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Posha wore a sexy hot pink dress, that clearly showed her baby bulge. Porsha also refrained from drinking any alcohol for the entire evening, MTO News confirmed.

And that's pretty rare, especially for the Bravo reality starlet. On October 1, it was reported that she was engaged to entrepreneur Dennis McKinley.

On March 22, , she gave birth to their daughter, Pilar Jhena. Williams and McKinley briefly split in June, but have reunited as of August.

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This study enrolled patients being treated for HER2 -amplified breast cancer, HER2-mutant non-small-cell lung cancer, and other advanced solid tumors.

While common toxicities included nausea , stomatitis , and anemia ; responses were noted. Everolimus is the second novel Rapamycin analog.

FDA approved everolimus for the treatment of advanced renal cell carcinoma after failure of treatment with sunitinib or sorafenib , subependymal giant cell astrocytoma SEGA associated with tuberous sclerosis TS , and progressive neuroendocrine tumors of pancreatic origin PNET.

Ridaforolimus AP, MK , or deforolimus, is the newest rapamycin analog and it is not a prodrug. Like rapalogs, they decrease protein translation , attenuate cell cycle progression, and inhibit angiogenesis in many cancer cell lines and also in human cancer.

In fact, they have been proven to be more potent than rapalogs. Even though these compounds have been effective in rapamycin-insensitive cell lines, they have only shown limited success in KRAS driven tumors.

This suggests that combinational therapy may be necessary for the treatment of these cancers. Another drawback is also their potential toxicity.

These facts have raised concerns about the long term efficacy of these types of inhibitors. Strong induction of apoptosis and autophagy has also been seen.

Despite good promising results, there are preclinical evidence that some types of cancers may be insensitive to this dual inhibition. The studies of rapamycin as immunosuppressive agent enabled us to understand its mechanism of action.

Direct impact of them on cancer cells depend on the concentration of the drug and certain cellular characteristics. The indirect way, is based on interaction with processes required for tumor angiogenesis.

Rapamycin and rapalogs crosslink the immunophilin FK binding protein, tacrolimus or FKBP, through its methoxy group. As a consequence, S6K1 dephosphorylates, which reduces protein synthesis and decreases cell mortality and size.

Rapamycin induces dephosphorylation of 4EBP1 as well, resulting in an increase in p27 and a decrease in cyclin D1 expression. Rapamycin has shown to induce cancer cell death by stimulating autophagy or apoptosis , but the molecular mechanism of apoptosis in cancer cells has not yet been fully resolved.

One suggestion of the relation between mTOR inhibition and apoptosis might be through the downstream target S6K1, which can phosphorylate BAD , a pro-apoptotic molecule, on Ser A G0-G1 cell-cycle blockage can be the consequence of inactivation of mTOR in hypoxia-activated pericytes and endothelial cells.

Pharmacologic down-regulation of mTOR pathway during chemotherapy in a mouse model prevents activation of primordial follicles, preserves ovarian function, and maintains normal fertility using clinically available inhibitors INK and RAD.

In that way, it helps to maintain fertility while undergoing chemotherapy treatments. These mTOR inhibitors, when administrated as pretreatment or co-treatment with standard gonadotoxic chemotherapy, helps to maintain ovarian follicles in their primordial state.

The pipecolate region of rapamycin structure seems necessary for rapamycin-binding to FKBP This step is required for further binding of rapamycin to the mTOR kinase, which is the key enzyme in many biological actions of rapamycin.

The high affinity of rapamycin binding to FKBP12 is explained by number of hydrogen bonds through two different hydrophobic binding pockets, and this has been revealed by X-ray crystal structure of the compound bound to the protein.

The structural characteristics common to temsirolimus and sirolimus; the pipecolic acid , tricarbonyl region from CC15, and lactone functionalities play the key role in binding groups with the FKBP The most important hydrogen bonds are the lactone carbonyl oxygen at C to the backbone NH of Ile56 , amide carbonyl at C to the phenolic group on the sidechain of Tyr82 , and the hydroxyl proton at the hemiketal carbon, C, to the sidechain of Asp Structural changes to the rapamycin structure can affect binding to mTOR.

This could include both direct and indirect binding as a part of binding to FKBP This domain consists of molecular regions that make hydrophobic interactions with the FKB domain and triene region from CC-6, methoxy group at C-7, and methyl groups at C, C and C All changes of the macrolide ring can have unpredictible effects on binding and therefore, make determination of SAR for rapalogs problematic.

Rapamycin contains no functional groups that ionize in the pH range and therefore, are rather insoluble in water. Nonetheless, the rapamycin analogs that have been approved for human use are modified at C hydroxyl group and show improvement in pharmacokinetic parameters as well as drug properties, for example, solubility.

Rapamycin and temsirolimus have similar chemical structures and bind to FKBP12, though their mechanism of action differs.

Temsirolimus is a dihydroxymethyl propionic acid ester of rapamycin, and its first derivative. Everolimus has O-2 hydroxyethyl chain substitution and deforolimus has a phosphine oxide substitution at position C in the lactone ring of rapamycin.

Deforolimus Ridaforolimus has C43 secondary alcohol moiety of the cyclohexyl group of Rapamycin that was substituted with phosphonate and phosphinate groups, preventing the high-affinity binding to mTOR and FKBP.

Computational modelling studies helped the synthesise of the compound. Treatment with mTOR inhibitors can be complicated by adverse events.

Additionally, interstitial lung disease is an adverse event of particular importance. Even fatalities have been described. Careful diagnosis and treatment, therefore, is essential.

Recently, a new diagnostic and therapeutic management approach has been proposed. Identification of predictive biomarkers of efficacy for tumor types that are sensitive to mTOR inhibitors remains a major issue.

To date, attempts to identify biomarkers of rapalog response have been unsuccessful. Clinical and translational data suggest that sensitive tumor types, with adequate parameters and functional apoptosis pathways, might not need high doses of mTOR inhibitors to trigger apoptosis.

In most cases, cancer cells might only be partially sensitive to mTOR inhibitors due to redundant signal transduction or lack of functional apoptosis signaling pathways.

In situations like this, high doses of mTOR inhibitors might be required. For future studies, it is recommended to exclude patients with low or negative p-AKT levels from trials with mTOR inhibitors.

Current data is insufficient to predict sensitivity of tumors to rapamycin. However, the existing data allows us to characterize tumors that might not respond to rapalogs.

Their development has been benefited from previous studies with PI3K-selective inhibitors. For example, Novartis has developed the compound NVPBE that was reported to inhibit tumor growth in various preclinical models.

It enhances antitumor activity of some other drugs such as vincristine. New mTOR-specific inhibitors came forth from screening and drug discovery efforts.

A series of these mTOR kinase inhibitors have been studied.

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