| A novel mechanism of sodium iodide symporter repression in differentiated thyroid cancer. | thyroid, |
| Proto-oncogene PBF/PTTG1IP regulates thyroid cell growth and represses radioiodide treatment. | thyroid, |
| The present study provides the first epidemiological evidence that functional regulatory variants of PTTG1IP were associated with the risk of ER-positive breast cancer, further supporting its relevance as one proto-oncogene in breast cancer. | breast, |
| Functional variable number of tandem repeats variation in the promoter of proto-oncogene PTTG1IP is associated with risk of estrogen receptor-positive breast cancer. | breast, |
| Manipulation of PBF/PTTG1IP phosphorylation status; a potential new therapeutic strategy for improving radioiodine uptake in thyroid and other tumors. | thyroid, |
| protooncogene PBF is a negative regulator of p53 function in thyroid tumorigenesis, in which PBF is generally overexpressed and p53 mutations are rare compared with other tumor types | thyroid, |
| The PTTG1-binding factor (PBF/PTTG1IP) regulates p53 activity in thyroid cells. | thyroid, |
| The proto-oncogene PBF binds p53 and is associated with prognostic features in colorectal cancer. | colorectal, |
| An entirely novel mechanism by which the proto-oncogene PBF binds NIS and alters its subcellular localisation, thereby regulating its ability to uptake iodide, is presented. | None |
| Data from mutant recombinant proteins suggest that proto-oncogene PBF is a phosphoprotein and highlight importance of tyrosine residue Y174 in both endocytosis of PBF and its interaction/co-localization with NIS/SLC5A5 (sodium-iodide symporter). | None |
| data reveal new insight into PBF function and confirm that, rather than being oncogenic, mutations in PBF are likely to be passenger effects, with overexpression of PBF the more important etiological event in human cancer | None |