Specific delivery of siRNA, ribozyme and multiple therapeutic molecules to cancer cells using RNA nanotechnology

2006 ◽  
Vol 2 (4) ◽  
pp. 293-294
Author(s):  
S. Guo ◽  
P. Guo
Keyword(s):  
Cancer Cells ◽  
Rna Nanotechnology ◽  
Therapeutic Molecules

Bacterial delivery of smart nanoparticles-loaded with therapeutic molecules into cancer cells

2005 ◽  
Vol 1 (3) ◽  
pp. 250
Author(s):  
D. Akin ◽  
K. Ragheb ◽  
J. Sturgis ◽  
A.K. Bhunia ◽  
P. Robinson ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Therapeutic Molecules

Gold nanoparticles and gold nanoparticle-conjugates for delivery of therapeutic molecules. Progress and challenges

2014 ◽  
Vol 2 (27) ◽  
pp. 4204-4220 ◽  
Author(s):  
I. Fratoddi ◽  
I. Venditti ◽  
C. Cametti ◽  
M. V. Russo
Keyword(s):  
Drug Delivery ◽  
Gold Nanoparticles ◽  
Cancer Cells ◽  
Gold Nanoparticle ◽  
Drug Delivery Vehicles ◽  
Selective Targeting ◽  
Therapeutic Molecules ◽  
Delivery Vehicles

Gold nanoparticles and their conjugates as drug delivery vehicles for selective targeting of cancer cells.

The topoisomerase II catalytic inhibitor ICRF-193 preferentially targets telomeres that are capped by TRF2

2015 ◽  
Vol 308 (5) ◽  
pp. C372-C377 ◽  
Author(s):  
Lianxiang Chen ◽  
Xiaowei Zhu ◽  
Yaru Zou ◽  
Jun Xing ◽  
Eric Gilson ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Topoisomerase Ii ◽  
Chromosome Instability ◽  
Telomere Dysfunction ◽  
Telomeric Dna ◽  
Published Evidence ◽  
Catalytic Inhibitor ◽  
Binding Factor ◽  
Therapeutic Molecules

The increased level of chromosome instability in cancer cells is not only a driving force for oncogenesis but also can be the Achille's heel of the disease since many chemotherapies kill cells by inducing a nontolerable rate of DNA damage. A wealth of published evidence showed that telomere stability can be more affected than the bulk of the genome by several conventional antineoplastic drugs. In the present study, HT1080 cell lines compromised for either telomere repeats binding factor 2 (TRF2) or POT1 were treated with ICRF-193 (3 μM, 24 h) or bleomycin (1 μM, 24 h). DNA damage was assayed by combining telomeric DNA staining of a (CCCTAA)n PNA probe with immunofluorescence of 53BP1 to score the rate of telomere colocalization with 53BP1 foci. We found that ICRF-193, but not bleomycin, leads to DNA damage preferentially at telomeres, which can be rescued by TRF2 inhibition. POT1 inhibition exacerbates telomere dysfunction induced by ICRF-193. Thus, ICRF-193 induces damage at telomeres properly capped by TRF2 but not by POT1. These findings are expected to broaden our view on the mechanism by which conventional therapeutic molecules act to eliminate cancer cells and how to use TRF2 and POT1 levels as surrogate markers for anti-topoisomerase II sensitivity.

Grb7-based molecular therapeutics in cancer

2003 ◽  
Vol 5 (14) ◽  
pp. 1-11 ◽  
Author(s):  
Stephanie C. Pero ◽  
Roger J. Daly ◽  
David N. Krag
Keyword(s):  
Cancer Cells ◽  
Tyrosine Kinases ◽  
Sh2 Domain ◽  
Whole Body ◽  
Invasive Potential ◽  
Src Homology 2 ◽  
Molecular Therapeutics ◽  
Anti Cancer ◽  
Therapeutic Molecules ◽  
Src Homology

Traditional anti-cancer drugs preferentially kill rapidly growing tumour cells rather than normal cells. However, most of these drugs have no preferential selection towards cancer cells and are taken up by the whole body, resulting in significant adverse side effects. Therapeutic molecules that could specifically inhibit undesirable phenotypes are an attractive way of eliminating cancer cells. There is a widespread effort to develop inhibitors against signal transduction molecules that play a key role in the proliferative, migratory and invasive properties of a cancer cell. Grb7 is an adaptor-type signalling protein that is recruited via its Src-homology 2 (SH2) domain to a variety of tyrosine kinases. Grb7 is overexpressed in breast, oesophageal and gastric cancers, and may contribute to the invasive potential of cancer cells. Molecular interactions involving Grb7 therefore provide attractive targets for therapeutic intervention.

scholarly journals Carbon Nanotubes in Cancer Therapy and Drug Delivery

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Abdelbary M. A. Elhissi ◽  
Waqar Ahmed ◽  
Israr Ul Hassan ◽  
Vinod. R. Dhanak ◽  
Antony D'Emanuele
Keyword(s):  
Carbon Nanotubes ◽  
Drug Delivery ◽  
Cancer Therapy ◽  
Cancer Cells ◽  
Surface Area ◽  
Biological Properties ◽  
Major Focus ◽  
Carrier System ◽  
Wide Range ◽  
Therapeutic Molecules

Carbon nanotubes (CNTs) have been introduced recently as a novel carrier system for both small and large therapeutic molecules. CNTs can be functionalized (i.e., surface engineered) with certain functional groups in order to manipulate their physical or biological properties. In addition to the ability of CNTs to act as carriers for a wide range of therapeutic molecules, their large surface area and possibility to manipulate their surfaces and physical dimensions have been exploited for use in the photothermal destruction of cancer cells. This paper paper will discuss the therapeutic applications of CNTs with a major focus on their applications for the treatment of cancer.

The metal-binding domain of IGFBP-3 selectively delivers therapeutic molecules into cancer cells

2009 ◽  
Vol 20 (1) ◽  
pp. 21-31 ◽  
Author(s):  
Anja Huq ◽  
Baljit Singh ◽  
Thea Meeker ◽  
Desmond Mascarenhas
Keyword(s):  
Cancer Cells ◽  
Metal Binding ◽  
Binding Domain ◽  
Metal Binding Domain ◽  
Therapeutic Molecules ◽  
Igfbp 3

Ultrastructural modification of cellular interactions in cancer tumor

1978 ◽  
Vol 36 (2) ◽  
pp. 318-319
Author(s):  
N. P. Dmitrieva
Keyword(s):  
Cancer Cells ◽  
Human Thyroid ◽  
Adjacent Cell ◽  
Main Role ◽  
Cellular Interactions ◽  
Electron Microscopic ◽  
Cancer Tumor ◽  
Normal Human ◽  
Characteristic Features

One of the most characteristic features of cancer cells is their ability to metastasia. It is suggested that the modifications of the structure and properties of cancer cells surfaces play the main role in this process. The present work was aimed at finding out what ultrastructural features apear in tumor in vivo which removal of individual cancer cells from the cell population can provide. For this purpose the cellular interactions in the normal human thyroid and cancer tumor of this gland electron microscopic were studied. The tissues were fixed in osmium tetroxide and were embedded in Araldite-Epon.In normal human thyroid the most common type of intercellular contacts was represented by simple junction formed by the parallelalignment of adjacent cell membranees leaving in between an intermembranes space 15-20 nm filled with electronlucid material (Fig. 1a). Sometimes in the basal part of cells dilatations of the intercellular space 40-50 nm wide were found (Fig. 1a). Here the cell surfaces may form single short microvilli.

Ultrastructural Localization Study of Carcinoembryonic Antigen (CEA) in Gastric Cancer: Immunoelectron Microscopic Observation

1990 ◽  
Vol 48 (3) ◽  
pp. 252-253
Author(s):  
Dong Yuming ◽  
Yang Guanglin ◽  
Wu Jifeng ◽  
Chen Xiaolin
Keyword(s):  
Gastric Cancer ◽  
Intestinal Metaplasia ◽  
Cancer Cells ◽  
Microscopic Observation ◽  
Biological Significance ◽  
Ultrastructural Localization ◽  
Mucinous Carcinoma ◽  
Surface Glycoprotein ◽  
Tubular Adenocarcinoma ◽  
Pap Method

On the basis of light microscopic observation, the ultrastructural localization of CEA in gastric cancer was studied by immunoelectron microscopic technique. The distribution of CEA in gastric cancer and its biological significance and the mechanism of abnormal distribution of CEA were further discussed.Among 104 surgically resected specimens of gastric cancer with PAP method at light microscopic level, the incidence of CEA(+) was 85.58%. All of mucinous carcinoma exhibited CEA(+). In tubular adenocarcinoma the incidence of CEA(+) showed a tendency to rising with the increase of degree of differentiation. In normal epithelia and intestinal metaplasia CEA was faintly present and was found only in the luminal surface. The CEA staining patterns in cancer cells were of three types--- cytoplasmic, membranous and weak reactive type. The ultrastructural localization of CEA in 14 cases of gastric cancer was studied by immunoelectron microscopic technique.There was a little or no CEA in the microvilli of normal epithelia. In intestinal metaplasia CEA was found on the microvilli of absorptive cells and among the mucus particles of goblet cells. In gastric cancer CEA was also distributed on the lateral and basal surface or even over the entire surface of cancer cells and lost their polarity completely. Many studies had proved that the alterations in surface glycoprotein were characteristic changes of tumor cells. The antigenic determinant of CEA was glycoprotein, so the alterations of tumor-associated surface glycoprotein opened up a new way for the diagnosis of tumors.

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