Sentence examples for mouse prostate tumor from inspiring English sources

The presence of iNKT cells in the tumor infiltrate prompted us to ask whether the mouse prostate tumor cells attract iNKT cells.

In the TRAMP mouse prostate tumor model, we found iNKT cells from cancer-bearing mice exhibit functional defects similar to those observed in humans.

Frozen nude mouse prostate tumor (PC3) xenograft sections were also processed accordingly.

By injecting so-called quantum dots into mice, a group of biomedical engineers gave mouse prostate tumors the equivalent of neon signs that could one day ease diagnosis and guide surgeon's hands.

We first tested whether mouse prostate tumors and the derived cell line TRAMP-C2 secrete CCL2.

In contrast, intracellular clusterin was also shown to inhibit prostate cancer cell proliferation, and clusterin knockout induced highly aggressive transgenic mouse prostate tumors [17].

In this context, our demonstration that MYC overexpression can convert AKT-activated mouse prostate tumors from rapalog-sensitive to rapalog-resistant has implications for clinical studies of PI3K-pathway inhibitors in men whose prostate cancers also harbor increased AKT signaling.

Recently, Pittoni et al. analyzed the role of MCs in transgenic mouse prostate tumors and showed that MCs exert different functions according to the tumor subtype [ 127].

Using comparative transcriptomic analyses, Ding et al. [ 26] identified the robust activation of the Tgfβ/Bmp-Smad4 signaling pathway in indolent Pten-null mouse prostate tumors.

Moreover, TGF-β1 has been shown to selectively induce MMP-9 activity in a subset of metastatic but not primary mouse prostate tumors, implying that this TGF-β1-induced response may be an important selection step in tumor progression [ 18].

We postulate that a combination of species-specific and cell type-specific gene regulation mechanisms could be involved in the differential expression of TSPY between human clinical prostate cancer and TgTSPY9/LADY mouse prostatic tumor.