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Targeting apoptosis pathways by natural compounds in cancer: marine compounds as lead structures and chemical tools for cancer therapy.
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Natural compounds derived from marine organisms and their synthetic derivates are an important source for new therapeutics for single agent or combined therapy with other chemotherapeutics to support the struggle against cancer.About:
This article is published in Cancer Letters.The article was published on 2013-05-28. It has received 88 citations till now. The article focuses on the topics: Discodermolide.read more
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Marine-sourced anti-cancer and cancer pain control agents in clinical and late preclinical development.
David J. Newman,Gordon M. Cragg +1 more
TL;DR: This review shows the compounds derived from marine sources that are currently in clinical trials against cancer and the use of marine-derived agents to ameliorate the pain from cancers in humans, and to act as an adjuvant in immunological therapies.
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Antitumor Peptides from Marine Organisms
TL;DR: In this review, the progress on studies of antitumor peptides from marine sources is provided; the biological properties and mechanisms of action of different marine peptides are described; information about their molecular diversity is presented.
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Stellettin B Induces G1 Arrest, Apoptosis and Autophagy in Human Non-small Cell Lung Cancer A549 Cells via Blocking PI3K/Akt/mTOR Pathway
Ran Wang,Qian Zhang,Xin Peng,Chang Zhou,Yuxu Zhong,Xi Chen,Yuling Qiu,Meihua Jin,Min Gong,Dexin Kong +9 more
TL;DR: The isolated stellettin B (Stel B) from marine sponge Jaspis stellifera is isolated, and it is demonstrated that it induced G1 arrest, apoptosis and autophagy at low concentrations in human NSCLC A549 cells, indicating the antitumor potential of Stel B by targeting PI3K/Akt/mTOR pathway.
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Kinase inhibitors of marine origin.
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Anticancer Properties of Lamellarins
TL;DR: The lead compound in the lamellarins family is lamellarin D, characterized as a potent inhibitor of both nuclear and mitochondrial topoisomerase I but also capable of directly interfering with mitochondria to trigger cancer cell death.
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The antitumoral compound Kahalalide F acts on cell lysosomes
TL;DR: The target for the antitumoral peptidic drug, Kahalalide F, has been studied in cultured cells, and in the presence of the compound, cells became impressively swollen, showing the formation of large vacuoles.
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A New, More Efficient, and Effective Process for the Synthesis of a Key Pentacyclic Intermediate for Production of Ecteinascidin and Phthalascidin Antitumor Agents
Eduardo J. Martinez,E. J. Corey +1 more
TL;DR: An efficient process is described for the synthesis of 5, a key intermediate for the synthesisation of the potent antitumor agents ecteinascidin 743 and phthalascidins from the readily available building blocks 3b and 4.
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Progress in the clinical development of new marine-derived anticancer compounds.
Jose Jimeno,Jose A. Lopez-Martin,Ana Ruiz-Casado,Miguel Izquierdo,P. J. Scheuer,Kenneth L. Rinehart +5 more
TL;DR: ET-743 (Yondelis) represents the first new agent developed against advanced pretreated soft tissue sarcoma in the past 25 years, and also harbors activity in women bearing pretreated ovarian cancer and a solid potential in combination therapy.
Journal Article
Inhibition of phorbol ester-induced T cell proliferation by bryostatin is associated with rapid degradation of protein kinase C.
TL;DR: It is proposed that Bryo inhibits PMA-induced T cell proliferation by causing rapid degradation of PKC, reflecting a requirement of persistent PKC stimulation for the activation of human T cells and progression through the cell cycle.
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Differential cytostatic and apoptotic effects of ecteinascidin-743 in cancer cells. Transcription-dependent cell cycle arrest and transcription-independent JNK and mitochondrial mediated apoptosis.
TL;DR: E ecteinascidin-743 is a very potent anticancer drug showing dose-dependent cytostatic and proapoptotic effects through activation of two different signaling pathways, namely a transcription-dependent pathway leading to cell cycle arrest andA transcription-independent route leading to rapid apoptosis that involves mitochondria, JNK, and caspase-3.