Clinicopathologic classification of endometrial cancer imperfectly reflects the tumor biology. Pathologic categorization - especially in high-grade tumors - results in an imprecise estimation of the risk of disease, recurrence, and death. Molecular subtyping is emerging as the standard of care in diagnosis and treatment of endometrial cancers. Molecular markers are important prognostic factors in tumor dissemination and early recurrence of endometrial cancers. TP53 mutation is an important prognostic factor for both serous and endometrioid cancers. The study aims to compare the clinical profile and overall survival of endometrial cancers with and without p53 mutation. Sixty-three patients who underwent surgical staging for carcinoma endometrium were included in the study.TP53 mutation status was determined based on p53 expression by immunohistochemistry (IHC) as a p53 wild or p53 mutant type. Data were analyzed for the clinical profile, p53 mutation status on IHC, histological pattern, tumor grade, stage of the disease, lymph node spread, recurrence pattern, treatment received, 2-year disease-free survival, and overall survival. Recurrence was noted in 12.7% patients after 2-year follow-up, of which 75% patients had p53 mutation. Significant association was seen between p53 expression and high-grade tumors, stage, cervical involvement, and adnexal involvement. The 2-year overall survival of the p53 wild type was 97.2% and the p53 mutant type was 91.7%. The 2-year disease-free survival for the p53 wild type was 94.3% and the disease-free survival of the p53 mutant variety was 83.5%. The 2-year disease-free survival for endometrioid carcinoma with p53 wild type was 100% and p53 mutant variety was 86.2% ( value 0.033). About 15.9% (10) patients were reassigned to the high-risk group needing chemotherapy and radiation according to the ESGO ESTRO 2021 consensus classification, due to their p53 mutation status. IHC to assess somatic p53 mutation may be done in endometrial biopsies irrespective of their histology. This may help to identify that the aggressive tumors thereby help in tailoring surgery, planning adjuvant treatment, and follow-up.
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http://dx.doi.org/10.1007/s13193-022-01523-9 | DOI Listing |
Urologie
January 2025
Klinik für Urologie, Uro-Onkologie, roboter-assistierte und spezielle urologische Chirurgie, Uniklinik Köln, Kerpener Str. 62, 50927, Köln, Deutschland.
Introduction: Prostate cancer guidelines recommend molecular analysis of biomaterial following resistance to first-line systemic therapy in order to identify druggable mutations. We report on our results of molecular analysis of tissue specimens via next generation sequencing (NGS) in men with metastatic castration resistant prostate cancer (mCRPC).
Patients And Methods: In all, 311 mCRPC patients underwent NGS analysis from biopsy samples of progressive metastatic lesions or archival radical prostatectomy specimens.
Elife
January 2025
Department of Neurology, Weill Institute for Neuroscience, University of California San Francisco, San Francisco, United States.
Mutations in Sonic Hedgehog (SHH) signaling pathway genes, for example, (SUFU), drive granule neuron precursors (GNP) to form medulloblastomas (MB). However, how different molecular lesions in the Shh pathway drive transformation is frequently unclear, and mutations in the cerebellum seem distinct. In this study, we show that fibroblast growth factor 5 (FGF5) signaling is integral for many infantile MB cases and that expression is uniquely upregulated in infantile MB tumors.
View Article and Find Full Text PDFFree Neuropathol
January 2024
NeuroMarkers, Houston, Texas, USA.
Glioblastoma is the most frequent and malignant primary brain tumor. Although the survival is generally dismal for glioblastoma patients, risk stratification and the identification of high-risk subgroups is important for prompt and aggressive management. The G1-G7 molecular subgroup classification based on the MAPK pathway activation has offered for the first time a non-redundant, all-inclusive classification of adult glioblastoma.
View Article and Find Full Text PDFBMC Res Notes
January 2025
Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 313 Ferst Drive, Atlanta, GA, 30332, USA.
Objective: Primary tumors of the brain and a large percent of malignant brain tumors are gliomas. Gliomas comprise high-grade gliomas like glioblastoma multiforme (GBMs), many of which have mutation in the tumor suppressor p53 gene and low-grade gliomas (LGGs). LGGs can progress to GBMs due to various factors.
View Article and Find Full Text PDFCancer Manag Res
January 2025
Department of Oncology, Anhui Chest Hospital, Hefei, 230022, People's Republic of China.
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths worldwide. Mutations within the TP53 gene represent critical molecular events in NSCLC, contributing to the tumorigenesis in the pulmonary epithelial tissues. TP53 is a widely researched prognostic indicator in NSCLC, and pathological investigations have revealed a weak to mild negative predictive effect for TP53.
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