MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1111/j.1349-7006.1993.tb02036.x

Медицинская библиотека · Japanese journal of cancer research : Gann · 1993

Loss of VLA-2 collagen receptor in breast carcinoma, facilitating invasion and metastasis.

Arihiro K, Inai K, Kurihara K, Takeda S, Kaneko M, Kuroi K, Toge T

СтатьяПеревод в очереди

Аннотация

The integrin VLA-2 as a collagen receptor and VLA-5 as a fibronectin receptor were detected immunohistochemically in normal, benign tumor and carcinoma tissues of the breast. Both proteins were also detected by Western-blot analysis in some carcinoma cases. Epithelial and myoepithelial cells of both normal breast and benign tumor were in all cases immunoreactive for VLA-2 in the plasma membrane. Carcinoma cells in the invasive component were not immunoreactive for VLA-2 in 31 (46%) of 67 cases. Carcinoma cells in the intraductal components were negative for VLA-2 in only 4 (11%) of 36 cases, while 20 cases (56%) showed weak expression and 12 cases (33%) showed strong expression. Metastatic carcinoma cells in the lymph nodes of 6 cases showed no immunoreactivity except in one case, whereas, again with the exception of one case, the carcinoma cells in the primary tumors did show VLA-2 expression. With regard to VLA-5, there was no difference in its expression in the invasive components and the intraductal components. These findings suggest that the loss of VLA-2 plays a role in the invasion and metastasis of breast carcinoma.

Для цитирования: Arihiro K, Inai K, Kurihara K, Takeda S, Kaneko M, Kuroi K, Toge T. Loss of VLA-2 collagen receptor in breast carcinoma, facilitating invasion and metastasis.. Japanese journal of cancer research : Gann. 1993. DOI: 10.1111/j.1349-7006.1993.tb02036.x.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

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.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.