Background: The p53 gene mutations have been associated with the development of human breast and canine mammary neoplasms; breast carcinoma patients with alterations of p53 gene are considered to have a poor prognosis. Mammary carcinoma represents the most common malignant tumor in female dogs. However, the prognostic significance of p53 gene mutation in the dog has been unclear.
Study Design: The alteration in exons 5-8 of p53 gene in 69 canine mammary carcinomas were investigated by PCR-SSCP with direct sequence analysis and statistically analyzed to compare with other clinicopathological parameters including age, neuter, tumor size, stage, histology, p53 expression, recurrence and death from carcinoma.
Results: 12 out of 69 (17%) carcinomas showed p53 gene mutations. After a follow-up period of 30 months, multivariate regression analysis revealed that p53 gene mutation was only an independent risk factor for increased risk of the recurrence and death from mammary carcinoma.
Conclusion: The p53 gene alterations might contribute to the prognostic status in canine mammary carcinomas, in a way comparable to that of human tumors.
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BMC Complement Med Ther
January 2025
Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, 31527, Egypt.
Background: Oral squamous cell carcinoma (OSCC) ranks as the sixth most common malignancy globally. Cisplatin is the standard chemotherapy for OSCC, but resistance often reduces its efficacy, necessitating new treatments with fewer side effects. Rumex dentatus L.
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January 2025
Department of Clinical Biochemistry, School of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran.
This study is designed to assess the effect of root extract of P. ginseng on kidney tissue injury attributed to cisplatin and its molecular mechanism involved in this process in the AKI rat model. Twenty-four male Wistar rats were randomly allocated into 4 experimental groups including: the control group, the cisplatin group, the extract 100 mg/kg group, and the extract 200 mg/kg group.
View Article and Find Full Text PDFZhonghua Bing Li Xue Za Zhi
February 2025
Department of Pathology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou 215002, China.
To investigate the clinicopathological characteristics of solid, endometrial-like and transitional (SET) cell growth subtype in high-grade serous ovarian carcinoma (HGSC). Clinical data of 25 cases of HGSC-SET were collected from January 2020 to March 2024 at the Affiliated Suzhou Hospital of Nanjing Medical University, and their histological features were analyzed. Immunohistochemical stains were used to analyze the expression of ER, PR, PAX8, WT-1, p16, p53 and Ki-67.
View Article and Find Full Text PDFZhonghua Bing Li Xue Za Zhi
February 2025
Department of Pathology, the First Affiliated Hospital of Air Force Medical University, Xi'an 710032, China.
To investigate the clinicopathological features, diagnosis, genetic alterations, and biological behaviors of hamartomatous inverted hyperplastic polyp (HIHP) in the gastrointestinal tract. The clinical, sonographic, endoscopic and pathologic data of 10 HIHP cases diagnosed at the First Affiliated Hospital of Air Force Medical University, Xi'an, China from January 2013 to March 2024 were collected. Their clinicopathological features and histological morphology were analyzed.
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January 2025
Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; The Brain Tumor Center, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Mutation or deletion of the deubiquitinase USP7 causes Hao-Fountain syndrome (HAFOUS), which is characterized by speech delay, intellectual disability, and aggressive behavior and highlights important unknown roles of USP7 in the nervous system. Here, we conditionally delete USP7 in glutamatergic neurons in the mouse forebrain, triggering disease-relevant phenotypes, including sensorimotor deficits, impaired cognition, and aggressive behavior. Although USP7 deletion induces p53-dependent neuronal apoptosis, most behavioral abnormalities in USP7 conditional knockout mice persist following p53 loss.
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