International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2010
A Unique case of primary squamous carcinoma of the salpinx associated with serous carcinoma of the omentum: a pathological and molecular study.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Giordano Giovanna, D'Adda Tiziana, Brigati Francesca, Lombardi Mariano, Raboni Sfefano
Аннотация
In this article, we report a case of primary squamous cell carcinoma of the salpinx (PSCCS) with immunohistochemical and molecular studies to evaluate the phenotype and define the etiopathogenesis of this neoplasm. A 77-year-old woman, 38 years postmenopausal, was admitted to the Department of Obstetrics and Gynecology for ascites. Her clinical history showed breast carcinoma and left salpingooophorectomy as a result of extrauterine pregnancy. Cytological examination of the free peritoneal fluid showed clusters of malignant cells consistent with ovarian carcinoma. Transvaginal ultrasonography and a pelvic computed tomography scan disclosed a right pelvic mass with solid and cystic areas, measuring 3.222.3 cm. The patient underwent exploratory laparotomy. Intraoperative findings showed a mass that had replaced the salpinx and enveloped the ovary and ureter. The surface of the omentum was covered in small white nodules. Pathological examination showed that the right pelvic mass corresponded to PSCCS, whereas the omental white nodules were primary serous carcinoma. On immunohistochemical analysis, the tubal neoplasm showed positivity to Ca-125, keratin 14, and p63 and negativity to WT1 and p16. The hyper-expression of the p53 protein was evident as nuclear positivity. Molecular study by polymerase chain reaction amplification of the tumor DNA did not show any signal for human papilloma virus DNA. In summary, in this case we showed that the PSCCS was not due to human papilloma virus infection, but in all probability due to other pathogenetic mechanisms that cause a mutation of the p53 tumor-suppressor gene.