Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42345 (mTOR)
 26,049 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although most patients with adult acute lymphoblastic leukaemia (ALL) can achieve a remission when treated with conventional, DNA-damaging chemotherapy, in more than half of all cases the disease relapses and ultimately results in death. Therefore, there is a substantial need for new antileukaemic drugs. Recent advances in the understanding of the molecular alterations in ALL have lead to the identification of new targets and the arrival of molecular-targeted therapies in the clinical setting. The prototype for this approach is the treatment of Philadelphia chromosome-positive ALL with imatinib mesylate. Here, the targeting of a molecular abnormality--inhibition of BCR-ABL tyrosine kinase--has turned a very poor-prognosis disease into one in which promising results are achieved. Promising new therapies are under development that target various goals, including the NOTCH signalling pathway, purine nucleoside phosphorylase activity, mammalian target of rapamycin and tyrosine kinase. This review outlines recent advances in the development of emerging drugs for the treatment of adult ALL. The recent advances in the understanding of the biology and pathogenesis of ALL have helped to determine prognosis and to plan the therapy of adult patients with ALL. Still, despite improved complete remission rates of 65-90% with current therapy, only 20-40% of patients can be considered cured. New therapeutic alternatives are needed to improve these results. With a better understanding of the disease, more target-specific therapies could be designed. The aim of this review is to highlight new pharmacotherapies and those emerging drug treatments for patients with adult ALL.
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PMID:Emerging drugs for adult acute lymphoblastic leukaemia. 1608 31

Peripheral T-cell non-Hodgkin's lymphomas are a diverse group of disorders, most of which carry a poor prognosis. Relapse is common following the administration of most currently available agents, and there are few effective options for salvage therapy. This article discusses a number of novel emerging therapies for the treatment of patients with T-cell non-Hodgkin's lymphomas, including the antimetabolite nelarabine, the purine nucleoside phosphorylase inhibitor forodesine, the pyrimidine analogue gemcitabine, and the fusion protein denileukin diftitox. Other therapies discussed for the treatment of patients with T-cell non-Hodgkin's lymphomas include bendamustine, gallium nitrate, and bortezomib, as well as the mammalian target of rapamycin inhibitors, small molecules that target the apoptotic pathways, immunomodulatory agents, and monoclonal antibodies.
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PMID:Clinical management of T-cell malignancies: current perspectives, key issues, and emerging therapies. 1808 45

The epidermal growth factor receptor (EGFR) is a well-studied receptor-tyrosine kinase that serves vital roles in regulation of organ development and cancer progression. EGFR not only exists on the plasma membrane, but also widely expressed in the nucleus, endosomes, and mitochondria. Most recently, several lines of evidences indicated that autophagy is regulated by EGFR in kinase-active and -independent manners. In this review, we summarized recent advances in our understanding of the functions of different subcellularly located EGFR on autophagy. Specifically, plasma membrane- and cytoplasm-located EGFR (pcEGFR) acts as a tyrosine kinase to regulate autophagy via the PI3K/AKT1/mTOR, RAS/MAPK1/3, and STAT3 signaling pathways. The kinase-independent function of pcEGFR inhibits autophagy by maintaining SLC5A1-regulated intracellular glucose level. Endosome-located EGFR phosphorylates and inhibits Beclin1 to suppress autophagy, while kinase-independent endosome-located EGFR releases Beclin1 from the Rubicon-Beclin1 complex to increase autophagy. Additionally, the nuclear EGFR activates PRKDC/PNPase/MYC signaling to inhibit autophagy. Although the role of mitochondria-located EGFR in autophagy is largely unexplored, the production of ATP and reactive oxygen species mediated by mitochondrial dynamics is most likely to influence autophagy.
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PMID:The roles of subcellularly located EGFR in autophagy. 2842 83