Experts and Doctors on sirolimus in United States


Locale: United States
Topic: sirolimus

Top Publications

  1. Crittenden M, Gough M, Chester J, Kottke T, Thompson J, Ruchatz A, et al. Pharmacologically regulated production of targeted retrovirus from T cells for systemic antitumor gene therapy. Cancer Res. 2003;63:3173-80 pubmed
    ..We hypothesize that this enhanced targeting to tumor sites is responsible for the efficiency of T cell-mediated retroviral gene transfer and that this principle can be used to enhance systemic therapies using immune-cell carriers. ..
  2. Goehring A, Rivers D, Sprague G. Urmylation: a ubiquitin-like pathway that functions during invasive growth and budding in yeast. Mol Biol Cell. 2003;14:4329-41 pubmed
    ..Moreover, these five genes have a role in invasive growth and display genetic interactions with the TOR pathway. In summary, our results suggest the urmylation pathway is involved in nutrient sensing and budding. ..
  3. O Reilly Zwald F, Brown M. Skin cancer in solid organ transplant recipients: advances in therapy and management: part I. Epidemiology of skin cancer in solid organ transplant recipients. J Am Acad Dermatol. 2011;65:253-261 pubmed publisher
    ..This review also highlights the concept of "field cancerization," represented by extensive areas of actinic damage and epidermal dysplasia, which accounts for increased risk of aggressive skin cancer development in susceptible patients. ..
  4. Leontieva O, Blagosklonny M. Yeast-like chronological senescence in mammalian cells: phenomenon, mechanism and pharmacological suppression. Aging (Albany NY). 2011;3:1078-91 pubmed
    ..We discuss that although CS does not mimic organismal aging, the same signal transduction pathways that drive CS also drive aging. ..
  5. Bukowski R. Temsirolimus: a safety and efficacy review. Expert Opin Drug Saf. 2012;11:861-79 pubmed publisher
    ..Studies in untreated favorable and intermediate risk clear cell and refractory mRCC patients are required. ..
  6. Dutta D, Xu J, Kim J, Dunn W, Leeuwenburgh C. Upregulated autophagy protects cardiomyocytes from oxidative stress-induced toxicity. Autophagy. 2013;9:328-44 pubmed publisher
    ..We conclude that autophagy induction by rapamycin could be utilized as a potential therapeutic strategy against oxidative stress-mediated damage in cardiomyocytes. ..
  7. Fluckey J, Pohnert S, Boyd S, Cortright R, Trappe T, Dohm G. Insulin stimulation of muscle protein synthesis in obese Zucker rats is not via a rapamycin-sensitive pathway. Am J Physiol Endocrinol Metab. 2000;279:E182-7 pubmed
    ..Furthermore, rapamycin inhibits protein synthesis in muscle of obese Zucker rats; however, stimulation of protein synthesis by insulin is not via a rapamycin-sensitive pathway...
  8. Baker A, Wang R, Mackman N, Luyendyk J. Rapamycin enhances LPS induction of tissue factor and tumor necrosis factor-alpha expression in macrophages by reducing IL-10 expression. Mol Immunol. 2009;46:2249-55 pubmed publisher
    ..In contrast, the decrease in LPS-induced TNFalpha and TF expression in PTEN(-/-) PMs also requires an IL-10-independent pathway. ..
  9. Houghton P. Everolimus. Clin Cancer Res. 2010;16:1368-72 pubmed publisher
    ..Further, biomarkers that predict tumor sensitivity are still elusive. The mechanism of action, preclinical antitumor activity, and clinical activity of everolimus against RCC are reviewed. ..

More Information

Publications183 found, 100 shown here

  1. Johnston P, Inwards D, Colgan J, LaPlant B, Kabat B, Habermann T, et al. A Phase II trial of the oral mTOR inhibitor everolimus in relapsed Hodgkin lymphoma. Am J Hematol. 2010;85:320-4 pubmed publisher
    ..Four patients experienced a Grade 3 or higher pulmonary toxicity. Everolimus has single-agent activity in relapsed/refractory HL and provides proof-of-concept that targeting the mTOR pathway in HL is clinically relevant. ..
  2. Blagosklonny M. The power of chemotherapeutic engineering: arresting cell cycle and suppressing senescence to protect from mitotic inhibitors. Cell Cycle. 2011;10:2295-8 pubmed
    ..By knowing the mechanisms of cell cycle arrest, death and senescence, we can design "rainbow combinations" that obediently kill or spare desired cells. Knowledge is power. ..
  3. Kirby S, Satoskar A, Brodsky S, Pope Harman A, Nunley D, Hitchcock C, et al. Histological spectrum of pulmonary manifestations in kidney transplant recipients on sirolimus inclusive immunosuppressive regimens. Diagn Pathol. 2012;7:25 pubmed publisher
    ..The virtual slide(s) for this article can be found here: ..
  4. Li S, Fang C, Aberle N, Ren B, Ceylan Isik A, Ren J. Inhibition of PI-3 kinase/Akt/mTOR, but not calcineurin signaling, reverses insulin-like growth factor I-induced protection against glucose toxicity in cardiomyocyte contractile function. J Endocrinol. 2005;186:491-503 pubmed
    ..Collectively, our data suggest that IGF-1 may provide cardiac protection against glucose in part through a PI-3 kinase/Akt/mTOR/ p70s6k-dependent and calcineurin-independent pathway. ..
  5. Chan L, Shen D, Wilkinson A, Patton W, Lai N, Chan E, et al. A novel image-based cytometry method for autophagy detection in living cells. Autophagy. 2012;8:1371-82 pubmed publisher
    ..The described image-based cytometry/fluorescent dye method should serve as a useful addition to the current arsenal of techniques available in support of autophagy-based drug discovery relating to various pathological disorders. ..
  6. Gardner E, Connis N, Poirier J, Cope L, Dobromilskaya I, Gallia G, et al. Rapamycin rescues ABT-737 efficacy in small cell lung cancer. Cancer Res. 2014;74:2846-56 pubmed publisher
    ..These data have direct translational implications for SCLC clinical trials. ..
  7. Slomiany M, Rosenzweig S. Hypoxia-inducible factor-1-dependent and -independent regulation of insulin-like growth factor-1-stimulated vascular endothelial growth factor secretion. J Pharmacol Exp Ther. 2006;318:666-75 pubmed
    ..In conclusion, IGF-1 regulates VEGF expression and secretion via HIF-1-dependent and -independent pathways. ..
  8. Chappelow A, Kaiser P. Neovascular age-related macular degeneration: potential therapies. Drugs. 2008;68:1029-36 pubmed
    ..Other potential therapies include pigment epithelium-derived factor-based therapies, nicotinic acetylcholine receptor antagonists, integrin antagonists and sirolimus. ..
  9. Nayak S, Cao O, Hoffman B, Cooper M, Zhou S, Atkinson M, et al. Prophylactic immune tolerance induced by changing the ratio of antigen-specific effector to regulatory T cells. J Thromb Haemost. 2009;7:1523-32 pubmed publisher
    ..This protocol may provide a marked advance in efforts seeking to improve clinical outcomes in disorders involving therapeutic protein replacement. ..
  10. Goc A, Choudhary M, Byzova T, Somanath P. TGF?- and bleomycin-induced extracellular matrix synthesis is mediated through Akt and mammalian target of rapamycin (mTOR). J Cell Physiol. 2011;226:3004-13 pubmed publisher
    ..These findings indicate the importance of the Akt-mTOR signaling pathway in TGF-mediated fibrogenic events in vivo. ..
  11. Blagosklonny M. Progeria, rapamycin and normal aging: recent breakthrough. Aging (Albany NY). 2011;3:685-91 pubmed
    ..Here I discuss four potential scenarios, comparing progeria with both normal and accelerated aging. This reveals further indications of rapamycin both for accelerated aging in obese and for progeria. ..
  12. Leontieva O, Demidenko Z, Gudkov A, Blagosklonny M. Elimination of proliferating cells unmasks the shift from senescence to quiescence caused by rapamycin. PLoS ONE. 2011;6:e26126 pubmed publisher
    ..Thus, p21 causes senescence passively, just by causing arrest, while still active mTOR drives senescent phenotype. ..
  13. Blagosklonny M. Rapamycin-induced glucose intolerance: hunger or starvation diabetes. Cell Cycle. 2011;10:4217-24 pubmed publisher
    ..If rapamycin is a CR-mimetic, no wonder it may, in certain models, induce "hunger diabetes." But will rapamycin prevent true type II diabetes? Here are some answers. ..
  14. Baar E, Carbajal K, Ong I, Lamming D. Sex- and tissue-specific changes in mTOR signaling with age in C57BL/6J mice. Aging Cell. 2016;15:155-66 pubmed publisher
    ..Our results demonstrate that aging does not result in increased mTOR signaling in most tissues and suggest that rapamycin does not promote lifespan by reversing or blunting such an effect. ..
  15. Chung T, Crilly K, Anderson W, Mukherjee J, Kiss Z. ATP-dependent choline phosphate-induced mitogenesis in fibroblasts involves activation of pp70 S6 kinase and phosphatidylinositol 3'-kinase through an extracellular site. Synergistic mitogenic effects of choline phosphate and sphingosine 1-phosphate. J Biol Chem. 1997;272:3064-72 pubmed
    ..The results indicate that in the presence of extracellular ATP and/or S1P, ChoP induces mitogenesis through an extracellular site by mechanisms involving the activation of pp70 S6 kinase and, to a lesser extent, PI 3'-kinase. ..
  16. Montanaro L, Pandolfi P. Initiation of mRNA translation in oncogenesis: the role of eIF4E. Cell Cycle. 2004;3:1387-9 pubmed
  17. Blagosklonny M. Aging-suppressants: cellular senescence (hyperactivation) and its pharmacologic deceleration. Cell Cycle. 2009;8:1883-7 pubmed
    ..How can growth inhibitors suppress senescence? May these aging-suppressants decelerate organismal aging? To answer these questions, we need to reconsider the meaning of aging. ..
  18. Blagosklonny M. Revisiting the antagonistic pleiotropy theory of aging: TOR-driven program and quasi-program. Cell Cycle. 2010;9:3151-6 pubmed publisher
    ..Early in life the TOR pathway drives developmental program, which persists later in life as an aimless quasi-program of aging and age-related diseases. ..
  19. Leontieva O, Blagosklonny M. DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re-activation of mTOR is associated with conversion to senescence. Aging (Albany NY). 2010;2:924-35 pubmed
    ..We conclude that induction of p53 does not activate the senescence program in quiescent cells. In cells with induced p53, re-activation of mTOR by serum stimulation causes senescence, as an equivalent of cellular growth. ..
  20. Shin H, Alani A, Cho H, Bae Y, Kolesar J, Kwon G. A 3-in-1 polymeric micelle nanocontainer for poorly water-soluble drugs. Mol Pharm. 2011;8:1257-65 pubmed publisher
    ..Collectively, these results suggest that PEG-b-PLA micelles carrying paclitaxel, 17-AAG, and rapamycin will provide a simple yet safe and efficacious 3-in-1 nanomedicine for cancer therapy. ..
  21. Carter C, Marzetti E, Leeuwenburgh C, Manini T, Foster T, Groban L, et al. Usefulness of preclinical models for assessing the efficacy of late-life interventions for sarcopenia. J Gerontol A Biol Sci Med Sci. 2012;67:17-27 pubmed publisher
    ..We finish by providing our perspective regarding the implications of this body of work and future areas of research that may also contribute to the ultimate goal of extending healthspan. ..
  22. Liu Y, Zhang X, Ringel M, Jhiang S. Modulation of sodium iodide symporter expression and function by LY294002, Akti-1/2 and Rapamycin in thyroid cells. Endocr Relat Cancer. 2012;19:291-304 pubmed publisher
  23. Ramakrishnan V, Kimlinger T, Haug J, Painuly U, Wellik L, Halling T, et al. Anti-myeloma activity of Akt inhibition is linked to the activation status of PI3K/Akt and MEK/ERK pathway. PLoS ONE. 2012;7:e50005 pubmed publisher
    ..These provide the basis for clinical evaluation of MK-2206 alone or in combination in MM and potential use of baseline pAkt and pErk as biomarkers for patient selection. ..
  24. Leontieva O, Paszkiewicz G, Blagosklonny M. Mechanistic or mammalian target of rapamycin (mTOR) may determine robustness in young male mice at the cost of accelerated aging. Aging (Albany NY). 2012;4:899-916 pubmed
    ..Our data suggest higher efficacy of rapamycin compared to fasting. Higher sensitivity of females to rapamycin may explain more pronounced life extension by rapamycin observed in females compared to males in several studies. ..
  25. Adams D, Trenor C, Hammill A, Vinks A, Patel M, Chaudry G, et al. Efficacy and Safety of Sirolimus in the Treatment of Complicated Vascular Anomalies. Pediatrics. 2016;137:e20153257 pubmed publisher
    ..No toxicity-related deaths occurred. Sirolimus was efficacious and well tolerated in these study patients with complicated vascular anomalies. Clinical activity was reported in the majority of the disorders. ..
  26. Argula R, Kokosi M, Lo P, Kim H, Ravenel J, Meyer C, et al. A Novel Quantitative Computed Tomographic Analysis Suggests How Sirolimus Stabilizes Progressive Air Trapping in Lymphangioleiomyomatosis. Ann Am Thorac Soc. 2016;13:342-9 pubmed publisher
    ..We speculate that a reduction in lymphangioleiomyomatosis cell burden around small airways and cyst walls alleviates progressive airflow limitation and facilitates cyst emptying. ..
  27. Bodkin C, Eidelman B. Sirolimus-induced posterior reversible encephalopathy. Neurology. 2007;68:2039-40 pubmed
  28. Bourcier M, Sherrod A, DiGuardo M, Vinik A. Successful control of intractable hypoglycemia using rapamycin in an 86-year-old man with a pancreatic insulin-secreting islet cell tumor and metastases. J Clin Endocrinol Metab. 2009;94:3157-62 pubmed publisher
    ..Rapamycin may provide a useful means of abrogating tumor growth and controlling hypoglycemia in malignant insulinomas by reducing the malignant beta-cell growth and proliferation as well as inhibiting insulin production. ..
  29. Djamali A, Samaniego M. Fibrogenesis in kidney transplantation: potential targets for prevention and therapy. Transplantation. 2009;88:1149-56 pubmed publisher
    ..Clinical trials are needed to examine the effect of these therapies on long-term outcomes. ..
  30. Fournier M, Paulson A, Pavelka N, Mosley A, Gaudenz K, Bradford W, et al. Delayed correlation of mRNA and protein expression in rapamycin-treated cells and a role for Ggc1 in cellular sensitivity to rapamycin. Mol Cell Proteomics. 2010;9:271-84 pubmed publisher
    ..A dynamic mRNA expression analysis of Deltaggc1 and wild-type cells treated with rapamycin revealed a key role for Ggc1p in the regulation of ribosome biogenesis and cell cycle progression under TOR control. ..
  31. Zhang Z, Wu X, Duan J, Hinrichs D, Wegmann K, Zhang G, et al. Low dose rapamycin exacerbates autoimmune experimental uveitis. PLoS ONE. 2012;7:e36589 pubmed publisher
    ..Thus, more research is needed to further define the mechanism by which low dose rapamycin augments the immune response. ..
  32. Arriola Apelo S, Neuman J, Baar E, Syed F, Cummings N, Brar H, et al. Alternative rapamycin treatment regimens mitigate the impact of rapamycin on glucose homeostasis and the immune system. Aging Cell. 2016;15:28-38 pubmed publisher
    ..Our results suggest that many of the negative side effects of rapamycin treatment can be mitigated through intermittent dosing or the use of rapamycin analogs. ..
  33. DICKINSON S, Janda J, Criswell J, Blohm Mangone K, Olson E, Liu Z, et al. Inhibition of Akt Enhances the Chemopreventive Effects of Topical Rapamycin in Mouse Skin. Cancer Prev Res (Phila). 2016;9:215-24 pubmed publisher
    ..Our findings indicate that patients taking rapamycin should avoid sun exposure, and that combining topical mTOR inhibitors and Akt inhibitors may be a viable chemoprevention option for individuals at high risk for cutaneous SCC. ..
  34. Lescrauwaet B, Miserocchi E, Thurau S, Bodaghi B, Duchateau L, Verstraeten T, et al. Association Between Visual Function Response and Reduction of Inflammation in Noninfectious Uveitis of the Posterior Segment. Invest Ophthalmol Vis Sci. 2017;58:3555-3562 pubmed publisher
    ..0009), and overall VFR (OR = 2.65; P < 0.0001). Inflammation reduction to a VH score of 0 or 0.5+ was significantly associated with improved visual function. Achieving a VH response of 0 or 0.5+ is a patient-relevant outcome. ..
  35. Sakakibara K, Liu B, Hollenbeck S, Kent K. Rapamycin inhibits fibronectin-induced migration of the human arterial smooth muscle line (E47) through the mammalian target of rapamycin. Am J Physiol Heart Circ Physiol. 2005;288:H2861-8 pubmed
    ..Taken together, our data demonstrate that rapamycin inhibits FN-induced SMC migration through a pathway that involves at least alpha(v)beta(3)-integrin, PI3K, mTOR, and S6K. ..
  36. Cruz R, Hedden L, Boyer D, Kharas M, Fruman D, Lee Fruman K. S6 kinase 2 potentiates interleukin-3-driven cell proliferation. J Leukoc Biol. 2005;78:1378-85 pubmed
    ..This is the first indication that S6K2 plays a role in IL-3-dependent cell proliferation. ..
  37. Zhou H, Liu H, Porvasnik S, Terada N, Agarwal A, Cheng Y, et al. Heme oxygenase-1 mediates the protective effects of rapamycin in monocrotaline-induced pulmonary hypertension. Lab Invest. 2006;86:62-71 pubmed
    ..This study demonstrates that HO-1 is critical for the antiproliferative and vascular protective effects of rapamycin in vitro and in vivo in monocrotaline-induced pulmonary hypertension. ..
  38. Zeng X, Kinsella T. Mammalian target of rapamycin and S6 kinase 1 positively regulate 6-thioguanine-induced autophagy. Cancer Res. 2008;68:2384-90 pubmed publisher
    ..Activated Akt is a well-known inhibitor of autophagy. In conclusion, our data indicate that mTOR-S6K1 positively regulates autophagy after MMR processing of 6-TG probably through its negative feedback inhibition of Akt. ..
  39. Yang L, Clarke M, Carlson B, Mladek A, Schroeder M, Decker P, et al. PTEN loss does not predict for response to RAD001 (Everolimus) in a glioblastoma orthotopic xenograft test panel. Clin Cancer Res. 2008;14:3993-4001 pubmed publisher
    ..These data suggest that loss of PTEN function is insufficient to adequately predict responsiveness to mTOR inhibitors in glioblastoma multiforme. ..
  40. Kim D, Kleinman D, Kanetaka T, Gerritsen M, Nivaggioli T, Weber D, et al. Rapamycin inhibits VEGF-induced microvascular hyperpermeability in vivo. Microcirculation. 2010;17:128-36 pubmed publisher
    ..This inhibition is (i) a direct effect on the endothelial barrier, and (ii) independent of arteriolar vasodilation. Rapamycin at 10 mg/kg stimulates effectors that increase microvascular permeability. ..
  41. Fernandez D, Perl A. mTOR signaling: a central pathway to pathogenesis in systemic lupus erythematosus?. Discov Med. 2010;9:173-8 pubmed
    ..Thus mTOR offers a window into diverse facets of lupus pathogenesis as well as a unifying narrative in our understanding of the therapeutic efficacy of rapamycin in SLE. ..
  42. Gedaly R, Angulo P, Hundley J, Daily M, Chen C, Evers B. PKI-587 and sorafenib targeting PI3K/AKT/mTOR and Ras/Raf/MAPK pathways synergistically inhibit HCC cell proliferation. J Surg Res. 2012;176:542-8 pubmed publisher
    ..The combination of PKI-587 and sorafenib has the advantage over monodrug therapy on inhibition of HCC cell proliferation by blocking both PI3K/AKT/mTOR and Ras/Raf/MAPK signaling pathways. ..
  43. Blagosklonny M. Cell cycle arrest is not yet senescence, which is not just cell cycle arrest: terminology for TOR-driven aging. Aging (Albany NY). 2012;4:159-65 pubmed
  44. Blagosklonny M. How to save Medicare: the anti-aging remedy. Aging (Albany NY). 2012;4:547-52 pubmed
    ..At the same time this advance could save Medicare as we know it. Here I discuss how anti-aging interventions could solve otherwise intractable political problems without tax increases or curtailment of health care benefits. ..
  45. Kondratov R, Kondratova A. Rapamycin in preventive (very low) doses. Aging (Albany NY). 2014;6:158-9 pubmed
  46. Mehta R, Tsymbalyuk N, Ivanova S, Stokum J, Woo K, Gerzanich V, et al. α-Endosulfine (ARPP-19e) Expression in a Rat Model of Stroke. J Neuropathol Exp Neurol. 2017;76:898-907 pubmed publisher
    ..In conjunction with recent studies suggesting a neuroprotective role, our data highlight a potential function for αEnsa within ischemic brain. ..
  47. Zhang J, Francois R, Iyer R, Seshadri M, Zajac Kaye M, Hochwald S. Current understanding of the molecular biology of pancreatic neuroendocrine tumors. J Natl Cancer Inst. 2013;105:1005-17 pubmed publisher
    ..Further advances in our understanding of the molecular mechanisms of PanNETs and improved preclinical models will assist in developing personalized therapy utilizing novel drugs to provide prolonged control or even cure the disease. ..
  48. Koh Y, Shah M, Agarwal K, McCarty S, Koo B, Brendel V, et al. Sorafenib and Mek inhibition is synergistic in medullary thyroid carcinoma in vitro. Endocr Relat Cancer. 2012;19:29-38 pubmed publisher
    ..In conclusion, sorafenib combined with a Mek inhibitor demonstrated synergy in MTC cells in vitro. Mechanisms of resistance to everolimus in MTC cells likely involved TORC2-dependent and TORC2-independent pathways. ..
  49. Huang X, Liu J, Withers B, Samide A, Leggas M, Dickson R. Reducing signs of aging and increasing lifespan by drug synergy. Aging Cell. 2013;12:652-60 pubmed publisher
    ..Thus, our data show that it ought to be possible to find pharmacological approaches to generate a synergistic reduction in the incidence of human age-related diseases to improve health quality in the elderly and enhance lifespan. ..
  50. Fang Y, Westbrook R, Hill C, Boparai R, Arum O, Spong A, et al. Duration of rapamycin treatment has differential effects on metabolism in mice. Cell Metab. 2013;17:456-62 pubmed publisher
    ..Our findings provide a likely explanation of the "rapamycin paradox" and support the potential causal importance of these metabolic alterations in longevity. ..
  51. Flechner S, Gurkan A, Hartmann A, Legendre C, Russ G, Campistol J, et al. A randomized, open-label study of sirolimus versus cyclosporine in primary de novo renal allograft recipients. Transplantation. 2013;95:1233-41 pubmed publisher
  52. Kluk M, Hla T. Role of the sphingosine 1-phosphate receptor EDG-1 in vascular smooth muscle cell proliferation and migration. Circ Res. 2001;89:496-502 pubmed
    ..Since EDG-1 is expressed in the pup-intimal phenotype of VSMCs, S1P signaling via EDG-1 may play a role in vascular diseases in which the proliferation and migration of VSMCs are dysregulated. ..
  53. Pandya K, Dahlberg S, Hidalgo M, Cohen R, Lee M, Schiller J, et al. A randomized, phase II trial of two dose levels of temsirolimus (CCI-779) in patients with extensive-stage small-cell lung cancer who have responding or stable disease after induction chemotherapy: a trial of the Eastern Cooperative Oncology Group (E. J Thorac Oncol. 2007;2:1036-41 pubmed
    ..No patients experienced lethal toxicities. Temsirolimus (CCI 779), given at 25 or 250 mg weekly, seemed not to increase the PFS in this patient population. ..
  54. Wang H, Zhang C, Rorick A, Wu D, Chiu M, Thomas Ahner J, et al. CCI-779 inhibits cell-cycle G2-M progression and invasion of castration-resistant prostate cancer via attenuation of UBE2C transcription and mRNA stability. Cancer Res. 2011;71:4866-76 pubmed publisher
  55. Paghdal K, Schwartz R. Sirolimus (rapamycin): from the soil of Easter Island to a bright future. J Am Acad Dermatol. 2007;57:1046-50 pubmed
    ..This review will focus on the pharmacology and potential uses of sirolimus. ..
  56. Tong J, Yan X, Zhu M, Du M. AMP-activated protein kinase enhances the expression of muscle-specific ubiquitin ligases despite its activation of IGF-1/Akt signaling in C2C12 myotubes. J Cell Biochem. 2009;108:458-68 pubmed publisher
    ..In addition, AMPK inhibition of mTOR may provide an additional explanation for the enhancement of UL expression by AMPK. ..
  57. Sekulic A, Hudson C, Homme J, Yin P, Otterness D, Karnitz L, et al. A direct linkage between the phosphoinositide 3-kinase-AKT signaling pathway and the mammalian target of rapamycin in mitogen-stimulated and transformed cells. Cancer Res. 2000;60:3504-13 pubmed
    ..Furthermore, the activation status of the PI3K-AKT pathway in cancer cells may be an important determinant of cellular sensitivity to the cytostatic effect of rapamycin. ..
  58. Carter A, Aggarwal M, Kopia G, Tio F, Tsao P, Kolata R, et al. Long-term effects of polymer-based, slow-release, sirolimus-eluting stents in a porcine coronary model. Cardiovasc Res. 2004;63:617-24 pubmed
    ..Long-term inhibition of neointimal hyperplasia is not sustained presumably due to delayed cellular proliferation despite increased levels of the cyclin-dependent kinase p27(kip1) in the vessel wall. ..
  59. Garcia J, Danielpour D. Mammalian target of rapamycin inhibition as a therapeutic strategy in the management of urologic malignancies. Mol Cancer Ther. 2008;7:1347-54 pubmed publisher
  60. Verma M, Awdishu L, Lane J, Park K, Bahur B, Lwin W, et al. Impact of single immunosuppressive drug withdrawal on lymphocyte immunoreactivity. J Surg Res. 2014;188:309-15 pubmed publisher
    ..In comparison, tacrolimus did not have a similar effect on lymphocyte proliferation or interleukin 17A secretion. Future analysis of sirolimus in diverse transplantation populations merits investigation. ..
  61. NIKIFOROV M. TOR-inhibitors as gero-suppressors. Aging (Albany NY). 2015;7:1030-1 pubmed
  62. Goehring A, Rivers D, Sprague G. Attachment of the ubiquitin-related protein Urm1p to the antioxidant protein Ahp1p. Eukaryot Cell. 2003;2:930-6 pubmed
    ..These results suggest that the conjugation of Urm1p to Ahp1p could regulate the function of Ahp1p in antioxidant stress response in Saccharomyces cerevisiae. ..
  63. Miller A, Brestoff J, Phelps C, Berk E, Reynolds T. Rapamycin does not improve insulin sensitivity despite elevated mammalian target of rapamycin complex 1 activity in muscles of ob/ob mice. Am J Physiol Regul Integr Comp Physiol. 2008;295:R1431-8 pubmed publisher
    ..These results indicate that the insulin resistance of OB mice is mediated, in part, by factors other than mTORC1. ..
  64. Goodman C, Frey J, Mabrey D, Jacobs B, Lincoln H, You J, et al. The role of skeletal muscle mTOR in the regulation of mechanical load-induced growth. J Physiol. 2011;589:5485-501 pubmed publisher
    ..Overall, these results demonstrate that CML activates several growth regulatory events, but only a few (e.g. hypertrophy) are fully dependent on mTOR signalling within the skeletal muscle cells. ..
  65. Morice W, Wiederrecht G, Brunn G, Siekierka J, Abraham R. Rapamycin inhibition of interleukin-2-dependent p33cdk2 and p34cdc2 kinase activation in T lymphocytes. J Biol Chem. 1993;268:22737-45 pubmed
    ..The inhibitory effects of RAP on the activation of cyclin E- and cyclin A-associated cyclin-dependent kinases suggest that one or both events participate in the regulation of T cell entry into S-phase. ..
  66. Mosley J, Poirier J, Seachrist D, Landis M, Keri R. Rapamycin inhibits multiple stages of c-Neu/ErbB2 induced tumor progression in a transgenic mouse model of HER2-positive breast cancer. Mol Cancer Ther. 2007;6:2188-97 pubmed
    ..In summary, data from this preclinical model of ErbB2/Neu-induced breast cancer show that inhibition of the mTOR pathway with rapamycin blocks multiple stages of ErbB2/Neu-induced tumorigenic progression. ..
  67. Rangaraju S, Verrier J, Madorsky I, Nicks J, Dunn W, Notterpek L. Rapamycin activates autophagy and improves myelination in explant cultures from neuropathic mice. J Neurosci. 2010;30:11388-97 pubmed publisher
    ..Together, these results support the potential use of RM and other autophagy-enhancing compounds as therapeutic agents for PMP22-associated demyelinating neuropathies. ..
  68. Blagosklonny M. Increasing healthy lifespan by suppressing aging in our lifetime: preliminary proposal. Cell Cycle. 2010;9:4788-94 pubmed
  69. Blagosklonny M. TOR-driven aging: speeding car without brakes. Cell Cycle. 2009;8:4055-9 pubmed
  70. Stelzer M, Pitot H, Liem A, Lee D, Kennedy G, Lambert P. Rapamycin inhibits anal carcinogenesis in two preclinical animal models. Cancer Prev Res (Phila). 2010;3:1542-51 pubmed publisher
    ..As has been seen in other cancers, rapamycin treatment led to an activation of the MAPK pathway. These results provide us cause to pursue further the evaluation of rapamycin as a therapeutic agent in the control of anal cancer. ..
  71. Leontieva O, Paszkiewicz G, Demidenko Z, Blagosklonny M. Resveratrol potentiates rapamycin to prevent hyperinsulinemia and obesity in male mice on high fat diet. Cell Death Dis. 2013;4:e472 pubmed publisher
    ..Given distinct mechanisms of action of rapamycin and resveratrol at clinically relevant doses, their combination warrants further investigation as a potential antiaging, antiobesity and antidiabetic modality. ..
  72. Eloy J, Petrilli R, Topan J, Antonio H, Barcellos J, Chesca D, et al. Co-loaded paclitaxel/rapamycin liposomes: Development, characterization and in vitro and in vivo evaluation for breast cancer therapy. Colloids Surf B Biointerfaces. 2016;141:74-82 pubmed publisher
    ..Therefore, we expect that the formulation developed herein might be a contribution for future studies focusing on the clinical combination of paclitaxel and rapamycin. ..
  73. Hu H, Chai Y, Wang L, Zhang J, Lee H, Kim S, et al. Pentagalloylglucose induces autophagy and caspase-independent programmed deaths in human PC-3 and mouse TRAMP-C2 prostate cancer cells. Mol Cancer Ther. 2009;8:2833-43 pubmed publisher
    ..The induction by PGG of caspase-independent programmed cell death in aggressive prostate cancer cell lines supports testing its merit as a potential drug candidate for therapy of caspase-resistant recurrent prostate cancer...
  74. Hansel D, Platt E, Orloff M, Harwalker J, Sethu S, Hicks J, et al. Mammalian target of rapamycin (mTOR) regulates cellular proliferation and tumor growth in urothelial carcinoma. Am J Pathol. 2010;176:3062-72 pubmed publisher
    ..01) compared with vehicle-injected mice. These findings indicate that mTOR pathway activation frequently occurs in UCC and that mTOR inhibition may be a potential means to reduce UCC growth. ..
  75. Haemel A, O Brian A, Teng J. Topical rapamycin: a novel approach to facial angiofibromas in tuberous sclerosis. Arch Dermatol. 2010;146:715-8 pubmed publisher
  76. Li J, Liu J, Song J, Wang X, Weiss H, Townsend C, et al. mTORC1 inhibition increases neurotensin secretion and gene expression through activation of the MEK/ERK/c-Jun pathway in the human endocrine cell line BON. Am J Physiol Cell Physiol. 2011;301:C213-26 pubmed publisher
    ..Our results identify a physiological link between mTORC1 and MEK/ERK signaling in controlling intestinal hormone gene expression and secretion. ..
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