Trichoblastoma: is a clinical or dermoscopic diagnosis possible?

BACKGROUND: Trichoblastoma is a rare benign skin tumour that must be differentiated from basal cell carcinoma for its benign course and favourable outcome. OBJECTIVES: To describe clinical and dermoscopic features of solitary primitive trichoblastoma and to compare them with trichoblastic basal cell carcinoma (tBCC). METHODS: Digital dermoscopic images of 19 trichoblastoma and 19 tBCC were compared and reviewed by a dermatologist experienced in dermoscopy. RESULTS: The most striking dermoscopic difference between trichoblastoma and tBCC was the presence of blue-grey globules and blue-grey ovoid nests that were found to be more frequent but not exclusive of tBCC. Arborizing vessels were found both in trichoblastoma and tBCC, with a lower frequency in the latter. CONCLUSION: Histology remains the gold standard to differentiate trichoblastoma from tBCC.

p14ARF promotes RB accumulation through inhibition of its Tip60-dependent acetylation.

p14ARF is a tumour suppressor which plays a critical role in p53-dependent or -independent cell growth control. Several studies have recently provided evidence that p14ARF can also interfere either directly or indirectly with some components of the RB signalling pathway to mediate its antiproliferative activity. The aim of this study was to explore the existence of direct relationships between p14ARF and RB proteins. We show that p14ARF promotes the accumulation of a hypoacetylated RB protein, when it is upregulated in a model of stable-inducible clones or physiologically induced following cell exposure to cytotoxic agents. Looking for the mechanisms involved in this process, we demonstrate that the histone acetyl transferase Tip60 directly interacts with RB and stimulates its degradation by the proteasome through acetylation of its C-terminus. Furthermore, and consistent with p14ARF-induced RB accumulation, we provide evidence that p14ARF prevents Tip60-mediated RB acetylation, therefore precluding its proteasomal degradation. Overall, our results identify a novel mechanism by which p14ARF controls the RB pathway to trigger its antiproliferative function.

The histone acetyltransferase, hGCN5, interacts with and acetylates the HIV transactivator, Tat.

Factor acetyltransferase activity associated with several histone acetyltransferases plays a key role in the control of transcription. Here we report that hGCN5, a well known histone acetyltransferase, specifically interacts with and acetylates the human immunodeficiency virus type 1 (HIV-1) transactivator protein, Tat. The interaction between Tat and hGCN5 is direct and involves the acetyltransferase and the bromodomain regions of hGCN5, as well as a limited region of Tat encompassing the cysteine-rich domain of the protein. Tat lysines 50 and 51, target of acetylation by p300/CBP, were also found to be acetylated by hGCN5. The acetylation of these two lysines by p300/CBP has been recently shown to stimulate Tat transcriptional activity and accordingly, we have found that hGCN5 can considerably enhance Tat-dependent transcription of the HIV-1 long terminal repeat. These data highlight the importance of the acetylation of lysines 50 and 51 in the function of Tat, since different histone acetyltransferases involved in distinct signaling pathways, GCN5 and p300/CBP, converge to acetylate Tat on the same site.

Control of the histone-acetyltransferase activity of Tip60 by the HIV-1 transactivator protein, Tat.

Tip60, a cellular histone-acetyltransferase, is known to interact with the HIV-1-encoded transactivator protein, Tat. In this work, we show that the interaction of Tat with Tip60 efficiently inhibits the Tip60 histone-acetyltransferase activity. Besides its histone-acetyltransferase activity, Tip60 can undergo an autoacetylation which is not affected by Tat interaction. Our data show that Tip60 does not significantly influence Tat-dependent transcriptional activation of the 5'-LTR of HIV, suggesting that its interaction with Tat affects some intrinsic cellular process. We were then able to identify a cellular gene, Mn-dependent superoxide dismutase (Mn-SOD), that has a Tip60-dependent transcriptional activity. Interestingly, the simultaneous expression of Tat and Tip60 abolishes the effect of Tip60 on the activity of the Mn-SOD promoter. We postulate that the HIV-1 transactivator, Tat, in targeting Tip60 hinders the expression of cellular genes (such as Mn-SOD) which normally interfere with the efficient replication and propagation of the virus.

[Long-lasting expansive gases in the treatment of rhegmatogenous retinal detachment associated with vitreoretinal proliferation]. / Les gaz expansifs de longue durée dans le traitement des décollements rétiniens rhegmatogènes associés à une prolifération vitréo-rétinienne.

Thirty two eyes of 32 patients affected with rhegmatogenous retinal detachment (R.D.) associated with proliferative vitreoretinopathy (P.V.R.) were operated on with combined external and endovitreal microsurgery. Internal tamponade was carried out with SF6 in 16 eyes and C3F8 in 16 eyes. All patients were followed for at least six months after the last surgical procedure. Permanent retinal reattachment was achieved in 56% of the eyes operated on with SF6 and 60% of the eyes operated on with C3F8. Surgical success was achieved with only one operation in those eyes operated on with C3F8. In contrast, 88% of the eyes successfully operated on with SF6, had more than one operation. The overall surgical results, whatever the gas used for internal tamponade, are as follows: surgical success was achieved in 83% of P.V.R. cases grade C1 and C2 (5 cases out of 6), 73% of P.V.R. cases grade C3 and D1 (11 cases out 15), and 20% of P.V.R. cases grade D2 and D3 (2 cases out of 10).