Current development of mTOR inhibitors as anticancer agents

By S. Faivre, Guido Kroemer, E. Raymond. Nature reviews. Drug discovery, 2006

998 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/2f05dd0ac0064a5d29f7a369a7fd58230906a9d0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

In Molecular Biology

In Pathology and Forensic Medicine

Citations in the corpus

Active-Site Inhibitors of mTOR Target Rapamycin-Resistant Outputs of mTORC1 and mTORC2 (2009, background): “As active site inhibitors of mTOR join rapamycin and its analogs in the clinic [22,27,30], it will be important to understand the distinct effects of these pharmacological agents on cellular and organismal physiology and to evaluate their efficacy in the treatment of disease and cancer caused by hyp”
Defining the role of mTOR in cancer. (2007, background): “…for combination therapy include gefitinib (Iressa, an EGFR inhibitor), imatinib mesylate (Gleevec, a BCR-ABL inhibitor), tamoxifen (estrogen receptor modulator), cisplatin (DNA damaging agent), and paclitaxel (microtubule stabilizer) (reviewed in Faivre et al., 2006; Granville et al., 2006).”
Targeting cancer with small molecule kinase inhibitors (2009, neutral): “, mTOR (also known as FRAP1 ), which is located in the PI3K–Akt signalling syste”
Targeting PI3K/Akt/mTOR Signaling in Cancer (2014, background): “However, clinical development of rapamycin as an anticancer agent was hampered by unfavorable pharmacokinetic properties (22).”
Tumor cell metabolism: cancer's Achilles' heel. (2008, background): “The preclinical and clinical evaluation of metabolic inhibitors for cancer therapy is in its infancy, perhaps with the notable exception of mTOR antagonists (Faivre et al., 2006) and (unfortunately rather nonspecific) activators of AMPK that are given as oral antidiabetics and reduce the incidence o”
The mTOR Signalling Pathway in Human Cancer (2012, background): “contributes to tumour growth, angiogenesis and metastasis [56].”
Tenets of PTEN tumor suppression. (2008, background): “…a number of tumor suppressor genes directly implicated in human cancer, the mTOR arm of the PTEN/PI3K/AKT pathway is emerging as an effective target for anti-cancer agents, especially in tumors in which the activity of the mTOR pathway is elevated (Faivre et al., 2006; Guertin and Sabatini, 2007).”
mTOR: a pharmacologic target for autophagy regulation. (2015, positive): “These rapalogs have a similar ability to inhibit mTORC1 with fewer immunosuppressive effects (93).”
The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “mTORC1 inhibitors failed to inhibit tumor progression in a variety of cancers, with the exception of kidney cancer, TSC-associated symptoms (Faivre et al., 2006) and brain tumors (Cloughesy et al.”
Regulation of autophagy by cytoplasmic p53 (2008, background): “, and the mammalian target of rapamycin (mTOR), which suppresses autophag”
The exploration of macrocycles for drug discovery — an underexploited structural class (2008, background): “Rapamycin (3) similarly controls the mTOR pathway through its interaction with FKBP12 to create a hybrid macrocycle–protein surface that facilitates the binding of FRAP”
Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma (2008, background): “Recently, mTOR inhibitors have shown clinical activity in metastatic kidney cancer, where the frequency of PTEN loss is low [50].”
Kinase-targeted cancer therapies: progress, challenges and future directions (2018, background): “Other examples of tumor cell survival kinases include MEK1 [54], MEK2 [54], mTOR [55], and S6 kinase [56] which are all downstream members of MAPK, PI3K–Akt and EGFR pathway, respectively.”