Adam Put, Katerina Smesny Trtkova, Marcel Mittak, Petra Herentinova, Jana Vaculova, Radoslava Cernekova, Jozef Skarda
Introduction: Large cell neuroendocrine carcinoma (LCNEC) is a subtype of non-small-cell lung carcinoma with poorly understood methylation characteristics, including the activity of DNA methyltransferases. Despite the pivotal role of DNA methyltransferases in epigenetic regulation, their expression profile in LCNEC remains unexplored. This study represents the first effort to evaluate the expression of DNMT1, DNMT3A, and DNMT3B genes in patients with LCNEC.
Materials and methods: We performed quantitative expression analyses of DNMT1, DNMT3A, and DNMT3B on formalin-fixed, paraffin-embedded tissue samples obtained from LCNEC patients. Normal lung tissues (n = 4) from healthy patients served as controls to determine differential expression levels.
Results: The analysis revealed upregulation of both DNMT1 and DNMT3A compared to control normal lung tissue. In addition, normalized expression values of DNMT3B were reduced compared to the analyzed DNMT1 and DNMT3A.
Conclusion: In this exploratory pilot of 18 LCNEC cases, DNMT1 and DNMT3A transcripts were frequently higher relative to a normal-lung calibrator, while DNMT3B results were inconclusive due to technical limitations and small sample size. These descriptive findings warrant validation in larger, isoform-resolved cohorts before clinical inference. Future research should prioritize investigating these DNA methyltransferases to explore their therapeutic implications. Moreover, future research should also aim to detect and characterize individual DNMT3B isoforms in LCNEC patients to further elucidate their specific contributions to the pathology of the disease.
{"title":"Altered DNA Methyltransferase Expression in Pulmonary Large-Cell Neuroendocrine Carcinoma: Pilot Experimental Data Targeted DNMT1, DNMT3A, and DNMT3B.","authors":"Adam Put, Katerina Smesny Trtkova, Marcel Mittak, Petra Herentinova, Jana Vaculova, Radoslava Cernekova, Jozef Skarda","doi":"10.1002/cnr2.70513","DOIUrl":"https://doi.org/10.1002/cnr2.70513","url":null,"abstract":"<p><strong>Introduction: </strong>Large cell neuroendocrine carcinoma (LCNEC) is a subtype of non-small-cell lung carcinoma with poorly understood methylation characteristics, including the activity of DNA methyltransferases. Despite the pivotal role of DNA methyltransferases in epigenetic regulation, their expression profile in LCNEC remains unexplored. This study represents the first effort to evaluate the expression of DNMT1, DNMT3A, and DNMT3B genes in patients with LCNEC.</p><p><strong>Materials and methods: </strong>We performed quantitative expression analyses of DNMT1, DNMT3A, and DNMT3B on formalin-fixed, paraffin-embedded tissue samples obtained from LCNEC patients. Normal lung tissues (n = 4) from healthy patients served as controls to determine differential expression levels.</p><p><strong>Results: </strong>The analysis revealed upregulation of both DNMT1 and DNMT3A compared to control normal lung tissue. In addition, normalized expression values of DNMT3B were reduced compared to the analyzed DNMT1 and DNMT3A.</p><p><strong>Conclusion: </strong>In this exploratory pilot of 18 LCNEC cases, DNMT1 and DNMT3A transcripts were frequently higher relative to a normal-lung calibrator, while DNMT3B results were inconclusive due to technical limitations and small sample size. These descriptive findings warrant validation in larger, isoform-resolved cohorts before clinical inference. Future research should prioritize investigating these DNA methyltransferases to explore their therapeutic implications. Moreover, future research should also aim to detect and characterize individual DNMT3B isoforms in LCNEC patients to further elucidate their specific contributions to the pathology of the disease.</p>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 3","pages":"e70513"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147484790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Male patients were twice as likely to develop gastric cancer (GC) compared to females, partly due to the protective effect of estrogen. However, the proportion of females increased in the young GC patients.
Aims: The study was designed to explore comprehensive molecular profiles of younger female GC patients, as well as develop a prognostic gene model for female GC patients.
Materials&methods: Gene expression and clinical data of GC and nontumor patients were downloaded from the Gene Expression Omnibus (GEO) database. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) were used to find molecular characteristics and potential mechanisms of younger female GC patients. The prognostic gene model containing six differential expressed genes (DEGs), which were between younger and older female patients, was established using Lasso-Cox regression. Its performance was validated by external validation. Then, receiver operating characteristic (ROC) curve was applied to determine the prognostic value of the prognostic gene model.
Results: Six GEO cohorts with 305 female GC patients (69 younger patients and 236 older patients) and 38 female nontumor patients were included. A total of 4557 DEGs between female GC patients and nontumor patients were identified, including 2212 upregulated genes and 2345 downregulated genes. Estrogen response early (p < 0.001) and estrogen response late (p < 0.001) were enriched in female GC patients. In KEGG analysis, aldosterone (p = 0.023) and relaxin pathways (p = 0.043) were concentrated in the younger group. Moreover, we further used the GSE84437 cohort to construct a prognostic gene model containing six genes, namely NREP, GAD1, SLCO4A1, KRT17, DEFB1, and P3H2, to predict the overall survival (OS) of female GC patients (AUC = 0.810). In the overall analysis of female GC patients, high-risk patients showed worse OS than low-risk patients (HR = 5.7688, 95% CI: 3.0108-11.0530, p < 0.001). Compared with older female patients, younger female patients had a higher tendency to be in the high-risk group (31.1% vs. 18.3%, p = 0.018).
Conclusions: In conclusion, we provided the comprehensive molecular profiles of younger female GC patients and found that there was a significant difference in enriched hormone-related pathways between the younger group and the older group. Compared with older female patients, younger female patients were more likely to be in the high-risk group, which showed worse OS than low-risk patients.
背景：男性患者发生胃癌（GC）的可能性是女性的两倍，部分原因是雌激素的保护作用。然而，女性在年轻胃癌患者中所占比例增加。目的：本研究旨在探索年轻女性GC患者的综合分子图谱，并建立女性GC患者预后的基因模型。材料与方法：从Gene expression Omnibus （GEO）数据库下载胃癌和非肿瘤患者的基因表达和临床数据。采用基因本体（GO）、京都基因与基因组百科全书（KEGG）和基因集富集分析（GSEA）等方法寻找年轻女性GC患者的分子特征和潜在机制。采用Lasso-Cox回归建立了包含6个差异表达基因（DEGs）的年轻和老年女性患者预后基因模型。通过外部验证对其性能进行了验证。然后应用受试者工作特征（ROC）曲线确定预后基因模型的预后价值。结果：6个GEO队列共纳入305例女性胃癌患者（年轻69例，老年236例）和38例女性非肿瘤患者。女性胃癌患者与非肿瘤患者共鉴定出4557个基因，其中上调基因2212个，下调基因2345个。结论：综上所述，我们提供了年轻女性GC患者的全面分子图谱，发现年轻组与老年组在丰富的激素相关通路上存在显著差异。与老年女性患者相比，年轻女性患者更有可能属于高危组，其OS表现较低危患者差。
{"title":"Molecular Characteristics, Potential Mechanisms, and Prognostic Gene Model of Younger Female Patients With Gastric Cancer.","authors":"Xiaoyi Luan, Lulu Zhao, Wanqing Wang, Penghui Niu, Xue Han, Zerong Wang, Xiaojie Zhang, Dongbing Zhao, Yingtai Chen","doi":"10.1002/cnr2.70469","DOIUrl":"10.1002/cnr2.70469","url":null,"abstract":"<p><strong>Background: </strong>Male patients were twice as likely to develop gastric cancer (GC) compared to females, partly due to the protective effect of estrogen. However, the proportion of females increased in the young GC patients.</p><p><strong>Aims: </strong>The study was designed to explore comprehensive molecular profiles of younger female GC patients, as well as develop a prognostic gene model for female GC patients.</p><p><strong>Materials&methods: </strong>Gene expression and clinical data of GC and nontumor patients were downloaded from the Gene Expression Omnibus (GEO) database. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) were used to find molecular characteristics and potential mechanisms of younger female GC patients. The prognostic gene model containing six differential expressed genes (DEGs), which were between younger and older female patients, was established using Lasso-Cox regression. Its performance was validated by external validation. Then, receiver operating characteristic (ROC) curve was applied to determine the prognostic value of the prognostic gene model.</p><p><strong>Results: </strong>Six GEO cohorts with 305 female GC patients (69 younger patients and 236 older patients) and 38 female nontumor patients were included. A total of 4557 DEGs between female GC patients and nontumor patients were identified, including 2212 upregulated genes and 2345 downregulated genes. Estrogen response early (p < 0.001) and estrogen response late (p < 0.001) were enriched in female GC patients. In KEGG analysis, aldosterone (p = 0.023) and relaxin pathways (p = 0.043) were concentrated in the younger group. Moreover, we further used the GSE84437 cohort to construct a prognostic gene model containing six genes, namely NREP, GAD1, SLCO4A1, KRT17, DEFB1, and P3H2, to predict the overall survival (OS) of female GC patients (AUC = 0.810). In the overall analysis of female GC patients, high-risk patients showed worse OS than low-risk patients (HR = 5.7688, 95% CI: 3.0108-11.0530, p < 0.001). Compared with older female patients, younger female patients had a higher tendency to be in the high-risk group (31.1% vs. 18.3%, p = 0.018).</p><p><strong>Conclusions: </strong>In conclusion, we provided the comprehensive molecular profiles of younger female GC patients and found that there was a significant difference in enriched hormone-related pathways between the younger group and the older group. Compared with older female patients, younger female patients were more likely to be in the high-risk group, which showed worse OS than low-risk patients.</p>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 3","pages":"e70469"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12954549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Randy S D'Amico, Patricia Avancena, Alon Kashanian, Rosivel Galvez, Deborah Gruber, Sami Saba, Avraham Zlochower, Manju Harshan, Morana Vojnic
Background: Pleomorphic xanthoastrocytomas (PXAs) are rare primary central nervous system (CNS) tumors that appear heterogeneous on imaging and histology and typically cause headaches or seizures on initial presentation. Alongside high rates of favorable prognosis after surgical excision exist similarly high rates of recurrence. Leptomeningeal spread on recurrence is even rarer and more challenging to diagnose.
Case: We describe a case of a 40-year-old man with a history of surgically resected PXA presenting 12 years later with persistent headaches and lower back pain. Imaging studies revealed arachnoiditis, and a subsequent brain biopsy was nondiagnostic. Serial CSF studies only revealed the presence of atypical cells too few to further characterize via standard histology studies, with rare small lymphocytes and monocytoid cells. Submitting these cells for next-generation sequencing ultimately revealed a BRAF V600E mutation typically found in PXAs, thereby confirming the diagnosis of leptomeningeal recurrence and revealing a therapeutic target.
Conclusion: This case highlights the utility of next-generation sequencing as a means of non-invasively diagnosing leptomeningeal disease in recurrent PXA and potentially in other cancer types as well.
{"title":"Identification of BRAF V600E Mutation in Cerebrospinal Fluid Aids in Diagnosing Leptomeningeal Carcinomatosis Arising From Pleomorphic Xanthoastrocytoma: A Case Report.","authors":"Randy S D'Amico, Patricia Avancena, Alon Kashanian, Rosivel Galvez, Deborah Gruber, Sami Saba, Avraham Zlochower, Manju Harshan, Morana Vojnic","doi":"10.1002/cnr2.70487","DOIUrl":"https://doi.org/10.1002/cnr2.70487","url":null,"abstract":"<p><strong>Background: </strong>Pleomorphic xanthoastrocytomas (PXAs) are rare primary central nervous system (CNS) tumors that appear heterogeneous on imaging and histology and typically cause headaches or seizures on initial presentation. Alongside high rates of favorable prognosis after surgical excision exist similarly high rates of recurrence. Leptomeningeal spread on recurrence is even rarer and more challenging to diagnose.</p><p><strong>Case: </strong>We describe a case of a 40-year-old man with a history of surgically resected PXA presenting 12 years later with persistent headaches and lower back pain. Imaging studies revealed arachnoiditis, and a subsequent brain biopsy was nondiagnostic. Serial CSF studies only revealed the presence of atypical cells too few to further characterize via standard histology studies, with rare small lymphocytes and monocytoid cells. Submitting these cells for next-generation sequencing ultimately revealed a BRAF V600E mutation typically found in PXAs, thereby confirming the diagnosis of leptomeningeal recurrence and revealing a therapeutic target.</p><p><strong>Conclusion: </strong>This case highlights the utility of next-generation sequencing as a means of non-invasively diagnosing leptomeningeal disease in recurrent PXA and potentially in other cancer types as well.</p>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 3","pages":"e70487"},"PeriodicalIF":1.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<div> <section> <h3> Background</h3> <p>Androgen insensitivity syndrome (AIS) is an X-linked recessive genetic disorder caused by mutations in the androgen receptor (AR) gene, leading to androgen resistance and disorders of sex development (DSD) in 46, XY individuals. It is classified into three phenotypes: complete (CAIS), partial (PAIS), and mild (MAIS). CAIS is characterized by normal external female genitalia, primary amenorrhea, and a 46, XY karyotype. While the risk of germ cell tumors (GCTs) in CAIS is generally low due to rapid germ cell depletion from absent AR responsiveness, GCTs still occur in adulthood, and clinical data on such cases remain limited—especially regarding detailed genetic profiling and long-term management outcomes.</p> </section> <section> <h3> Case</h3> <p>This study presents two adult CAIS patients with GCTs, managed at one tertiary hospital in Beijing, China, between 2020 and 2022. Both patients were raised as females and presented with primary amenorrhea:</p> </section> <section> <h3> Case 1</h3> <p>A 43-year-old married woman with a 5-year history of abdominal distension and 5-month history of impaired bowel movements. Preoperative imaging revealed bilateral pelvic masses (left: 7.7 × 6.4 cm; right: 2.2 × 2.0 cm), and laboratory tests showed elevated testosterone, LH, FSH, AFP, and β-HCG. She underwent 3-dimensional laparoscopic pelvic lumpectomy; histopathology confirmed left seminoma and right testicular tissue dysplasia. Whole exome sequencing (WES) identified four AR gene mutations (c.171_191del, c.255_257del, c.1368_1369insGGC, c.T2723C).</p> </section> <section> <h3> Case 2</h3> <p>A 31-year-old unmarried woman with a history of bilateral inguinal hernia repair (age 2) and prior right pelvic lumpectomy (1 year 8 months prior, with histopathology confirming seminoma). She presented for management of a residual left pelvic mass (3.4 × 2.0 cm). Laboratory tests showed elevated testosterone, LH, and FSH; AFP and β-HCG were normal. She underwent three-dimensional laparoscopic left pelvic lumpectomy; histopathology confirmed intratubular germ cell neoplasia. WES identified three AR gene mutations (c.171_179del, c.255_257del, c.G2495A).</p> </section> <section> <h3> Conclusion</h3> <p>The two cases highlight the importance of integrating clinical, imaging, hormonal, and genetic data for diagnosing CAIS with GCTs. WES effectively identified multiple AR mutations, which may contribute to the severe CAIS phenotype and
{"title":"Clinical Characteristics and Management of Two Cases of Complete Androgen Insensitivity Syndrome With Germ Cell Tumors","authors":"Fangming Wang, Dong Wang, Jianxing Li, Nianzeng Xing","doi":"10.1002/cnr2.70491","DOIUrl":"10.1002/cnr2.70491","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Androgen insensitivity syndrome (AIS) is an X-linked recessive genetic disorder caused by mutations in the androgen receptor (AR) gene, leading to androgen resistance and disorders of sex development (DSD) in 46, XY individuals. It is classified into three phenotypes: complete (CAIS), partial (PAIS), and mild (MAIS). CAIS is characterized by normal external female genitalia, primary amenorrhea, and a 46, XY karyotype. While the risk of germ cell tumors (GCTs) in CAIS is generally low due to rapid germ cell depletion from absent AR responsiveness, GCTs still occur in adulthood, and clinical data on such cases remain limited—especially regarding detailed genetic profiling and long-term management outcomes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case</h3>\u0000 \u0000 <p>This study presents two adult CAIS patients with GCTs, managed at one tertiary hospital in Beijing, China, between 2020 and 2022. Both patients were raised as females and presented with primary amenorrhea:</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case 1</h3>\u0000 \u0000 <p>A 43-year-old married woman with a 5-year history of abdominal distension and 5-month history of impaired bowel movements. Preoperative imaging revealed bilateral pelvic masses (left: 7.7 × 6.4 cm; right: 2.2 × 2.0 cm), and laboratory tests showed elevated testosterone, LH, FSH, AFP, and β-HCG. She underwent 3-dimensional laparoscopic pelvic lumpectomy; histopathology confirmed left seminoma and right testicular tissue dysplasia. Whole exome sequencing (WES) identified four AR gene mutations (c.171_191del, c.255_257del, c.1368_1369insGGC, c.T2723C).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case 2</h3>\u0000 \u0000 <p>A 31-year-old unmarried woman with a history of bilateral inguinal hernia repair (age 2) and prior right pelvic lumpectomy (1 year 8 months prior, with histopathology confirming seminoma). She presented for management of a residual left pelvic mass (3.4 × 2.0 cm). Laboratory tests showed elevated testosterone, LH, and FSH; AFP and β-HCG were normal. She underwent three-dimensional laparoscopic left pelvic lumpectomy; histopathology confirmed intratubular germ cell neoplasia. WES identified three AR gene mutations (c.171_179del, c.255_257del, c.G2495A).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The two cases highlight the importance of integrating clinical, imaging, hormonal, and genetic data for diagnosing CAIS with GCTs. WES effectively identified multiple AR mutations, which may contribute to the severe CAIS phenotype and ","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12927923/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rui Chen, Tao Zhang, Jingru Yang, Longxia Zhang, Fei Su
Background
Colon adenocarcinoma (COAD), although the third-most common type of gastrointestinal tumors, still lacks specific biomarkers for early diagnosis, treatment, and prognosis.
Aims
This study aimed to evaluate the CD276 in tumorigenesis, prognosis and immunity for colon adenocarcinoma.
Methods and Results
The CD276 expression in colon adenocarcinoma was established by using RNA-sequencing transcriptomic data of The Cancer Genome Atlas (TCGA) databases. The biological functions of CD276 were evaluated using the Metascape database and Gene Set Enrichment Analysis (GSEA). The association between CD276 and immune cell infiltration was investigated by TIMER website. Correlation analysis was performed between CD276 expression and clinicopathological characteristics. CD276 expression was significantly elevated in colon adenocarcinoma tumor (p < 0.0001). High CD276 was associated with microsatellite instability (MSI) status, patients' survival, and disease progression. Cox regression analysis revealed that CD276 was a risk factor for overall survival [hazard ratio (HR): 1.848, p = 2.64E−03], disease-specific survival (HR: 2.406, p = 5.35E−04), and progression-free interval (HR: 1.772, p = 2.04E−03). Moreover, CD276 level was significantly associated with tumor immune cell infiltration, biomarkers of immune cells, and immune checkpoint expression.
Conclusions
Our analyses indicated that increased CD276 may contribute to colon adenocarcinoma development by activating tumor-promoting signal pathways and altering the immune microenvironment.
背景：结肠腺癌（COAD）虽然是第三常见的胃肠道肿瘤类型，但仍然缺乏用于早期诊断、治疗和预后的特异性生物标志物。目的：探讨CD276在结肠腺癌发生、预后及免疫中的作用。方法与结果：利用美国癌症基因组图谱（The Cancer Genome Atlas， TCGA）数据库的rna测序转录组数据，建立CD276在结肠腺癌中的表达。利用metscape数据库和基因集富集分析（GSEA）对CD276的生物学功能进行了评估。通过TIMER网站研究了CD276与免疫细胞浸润的关系。分析CD276表达与临床病理特征的相关性。结论：我们的分析表明，CD276的增加可能通过激活促瘤信号通路和改变免疫微环境来促进结肠腺癌的发展。
{"title":"The Bioinformatics and Experimental Analysis of CD276 for Prognosis and Immune Infiltrates in Colon Adenocarcinoma","authors":"Rui Chen, Tao Zhang, Jingru Yang, Longxia Zhang, Fei Su","doi":"10.1002/cnr2.70503","DOIUrl":"10.1002/cnr2.70503","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Colon adenocarcinoma (COAD), although the third-most common type of gastrointestinal tumors, still lacks specific biomarkers for early diagnosis, treatment, and prognosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This study aimed to evaluate the CD276 in tumorigenesis, prognosis and immunity for colon adenocarcinoma.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>The CD276 expression in colon adenocarcinoma was established by using RNA-sequencing transcriptomic data of The Cancer Genome Atlas (TCGA) databases. The biological functions of CD276 were evaluated using the Metascape database and Gene Set Enrichment Analysis (GSEA). The association between CD276 and immune cell infiltration was investigated by TIMER website. Correlation analysis was performed between CD276 expression and clinicopathological characteristics. CD276 expression was significantly elevated in colon adenocarcinoma tumor (<i>p</i> < 0.0001). High CD276 was associated with microsatellite instability (MSI) status, patients' survival, and disease progression. Cox regression analysis revealed that CD276 was a risk factor for overall survival [hazard ratio (HR): 1.848, <i>p</i> = 2.64E−03], disease-specific survival (HR: 2.406, <i>p</i> = 5.35E−04), and progression-free interval (HR: 1.772, <i>p</i> = 2.04E−03). Moreover, CD276 level was significantly associated with tumor immune cell infiltration, biomarkers of immune cells, and immune checkpoint expression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our analyses indicated that increased CD276 may contribute to colon adenocarcinoma development by activating tumor-promoting signal pathways and altering the immune microenvironment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12928083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer globally. For locally advanced cases when upfront surgery or radiation are not feasible, a platinum agent (carboplatin or cisplatin) with 5-fluorouracil (carbo-5FU) and immunotherapy is the standard of care. We present the first documented case of acute gout flare in a HNSCC patient after initiation of carboplatin-5-fluorouracil.
Case
A 67-year-old male patient with a remote history of gout and recurrent HPV-associated oropharyngeal squamous cell carcinoma (OSCC) presented for evaluation and management of local recurrence. He underwent right tonsillectomy, chemoradiation, and naturopathic therapy over the past 9 years, but the OSCC recurred in the right neck. As the patient was deemed a poor surgical candidate and declined radiation therapy, he was counseled on treatment options and elected to proceed with palliative systemic carbo-5FU therapy but experienced an acute gout flare after cycle 1. Uric acid was checked and found to be elevated at 9.3. He then started prednisone, allopurinol, and intravenous hydration for gout control, and his initially elevated uric acid levels normalized over the next 5 weeks.
Conclusions
Our case describes the first documented incidence of gout flare precipitated by carbo-5FU, but also demonstrates a successful pharmacological treatment approach to control chemotherapy-induced gout.
{"title":"Acute Gout Flare After Carboplatin/5-Fluorouracil for Locally Advanced Head and Neck Squamous Cell Carcinoma","authors":"Henry Zou, Anas Al Janadi, Zeyad Sako","doi":"10.1002/cnr2.70497","DOIUrl":"10.1002/cnr2.70497","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer globally. For locally advanced cases when upfront surgery or radiation are not feasible, a platinum agent (carboplatin or cisplatin) with 5-fluorouracil (carbo-5FU) and immunotherapy is the standard of care. We present the first documented case of acute gout flare in a HNSCC patient after initiation of carboplatin-5-fluorouracil.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case</h3>\u0000 \u0000 <p>A 67-year-old male patient with a remote history of gout and recurrent HPV-associated oropharyngeal squamous cell carcinoma (OSCC) presented for evaluation and management of local recurrence. He underwent right tonsillectomy, chemoradiation, and naturopathic therapy over the past 9 years, but the OSCC recurred in the right neck. As the patient was deemed a poor surgical candidate and declined radiation therapy, he was counseled on treatment options and elected to proceed with palliative systemic carbo-5FU therapy but experienced an acute gout flare after cycle 1. Uric acid was checked and found to be elevated at 9.3. He then started prednisone, allopurinol, and intravenous hydration for gout control, and his initially elevated uric acid levels normalized over the next 5 weeks.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our case describes the first documented incidence of gout flare precipitated by carbo-5FU, but also demonstrates a successful pharmacological treatment approach to control chemotherapy-induced gout.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12922451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146257538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wanhua An, Shuli Guo, Sizhe Liu, Pengli Xiao, Emma Mi, Huirui Wang
Background
The pathogenesis of diffuse large B-cell lymphoma (DLBCL) remains unclear. Zinc finger protein 382 (ZNF382) expression is significantly downregulated in DLBCL, which is associated with poor prognosis. However, the underlying mechanisms remain unknown.
Aims
To investigate the association between DNA methylation of the promoter region of ZNF382 and ZNF382 expression with the occurrence and progression of DLBCL and to analyze the clinical significance of ZNF382 in DLBCL.
Methods and Results
DLBCL cell lines and reactive hyperplastic lymph node tissues were used as the experimental subjects. Methylation-specific polymerase chain reaction and reverse-transcription polymerase chain reaction analyses revealed significantly higher methylation of the promoter region of ZNF382 (p < 0.0001), whereas ZNF382 mRNA expression was significantly lower (p < 0.01) in DLBCL cells compared with those in reactive hyperplastic lymph node tissues. Cells were treated with the demethylating agent decitabine (DAC), and the methylation status of the promoter and expression levels of ZNF382 were determined. ZNF382 promoter methylation was significantly reduced (p < 0.01) in DLBCL cells, whereas ZNF382 mRNA expression was significantly increased (p < 0.01) compared with those in the control cells. Furthermore, compared with that in the blank control group, the apoptosis rate of DLBCL cells was significantly increased following DAC intervention (p < 0.01). A cell model of ZNF382 overexpression was constructed, and its proliferation, migration, and clonogenic capacities were detected using CCK-8, Transwell, and soft agar assays, respectively. Compared with those of the vector control group, the cell proliferation, migration, and clone formation abilities of the ZNF382 overexpression group were significantly inhibited (p < 0.01).
Conclusion
DNA hypermethylation in the promoter region of ZNF382 and low ZNF382 mRNA expression are closely related to the occurrence and progression of DLBCL. Moreover, ZNF382 overexpression significantly increased apoptosis and inhibited cell proliferation, migration, and clone formation. Therefore, ZNF382 has potential as a therapeutic target in the treatment of DLBCL.
{"title":"DNA Hypermethylation of the ZNF382 Promoter Region and Low mRNA Expression of ZNF382 Promote Diffuse Large B-Cell Lymphoma Occurrence and Progression","authors":"Wanhua An, Shuli Guo, Sizhe Liu, Pengli Xiao, Emma Mi, Huirui Wang","doi":"10.1002/cnr2.70502","DOIUrl":"10.1002/cnr2.70502","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The pathogenesis of diffuse large B-cell lymphoma (DLBCL) remains unclear. Zinc finger protein 382 (<i>ZNF382</i>) expression is significantly downregulated in DLBCL, which is associated with poor prognosis. However, the underlying mechanisms remain unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>To investigate the association between DNA methylation of the promoter region of <i>ZNF382</i> and <i>ZNF382 expression</i> with the occurrence and progression of DLBCL and to analyze the clinical significance of <i>ZNF382</i> in DLBCL.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>DLBCL cell lines and reactive hyperplastic lymph node tissues were used as the experimental subjects. Methylation-specific polymerase chain reaction and reverse-transcription polymerase chain reaction analyses revealed significantly higher methylation of the promoter region of <i>ZNF382</i> (<i>p</i> < 0.0001), whereas <i>ZNF382</i> mRNA expression was significantly lower (<i>p</i> < 0.01) in DLBCL cells compared with those in reactive hyperplastic lymph node tissues. Cells were treated with the demethylating agent decitabine (DAC), and the methylation status of the promoter and expression levels of <i>ZNF382</i> were determined. <i>ZNF382</i> promoter methylation was significantly reduced (<i>p</i> < 0.01) in DLBCL cells, whereas <i>ZNF382</i> mRNA expression was significantly increased (<i>p</i> < 0.01) compared with those in the control cells. Furthermore, compared with that in the blank control group, the apoptosis rate of DLBCL cells was significantly increased following DAC intervention (<i>p</i> < 0.01). A cell model of <i>ZNF382</i> overexpression was constructed, and its proliferation, migration, and clonogenic capacities were detected using CCK-8, Transwell, and soft agar assays, respectively. Compared with those of the vector control group, the cell proliferation, migration, and clone formation abilities of the <i>ZNF382</i> overexpression group were significantly inhibited (<i>p</i> < 0.01).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>DNA hypermethylation in the promoter region of <i>ZNF382</i> and low <i>ZNF382</i> mRNA expression are closely related to the occurrence and progression of DLBCL. Moreover, <i>ZNF382</i> overexpression significantly increased apoptosis and inhibited cell proliferation, migration, and clone formation. Therefore, <i>ZNF382</i> has potential as a therapeutic target in the treatment of DLBCL.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12920067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fabio Murtas, Benedetta Chiusole, Ilaria Tortorelli, Silvia Finotto, Marta Burei, Marina Coppola, Antonella Galiano, Maital Bolshinsky, Elena Bellan, Marta Sbaraglia, Angelo Paolo Dei Tos, Antonella Brunello
Background
Ewing sarcoma is a rare primary mesenchymal tumor of the bone that requires an intensive multimodal therapeutic approach. Multidrug chemotherapy regimens are also the backbone for relapsing/recurring Ewing sarcoma treatment, yet when the disease relapses as bone marrow infiltration, combination chemotherapy might be difficult to administer and prognosis is poor.
Case
This report describes the case of a 22-year-old patient with Ewing sarcoma who developed severe pancytopenia due to bone marrow infiltration, and who was treated with high-dose continuous infusion ifosfamide, obtaining both clinical, radiological, and hematological response lasting for about 7 months.
Conclusion
To our knowledge, this is the first described case of a patient with bone marrow infiltration from Ewing sarcoma presenting with severe thrombocytopenia successfully managed with low-dose continuous infusion ifosfamide, providing almost 7 months of progression-free survival. Considering the very dismal prognosis of Ewing sarcoma relapsing with bone marrow infiltration, this case might be of help when decision-making is required in this setting.
{"title":"High-Dose Continuous Infusion Ifosfamide as Effective Palliation in a Patient With Relapsed Ewing Sarcoma With Bone Marrow Infiltration and Severe Thrombocytopenia: A Case Report","authors":"Fabio Murtas, Benedetta Chiusole, Ilaria Tortorelli, Silvia Finotto, Marta Burei, Marina Coppola, Antonella Galiano, Maital Bolshinsky, Elena Bellan, Marta Sbaraglia, Angelo Paolo Dei Tos, Antonella Brunello","doi":"10.1002/cnr2.70468","DOIUrl":"10.1002/cnr2.70468","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Ewing sarcoma is a rare primary mesenchymal tumor of the bone that requires an intensive multimodal therapeutic approach. Multidrug chemotherapy regimens are also the backbone for relapsing/recurring Ewing sarcoma treatment, yet when the disease relapses as bone marrow infiltration, combination chemotherapy might be difficult to administer and prognosis is poor.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case</h3>\u0000 \u0000 <p>This report describes the case of a 22-year-old patient with Ewing sarcoma who developed severe pancytopenia due to bone marrow infiltration, and who was treated with high-dose continuous infusion ifosfamide, obtaining both clinical, radiological, and hematological response lasting for about 7 months.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>To our knowledge, this is the first described case of a patient with bone marrow infiltration from Ewing sarcoma presenting with severe thrombocytopenia successfully managed with low-dose continuous infusion ifosfamide, providing almost 7 months of progression-free survival. Considering the very dismal prognosis of Ewing sarcoma relapsing with bone marrow infiltration, this case might be of help when decision-making is required in this setting.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12914222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marzieh Rahimi, Mohammadreza Mamaghani-Ghazijahani, Fatemeh Shahabi, Majid Ansari, Mahdie Ghiyasi Noei, Mina Alvandipour, Abbas Abdollahi
Background
Neoadjuvant chemoradiotherapy (nCRT) has been shown to improve prognosis in patients with locally advanced rectal cancer (LARC). However, there is still debate regarding the optimal time of surgery following nCRT.
Aims
This exploratory study aimed to investigate whether there is a difference in oncological outcomes between patients with LARC who undergo surgery within 6 weeks of nCRT and those who wait longer than 6 weeks.
Methods and Results
This retrospective study included patients with rectal tumors who underwent nCRT followed by laparoscopic surgery during 2011–2020. Based on the time interval, the study participants were divided into two groups: ≤ 6 weeks and > 6 weeks. Receiver Operating Characteristics and Kaplan–Meier survival curves were employed to evaluate the effect of time interval on overall survival (OS) and recurrence-free survival (RFS). Cox regression analysis was used to identify the prognostic factors of RFS and OS. A total of 175 patients were included in our study with a mean ± SD age of 56.1 ± 12.9 years. The median (interquartile range) follow-up time was 71 (63) months. There was no difference in demographic and clinical variables between the two groups. Neither pCR, OS, nor RFS was affected by the nCRT-surgery interval. Multivariable Cox regression analysis showed that patients with ypStage III had a mortality and recurrence hazard of 7.6 and 3.3 times higher than those with pCR (p < 0.001, p = 0.018, respectively). Additionally, those who underwent abdominoperineal resection (APR) were 5.8 times more at risk of developing recurrence (p = 0.001).
Conclusion
The present study revealed that pCR rates, OS, and RFS were not affected by the nCRT-surgery interval within the cohort studied. In addition, the time interval of more than 6 weeks may be safe, as no substantial difference in postoperative complications was observed between groups. The ypTNM staging was an independent predictor of OS and RFS. Moreover, APR was considered an important prognostic factor for RFS. These findings require further investigation by multicenter, large-scale studies in the future.
{"title":"The Impact of Time Interval to Surgery After Neoadjuvant Chemoradiotherapy on Oncological Outcomes: A Long-Term Follow-Up Study on Rectal Cancer Patients","authors":"Marzieh Rahimi, Mohammadreza Mamaghani-Ghazijahani, Fatemeh Shahabi, Majid Ansari, Mahdie Ghiyasi Noei, Mina Alvandipour, Abbas Abdollahi","doi":"10.1002/cnr2.70493","DOIUrl":"10.1002/cnr2.70493","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Neoadjuvant chemoradiotherapy (nCRT) has been shown to improve prognosis in patients with locally advanced rectal cancer (LARC). However, there is still debate regarding the optimal time of surgery following nCRT.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This exploratory study aimed to investigate whether there is a difference in oncological outcomes between patients with LARC who undergo surgery within 6 weeks of nCRT and those who wait longer than 6 weeks.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>This retrospective study included patients with rectal tumors who underwent nCRT followed by laparoscopic surgery during 2011–2020. Based on the time interval, the study participants were divided into two groups: ≤ 6 weeks and > 6 weeks. Receiver Operating Characteristics and Kaplan–Meier survival curves were employed to evaluate the effect of time interval on overall survival (OS) and recurrence-free survival (RFS). Cox regression analysis was used to identify the prognostic factors of RFS and OS. A total of 175 patients were included in our study with a mean ± SD age of 56.1 ± 12.9 years. The median (interquartile range) follow-up time was 71 (63) months. There was no difference in demographic and clinical variables between the two groups. Neither pCR, OS, nor RFS was affected by the nCRT-surgery interval. Multivariable Cox regression analysis showed that patients with ypStage III had a mortality and recurrence hazard of 7.6 and 3.3 times higher than those with pCR (<i>p</i> < 0.001, <i>p</i> = 0.018, respectively). Additionally, those who underwent abdominoperineal resection (APR) were 5.8 times more at risk of developing recurrence (<i>p</i> = 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The present study revealed that pCR rates, OS, and RFS were not affected by the nCRT-surgery interval within the cohort studied. In addition, the time interval of more than 6 weeks may be safe, as no substantial difference in postoperative complications was observed between groups. The ypTNM staging was an independent predictor of OS and RFS. Moreover, APR was considered an important prognostic factor for RFS. These findings require further investigation by multicenter, large-scale studies in the future.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12914080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vahid Mohammadkarimi, Abolfazl Khalafi-Nezhad, Bijan Najafi, Nazanin Alemzadeh, Zahra Ghanbarinasab, Reza Vahid
Background
Tyrosine kinase inhibitors (TKIs) used in chronic myeloid leukemia (CML) are associated with a spectrum of cardiovascular toxicities, including hypertension, atrial fibrillation, impaired cardiac function, heart failure, and arterio-occlusive events. Among these, nilotinib has been particularly linked to peripheral arterial disease and thromboembolic complications.
Case
We report the case of a 53-year-old male patient who initially presented with fatigue, malaise, and mild left upper quadrant abdominal pain. Bone marrow aspiration confirmed CML with the presence of the BCR::ABL1 fusion gene. The patient was started on nilotinib therapy. After 8 months of treatment, he developed unilateral blurred vision and sixth nerve palsy, which were attributed to a retinal arterial occlusion. No prior cardiovascular risk factors were documented. Nilotinib therapy was discontinued, and the patient was switched to dasatinib, leading to gradual improvement of visual symptoms.
Conclusion
This case underlines the importance of considering rare but severe arterio-occlusive complications, such as retinal artery thrombosis, among the cardiovascular toxicities of nilotinib. Careful cardiovascular monitoring and early recognition of such events are crucial to optimize patient safety and treatment outcomes in CML management.
{"title":"Nilotinib-Induced Retinal Artery Thrombosis in a Patient With Chronic Myeloid Leukaemia: A Rare Case","authors":"Vahid Mohammadkarimi, Abolfazl Khalafi-Nezhad, Bijan Najafi, Nazanin Alemzadeh, Zahra Ghanbarinasab, Reza Vahid","doi":"10.1002/cnr2.70501","DOIUrl":"10.1002/cnr2.70501","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Tyrosine kinase inhibitors (TKIs) used in chronic myeloid leukemia (CML) are associated with a spectrum of cardiovascular toxicities, including hypertension, atrial fibrillation, impaired cardiac function, heart failure, and arterio-occlusive events. Among these, nilotinib has been particularly linked to peripheral arterial disease and thromboembolic complications.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case</h3>\u0000 \u0000 <p>We report the case of a 53-year-old male patient who initially presented with fatigue, malaise, and mild left upper quadrant abdominal pain. Bone marrow aspiration confirmed CML with the presence of the <i>BCR::ABL1</i> fusion gene. The patient was started on nilotinib therapy. After 8 months of treatment, he developed unilateral blurred vision and sixth nerve palsy, which were attributed to a retinal arterial occlusion. No prior cardiovascular risk factors were documented. Nilotinib therapy was discontinued, and the patient was switched to dasatinib, leading to gradual improvement of visual symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This case underlines the importance of considering rare but severe arterio-occlusive complications, such as retinal artery thrombosis, among the cardiovascular toxicities of nilotinib. Careful cardiovascular monitoring and early recognition of such events are crucial to optimize patient safety and treatment outcomes in CML management.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9440,"journal":{"name":"Cancer reports","volume":"9 2","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12911114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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