Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
The morbidity and mortality rates of prostate cancer (PCa) are high among elderly men worldwide. Several factors, such as heredity, obesity, and environment are associated with the occurrence of PCa. Cigarette smoking, which is also an important factor in the development of PCa, can lead to genetic alterations and consequently promote PCa development. However, the smoking-induced genetic alterations in PCa are unclear. This study aimed to identify the potential smoking-related genes associated with PCa development. The smoking-related differentially expressed genes (DEGs) were identified using the Gene Expression Omnibus (GEO) which included lots of PCa datasets. DEGs were subjected to protein–protein interaction (PPI) network analysis to identify the hub genes. The pathways in which these hub genes were enriched were identified. The Cancer Genome Atlas (TCGA) dataset was used to examine the expression of smoking-related genes in PCa samples and estimate their value in predicting tumor progression and prognosis. In total, 110 smoking-related DEGs were got from GSE68135 dataset which included microarray data of PCa patients with smoking or not and 14 smoking-related key genes associated with PCa were identified from PPI network. The expression of the following seven key genes was altered in TCGA PCa patients: EWSR1 , SRSF6 , COL6A3 , FBLN1 , DCN, CYP2J2 , and PLA2G2A . EWSR1 , SRSF6 , FBLN1 , and CYP2J2 also influenced PCa progression. Additionally, EWSR1 influenced disease-free survival. In the logistic regression model, CYP2J2 , which exhibited the highest risk scores, was identified as the risk gene for PCa. We also found one of the smoking-related genes: EWSR1 was truly upregulated in clinical PCa patients and influenced PCa cells invasion and proliferation. This study identified the function of smoking-related genes involved in the progression of PCa. Supplementary Information The online version contains supplementary material available at 10.1007/s12672-024-01645-2.
The morbidity and mortality rates of prostate cancer (PCa) are high among elderly men worldwide. Several factors, such as heredity, obesity, and environment are associated with the occurrence of PCa. Cigarette smoking, which is also an important factor in the development of PCa, can lead to genetic alterations and consequently promote PCa development. However, the smoking-induced genetic alterations in PCa are unclear. This study aimed to identify the potential smoking-related genes associated with PCa development. The smoking-related differentially expressed genes (DEGs) were identified using the Gene Expression Omnibus (GEO) which included lots of PCa datasets. DEGs were subjected to protein–protein interaction (PPI) network analysis to identify the hub genes. The pathways in which these hub genes were enriched were identified. The Cancer Genome Atlas (TCGA) dataset was used to examine the expression of smoking-related genes in PCa samples and estimate their value in predicting tumor progression and prognosis. In total, 110 smoking-related DEGs were got from GSE68135 dataset which included microarray data of PCa patients with smoking or not and 14 smoking-related key genes associated with PCa were identified from PPI network. The expression of the following seven key genes was altered in TCGA PCa patients: EWSR1 , SRSF6 , COL6A3 , FBLN1 , DCN, CYP2J2 , and PLA2G2A . EWSR1 , SRSF6 , FBLN1 , and CYP2J2 also influenced PCa progression. Additionally, EWSR1 influenced disease-free survival. In the logistic regression model, CYP2J2 , which exhibited the highest risk scores, was identified as the risk gene for PCa. We also found one of the smoking-related genes: EWSR1 was truly upregulated in clinical PCa patients and influenced PCa cells invasion and proliferation. This study identified the function of smoking-related genes involved in the progression of PCa. Supplementary Information The online version contains supplementary material available at 10.1007/s12672-024-01645-2.
Spindle cell/sclerosing rhabdomyosarcoma is an infrequent subtype of rhabdomyosarcoma according to the World Health Organization Classification of Soft Tissue and Bone Tumours, which includes a novel category of intraosseous spindle-cell rhabdomyosarcomas (ISCRMS) with EWSR1:: or FUS::TFCP2 fusions. We report a case of ISCRMS with EWSR1::TFCP2 fusion presenting in the femur mimicking osteosarcoma in this unusual primary location. We present an 18-year-old male with relapsed widely metastatic sarcoma, morphologically identical to osteosarcoma responding poorly to chemotherapy, initially presenting in the distal femur. Sections showed a high-grade malignant neoplasm with sheets of epithelioid and spindled cells without obvious rhabdomyoblastic differentiation morphologically containing focal areas resembling new bone/osteoid formation. Molecular sequencing identified t(12;22) EWSR1::TFCP2. The tumor cells were diffusely positive for pancytokeratin, MyoD1, and ALK by retrospective immunohistochemistry. Desmin and SATB2 were focally positive. Myogenin was negative, and INI-1 expression was retained. ISCRMS commonly involves craniofacial and pelvic bones, but rarely originates in long bones, as in this case. Initially, osteosarcoma was the primary diagnostic consideration based on distal long bone location, patient age, and evidence of osteoid formation. Distinction between the two entities may be nearly impossible on morphologic grounds alone, which presents a diagnostic pitfall without molecular or extensive immunoprofiling data.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.