Sentence examples for transition of breast from inspiring English sources

Wang D, Lu P, Zhang H, Luo M, Zhang X, Wei X et al. Oct-4 and Nanog promote the epithelial-mesenchymal transition of breast cancer stem cells and are associated with poor prognosis in breast cancer patients.

Recently, we have focused on defining the proteolytic pathways that function in the transition of breast cancer from the pre-invasive lesions of ductal carcinoma in situ (DCIS) to invasive ductal carcinomas (IDCs).

The molecular mechanism associated with the transition of breast tumours to steroid hormone-independent growth is poorly understood.

We selected five genes (CAV1, DHFR, TYMS, VIM, ZEB1) known to be associated with drug sensitivity and the epithelial-mesenchymal transition of breast cancer [ 25- 29].

On an individual gene basis, our data match the results presented in a study determining gene-expression profiles during the transition of breast tumors to invasive stages [ 56].

Since rapamycin blocks the estrogen-driven transition of breast cancer cells from the G1 to S phases of the cell cycle [ 20], further studies in breast cancer may be warranted.

Breast carcinogenesis, with the transition of normal breast epithelial cells through hyperplasia to invasive cancer, is increasingly well understood [ 1, 2], but there is uncertainty as to the exact mechanisms of tumour initiation and in which cells these first steps occur [ 3].

Donnarumma et al. showed that in breast cancer, CAF-derived EVs contain three miRNAs (miR-21-5p, -378e, 143-3p) that induce stemness and epithelial mesenchymal transition (EMT) of breast cancer cells, regulating the development of an aggressive cancer phenotype [42].

The epithelial-mesenchymal transition (EMT) of breast cancer cells was analyzed by wound-healing assay and Western blot of snail, vimentin and E-cadherin expression.

Our observations suggest that after an initial loss of MUC4 levels during the transition of normal breast tissue to primary tumor, the re-establishment of elevated MUC4 levels confers an advantage to metastasizing breast tumor cells by promoting the acquisition of cellular properties associated with malignancy.

The observations described here provide strong evidence that MUC4 becomes re-expressed during the transition of primary breast tumor to metastatic lesion.