scholarly journals High mitochondrial accumulation of new gadolinium(iii) agents within tumour cells

2014 ◽  
Vol 50 (18) ◽  
pp. 2252-2254 ◽  
Author(s):  
Daniel E. Morrison ◽  
Jade B. Aitken ◽  
Martin D. de Jonge ◽  
Joseph A. Ioppolo ◽  
Hugh H. Harris ◽  
...  
Keyword(s):  
Tumour Cell ◽  
Tumour Cells

The first tumour-cell selective mitochondrial agents containing GdIII which can deliver greater than 1010 Gd atoms per tumour cell are reported.

scholarly journals Monoclonal Antibodies as Immune Modulators for Cancer Therapy

1992 ◽  
Vol 3 (suppl b) ◽  
pp. 20-25
Author(s):  
Robert O Dillman
Keyword(s):  
Monoclonal Antibodies ◽  
Cancer Therapy ◽  
Immune Cells ◽  
Tumour Cell ◽  
Interleukin 2 ◽  
Tumour Cells ◽  
Host Immune System ◽  
Biological Behaviour ◽  
Immune Modulators ◽  
The Status

Monoclonal antibodies may modulate immune and/or biological responses alone, or as carriers of specific agents. Monoclonal antibodies directed against tumours may be indirectly cytotoxic by modulation of antibody-dependent, cell-mediated cytotoxicity or complement-mediated cytotoxicity. Monoclonal antibodies directed against certain tumour cell receptors may alter the biological behaviour of tumour cells such as blocking or downregulation of growth factors essential to tumour cell proliferation. Monoclonal antibodies directed to certain receptors on host immune cells. such as the CD3 receptor on T lymphocytes. may activate those cells and increase their cytotoxicity. Antitumour monoclonal antibodies can serve as carriers of interferons, interleukin-2, tumour necrosis factor and other lymphokines and cytokines to modulate selectively the cytotoxic potential of immune cells in the vicinity of tumour cells. Cytotoxic chemotherapy agents conjugated to antitumour monoclonal antibodies may be processed differently so that they bypass certain mechanisms of drug resistance. The penultimate application of monoclonal antibodies in cancer therapy is to combine various monoclonal antibodies and immunoconjugates for selective combination therapy based on known antigenic tumour cell determinants and the status of the host immune system.

scholarly journals Cellular Automaton Simulation of Tumour Growth – Equivocal Relationships between Simulation Parameters and Morphologic Pattern Features

1998 ◽  
Vol 17 (2) ◽  
pp. 71-82 ◽  
Author(s):  
Josef Smolle
Keyword(s):  
Cell Adhesion ◽  
Cellular Automaton ◽  
Cell Motility ◽  
Tumour Cell ◽  
Growth Control ◽  
Tumour Cells ◽  
Reliable Estimate ◽  
Morphometric Features ◽  
Simulation Parameter ◽  
Simulation Parameters

Objective:To develop an interpretation procedure which estimates simulation parameters (tumour cell motility, tumour cell adhesion, autocrine and paracrine growth control, stroma destruction) of simulated patterns solely based on morphometric features of the morphologic pattern.Methods:A cellular automaton computer simulation program was developed which produces morphologic patterns by growth of a seed of tumour cells. At the beginning of each simulation run certain simulation parameters are assigned to the tumour cells. After the run has been completed, the resulting pattern is evaluated by a set of morphometric features. Simulation parameters and resulting morphometric features of 27,800 simulations were stored in a database and were used for the evaluation of potential relationships.Results:Correlation analysis showed highly significant correlations between morphometric features on the one hand and the preset simulation parameters (tumour cell motility, tumour cell adhesion, autocrine and paracrine growth control, stroma destruction) on the other. Correlation coefficients, however, varied from 0.72 to 0.99. When only one simulation parameter varied while all others were kept constant, morphometric features yielded a highly reliable estimate of the particular simulation parameter. When variability was extended to 4 simulation parameters, morphometric features were less effective in estimating the setting of the parameters. Though in all patterns tested several possible simulation parameter constellations could be ruled out, morphometric features were usually compatible with more than one set of simulation parameters thus preventing a straightforward interpretation.Conclusions:Though simulation parameters significantly and reproducibly influence the resulting morphologic pattern as characterized by morphometric features, estimates of the simulation parameters based on morphometric features yield equivocal results.

Circulating tumour cells and lung microvascular tumour cell retention in patients with metastatic breast and cervical cancer

2015 ◽  
Vol 356 (2) ◽  
pp. 872-879 ◽  
Author(s):  
Dieter J.E. Peeters ◽  
Anja Brouwer ◽  
Gert G. Van den Eynden ◽  
Annemie Rutten ◽  
Wendy Onstenk ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Tumour Cell ◽  
Metastatic Breast ◽  
Tumour Cells ◽  
Circulating Tumour Cells ◽  
Cell Retention ◽  
Breast And Cervical Cancer

scholarly journals The antimicrobial peptide Defensin cooperates with Tumour Necrosis Factor to drive tumour cell death in Drosophila

2019 ◽  
Author(s):  
Jean-Philippe Parvy ◽  
Yachuan Yu ◽  
Anna Dostalova ◽  
Shu Kondo ◽  
Alina Kurjan ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumour Necrosis Factor ◽  
Tumour Cell ◽  
Tumour Necrosis ◽  
Tumour Progression ◽  
Tumour Cells ◽  
Tumour Regression ◽  
Necrosis Factor

AbstractAntimicrobial peptides (AMPs) are small cationic molecules best known as mediators of the innate defence against microbial infection. While in vitro and ex vivo evidence suggest AMPs’ capacity to kill cancer cells, in vivo demonstration of an anti-tumour role of endogenous AMPs is lacking. Using a Drosophila model of tumourigenesis, we demonstrate a role for the AMP Defensin in the control of tumour progression. Our results reveal that Tumour Necrosis Factor mediates exposure of phosphatidylserine (PS), which makes tumour cells selectively sensitive to the action of Defensin remotely secreted from tracheal and fat tissues. Defensin binds tumour cells in PS-enriched areas, provoking cell death and tumour regression. Altogether, our results provide the first in vivo demonstration for a role of an endogenous AMP as an anti-cancer agent, as well as a mechanism that explains tumour cell sensitivity to the action of AMPs.

scholarly journals Optical Cellular Micromotion: A New Paradigm to Measure Tumour Cells Invasion in 3D Tumour Environments

2021 ◽  
Author(s):  
Zhaobin Guo ◽  
Chih-Tsung Yang ◽  
Chia-Chi Chien ◽  
Luke Selth ◽  
Pierre Bagnaninchi ◽  
...  
Keyword(s):  
Single Cell ◽  
Cell Invasion ◽  
Tumour Cell ◽  
Single Cells ◽  
Three Dimensional ◽  
Tumour Cells ◽  
Digital Holographic Microscopy ◽  
New Paradigm ◽  
Cell Invasiveness

Measuring tumour cell invasiveness through three-dimensional (3D) tissues, particularly at the single cell level, can provide important mechanistic understanding and assist in identifying therapeutic targets of tumour invasion. However, current experimental approaches, including standard in vitro invasion assays, have limited physiological relevance and offer insufficient insight about the vast heterogeneity in tumour cell migration through tissues. To address these issues, here we report on the concept of optical cellular micromotion, where digital holographic microscopy (DHM) is used to map the optical thickness fluctuations at sub-micron scale within single cells. These fluctuations are driven by the dynamic movement of subcellular structures including the cytoskeleton and inherently associated with the biological processes involved in cell invasion within tissues. We experimentally demonstrate that the optical cellular micromotion correlates with tumour cells motility and invasiveness both at the population and single cell levels. In addition, the optical cellular micromotion significantly reduced upon treatment with migrastatic drugs that inhibit tumour cell invasion. These results demonstrate that micromotion measurements can rapidly and non-invasively determine the invasive behaviour of single tumour cells within tissues, yielding a new and powerful tool to assess the efficacy of approaches targeting tumour cell invasiveness.

Spatiotemporal Quantification of Metastatic Tumour Cell Growth and Distribution in Lymph Nodes by Whole-Mount Tissue 3D Imaging

2021 ◽  
Author(s):  
Zhi-Gang Zhang ◽  
Jun Li ◽  
Chun-Jie Xu ◽  
Guang-Ang Tian ◽  
Qing Li ◽  
...  
Keyword(s):  
Cell Growth ◽  
Lymph Nodes ◽  
Tumour Cell ◽  
3D Imaging ◽  
Lymphatic Vessels ◽  
Tumour Cells ◽  
Diagnostic Methods ◽  
Metastatic Tumour ◽  
Whole Mount ◽  
Tumour Cell Growth

Abstract Lymph nodes (LNs) are a common site of metastasis in many solid cancers. Tumour cells can migrate to LNs for further metastatic colonization of distant organs, indicating poor prognosis and requiring different clinical interventions. The current histopathological diagnostic methods used for the detection of clinical lymph node metastasis (LNM) still have some limitations, such as incomplete observation. To obtain a complete picture of tumour-metastasized LNs at spatial and temporal scales, we used 3D imaging of solvent-cleared organs (uDISCO) and 3D rapid immunostaining. MC38 cells tagged with EGFP were injected into the left footpad of C57BL/6 mice. Draining lymph nodes (DLNs) obtained from these mice were cleared using uDISCO. Metastatic colorectal cancer (CRC) cells in various regions of DLNs from mice at different time points were quantified using whole-mount tissue 3D imaging. The results revealed several stages of tumour cell growth and distribution in LNs: 1) invasion of lymphatic vessels (LVs) and blood vessels (BVs); 2) dispersion outside LVs and BVs for proliferation and expansion; and 3) re-entry into BVs and efferent lymphatic vessels (ELVs) for further distant metastasis. Moreover, these data demonstrated that mouse fibroblast cells (MFCs) could not only promote the LNM of tumour cells but could also metastasize to LNs together with tumour cells, thus providing a “soil” for tumour cell colonization. In conclusion, whole-mount tissue 3D imaging and spatiotemporal analysis of LNM may together constitute an auxiliary method to improve the accuracy of clinical LNM detection in the future.

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