Identification of the potential novel biomarkers as susceptibility gene for Wilms tumor

Liu, Li; Song, Zhe; Gao, Xudong; Chen, Xian; Wu, Xiaobin; Wang, Mi; Hong, Yu-De

doi:10.1186/s12885-021-08034-w

Cited by 6 publications

(6 citation statements)

References 43 publications

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“…Despite advances in treatment strategies and the favorable prognosis of most patients with WT, the mortality rate is still 10% ( 9 ). Poor outcomes have been reported for advanced, bilateral and recurrent WT ( 10 ). Therefore, it is critical to identify novel prognostic factors for WT to guide the development of individualized treatment strategies.…”

Section: Discussionmentioning

confidence: 99%

Prognostic role of primary tumor size in Wilms tumor

Li,

Zhang,

Yuan

et al. 2024

Oncol Lett

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Wilms tumor (WT) is the most common childhood malignant kidney tumor. The aim of the present study was to determine the impact of primary tumor size on the survival of patients with WT. The data of 1,523 patients diagnosed with WT between 2000 and 2017 were retrieved from the Surveillance, Epidemiology, and End Results database. Receiver operating characteristic curves were plotted to determine the optimal cut-off value of primary tumor size. Overall survival (OS) and cancer-specific survival (CSS) were analyzed using the Kaplan-Meier method and the Cox proportional hazards regression model. The optimal cut-off value for primary tumor size was found to be 11.15 cm. No significant difference in the distribution of tumor size was detected between male and female patients. However, lymph node metastasis and distant metastasis were significantly more frequent in patients whose tumor was ≥11.15 cm in size compared with those with smaller tumors. In addition, patients with larger tumors exhibited significantly worse OS and CSS rates compared with those with smaller tumors. Furthermore, primary tumor size was identified as an independent prognostic factor for OS and CSS in the multivariate analyses. In summary, the present study indicates that primary tumor size is an independent prognostic factor for patients with WT, and tumors ≥11.15 cm are associated with worse OS and CSS.

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Section: Discussionmentioning

confidence: 99%

Prognostic role of primary tumor size in Wilms tumor

Li,

Zhang,

Yuan

et al. 2024

Oncol Lett

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“…WGCNA, a scale-free network distribution approach, is powerful data-driven tool to study gene expression pattern in samples from different cohorts [ 77 ]. Using WGCNA, we were able to validate the DEG pathway signatures in BWS-WT.…”

Section: Discussionmentioning

confidence: 99%

“…Modules enriched for altered-11p15 nonBWS-WT trait mainly showed enrichment of cell cycle and metabolic processes. Many other studies on WT using the WGCNA approach have showed enrichment of cell cycle related processes, indicating it as a major molecular signature for WT [ 77 – 79 ]. Along with metabolic pathway enrichment, Wang et al have also shown enrichment of PI3K-Akt, FoxO, p53, and TNF signaling pathways, along with many other cancer related pathways in WT, using the WGCNA approach [ 78 ].…”

Section: Discussionmentioning

confidence: 99%

Cancer predisposition signaling in Beckwith-Wiedemann Syndrome drives Wilms tumor development

Nirgude,

Naveh,

Kavari

et al. 2023

Br J Cancer

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Background Wilms tumor (WT) exhibits structural and epigenetic changes at chromosome 11p15, which also cause Beckwith-Wiedemann Syndrome (BWS). Children diagnosed with BWS have increased risk for WT. The aim of this study is to identify the molecular signaling signatures in BWS driving these tumors. Methods We performed whole exome sequencing, methylation array analysis, and gene expression analysis on BWS-WT samples. Our data were compared to publicly available nonBWS data. We categorized WT from BWS and nonBWS patients by assessment of 11p15 methylation status and defined 5 groups– control kidney, BWS-nontumor kidney, BWS-WT, normal-11p15 nonBWS-WT, altered-11p15 nonBWS-WT. Results BWS-WT samples showed single nucleotide variants in BCORL1, ASXL1, ATM and AXL but absence of recurrent gene mutations associated with sporadic WT. We defined a narrow methylation range stratifying nonBWS-WT samples. BWS-WT and altered-11p15 nonBWS-WT showed enrichment of common and unique molecular signatures based on global differential methylation and gene expression analysis. CTNNB1 overexpression and broad range of interactions were seen in the BWS-WT interactome study. Conclusion While WT predisposition in BWS is well-established, as are 11p15 alterations in nonBWS-WT, this study focused on stratifying tumor genomics by 11p15 status. Further investigation of our findings may identify novel therapeutic targets in WT oncogenesis.

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“…Nephroblastoma is the most common childhood abdominal malignancy and approximately 15% of patients will experience recurrence with a 40 to 80% overall survival rate [21]. Although the diagnosis and therapeutic effects have significantly improved, long-term survival rate remains low in patients with nephroblastoma with high mortality rate [22].…”

Section: Discussionmentioning

confidence: 99%

S100A16 cooperates with DEPDC1 to promote the progression and angiogenesis of nephroblastoma through PI3K/Akt/mTOR pathway

Geng,

Xu,

et al. 2023

pjp

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S100 calcium-binding protein A16 (S100A16) has previously been reported to play a role in tumor cells. Nevertheless, the role that S100A16 played in nephroblastoma cells remains obscure. The expression of S100A16 and DEPDC1 were detected via RT-q PCR and western blotting. Cell transfection was performed to overexpress DEPDC1 or interfere S100A16. CCK8 was applied for the assessment of cell viability. The apoptotic level and the capabilities of WiT49 cells to proliferate, invade and migrated were appraised utilizing Tunel, colony formation Transwell, and wound healing, separately. The angiogenesis was estimated through tube formation assay. Co-immunoprecipitation (CO-IP) was performed to examine the targeted binding of S100A16 to DEPDC1. The contents of PI3K/Akt/mTOR pathway-related proteins were resolved by virtue of western blot. S100A16 and DEPDC1 expression levels were significantly increased in nephroblastoma cell lines. S100A16 deletion suppressed nephroblastoma cell proliferative, invasive, migrative and angiogenetic capabilities but facilitated the apoptotic level. Moreover, S100A16 could bind DEPDC1, DEPDC1 overexpression partially reversed the inhibitory effect of S100A16 interference on nephroblastoma cell. DEPDC1 overexpression also partially counteracted the suppressive impacts of S100A16 interference on PI3K/Akt/mTOR pathway-related proteins. S100A16 synergistic with DEPDC1 promotes the progression and angiogenesis of nephroblastoma cell through the PI3K/Akt/mTOR pathway.

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Identification of the potential novel biomarkers as susceptibility gene for Wilms tumor

Cited by 6 publications

References 43 publications

Prognostic role of primary tumor size in Wilms tumor

Prognostic role of primary tumor size in Wilms tumor

Cancer predisposition signaling in Beckwith-Wiedemann Syndrome drives Wilms tumor development

S100A16 cooperates with DEPDC1 to promote the progression and angiogenesis of nephroblastoma through PI3K/Akt/mTOR pathway

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