<b>Purpose:</b> This study was undertaken to conduct a comprehensive investigation of the role of DNA damage repair (DDR) defects in poor outcome ER<sup>+</sup> disease.<b>Experimental Design:</b> Expression and mutational status of DDR genes in ER<sup>+</sup> breast tumors were correlated with proliferative response in neoadjuvant aromatase inhibitor therapy trials (discovery dataset), with outcomes in METABRIC, TCGA, and Loi datasets (validation datasets), and in patient-derived xenografts.
<b>Purpose:</b> To evaluate the ability of texture analysis of breast dynamic contrast enhancement-magnetic resonance (DCE-MR) images in differentiating human epidermal growth factor receptor 2 (HER2) 2+ status of breast tumors.
<i>Conclusions</i>: Our results indicated that miR-200c/141 played biphasic roles in breast tumor progression via affecting the BCSC heterogeneity, suggesting targeting BCSC heterogeneity to simultaneously restrict breast cancer initiation and metastasis could be a promising therapeutic strategy for breast cancer.
<i>In vitro</i> transfection of PLK1 and HSF1 siRNA into PKL1- and HSF1-positive human breast tumor MDA-MB-231 and human cervical carcinoma HeLa cells inhibited cell growth via suppression of PLK1 and HSF1 mRNA expression, respectively.
<i>In vitro</i> transfection of PLK1 and HSF1 siRNA into PKL1- and HSF1-positive human breast tumor MDA-MB-231 and human cervical carcinoma HeLa cells inhibited cell growth via suppression of PLK1 and HSF1 mRNA expression, respectively.
<i>In vivo</i>, IL-17B induced resistance to paclitaxel and treatment with an anti-IL-17RB neutralizing antibody completely restored breast tumor chemosensitivity, leading to tumor shrinkage.
<i>in-silico</i> analysis finds that CXCL12-CXCR4 is associated with an increased expression of PDZK1, PI3k and Akt which lead the breast tumor towards metastasis.
<i>in-silico</i> analysis finds that CXCL12-CXCR4 is associated with an increased expression of PDZK1, PI3k and Akt which lead the breast tumor towards metastasis.
<i>in-silico</i> analysis finds that CXCL12-CXCR4 is associated with an increased expression of PDZK1, PI3k and Akt which lead the breast tumor towards metastasis.
<i>in-silico</i> analysis finds that CXCL12-CXCR4 is associated with an increased expression of PDZK1, PI3k and Akt which lead the breast tumor towards metastasis.
<i>in-silico</i> analysis finds that CXCL12-CXCR4 is associated with an increased expression of PDZK1, PI3k and Akt which lead the breast tumor towards metastasis.
<i>in-silico</i> analysis finds that CXCL12-CXCR4 is associated with an increased expression of PDZK1, PI3k and Akt which lead the breast tumor towards metastasis.
<i>in-silico</i> analysis finds that CXCL12-CXCR4 is associated with an increased expression of PDZK1, PI3k and Akt which lead the breast tumor towards metastasis.
<sup>89</sup>Zr-UiO-66 was further functionalized with pyrene-derived polyethylene glycol (Py-PGA-PEG) and conjugated with a peptide ligand (F3) to nucleolin for targeting of triple-negative breast tumors.
(2018) show that HER2 signaling promotes ABL-mediated phosphorylation of the mitochondrial creatine kinase (MtCK1), providing ATP to support breast tumor growth.
(2018) show that HER2 signaling promotes ABL-mediated phosphorylation of the mitochondrial creatine kinase (MtCK1), providing ATP to support breast tumor growth.
1-kb segment of the p53 tumor suppressor gene (54.5% G+C) containing exons 5-9, including the intervening introns, was screened in a blinded analysis of 48 samples from human breast tumors containing known wild-type or mutant p53 genes.
2/2 ovarian and 2/9 breast tumors carried MSH2 somatic mutations possible pathogenics (4/11, 36%): a missense mutation in exon 3 (p.G162R), a duplication of exon 1 and a deletion of exon 2.
35 pairs of breast tumors and normal tissues were selected to real-time quantitative polymerase chain reaction (RT-qPCR) to validate LINC00673 is overexpressed in tumor tissues.
4), induces normalization and regression of the vasculature in an experimental human breast tumour that overexpresses HER2 in mice, and that it works by modulating the effects of different pro- and anti-angiogenic factors.