PubMed · 1038764
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B Westgate. 1975. Breast prostheses.. https://pubmed.ncbi.nlm.nih.gov/1038764/
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Using an approach based on the co-amplification of wild-type and exon deleted progesterone receptor (PR) variant cDNAs, we identified exon-deleted PR variant mRNAs in both normal and neoplastic human breast tissues. Several naturally occurring variants, whose sequences revealed precise whole exon deletions, may encode putative PR-like proteins which lack some functional domains of the wild-type PR molecule. We suggest that these PR variant proteins could have a pathophysiological role in progestin action, as suggested for estrogen receptor variant proteins.
Women who have undergone augmentation mammoplasty with silicone gel implants may present for routine breast cancer screening or with palpable breast lumps. Conventional mammography supplemented by additional displaced or Eklund view is usually sufficient to detect most abnormalities. Ultrasonographic evaluation may be performed as an ancillary technique to characterize palpable lumps or nonpalpable lesions detected on mammography. In patients suspected of having implant rupture, conventional mammography and displaced views are performed. If clinical findings warrant, magnetic resonance imaging may be performed to detect intracapsular and extracapsular rupture and migration of silicone globules to the axilla, branchial plexus and adjacent structures.
Rb protein is a critical regulator of entry into the cell cycle, and loss of Rb function by deletions, mutations, or interaction with DNA viral oncoproteins leads to oncogenic transformation. We have shown that the human papilloma virus (HPV)-16 E7 gene is sufficient to induce the immortalization of mammary epithelial cells (MECs). Surprisingly, the steady-state level of Rb protein in these immortal cells was drastically decreased. Here, we used pulse-chase analysis to show that the in vivo loss of Rb protein in E7-immortalized MECs is a consequence of enhanced degradation. Expression of HPV16 E7 in a cell line with a temperature-sensitive mutation in the E1 enzyme of the ubiquitin pathway demonstrated that degradation of Rb was ubiquitin dependent. Treatment of E7-immortalized MECs with aldehyde inhibitors of proteasome-associated proteases led to a marked stabilization of Rb protein, particularly the hypophosphorylated form. Taken together, our results provide evidence for HPV-16 E7-induced enhanced degradation of Rb protein via a ubiquitin-proteasome pathway and suggest a second mechanism of oncogenic transformation by E7, in addition to its previously identified ability to sequester Rb from E2F. Our analyses also show that normal Rb levels are regulated by the ubiquitin-proteasome degradation pathway.