Enzymatic activatable self-assembled peptide nanowire for targeted therapy and fluorescence imaging of tumors

2016 ◽  
Vol 52 (18) ◽  
pp. 3631-3634 ◽  
Author(s):  
Ying Tang ◽  
Zhan Wu ◽  
Chong-Hua Zhang ◽  
Xiao-Li Zhang ◽  
Jian-Hui Jiang
Keyword(s):  
Targeted Therapy ◽  
Cancer Therapy ◽  
Fluorescence Imaging ◽  
Cytotoxic Agents ◽  
Targeted Cancer Therapy ◽  
Self Assembled

An activatable theranostic approach based on self-assembled peptide nanostructures with surface-displayed activatable cytotoxic agents for targeted cancer therapy was developed.

pH-Responsive de-PEGylated nanoparticles based on triphenylphosphine–quercetin self-assemblies for mitochondria-targeted cancer therapy

2017 ◽  
Vol 53 (62) ◽  
pp. 8790-8793 ◽  
Author(s):  
Lei Xing ◽  
Jin-Yuan Lyu ◽  
Yue Yang ◽  
Peng-Fei Cui ◽  
Liu-Qing Gu ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Coordination Bond ◽  
The Self ◽  
Targeted Cancer Therapy ◽  
Ph Responsive ◽  
Pegylated Nanoparticles ◽  
Self Assembled

The self-assembled nanosystem formulated with amphiphilic TPP–Que and PBA–PEG through a coordination bond could balance the dilemma of PEGylation.

Genetically engineered and self-assembled oncolytic protein nanoparticles for targeted cancer therapy

Biomaterials ◽  
2017 ◽  
Vol 120 ◽  
pp. 22-31 ◽  
Author(s):  
Joong-jae Lee ◽  
Jung Ae Kang ◽  
Yiseul Ryu ◽  
Sang-Soo Han ◽  
You Ree Nam ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Genetically Engineered ◽  
Targeted Cancer Therapy ◽  
Protein Nanoparticles ◽  
Self Assembled

Self-assembled nanoparticles comprising aptide–SN38 conjugates for use in targeted cancer therapy

2016 ◽  
Vol 27 (48) ◽  
pp. 48LT01 ◽  
Author(s):  
Hyungjun Kim ◽  
Yonghyun Lee ◽  
Sukmo Kang ◽  
Minsuk Choi ◽  
Soyoung Lee ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Targeted Cancer Therapy ◽  
Self Assembled

scholarly journals Targeted cancer therapy induces APOBEC fuelling the evolution of drug resistance

2020 ◽  
Author(s):  
Manasi K. Mayekar ◽  
Deborah R. Caswell ◽  
Natalie I. Vokes ◽  
Emily K. Law ◽  
Wei Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Targeted Therapy ◽  
Cancer Therapy ◽  
De Novo ◽  
Tumour Progression ◽  
Genetic Alterations ◽  
Model Systems ◽  
Clinical Samples ◽  
Targeted Cancer Therapy

Introductory paragraphThe clinical success of targeted cancer therapy is limited by drug resistance that renders cancers lethal in patients1-4. Human tumours can evolve therapy resistance by acquiring de novo genetic alterations and increased heterogeneity via mechanisms that remain incompletely understood1. Here, through parallel analysis of human clinical samples, tumour xenograft and cell line models and murine model systems, we uncover an unanticipated mechanism of therapy-induced adaptation that fuels the evolution of drug resistance. Targeted therapy directed against EGFR and ALK oncoproteins in lung cancer induced adaptations favoring apolipoprotein B mRNA-editing enzyme, catalytic polypeptide (APOBEC)-mediated genome mutagenesis. In human oncogenic EGFR-driven and ALK-driven lung cancers and preclinical models, EGFR or ALK inhibitor treatment induced the expression and DNA mutagenic activity of APOBEC3B via therapy-mediated activation of NF-κB signaling. Moreover, targeted therapy also mediated downregulation of certain DNA repair enzymes such as UNG2, which normally counteracts APOBEC-catalyzed DNA deamination events. In mutant EGFR-driven lung cancer mouse models, APOBEC3B was detrimental to tumour initiation and yet advantageous to tumour progression during EGFR targeted therapy, consistent with TRACERx data demonstrating subclonal enrichment of APOBEC-mediated mutagenesis. This study reveals how cancers adapt and drive genetic diversity in response to targeted therapy and identifies APOBEC deaminases as future targets for eliciting more durable clinical benefit to targeted cancer therapy.

scholarly journals Finding a Place for Tumor-specific T Cells in Targeted Cancer Therapy

2004 ◽  
Vol 200 (12) ◽  
pp. 1533-1537 ◽  
Author(s):  
Stanley R. Riddell
Keyword(s):  
T Cells ◽  
Targeted Therapy ◽  
Cancer Therapy ◽  
Cell Surface ◽  
Adoptive Transfer ◽  
Cancer Therapeutics ◽  
Targeted Cancer Therapy ◽  
Normal Cells ◽  
Mhc Molecules ◽  
Recent Success

A goal in cancer therapeutics is to develop targeted modalities that distinguish malignant from normal cells. T cells can discriminate diseased cells based on subtle alterations in peptides displayed in association with MHC molecules at the cell surface. Recent success using the adoptive transfer of tumor-specific T cells has fueled optimism that this approach may find a place as a targeted therapy for some human cancers.

Self-assembled micelles of a multi-functional amphiphilic fusion (MFAF) peptide for targeted cancer therapy

2015 ◽  
Vol 6 (18) ◽  
pp. 3512-3520 ◽  
Author(s):  
Yin-Jia Cheng ◽  
Hong Cheng ◽  
Xin Zhao ◽  
Xiao-Ding Xu ◽  
Ren-Xi Zhuo ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Tumor Cells ◽  
Tumor Targeting ◽  
Targeted Cancer Therapy ◽  
Self Assembled

A new MFAF peptide was designed and prepared. The micelles of this MFAF peptide can efficiently use their tumor-targeting, membrane-penetrating and endosome-escaping functions to deliver the drug into targeted tumor cells, leading to the apoptosis of tumor cells.

scholarly journals Induction of a SALL4-dependency for targeted cancer therapy

2020 ◽  
Author(s):  
Junyu Yang ◽  
Chong Gao ◽  
Miao Liu ◽  
Zhiyuan Chen ◽  
Yao-Chung Liu ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Targeted Cancer Therapy ◽  
Proof Of Concept ◽  
Promising Target ◽  
Deacetylase Inhibitor ◽  
Exogenous Expression ◽  
Pre Treatment

AbstractOncofetal protein SALL4 is critical for tumor cell survival, making it a promising target in cancer therapy. However, it is detectable only in a subset of cancer patients, which limits the therapeutic impact of a SALL4 targeted therapy. Here we report that SALL4 can be activated and/or upregulated pharmacologically by hypomethylating agents, such as 5-Aza-2’-deoxycytidine (DAC), which are used clinically, and that SALL4 negative cancer cells become SALL4 dependent following exogenous expression of SALL4. In addition, the histone deacetylase inhibitor Entinostat (ENT) negatively regulates SALL4 expression by upregulating miR-205. Both ENT and miR-205 treatment induced cell apoptosis, rescuable by SALL4 expression or miR-205 inhibition. Finally, DAC pre-treatment sensitizes SALL4 negative cancer cell lines to ENT both in culture and in vivo by upregulating SALL4. Overall, we propose a framework whereby the scope of targeted therapy can be expanded by sensitizing cancer cells to treatment by target induction and engineered dependency.SignificanceThis proof of concept study demonstrates that targeted cancer therapy can be achieved by inducing a targetable gene establishing a survival-dependency for cancer cells. For SALL4, sequential treatment of DAC and ENT could expand the scope of SALL4 targeted cancer therapy.

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