssGSEA exhibited a positive correlation between NCAPH and DNA repair, G₂M checkpoint, tumor cell proliferation and the PI3K/AKT/mTOR pathway. NCAPH expression exhibited a significant negative correlation with CD8+ T cell infiltration, whereas positive correlations were observed with CD4+ T helper 2 cell infiltration, CD163 and programmed death-ligand 1. In addition, high NCAPH expression was found to predict reduced 5-year overall survival and exhibited certain diagnostic efficacy (area under the curve=0.628). Overall, NCAPH may promote endometrial carcinogenesis through dysregulation of mitotic processes, induction of chromosomal instability as well as modulation of the tumor immune microenvironment and thus may serve as both a prognostic biomarker and a therapeutic target in EC.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"341"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295882","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}

{"title":"RTA-408 induces JNK-dependent apoptosis and autophagy in breast cancer cells.","authors":"Yu-Jen Chen, Hung-Pei Tsai, Mei-Yin Chen, I-Hsiang Chen, Wei-Chieh Chen, Tzu-Ting Tseng, Chen-Yu Wang, Jia-Hau Lee","doi":"10.3892/ol.2026.15692","DOIUrl":"10.3892/ol.2026.15692","url":null,"abstract":"<p><p>RTA-408 is a synthetic activator of the nuclear factor erythroid 2-related factor 2 pathway with antioxidant and anti-inflammatory act2ivity, but its antitumor effects in breast cancer (BC) have not fully been defined. The present study evaluated the antiproliferative efficacy and underlying mechanisms of RTA-408 in BC cells. Estrogen receptor-positive MCF-7 and triple-negative MDA-MB-231 BC cells were exposed to 0-1,000 nM RTA-408 for 72 h in standard serum-containing culture medium. Cell viability was quantified using a tetrazolium-based colorimetric assay and apoptosis was evaluated by the Muse^® Annexin V & Dead Cell assay based on Annexin V and 7-amino-actinomycin D staining; the expression levels of JNK, p38, ERK, beclin-1, microtubule-associated protein 1 light chain 3B (LC3B), p62/sequestosome 1 (SQSTM1) and poly (ADP-ribose) polymerase (PARP) were assessed by western blotting. Pathway dependence was examined using the JNK inhibitor SP600125. Results showed that RTA-408 reduced cell viability in a concentration-dependent manner, with an IC₅₀ of ~400 nM, decreasing survival to 28% in MCF-7 cells and 22% in MDA-MB-231 cells at 1,000 nM. RTA-408 increased annexin V⁺ apoptotic fractions, enhanced PARP cleavage and increased beclin-1, LC3B and p62/SQSTM1 levels. RTA-408 markedly enhanced JNK phosphorylation, with more modest activation of p38 and ERK. Pharmacological inhibition with SP600125 attenuated JNK phosphorylation, reduced apoptotic responses and diminished autophagy-associated marker accumulation, supporting the notion that JNK signaling contributes, at least in part, to these effects. These findings indicate that RTA-408 exerts nanomolar antiproliferative activity in both hormone receptor-positive and triple-negative BC cells through a JNK-dependent mechanism that simultaneously engages apoptosis and autophagy, supporting further <i>in vivo</i> and translational investigation.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"337"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295880","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}

{"title":"Tanshinone IIA suppresses cancer metastasis by modulating tumor cell-platelet-endothelial cell interactions.","authors":"Judan Xu, Lin Luo, Feiyang Li, Siying Wang, Chengbin Fu, Guihua Wang, Yanhong Wang, Yusheng Lu","doi":"10.3892/ol.2026.15694","DOIUrl":"10.3892/ol.2026.15694","url":null,"abstract":"<p><p>Hematogenous metastasis is a major cause of cancer-related mortality and depends on coordinated interactions between circulating tumor cells, platelets and vascular endothelial cells. Targeting this metastatic microenvironment represents a promising strategy to limit tumor dissemination. Tanshinone IIA (Tan IIA), a bioactive compound derived from <i>Salvia miltiorrhiza</i>, has anti-tumor activity, however, its effects on tumor cell-platelet-endothelial interactions during metastasis remain incompletely understood. In the present study, Tan IIA was evaluated at low, non-cytotoxic concentrations to assess its influence on metastatic processes rather than direct tumor cell killing. In assessments of cell viability and the cell cycle, Tan IIA exhibited minimal effects on the viability of tumor and endothelial cells, while significantly suppressing tumor cell migration and invasion <i>in vitro</i>. Mechanistically, Tan IIA decreased CD29 expression on tumor cells, inhibited platelet activation, as indicated by decreased P-selectin expression, and attenuated tumor cell-platelet aggregate formation. Tan IIA diminished TNF-α-induced upregulation of endothelial adhesion molecules intercellular adhesion molecule-1 and E-selectin, resulting in decreased tumor cell adhesion to endothelial monolayers by inhibiting the NF-κB signaling pathway. These coordinated effects resulted in a significant reduction in pulmonary metastatic burden and prolonged survival in mouse models of hematogenous metastasis, without evidence of overt systemic toxicity. Collectively, these findings indicated that Tan IIA suppresses metastatic dissemination primarily by modulating interactions between tumor cells, platelets and endothelial cells, highlighting its potential as a pharmacological agent targeting the metastatic microenvironment.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"338"},"PeriodicalIF":2.1,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280531/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295388","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}

{"title":"Cepharanthine suppresses lung adenocarcinoma through targeting glutathione peroxidase 4.","authors":"Ruoxue Cao, Sun Kang, Kun Wang, Yan Wang, Minghui Li, Qian Liu, Ying Zhang, Mei Fu","doi":"10.3892/ol.2026.15686","DOIUrl":"10.3892/ol.2026.15686","url":null,"abstract":"<p><p>Lung cancer poses a marked threat to global health, with lung adenocarcinoma (LUAD) being a predominant subtype. Despite their availability, treatment options often fall short of expectations. In this context, Traditional Chinese Medicine, known for its multifaceted therapeutic effects and favorable safety profile, has emerged as a promising alternative. In particular, cepharanthine (CEP), a bisbenzylisoquinoline alkaloid derived from <i>Stephania cepharantha</i>, has demonstrated the ability to suppress the proliferation of a range of tumor cells. However, the precise mechanisms by which CEP impacts LUAD remain to be elucidated. The present study focused on the anti-tumor effects of CEP on LUAD. Cellular experiment analysis revealed that CEP exhibited an IC₅₀ value of 6.810 µM for the H1299 cell line and 9.041 µM for the PC-9 cell line, with minimal toxicity to normal BEAS-2B cells. Bioinformatics analysis identified three potential target genes for CEP, namely glutathione peroxidase 4 (GPX4), tyrosyl-DNA phosphodiesterase 1 and carbonic anhydrase 4, among which CEP significantly suppressed the expression of GPX4 in LUAD cells. Further validation showed that the impact of CEP on cell proliferation, apoptosis and invasiveness was diminished in cells with GPX4 knockdown. <i>In vivo</i> experiments demonstrated that CEP could inhibit the growth of subcutaneously transplanted tumors in mice, however its therapeutic effect was reduced in GPX4 gene knockout mice bearing GPX4-knockdown tumors. In summary, CEP may exert its anti-LUAD effects by targeting GPX4, thereby offering a novel therapeutic strategy for LUAD treatment.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"331"},"PeriodicalIF":2.1,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13273163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148278289","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}

{"title":"Undifferentiated pelvic sarcoma 5 years post-radiochemotherapy for rectal adenocarcinoma: A case report.","authors":"Yang Yang, Yubin Long","doi":"10.3892/ol.2026.15684","DOIUrl":"10.3892/ol.2026.15684","url":null,"abstract":"<p><p>Radiation-induced sarcoma (RIS) is a rare, life-threatening late complication of radiotherapy, typically diagnosed 3-5 years post-treatment. It is associated with a poor prognosis and poses diagnostic challenges due to non-specific imaging and clinical features that mimic tumor recurrence. As the long-term survival rates of patients with rectal cancer improve, recognizing late-onset treatment-related malignancies becomes increasingly paramount. The present study describes the case of a 62-year-old male patient who presented to Shaoyang Central Hospital (Shaoyang, Hunan, China) in February 2019 and underwent neoadjuvant chemoradiotherapy followed by radical resection for rectal adenocarcinoma in June 2019. After 5 years, he presented with buttock pain in December 2024. Computed tomography (CT) imaging revealed a sacrococcygeal soft tissue mass within the prior radiation field. A biopsy confirmed an undifferentiated sarcoma, histologically distinct from the primary carcinoma, fulfilling modified Cahan criteria for RIS. Despite diagnosis, the patient declined further treatment due to concerns about toxicity and exhibited disease progression. A follow-up examination in June 2025 showed that the masses had increased in number and size. The present case underscores the importance of long-term surveillance in rectal cancer survivors. A re-biopsy of suspicious masses is key to differentiate RIS from recurrence. Early recognition may improve patient outcomes, although current therapeutic options, such as standard radiotherapy and chemotherapy, remain limited. Immunotherapy and targeted therapy are considered as second-line treatment options. However, due to factors such as physical and financial conditions, this patient did not choose to continue the treatment.</p>","PeriodicalId":19503,"journal":{"name":"Oncology Letters","volume":"32 2","pages":"329"},"PeriodicalIF":2.1,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13273503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148278245","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}