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Does ionizing radiation stimulate cancer invasion and metastasis?

Indira Madani UGent, Wilfried De Neve UGent and Marc Mareel UGent (2008) BULLETIN DU CANCER. 95(3). p.292-300
abstract
Radiotherapy (RT) is a form of local treatment used mainly for malignant tumors. Such tumors originate from mutated stein cells, During their development they do attract a variety of host cells, coined tumor-associated host cells. Malignant tumors are characterized by uncontrolled growth,. invasion and metastasis'. the latter being the major cause of death of patients, even when their primary tumor is under control. RT inhibits growth. There are, however. clinical data suggesting that, under some circumstances, it may stimulate metastasis. DNA is a target of ionizing radiation (IR), though not the only one. IR produces cascades of growth factors and chemokines; it activates molecules initiating multiple signaling pathways that modulate several cellular Junctions. We consider cancer as a network of ecosystems, including at least the founder primary tumor, the site of metastasis and the hone marrow. As these ecosystems are in continuous communication, it is not surprising that R T of the primary tumor influences metastasis. Indeed, experiments with cells in culture and with animal tumors have shown that IR stimulates invasion and metastasis and activates pro-invasive and prometastatic cellular activities through upregulation of key molecules. At certain doses and within certain time frames, IR enhances the activities of the tumor-associated host cells that support invasion and metastasis, namely: endothelial cells building new vessels; leucocytes and macrophages causing inflammation; myofibroblasts initiating desmoplasia; osteoblasts and osteoclasts establishing hone metastasis; nerve cells producing efferent growth- and invasion-promoting molecules. Techniques such as spatially fractioned radiotherapy and hadron therapy may have different effects on metastasis. Taking into consideration the dose- and time-dependency of the IR-induced tumor-associated host cell reactions, these techniques, as well as the conventional ones, should he combined with repetitive biological imaging, reevaluation of planning and eventual replanning during the course of the treatment.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
metastasis, radiotherapy, tumor-associated host cells, pro-invasive signaling, tumor ecosystems, SQUAMOUS-CELL CARCINOMA, INTENSITY-MODULATED RADIOTHERAPY, MATRIX-METALLOPROTEINASE INHIBITOR, ENDOTHELIAL GROWTH-FACTOR, NECK-CANCER, IN-VITRO, NASOPHARYNGEAL CARCINOMA, DISTANT METASTASES, RANDOMIZED-TRIAL, ADVANCED HEAD
journal title
BULLETIN DU CANCER
Bull. Cancer
volume
95
issue
3
pages
292 - 300
Web of Science type
Review
Web of Science id
000254784800012
JCR category
ONCOLOGY
JCR impact factor
1.094 (2008)
JCR rank
131/141 (2008)
JCR quartile
4 (2008)
ISSN
0007-4551
language
English
UGent publication?
yes
classification
A1
id
439656
handle
http://hdl.handle.net/1854/LU-439656
date created
2008-11-13 05:55:00
date last changed
2014-02-21 11:08:03
@article{439656,
  abstract     = {Radiotherapy (RT) is a form of local treatment used mainly for malignant tumors. Such tumors originate from mutated stein cells, During their development they do attract a variety of host cells, coined tumor-associated host cells. Malignant tumors are characterized by uncontrolled growth,. invasion and metastasis'. the latter being the major cause of death of patients, even when their primary tumor is under control. RT inhibits growth. There are, however. clinical data suggesting that, under some circumstances, it may stimulate metastasis. DNA is a target of ionizing radiation (IR), though not the only one. IR produces cascades of growth factors and chemokines; it activates molecules initiating multiple signaling pathways that modulate several cellular Junctions. We consider cancer as a network of ecosystems, including at least the founder primary tumor, the site of metastasis and the hone marrow. As these ecosystems are in continuous communication, it is not surprising that R T of the primary tumor influences metastasis. Indeed, experiments with cells in culture and with animal tumors have shown that IR stimulates invasion and metastasis and activates pro-invasive and prometastatic cellular activities through upregulation of key molecules. At certain doses and within certain time frames, IR enhances the activities of the tumor-associated host cells that support invasion and metastasis, namely: endothelial cells building new vessels; leucocytes and macrophages causing inflammation; myofibroblasts initiating desmoplasia; osteoblasts and osteoclasts establishing hone metastasis; nerve cells producing efferent growth- and invasion-promoting molecules. Techniques such as spatially fractioned radiotherapy and hadron therapy may have different effects on metastasis. Taking into consideration the dose- and time-dependency of the IR-induced tumor-associated host cell reactions, these techniques, as well as the conventional ones, should he combined with repetitive biological imaging, reevaluation of planning and eventual replanning during the course of the treatment.},
  author       = {Madani, Indira and De Neve, Wilfried and Mareel, Marc},
  issn         = {0007-4551},
  journal      = {BULLETIN DU CANCER},
  keyword      = {metastasis,radiotherapy,tumor-associated host cells,pro-invasive signaling,tumor ecosystems,SQUAMOUS-CELL CARCINOMA,INTENSITY-MODULATED RADIOTHERAPY,MATRIX-METALLOPROTEINASE INHIBITOR,ENDOTHELIAL GROWTH-FACTOR,NECK-CANCER,IN-VITRO,NASOPHARYNGEAL CARCINOMA,DISTANT METASTASES,RANDOMIZED-TRIAL,ADVANCED HEAD},
  language     = {eng},
  number       = {3},
  pages        = {292--300},
  title        = {Does ionizing radiation stimulate cancer invasion and metastasis?},
  volume       = {95},
  year         = {2008},
}

Chicago
Madani, Indira, Wilfried De Neve, and Marcus Mareel. 2008. “Does Ionizing Radiation Stimulate Cancer Invasion and Metastasis?” Bulletin Du Cancer 95 (3): 292–300.
APA
Madani, I., De Neve, W., & Mareel, M. (2008). Does ionizing radiation stimulate cancer invasion and metastasis? BULLETIN DU CANCER, 95(3), 292–300.
Vancouver
1.
Madani I, De Neve W, Mareel M. Does ionizing radiation stimulate cancer invasion and metastasis? BULLETIN DU CANCER. 2008;95(3):292–300.
MLA
Madani, Indira, Wilfried De Neve, and Marcus Mareel. “Does Ionizing Radiation Stimulate Cancer Invasion and Metastasis?” BULLETIN DU CANCER 95.3 (2008): 292–300. Print.