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Testicular tumors are the most common malignancy of young men and tumors affecting the testis are caused by somatic mutations in germ or germ-like cells. The PI3K pathway is constitutively activated in about one third of testicular cancers. To investigate the role of the PI3K pathway in transforming stem-like cells in the testis, we investigated tumors derived from mice with post-natal, constitutive activation of PI3K signaling and homozygous deletion of tumor suppressor Pten, targeted to nestin expressing cells.

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Article Synopsis
  • The study discusses two rare cases of postmenopausal women experiencing rapid virilization and high testosterone levels, despite negative imaging results for ovarian masses.
  • Both patients underwent hormone profiling and inconclusive imaging, leading to a suspicion of ovarian tumors, prompting surgical intervention through laparoscopic oophorectomy.
  • Histological examination after surgery confirmed Leydig cell tumors in one patient and thecoma in the other, with testosterone levels normalizing and symptoms improving post-surgery, emphasizing the need for thorough evaluation of androgen excess in postmenopausal women.
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  • This study analyzes 37 ovarian Sertoli-Leydig cell tumors (SLCT) with a focus on their morphology, immunohistochemistry, and molecular features, categorizing them into well, moderately, and poorly differentiated tumors.
  • High levels of sex cord markers were found, along with variable expression of other markers, and notable mutations like DICER1 (54.5%) and FOXL2 (6%) were identified, suggesting important diagnostic and predictive implications.
  • Differences in mRNA expression profiles between DICER1 and non-DICER1 tumors highlight the distinct molecular characteristics of SLCTs, indicating that well-differentiated tumors could represent a unique subtype apart from the others.
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  • * The tumors included various types, such as aortic and carotid body PGLs, thyroid cancer, and other growths, with one aortic body tumor showing malignant traits.
  • * No genetic mutations were found in the SDHD gene subunits analyzed, indicating that other genetic factors may contribute to tumor development, prompting further research in this area.
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