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Zhongguo fei'ai zazhi (Online) ; Zhongguo fei'ai zazhi (Online);(12): 365-371, 2021.
Artículo en Chino | WPRIM | ID: wpr-880282

RESUMEN

Multiple primary lung cancer (MPLC) refers to lung cancer in which two or more primary lesions occurred simultaneously or successively in different parts of the same patient's lungs. The diagnosis interval is 6 months. MPLC is divided into synchronous MPLC (sMPLC) and metachronous MPLC (mMPLC). sMPLC and intrapulmonary metastasis (IM) are different in treatment strategies and prognosis. However, there are many controversies about the distinction between the two in clinical practice. This article summarizes the current main methods of diagnosing MPLC, and focuses on the latest research progress in distinguishing MPLC from IM. It aims to provide a theoretical basis for accurate diagnosis and treatment of patients with multifocal lung cancer.
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2.
Artículo en Chino | WPRIM | ID: wpr-524004

RESUMEN

Objective To study the effects and its mechanism of fentanyl(Fen) on the proliferation and cell cycle of human breast carcinoma line MCF-7. Methods MCF-7 cells were cultured in the medium with Fen, naloxone(Nx) or both the medicines at different concentration for different time. MTT method was employed to evaluate the level of the cell proliferation. The distribution of the cell cycle was detected with the flow cytometry (FCM). The expression levels of p53 and p21/WAF1 in the cells were determined by SP immunocytochemical staining method. Results Fen at≥0.1?mol/L concentration inhibited MCF-7 cells proliferation in dose- and time-dependent manners, and its IC 50 for 72h was 0.81?0.02 ?mol/L. However, the antiprolifeative effect of Fen was not antagonized by Nx. Fen significantly enhanced the ratio of G 0/G 1 phase MCF-7 cells, and decreased the proliferation index of MCF-7 cells in dose-dependent manner. Fen also upregulated the expression of p53 and p21/WAF1 in MCF-7 cells. Conclusion The data suggested that the inhibitory effect of Fen on MCF-7 cell growth might be mediated by blocking cell cycle progression from G 1 to S phase, and upregulating the expression of p53 and p21/WAF1.

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