Objective: To analyze the clinical features, diagnosis, treatment, and prognosis of epithelioid sarcoma (ES).
Methods: The clinical data of 13 cases with epithelioid sarcoma in the Tianjin Medical University Cancer Institute and Hospital from March 1995 to December 2009 were collected and analyzed. There were 10 males and 3 females in the group, with an average age of 41.5 years (range: 13 to 68 years). Nine patients had classic ES and 4 had proximal-type ES. Surgery was the mainstay of treatment. After the operation, four patients received radiotherapy, five received chemotherapy, and one received chemoradiotherapy.
Results: Of the 13 cases, only 1 had multi-locus lesion. The average tumor size was (6.07 ± 1.34) cm. The lymph node involvement was found in 46.2% of the patients. Local and distant failure occurred in 50% and 30% patients, respectively. The most common site for dissemination was the lung. Four cases died within 3 years after initial operation. The 1-, 2-, 5-, 10-year overall survival rates of the 11 cases were 72.7%, 54.5%, 27.3% and 9.1%, respectively, with a median survival time of 27 months.
Conclusions: Epithelioid sarcoma is a rare disease. The prognosis for patients with epithelioid sarcoma is poor because of a high propensity for local recurrence, lymph node metastases, and/or distant metastases. The definite diagnosis depends mainly on the pathologic examination. Wide surgical excision is the mainstay treatment, and radiation and chemotherapy have been used occasionally as adjuvant therapy but have had limited success.
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Pathol Oncol Res
January 2025
Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.
The () gene family is of rising importance as their fusions are oncogenic, and specific target drugs are available to inhibit the chimera proteins. Pan-TRK antibody, which shows the overexpression of the genes, is a useful tool to detect tumors with or without gene alterations, due to high negative predictive value. Though it is well known that pan-TRK immunopositivity is usually not connected to fusion, the role of other possible genetic alterations is under-researched.
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Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Front Microbiol
January 2025
Departments of Otorhinolaryngology-Head and Neck Surgery and Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Oncogenic gamma herpesviruses, including Epstein-Barr Virus (EBV) and Kaposi's Sarcoma-associated Herpesvirus (KSHV), are opportunistic cancer-causing viruses and induces oncogenesis through complex mechanisms, which involves manipulation of cellular physiology as well as epigenetic and epitranscriptomic reprogramming. In this review, we describe the intricate processes by which these viruses interact with the epigenetic machinery, leading to alterations in DNA methylation, histone modifications, and the involvement of non-coding RNAs. The key viral proteins such as EBNA1 and LMP1 encoded by EBV; LANA and vGPCR encoded by KSHV; play pivotal roles in these modifications by interacting with host factors, and dysregulating signaling pathways.
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Department of Radiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
The goal of this study was to summarize the radiological findings and clinical characteristics of mediastinal Ewing sarcoma/primitive neuroectodermal tumor (ES/PNET) in children. A retrospective review was conducted on the clinical and imaging data of 6 children with primary mediastinal ES/PNET that was confirmed by pathology. There were 3 girls and 3 boys in this study, aged between 2 and 11 years old.
View Article and Find Full Text PDFMol Oncol
January 2025
Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Italy.
Specific reactive oxygen species activate the GTPase Kirsten rat sarcoma virus (KRAS) by reacting with cysteine 118 (C118), leading to an electron transfer between C118 and nucleoside guanosine diphosphate (GDP), which causes the release of GDP. Here, we have mimicked permanent oxidation of human KRAS at C118 by replacing C118 with aspartic acid (C118D) in KRAS to show that oncogenic mutant KRAS is selectively inhibited via oxidation at C118, both in vitro and in vivo. Moreover, the combined treatment of hydrogen-peroxide-producing pro-oxidant paraquat and nitric-oxide-producing inhibitor N(ω)-nitro-l-arginine methyl ester selectively inhibits human mutant KRAS activity by inducing oxidization at C118.
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