After rapamycin, TORC1 and TORC2 specific inhibitors were introduced in the phase of clinical trial for the treatment of angiomyolipomas (TSC / no-TSC). I was expecting some better results from the new drugs that inhibit TORC2 (involved in the organization of actin). I thought in fact, after the first brilliant results with the use of rapamycin, that residual disease could be in part due to the permanence of spindle muscle cells perhaps also for a modulation from epithelioid to spindle cell (with immunophenotypic characteristics of the "perivascular epithelioid cell-PEC"). I imagined that inhibitors of TORC2 could solve this problem (if my idea was correct). Currently our hypothesis of a phenotypic modulation of PEC (in the visceral lesions of TSC) has been accepted. The PEC is modulated by a smooth muscle cell (with progesterone receptors) up to a huge epithelioid cell (HMB-45 positive) in which are obvious metabolic and autophagic alterations.
I would like to know if you know what the immunophenotype of residual lesions of angiomyolipomas after treatment with mTOR inhibitors is. In particular, if the spindle cells are positive for the progesterone receptors. I think it would also be important, as well as the understanding of the mechanisms of regression, to assess the ability to run hormone therapy after mTOR inhibitors.
https://www.researchgate.net/publication/5768738_PEComas_the_past_the_present_and_the_future
Article PEComas: The past, the present and the future
LAM also accompanied by tuberous sclerosis also shows much the same pathological change after the treatment with mTOR or calcineurin inhibitor.
I could not find any specific work on PP242 and Tuberous Sclerosis and / or lymphangioleiomyomatosis. Can someone tell me something about ?
Article PP242 Counteracts Glioblastoma Cell Proliferation, Migration...
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