{"title":"Incidence and Prognostic Value of TP53, STK11, and KEAP1 Mutations Between <i>De Novo</i> Versus Recurrent Actionable Mutation-Negative Non-Small Cell Lung Cancer: A Single-Center Retrospective Study.","authors":"Jorge Raul Vazquez-Urrutia, Natasha Venugopal, Junjia Zhu, Takefumi Komiya","doi":"10.14740/wjon2761","DOIUrl":"10.14740/wjon2761","url":null,"abstract":"<p><strong>Background: </strong>In non-small cell lung cancer (NSCLC), mutations in TP53, STK11, and KEAP1 are common in tumors lacking actionable oncogenic drivers and have been associated with poor outcomes, though their prognostic impact remains context-dependent. We evaluated the incidence and prognostic significance of these mutations in actionable mutation-negative NSCLC, stratified by <i>de novo</i> versus recurrent disease.</p><p><strong>Methods: </strong>We retrospectively analyzed 119 adult patients with NSCLC and available next-generation sequencing (NGS) results treated at our center through 2024. Cases with actionable mutations were excluded. Patients were classified as <i>de novo</i> (n = 82) or recurrent (n = 37) based on the disease status at the point of analysis. Between-group comparisons were done using Fisher's exact and Wilcoxon Rank-sum test. Overall survival and progression-free survival were assessed. All tests were two-sided and a P value < 0.05 was considered statistically significant.</p><p><strong>Results: </strong>TP53 mutations were most frequent (61% <i>de novo</i> vs. 54% recurrent; P > 0.05). STK11 and KEAP1 mutations occurred at similar rates between groups (5-15%; P > 0.05). Baseline clinical characteristics were balanced. No significant differences in overall or progression-free survival were observed by mutational status in either cohort.</p><p><strong>Conclusion: </strong>In this real-world cohort of actionable mutation-negative NSCLC cases, we did not detect significant prognostic associations for TP53, STK11, and KEAP1 mutations, and their incidence was similar between <i>de novo</i> and recurrent disease. These findings underscore the need for larger studies to evaluate the prognostic utility of these mutations in this clinical context.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"310-321"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943335","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}
Mariana Chantre-Justino, Rafaele Tavares Silvestre, Lucas Delmonico, Gilda Alves, Maria Helena Faria Ornellas, Caroline Rotilho, Amanda Cavalcanti, Jamila Alessandra Perini, Nina Carrossini Bastos, Eliane Luz, Rafael Pinheiro, Bruna Canteri Delocco, Anabela Cunha Caruso, Ana Cristina de Sa Lopes, Walter Meohas
{"title":"Detection of Longer Leukocyte Telomere Length in Patients With Bone Sarcomas.","authors":"Mariana Chantre-Justino, Rafaele Tavares Silvestre, Lucas Delmonico, Gilda Alves, Maria Helena Faria Ornellas, Caroline Rotilho, Amanda Cavalcanti, Jamila Alessandra Perini, Nina Carrossini Bastos, Eliane Luz, Rafael Pinheiro, Bruna Canteri Delocco, Anabela Cunha Caruso, Ana Cristina de Sa Lopes, Walter Meohas","doi":"10.14740/wjon2684","DOIUrl":"10.14740/wjon2684","url":null,"abstract":"<p><strong>Background: </strong>Bone sarcomas are rare and heterogeneous malignant neoplasms of mesenchymal origin, often associated with poor clinical outcomes. Being rare neoplasms, a comprehensive analysis of the molecular mechanisms involved in the tumor biology of bone sarcomas is still lacking. Telomeres are repetitive nucleotide sequences (TTAGGG)n at chromosome ends playing an essential role in genome stability, and their dysfunction has been associated with several human diseases, including cancer. This study aimed to assess telomere dynamics in pediatric and adult patients with bone sarcomas.</p><p><strong>Methods: </strong>The measurements of relative telomere length (RTL) in peripheral blood leukocytes were evaluated by quantitative polymerase chain reaction (qPCR) in 44 patients with newly diagnosed, histologically confirmed, treatment-naive bone sarcomas. The control group comprised 50 cancer-free individuals.</p><p><strong>Results: </strong>Overall, we observed significantly longer RTL in patients compared to controls (P = 0.02). RTL was also significantly longer in male patients compared to male controls (P = 0.01). Among patients, no significant association was observed between RTL and age group (pediatric vs. adult), sex (male vs. female), and outcome events (recurrence, metastasis or death).</p><p><strong>Conclusions: </strong>Our findings indicate that longer leukocyte telomere length in patients, compared with cancer-free controls, may be associated with increased susceptibility to bone sarcoma.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"337-346"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147964509","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}
{"title":"Omission of Sentinel Lymph Node Biopsy in Early-Stage Breast Cancer: Expanding Evidence in Clinically Node-Negative and Neoadjuvant Therapy Responders.","authors":"Abigail Grapes, Jessica Young, Kazuaki Takabe","doi":"10.14740/wjon2776","DOIUrl":"10.14740/wjon2776","url":null,"abstract":"<p><p>Management of the axilla in early-stage breast cancer has progressively evolved toward less invasive approaches, as advances in tumor biology, imaging, and local and systemic therapies have improved outcomes while highlighting the morbidity associated with axillary surgery. Sentinel lymph node biopsy, once considered essential for staging, is increasingly being questioned in select patients with clinically node-negative disease. This review summarizes current evidence evaluating omission of sentinel lymph node biopsy in early-stage breast cancer, including its impact on oncologic outcomes, quality of life, and implementation in clinical practice. Multiple retrospective studies and randomized controlled trials have demonstrated that omission of axillary surgery does not compromise survival outcomes in carefully selected patients with hormone receptor (HR)-positive/human epidermal growth factor receptor 2 (HER2)-negative tumors. These findings informed the 2016 Choosing Wisely<sup>®</sup> recommendation by the Society of Surgical Oncology to avoid routine sentinel lymph node biopsy in women over 70 years of age with clinically node-negative disease. While implementation of this guideline was slower than expected, subsequent studies have explored whether sentinel lymph node biopsy can be safely omitted in a broader group of women with early-stage, HR-positive/HER2-negative invasive breast cancers, who are clinically node-negative on physical exam and preoperative axillary ultrasound. This led to the development of several prospective trials, including SOUND (Sentinel Node vs Observation After Axillary Ultra-Sound), INSEMA (Intergroup Sentinel Mamma), NAUTILUS (No Axillary Surgical Treatment in Clinically Lymph Node Negative Patients on Ultrasonography After Neoadjuvant Chemotherapy), BOOG 2013-08 (Dutch Breast Cancer Research Group 2013-08), OMSLNB (Omission of Sentinel Lymph Node Biopsy), VENUS, and SOAPET (Sentinel node biopsy vs. observation after axillary PET). While many of these trials remain ongoing, results of the SOUND and INSEMA trials demonstrate no difference in survival outcomes following omission of sentinel lymph node biopsy in postmenopausal women with low grade, HR-positive/HER2-negative tumors less than 2 cm in size, and these findings are increasingly being incorporated into clinical practice. Advancements in neoadjuvant therapies have resulted in increasing rates of pathologic complete response in the breast in clinically node-negative women with HER2-positive and triple-negative breast cancers, raising the possibility that sentinel lymph node biopsy may be safely omitted in this population as well. This is being investigated in the EUBREAST-01 (European Breast Cancer Research Association of Surgical Trialists), ASICS (Avoiding Sentinel lymph node biopsy In select Clinical node negative breast cancer patients after neoadjuvant Systemic therapy), ASLAN (Avoid Axillary Sentinel Lymph Node Biopsy After Neoadjuvant Chemotherapy","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"292-309"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147964524","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}
{"title":"De-Escalation of Axillary Surgery: A Review of Choosing Wisely Guideline Evidence.","authors":"Abigail Grapes, Jessica Young, Kazuaki Takabe","doi":"10.14740/wjon2710","DOIUrl":"10.14740/wjon2710","url":null,"abstract":"<p><p>Management of the axilla in early stage breast cancer has shifted toward less invasive approaches as evidence demonstrates equivalent oncologic outcomes with reduced morbidity. In older women with biologically favorable disease, the value of axillary staging has been increasingly questioned. This review outlines the evolution of axillary surgery from axillary lymph node dissection to sentinel lymph node biopsy and subsequent omission strategies. We synthesize the available evidence presented defining when omission of sentinel lymph node biopsy is safe and how it can be implemented in practice. The Society of Surgical Oncology 2016 Choosing Wisely<sup>®</sup> guideline advises against routine sentinel lymph node biopsy in women ≥ 70 years with clinically node-negative, hormone receptor-positive/human epidermal growth factor receptor 2 (HER2)-negative invasive breast cancer receiving endocrine therapy. Across studies, omission of sentinel lymph node biopsy in appropriately selected patients is associated with low axillary recurrence rates without compromise in disease-free, breast cancer-specific, or overall survival. Although regional recurrence is modestly increased without axillary staging, these events are uncommon and typically amenable to salvage therapy. Despite strong evidence and professional endorsement, implementation of this recommendation remains inconsistent, with persistently high utilization of sentinel lymph node biopsy among women eligible for omission. Contemporary data indicate that adjuvant therapy decisions in hormone receptor-positive disease are driven primarily by tumor biology, with nodal status altering management in a minority of postmenopausal women. We propose a structured clinical decision framework incorporating tumor biology, physiologic rather than chronological age, competing mortality risk, and planned endocrine therapy. When nodal status is unlikely to influence treatment, omission of sentinel lymph node biopsy is a safe, evidence-based refinement that reduces morbidity without compromising survival. Multidisciplinary coordination is essential to optimize adjuvant therapy while minimizing low-value surgical care.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"277-291"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943299","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}
Imrana Tanvir, Amber Hassan, Bushra Nisar, Sadia Khan, Maryam Altaf, Humaira Waseem, Hussain Noorwali, Ali A Mousa, Amany Fathaddin, Ragdah Arif, Mohammed M Karami, Majid Almansouri
{"title":"Immunohistochemistry as a Cornerstone in Lung Cancer Diagnosis: Subtyping Based on the 2021 World Health Organization Classification and Its Practical Application.","authors":"Imrana Tanvir, Amber Hassan, Bushra Nisar, Sadia Khan, Maryam Altaf, Humaira Waseem, Hussain Noorwali, Ali A Mousa, Amany Fathaddin, Ragdah Arif, Mohammed M Karami, Majid Almansouri","doi":"10.14740/wjon2757","DOIUrl":"10.14740/wjon2757","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is the leading cause of cancer-related deaths worldwide, and precise histological classification is vital for therapy decisions. Given diagnostic limitations with small biopsies, immunohistochemistry (IHC) enhances accuracy. This study evaluated the diagnostic value of IHC markers in subtyping lung tumors per the 2021 World Health Organization (WHO) classification and differentiating primary from metastatic lesions.</p><p><strong>Methods: </strong>A prospective study was conducted on 151 lung biopsy specimens over 18 months. All samples were processed using standard histopathological techniques and an IHC panel comprising thyroid transcription factor-1 (TTF-1), napsin A, cytokeratin (CK)7, CK5/6, P63, synaptophysin, and chromogranin. Additional markers (estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), PAX-8, PAX-2, CD10) were applied for metastatic differentiation. Statistical correlation analysis between lineage-specific markers was performed to assess diagnostic concordance.</p><p><strong>Results: </strong>Adenocarcinoma was the most prevalent subtype (58.3%), followed by neuroendocrine neoplasms (17.2%), metastatic lesions (13.2%), adenosquamous carcinoma (6.0%), and squamous cell carcinoma (2.6%). Rare entities included carcinosarcoma and mucoepidermoid carcinoma (each 1.3%). TTF-1 and napsin A were highly specific for adenocarcinoma (85% and 94%, respectively), whereas CK5/6 and P63 confirmed squamous differentiation (100% each). Synaptophysin and chromogranin were positive in 96% and 100% of neuroendocrine tumors, respectively. Correlation analysis demonstrated strong marker concordance: TTF-1 vs napsin A (r = 0.88, P < 0.001), P63 vs CK5/6 (r = 0.93, P < 0.001), and synaptophysin vs chromogranin (r = 0.87, P < 0.001). All metastatic lesions were TTF-1 negative, confirming their extrapulmonary origin.</p><p><strong>Conclusions: </strong>Combining IHC with histopathology markedly improves diagnostic precision and consistency in lung tumor classification. Lineage-specific markers validate the IHC panel's reliability, distinguishing adenocarcinoma, squamous, and neuroendocrine types while differentiating primary from metastatic lesions. This integrative approach supports WHO-aligned precision diagnostics and guides individualized therapeutic strategies.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 3","pages":"419-427"},"PeriodicalIF":2.3,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13171280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147964501","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}
Zhi Nuo Zheng, Xiao Han Ye, Xiao Ban Shen, Tao Li, Jie Guo
{"title":"Advances in Targeted Therapy for Human Epidermal Growth Factor Receptor 2-Low Tumors: From Trastuzumab to Antibody-Drug Conjugates.","authors":"Zhi Nuo Zheng, Xiao Han Ye, Xiao Ban Shen, Tao Li, Jie Guo","doi":"10.14740/wjon2718","DOIUrl":"10.14740/wjon2718","url":null,"abstract":"<p><p>The assessment of human epidermal growth factor receptor 2 (HER2) expression status has evolved from the traditional binary classification of positive/negative to a continuum that includes HER2-low expression. This shift has redefined the treatment landscape for approximately half of breast cancer patients. Trastuzumab, the cornerstone monoclonal antibody targeting HER2, significantly improves outcomes in HER2-high patients by blocking downstream signaling pathways and mediating antibody-dependent cellular cytotoxicity. However, its efficacy remains limited in tumors with low HER2 expression. In recent years, the emergence of antibody-drug conjugates (ADCs) has overcome this limitation. Represented by trastuzumab deruxtecan (T-DXd), a new generation of ADCs has successfully extended therapeutic benefits to HER2-low tumors through high drug-to-antibody ratios, cleavable linkers, and potent bystander effects. T-DXd has been established as the new standard of care for previously treated patients. This review systematically outlines the evolution of HER2 expression profiles, the mechanism of action and limitations of trastuzumab, and focuses on analyzing the breakthrough role of ADCs centered on trastuzumab emtansine (T-DM1) and T-DXd in HER2-low tumors, key clinical evidence, and adverse reaction management. Additionally, it explores the application prospects of combination strategies involving ADCs with chemotherapy and immunotherapy. Finally, the article summarizes challenges facing the current treatment paradigm and outlines future directions for standardized testing and novel therapeutic development.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"129-142"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445670","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}
{"title":"Analysis of Prognosis and Immune Microenvironment of Protein Kinase C Substrate 80K-H in Diabetic Lung Cancer Patients.","authors":"Xiang Ying Li, Yue Feng, Cun Feng Li, Hong Qiao","doi":"10.14740/wjon2663","DOIUrl":"10.14740/wjon2663","url":null,"abstract":"<p><strong>Background: </strong>A substantial association has been established between diabetes and an elevated risk of lung cancer. This study aimed to elucidate the prognosis and characterize alterations in the immune microenvironment linked to the protein kinase C substrate 80K-H (<i>PRKCSH</i>) gene in the context of diabetic lung cancer.</p><p><strong>Methods: </strong>The expression profile of receptor for advanced glycation end products (RAGE) genes in lung adenocarcinoma (LUAD) and diabetic cohorts was analyzed utilizing data from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO). The methodological framework included single-sample gene set enrichment analysis (ssGSEA), hallmark pathway enrichment analysis, Pearson's correlation, and Wilcoxon tests, employing data from the Cancer Single Cell State Atlas (CancerSEA), tracking tumor immunophenotype (TIP) meta-server, and the Genomics of Drug Sensitivity in Cancer (GDSC) platform. <i>PRKCSH</i>-targeting small interfering RNA (siRNA) was synthesized and transfected into A549 cells. Functional validation of PRKCSH was conducted using real-time quantitative polymerase chain reaction (RT-qPCR), Western blotting, methylthiazolyldiphenyl-tetrazolium bromide (MTT) assays and flow cytometry.</p><p><strong>Results: </strong>The analysis identified five RAGE genes with dysregulated expression in both diabetic and LUAD conditions, which were significantly associated with the activation of signaling pathways and patterns of immune cell enrichment in diabetes. PRKCSH has been identified as an independent prognostic marker in LUAD, with associations with key biological processes such as cell cycle regulation, genomic instability responses, inflammatory mediation, and stem cell characteristics. Comprehensive pathway analysis revealed inverse relationships between PRKCSH expression and immune-related molecular mechanisms. Detailed immune profiling indicated reduced infiltration levels of various immune cell populations in association with elevated PRKCSH expression. Notably, increased PRKCSH activity in LUAD was linked to enhanced enzymatic pathway responses and greater therapeutic sensitivity to specific enzyme inhibitors. Experimental validation via gene silencing demonstrated that suppression of PRKCSH effectively reduced malignant cell proliferation while promoting apoptotic mechanisms in lung cancer models.</p><p><strong>Conclusions: </strong>This extensive investigation positioned PRKCSH as a critical prognostic biomarker and a promising therapeutic target for personalized immunotherapeutic strategies in the management of LUAD.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"157-177"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445729","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}
Milder Bravo-Davila, Dayana Espinoza-Rodrigez, Javier Orejon-Huarancca, Richard Junior Zapata Dongo
{"title":"Characterization of Acute Myeloid Leukemia With t(16;21) Translocation: Cytogenetic, Molecular, and Immunophenotypic Findings.","authors":"Milder Bravo-Davila, Dayana Espinoza-Rodrigez, Javier Orejon-Huarancca, Richard Junior Zapata Dongo","doi":"10.14740/wjon2700","DOIUrl":"10.14740/wjon2700","url":null,"abstract":"<p><strong>Background: </strong>Acute myeloid leukemia (AML) with t(16;21) translocation is an infrequent hematological neoplasia. This study aimed to describe the cytogenetic, molecular and immunophenotypic profiles of this disease.</p><p><strong>Methods: </strong>We conducted a descriptive observational study using secondary data. AML cases with the t(16;21) translocation were identified from the Mitelman database and systematic searches in PubMed, Scopus, SciELO and Genetics and Cytogenetics in Oncology and Hematology databases. Cytogenetic, molecular, immunophenotypic and clinical variables were extracted. We performed descriptive and survival statistical analyses at 2 and 5 years.</p><p><strong>Results: </strong>We identified 103 cases with AML with t(16;21). Most cases were t(16;21)(p11;q22) (n = 90, 87.4%), with recurrent additional abnormalities including +10 (14.4%), -16 (7.8%), add(11) (5.6%), and del(6) (4.4%), while t(16;21)(q24;q22) cases mainly showed +8 (45.5%) and del(9) (18.2%). <i>FUS</i>::<i>ERG</i> was reported in 62.2% of t(16;21)(p11;q22) cases, whereas <i>RUNX1</i>::<i>RUNX1T3</i> was detected in 72.2% of t(16;21)(q24;q22). Immunophenotypically, t(16;21)(p11;q22) cases expressed (among the cases evaluated) cluster of differentiation (CD)13 (100%), CD33 (96.6%), CD34 (98.0%), CD56 (93.0%), and MPO (84.8%), while all evaluated t(16;21)(q24;q22) cases were positive for CD13, CD33, CD34, and MPO. Relapse information was missing for a substantial proportion of cases; among those with available data (65.0%), relapse occurred in 51 cases (76.1%). The 5-year mortality rate was significantly higher in the t(16;21)(p11;q22) group than in the t(16;21)(q24;q22) group (P = 0.012), with no significant difference at 2 years.</p><p><strong>Conclusions: </strong>The cytogenetic, molecular, and immunophenotypic characteristics of AML with t(16;21) vary according to the chromosomal breakpoint. The t(16;21)(p11;q22) translocation was the most frequently reported and was frequently associated with CD56 expression. The findings suggest that patients with t(16;21)(p11;q22) exhibited lower 5-year survival compared with the other group, highlighting the unfavorable outcomes observed in reported cases.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"178-190"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445750","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}
Shuang Liu, Kun Chen, Yue Qi Wang, Xiao Yu Gu, Zhi He, Chen Zhang, Guo Qiu Wu, Su Su Luo, Xing Jin
{"title":"Bidirectional Mendelian Randomization Analysis Reveals Causal Associations Between Autoimmune Diseases and Colorectal Cancer.","authors":"Shuang Liu, Kun Chen, Yue Qi Wang, Xiao Yu Gu, Zhi He, Chen Zhang, Guo Qiu Wu, Su Su Luo, Xing Jin","doi":"10.14740/wjon2732","DOIUrl":"10.14740/wjon2732","url":null,"abstract":"<p><strong>Background: </strong>Observational studies have reported associations between autoimmune diseases (AIDs) and colorectal cancer (CRC), but whether these relationships are causal remains unclear.</p><p><strong>Methods: </strong>We performed a bidirectional two-sample Mendelian randomization (MR) analysis to evaluate the causal effects of eight prevalent AIDs-systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), ankylosing spondylitis (AS), gout, multiple sclerosis (MS), celiac disease (CD), eczema, and asthma-on CRC risk, and to examine the possibility of reverse causation. Genome-wide association study (GWAS) summary statistics from individuals of European ancestry were analyzed. The inverse-variance weighted (IVW) approach served as the primary MR estimator, with MR-Egger regression and the weighted median method applied as complementary analyses. Robustness was further evaluated through sensitivity analyses, including assessments of heterogeneity and horizontal pleiotropy.</p><p><strong>Results: </strong>Genetically predicted CD was associated with a reduced risk of CRC (IVW odds ratio (OR) = 0.94; 95% confidence interval (CI), 0.89-0.99; P = 0.028). Genetically predicted RA was associated with an increased risk of CRC (IVW OR = 1.06; 95% CI, 1.02-1.11; P = 0.004). No significant causal associations were observed for the other AIDs. Reverse MR provided no evidence that genetic liability to CRC causally influenced the risk of these AIDs. Sensitivity analyses supported the stability of the findings.</p><p><strong>Conclusions: </strong>This bidirectional MR study provides genetic evidence supporting unidirectional, modest causal effects of specific AIDs (CD and RA) on CRC risk. Further studies are warranted to clarify underlying mechanisms, including immune dysregulation, inflammation, and dietary factors, and to determine clinical implications.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"256-267"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147445705","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}
{"title":"Clinical Outcomes and Prognostic Factors in Metastatic Triple-Negative Breast Cancer: A Real-World Data Analysis.","authors":"Moe Itakura, Yoshiya Horimoto, Yumiko Ushiyama, Yuko Ueki, Yumiko Ishizuka, Yoichi Koyama, Kyoko Orimoto, Hiroki Kusama, Takahiko Kawate, Takashi Ishikawa, Junichiro Watanabe, Goro Kutomi","doi":"10.14740/wjon2713","DOIUrl":"10.14740/wjon2713","url":null,"abstract":"<p><strong>Background: </strong>Metastatic triple-negative breast cancer (mTNBC) is associated with poor outcomes, and therapeutic strategies remain challenging. This study analyzed real-world data to clarify clinical characteristics, treatment patterns, and survival outcomes, focusing on treatment feasibility at metastatic diagnosis.</p><p><strong>Methods: </strong>A retrospective analysis was conducted on 96 Japanese women who developed distant metastasis after curative surgery and met the inclusion criteria for the final analysis. Patients who were unable to receive drug treatment due to poor condition were defined as the non-treated group and compared with the treated group, who received at least 4 weeks of systemic therapy. Overall survival was assessed using the Cox proportional hazard model.</p><p><strong>Results: </strong>Overall, 31% of patients could not receive systemic treatment due to poor condition. The non-treated group was more frequently diagnosed after presenting with symptoms and had a higher prevalence of poor performance status and brain metastasis (P < 0.001). Among the 66 treated patients, the median overall survival was 14 months with an average of 2.2 treatment lines. In exploratory Cox analyses, the number of metastatic organs and treatment with paclitaxel plus bevacizumab were associated with overall survival. Several patients experienced prolonged treatment with oral 5-fluorouracil.</p><p><strong>Conclusions: </strong>A significant proportion of patients were diagnosed with mTNBC after symptom onset, limiting therapeutic intervention. Diagnosing mTNBC before symptomatic deterioration may expand treatment opportunities. Prospective evaluation of follow-up strategies and biomarkers is required, and further research should clarify treatment positioning, including paclitaxel plus bevacizumab and maintenance therapy with oral agents for biologically low-grade cases.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"17 2","pages":"268-276"},"PeriodicalIF":2.3,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444167","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}