{"title":"Angiogenesis Is Associated With Aggressive Biology That Counterbalances With Tumor Immunogenicity in Hepatocellular Carcinoma.","authors":"Raj Vaghjiani, Rongrong Wu, Kaity H Tung, Takashi Ishikawa, Kazuaki Takabe","doi":"10.14740/wjon2009","DOIUrl":"10.14740/wjon2009","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is an arterialized tumor; thus, anti-angiogenesis targeted therapy is in clinical practice. Herein, we hypothesized that HCC with high angiogenesis is biologically aggressive with worse survival.</p><p><strong>Methods: </strong>Angiogenesis score (AS) was derived from the Molecular Signatures Database (MSigDB) Hallmark Angiogenesis Gene Set, and median was used to divide high versus low groups. Transcriptome of HCC patients of The Cancer Genome Atlas (TCGA, n = 386) and GSE76427 (n = 115) cohorts were analyzed.</p><p><strong>Results: </strong>High AS correlated with angiogenesis-related gene expressions. Both microvascular and lymphatic endothelial cell infiltrations were higher in high angiogenesis HCC. Surprisingly, no survival difference was seen with varying levels of angiogenesis. High angiogenesis significantly enriched tumor aggravating signaling pathways: glycolysis, Notch, Hedgehog, KRAS, epithelial mesenchymal transition, and transforming growth factor-beta (TGF-β) in Gene Set Enrichment Analysis (GSEA), but also infiltrated less CD8<sup>+</sup> T cells and T-helper 1 cells, and higher M1 macrophages and conventional dendritic cells (cDCs) with elevated cytolytic activity score in both cohorts. In agreement, immune response-related gene sets: inflammatory response, tumor necrosis factor-alpha (TNF-α) signaling, allograft rejection, interferon-alpha, and interferon-gamma were all enriched to high angiogenesis HCC. Programmed cell death protein 1 (PD1), programmed death ligand 1 (PD-L1), programmed death ligand 2 (PD-L2), and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) were higher in high angiogenesis HCC in TCGA, but not in GSE76427 cohort.</p><p><strong>Conclusions: </strong>Angiogenesis quantified using transcriptome of HCC patients demonstrated that it is associated with aggressive biology but also with tumor immunogenicity and immune response that counterbalance and did not reflect in survival. Given high expression of immune checkpoint molecules, we cannot help but speculate that immunotherapy may be useful for high angiogenesis HCC patients.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 2","pages":"173-181"},"PeriodicalIF":2.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755232","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}
Kyla Wright, Michael A Mederos, Irene R Riahi, Bita V Naini, Jena Depetris, Mark D Girgis
{"title":"Solitary Synchronous Biliary Metastasis in Colorectal Adenocarcinoma.","authors":"Kyla Wright, Michael A Mederos, Irene R Riahi, Bita V Naini, Jena Depetris, Mark D Girgis","doi":"10.14740/wjon2008","DOIUrl":"10.14740/wjon2008","url":null,"abstract":"<p><p>Malignant biliary obstruction can, in rare cases, arise from metastases to the biliary tree from distant primary tumors. This phenomenon often poses a diagnostic challenge, as bile duct metastases may clinically and radiologically mimic primary biliary tumors, such as cholangiocarcinoma. We present a unique case of solitary, synchronous intraductal biliary metastasis in a patient with colorectal adenocarcinoma that led to biliary obstruction. The patient initially presented with a new diagnosis of colon cancer at the hepatic flexure and was found, on cross-sectional imaging, to have biliary obstruction due to an intraductal mass. Initially, the nature of the intraductal lesion was uncertain; however, it was ultimately confirmed through histopathological examination to be metastatic colorectal adenocarcinoma. This case underscores the difficulty of distinguishing metastatic biliary obstruction from primary biliary tumors and highlights the importance of considering metastatic disease in atypical presentations of biliary masses. We discuss several key radiologic and histopathological features that may help differentiate intraductal colorectal adenocarcinoma metastases from primary biliary tumors.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 2","pages":"227-234"},"PeriodicalIF":2.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755146","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}
Nur Qodir, Didit Pramudhito, Zen Hafy, Muhammad Baharul Iman, Fara Syafira, Putri Mahirah Afladhanti, Raehan Satya Daenasa, Bima Indra
{"title":"Tumor Necrosis Factor-Alpha and Its Association With Breast Cancer: A Systematic Review.","authors":"Nur Qodir, Didit Pramudhito, Zen Hafy, Muhammad Baharul Iman, Fara Syafira, Putri Mahirah Afladhanti, Raehan Satya Daenasa, Bima Indra","doi":"10.14740/wjon2532","DOIUrl":"10.14740/wjon2532","url":null,"abstract":"<p><strong>Background: </strong>Tumor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine implicated in the pathogenesis and progression of various cancers, including breast cancer. Elevated TNF-α levels have been associated with cancer progression, metastasis, and treatment outcomes. This systematic review aimed to synthesize existing evidence on the relationship between TNF-α levels and breast cancer.</p><p><strong>Methods: </strong>A systematic search of observational studies published from inception to June 2024 was conducted in PubMed, ScienceDirect, Sage Journals, and Google Scholar to identify studies examining TNF-α levels in breast cancer patients compared to healthy controls, as well as its association with metastasis, response to chemotherapy, and survival outcomes. Inclusion criteria were applied to select eligible studies, resulting in nine studies that met the criteria for this review.</p><p><strong>Results: </strong>Eight eligible studies reported that breast cancer patients exhibited higher TNF-α levels than healthy controls. Two studies indicated that TNF-α levels were elevated in patients with metastatic breast cancer. Additionally, two studies found that patients with higher TNF-α levels tended to have a poorer response to chemotherapy. One study revealed that patients with elevated TNF-α levels had a lower mean survival time.</p><p><strong>Conclusions: </strong>Elevated TNF-α levels are significantly associated with breast cancer progression, metastasis, and poorer treatment outcomes. These findings underscore the potential of TNF-α as a biomarker for breast cancer prognosis and therapeutic response. Further research is warranted to explore the underlying mechanisms and validate TNF-α as a target for therapeutic intervention in breast cancer management.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 2","pages":"143-151"},"PeriodicalIF":2.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143754709","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":"Should All Low-Grade Ductal Carcinoma <i>In Situ</i> Be Excised? Implications and Challenges of the COMET Trial.","authors":"Hiroki Kusama, Yoshiya Horimoto, Kazuaki Takabe, Takashi Ishikawa","doi":"10.14740/wjon2562","DOIUrl":"10.14740/wjon2562","url":null,"abstract":"","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 2","pages":"239-241"},"PeriodicalIF":2.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755145","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}
Nan Yang Zhang, Wen Yuan Liu, Ke Hua Fang, Xiao Tian Chang
{"title":"Increased Sirtuin 6 Activity in Tumor Cells Can Prompt CD4-Positive T-Cell Differentiation Into Regulatory T Cells and Impede Immune Surveillance in the Microenvironment.","authors":"Nan Yang Zhang, Wen Yuan Liu, Ke Hua Fang, Xiao Tian Chang","doi":"10.14740/wjon2547","DOIUrl":"10.14740/wjon2547","url":null,"abstract":"<p><strong>Background: </strong>Sirtuin 6 (Sirt6) is expressed at increased levels in many tumors and may be involved in immunoregulation. The present study investigated how Sirt6 in tumor cells affects immune surveillance.</p><p><strong>Methods: </strong>The human tumor cell lines A2780, HeLa, Huh7, MBA-MD-231, SMMC-7721 and SW480 were incubated with UBCS039, a target-selective activator of Sirt6, to stimulate Sirt6 activity. These cells, following washing to remove residual UBCS039, were cultured with human naive CD4<sup>+</sup> T cells in the Transwell to observe the T cell differentiation. Regulatory T cells (Tregs) among CD4<sup>+</sup> T cells and the levels of various cytokines and adenosine (ADO), an immunosuppressive metabolite, in the culture medium, were measured via flow cytometry. The treated tumor cells were examined via transcriptomic analysis. The transcriptomic results, as well as programmed cell death protein-1 (PD-1), programmed cell death-ligand 1 (PD-L1) and Sirt6 expression in tumor cells and CD4<sup>+</sup> T cells were verified via real-time polymerase chain reaction (PCR).</p><p><strong>Results: </strong>Following culture with UBSC039-pretreated tumor cells, the proportion of Tregs among CD4<sup>+</sup> T cells was significantly increased. PD-L1 and Sirt6 expressions in UBS039-pretreated tumor cells and PD-1 expression in cocultured CD4<sup>+</sup> T cells were also increased. Moreover, the ADO level increased, and the interleukin (IL)-10, interferon (IFN)-α2, IFN-γ and monocyte chemoattractant protein-1 (MCP-1) levels decreased in the coculture medium. Transcriptomic analysis revealed significant downregulation of the antitumor genes <i>BASP1</i>, <i>CPS1</i>, <i>GNG11</i>, <i>MFAP5</i>, <i>NNMT</i> and <i>SMOC1</i>, upregulation of the tumor-promoting genes <i>FOXA2</i>, <i>GSTP1</i>, <i>RASEF</i> and <i>ZNF844</i>, and activation of adherens junctions, tumor necrosis factor (TNF)-signaling and the circadian rhythm pathway in UBCS039-pretreated SMMC-7721 cells. The above results were verified in all six cell lines.</p><p><strong>Conclusions: </strong>The present study suggested that increased Sirt6 expression and activity in tumor cells can suppress immune surveillance by increasing Treg, ADO, PD-1 and PD-L1 levels, decreasing IFN-γ production, and altering tumor-promoting and antitumor gene expression in the microenvironment.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 2","pages":"182-199"},"PeriodicalIF":2.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755138","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":"CD19 Expression in B-Cell Lymphomas and Clinical Considerations in the Evolving Landscape of CD19-Targeted Therapy.","authors":"Joseph P Marshalek, Xin Qing, Sarah Tomassetti","doi":"10.14740/wjon2534","DOIUrl":"10.14740/wjon2534","url":null,"abstract":"","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 2","pages":"235-238"},"PeriodicalIF":2.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755234","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}
Bryant Ng, Armeyra Devani Ferintasari, Susanna Hilda Hutajulu, Yufi Kartika Astari, Juan Adrian Wiranata, Suwardjo Suwardjo, Irianiwati Widodo, Lina Choridah, Wigati Dhamiyati, Mardiah Suci Hardianti, Kartika Widayati Taroeno-Hariadi
{"title":"Patterns, Predictors, and Prognostic Implication of Treatment-Related Amenorrhea in Patients With Breast Cancer.","authors":"Bryant Ng, Armeyra Devani Ferintasari, Susanna Hilda Hutajulu, Yufi Kartika Astari, Juan Adrian Wiranata, Suwardjo Suwardjo, Irianiwati Widodo, Lina Choridah, Wigati Dhamiyati, Mardiah Suci Hardianti, Kartika Widayati Taroeno-Hariadi","doi":"10.14740/wjon1991","DOIUrl":"10.14740/wjon1991","url":null,"abstract":"<p><strong>Background: </strong>Treatment-related amenorrhea (TRA) is a common side effect of treatment in premenopausal patients with breast cancer, with important consequences for patient counseling and management. Its occurrence and potential influence on survival outcomes remain active areas of investigation. This study aimed to evaluate the incidence, risk factors, and prognostic significance of TRA in patients with breast cancer.</p><p><strong>Methods: </strong>This is a retrospective cohort study. Patients were interviewed during and after chemotherapy to assess their menstrual status. Sociodemographic, clinical, and treatment data of patients were also collected. TRA was classified into early amenorrhea (EA) and late amenorrhea (LA) based on the duration of amenorrhea. Univariable and multivariable logistic regression were used to identify risk factors of EA and LA. Kaplan-Meier curves and Cox proportional hazards analyses were used to investigate the impact of EA and LA on 3-year overall survival (OS).</p><p><strong>Results: </strong>There were 81 patients who were eligible for the final analysis. Of these subjects, 14 (17.3%) developed no amenorrhea, 67 (82.7%) developed EA, and 45 (55.6%) developed LA. We did not find any significant independent risk factor for EA. Age > 45 years (odds ratio (OR): 4.00; confidence interval (CI): 1.23 - 13.01; P = 0.021) and the usage of hormonal therapy (OR: 4.96; CI: 1.58 - 15.53; P = 0.006) independently significantly increase the risk of LA, whereas a metastatic disease status decreased the risk (OR: 0.20; CI: 0.04 - 0.90; P = 0.036). Both EA (hazard ratio (HR) = 0.262, CI: 0.105 - 0.653; P = 0.002) and LA (HR = 0.234, CI: 0.091 - 0.604; P = 0.001) were associated with an improved 3-year OS rate.</p><p><strong>Conclusions: </strong>Age > 45 years and the usage of hormonal therapy are risk factors for LA, while metastatic disease was associated with a decreased risk. Both EA and LA had a significant association with favorable 3-year OS. These findings enable clinicians to provide personalized guidance, tailor treatment strategies, and improve the outcomes of premenopausal patients with breast cancer. Standardization of how TRA is defined and assessed in future studies is essential to improve comparability and enhance the understanding of its clinical implications.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 2","pages":"200-209"},"PeriodicalIF":2.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755142","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}
Ying Zhou, Rui Sun, Zi Wen Zhang, Xin Yi He, Lin Li, Chun Jing Zhang, Ying Liu, Hai Tao Yu
{"title":"Proliferation Inhibited by Genipin in Human Leukemia K562 Cells: Involvement of Uncoupling Protein 2 in Mitochondrial Damage.","authors":"Ying Zhou, Rui Sun, Zi Wen Zhang, Xin Yi He, Lin Li, Chun Jing Zhang, Ying Liu, Hai Tao Yu","doi":"10.14740/wjon1975","DOIUrl":"10.14740/wjon1975","url":null,"abstract":"<p><strong>Background: </strong>Uncoupling protein 2 (UCP2) is essential for maintaining redox homeostasis and regulating energy metabolism. Abnormal expression of UCP2 has been associated with various tumors, including leukemia. Genipin (GEN), a specific inhibitor of UCP2, has a long history of use in traditional Chinese medicine. However, the precise role and underlying mechanisms of UCP2 in the inhibition of leukemia cells by GEN remain inadequately understood. This study focuses on the expression levels of UCP2 in myeloid leukemia (ML) and investigates the effects of GEN on the proliferation, mitochondrial function, and energy metabolism of the chronic myeloid leukemia (CML) cell line K562.</p><p><strong>Methods: </strong>The expression of UCP2 in clinical samples and cell lines (HL-60, U937, and K562) was confirmed using real-time quantitative polymerase chain reaction (qPCR) and western blot. The effects of GEN on K562 cell viability, morphology, and apoptosis were assessed through a cell counting kit-8 (CCK-8), Wright-Giemsa staining, and an annexin V-fluorescein isothiocyanate/propidium iodide (FITC/PI) apoptosis detection kit. Additionally, the impact of GEN on mitochondrial function and energy metabolism, including reactive oxygen species (ROS), mitochondrial membrane permeability transition pore (MPTP), lactic acid (LA), oxygen consumption rate (OCR), and adenosine triphosphate (ATP) levels in K562 cells, was also examined.</p><p><strong>Results: </strong>The results showed that UCP2 was differentially expressed in clinical samples from patients with ML. Among the three cell lines examined, K562 cells exhibited a significantly higher expression level of UCP2. Functionally, GEN markedly inhibited K562 cell viability while promoting K562 cell differentiation and apoptosis. Mechanistically, UCP2 mRNA and protein expression levels were inhibited by GEN in K562 cells in a concentration- and time-dependent manner. Additionally, GEN dramatically increased ROS generation and induced mitochondrial MPTP opening in K562 cells. Furthermore, GEN significantly reduced LA production in K562 cells and markedly increased OCR and ATP production.</p><p><strong>Conclusion: </strong>The results suggest that UCP2 is differentially expressed in ML patients and cell lines; GEN, a UCP2 inhibitor, induces mitochondrial damage and metabolic remodeling, thereby inhibiting proliferation and promoting apoptosis in K562 cells, and thus could be suggested as an adjuvant of an antitumor metabolic therapy.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 1","pages":"83-94"},"PeriodicalIF":2.1,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11750759/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029497","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":"<i>VEGFA</i> Gene Expression in Breast Cancer Is Associated With Worse Prognosis, but Better Response to Chemotherapy and Immunotherapy.","authors":"Pia Sharma, Kohei Chida, Rongrong Wu, Kaity Tung, Kenichi Hakamada, Takashi Ishikawa, Kazuaki Takabe","doi":"10.14740/wjon1993","DOIUrl":"10.14740/wjon1993","url":null,"abstract":"<p><strong>Background: </strong>Vascular endothelial growth factor-A (VEGFA) is a key inducer of angiogenesis, responsible for generating new blood vessels in the tumor microenvironment (TME) and facilitating metastasis. Notably, Avastin, which targets VEGFA, failed to demonstrate any significant benefit in clinical trials for breast cancer (BC). This study aimed to investigate the clinical relevance of <i>VEGFA</i> gene expression in BC.</p><p><strong>Methods: </strong>A total of 7,336 BC patients across eight independent cohorts: ISPY2 (GSE173839), Sweden Cancerome Analysis Network-Breast (SCAN-B) (GSE96058), Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), GSE25066, GSE163882, GSE34138, GSE20194, and The Cancer Genome Atlas (TCGA), were analyzed. The calculated median <i>VEGFA</i> expression level was used to stratify these cohorts into high and low groups.</p><p><strong>Results: </strong>High <i>VEGFA</i> was associated with worse disease-free, disease-specific, and overall survival in the METABRIC cohort, with findings supported by the SCAN-B cohort, which also showed worse overall survival (all P < 0.02). High <i>VEGFA</i> expression was seen in triple-negative breast cancer (TNBC) but not in BC with lymph node metastasis. Additionally, there was a significant correlation between high <i>VEGFA</i> expression and higher silent and non-silent mutations, single-nucleotide variant (SNV) neoantigens, homologous recombination defect, intratumoral heterogeneity, in the TCGA cohort. In the TCGA, METABRIC, and SCAN-B cohorts, high <i>VEGFA</i> BC was also associated with higher cell proliferation: higher Ki67 gene expression, higher Nottingham histological grade, and consistent enrichment of all the Hallmark cell proliferation-related gene sets. Unexpectedly, the angiogenesis gene set was not enriched in any of the cohorts and showed no association with infiltrations of lymphatic or blood vascular endothelial cells besides pericytes. High <i>VEGFA</i> BC had significantly less infiltration of anti-cancer immune cells but higher infiltration of pro-cancer immune cells in TCGA, METABRIC, and SCAN-B cohorts. Interestingly, BC, which had a pathological complete response (pCR) after anthracycline- and taxane-based neoadjuvant therapy, was associated with significantly heightened <i>VEGFA</i> expression in both estrogen receptor (ER)+/human epidermal growth factor receptor 2 (HER2)- and TNBC subtypes in the GSE25066 cohort and after immunotherapy in ER+/ HER2- subtype, but not TNBC in the ISPY2 cohort.</p><p><strong>Conclusions: </strong>Our research indicates that high <i>VEGFA</i> BC confers high cell proliferation, reduced immune cell infiltration, and poorer survival, but allows better response to anthracycline- and taxane-based chemotherapy, and immunotherapy.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 1","pages":"120-130"},"PeriodicalIF":2.2,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11750749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143030037","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}
Bann Siang Yeo, Wen Xuan Lee, Rozi Mahmud, Geok Chin Tan, Mohamed Ibrahim Abdul Wahid, Yoke Kqueen Cheah
{"title":"MicroRNA-155 as Biomarker and Its Diagnostic Value in Breast Cancer: A Systematic Review.","authors":"Bann Siang Yeo, Wen Xuan Lee, Rozi Mahmud, Geok Chin Tan, Mohamed Ibrahim Abdul Wahid, Yoke Kqueen Cheah","doi":"10.14740/wjon1955","DOIUrl":"10.14740/wjon1955","url":null,"abstract":"<p><p>The investigation of microRNAs (miRNAs) for the purpose of identifying biomarkers and new treatments for breast cancer has been gaining traction from scientists in recent years. Of all the miRNAs, miR-155 has been reportedly involved in breast cancer development as it regulates various cellular processes such as glucose uptake, proliferation, metastasis, and migration. Various efforts have been done towards researching miR-155 as a biomarker in breast cancer; however, the results were varied. The objective of the current systematic review is to compile and summarize information regarding miR-155 as a potential diagnostic biomarker for breast cancer. All eligible studies were found from SCOPUS and PubMed databases. Out of the 376 potential eligible records, only 26 original articles were selected for further assessment according to inclusion and exclusion criteria. The expressions of miR-155 in serum, plasma, biopsy, urine, nipple aspirate fluid, serum exosomes, and peripheral blood mononuclear cells were recorded and analyzed. Besides that, the expression of miR-155 was also correlated to clinicopathological features in breast cancer patients. The area under the curve (AUC) values from receiver operating characteristic (ROC) analysis used to evaluate diagnostic sensitivity and specificity of miR-155 as a diagnostic biomarker were also recorded. The limitations such as the small sampling size, the unemployment of internal controls for quantitative real-time polymerase chain reaction (RT-qPCR), and inconsistency of sensitivity as well as specificity values of miR-155 as a biomarker have been discussed. The present study proposed that miR-155 is a good diagnostic biomarker for breast cancer; however, further clinical research is required to assess the validity of miR-155 as a potential biomarker to translate the research outcomes into clinical practice.</p>","PeriodicalId":46797,"journal":{"name":"World Journal of Oncology","volume":"16 1","pages":"1-15"},"PeriodicalIF":2.1,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11750751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029401","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}