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Cancer: More of polygenic disease and less of multiple mutations? A quantitative viewpoint.

Bredberg, Anders LU (2011) In Cancer Okt. p.440-445
Abstract
The focus of cancer research is on cancer-specific mutations, with most clinical trials involving targeted drugs. Huge numbers of DNA lesions and tumor resistance events, in each of the >10(13) cells of a human individual, form a striking contrast to the low, and also very narrow, cancer incidence window (10(-1)-10(0)). A detailed consideration of these quantitative observations seems to question the present paradigm, while suggesting that a systemic regulatory network mechanism is a stronger determinant for overt cancer disease, as compared with cancer-specific gene products. If we shall ever achieve major improvements in survival, we must gain understanding of this systemic network, rather than targeting therapy to a limited set of... (More)
The focus of cancer research is on cancer-specific mutations, with most clinical trials involving targeted drugs. Huge numbers of DNA lesions and tumor resistance events, in each of the >10(13) cells of a human individual, form a striking contrast to the low, and also very narrow, cancer incidence window (10(-1)-10(0)). A detailed consideration of these quantitative observations seems to question the present paradigm, while suggesting that a systemic regulatory network mechanism is a stronger determinant for overt cancer disease, as compared with cancer-specific gene products. If we shall ever achieve major improvements in survival, we must gain understanding of this systemic network, rather than targeting therapy to a limited set of molecules or mutations. This may give us new opportunities for development of highly potent therapeutic tools. Cancer 2010. © 2010 American Cancer Society. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cancer
volume
Okt
pages
440 - 445
publisher
John Wiley & Sons
external identifiers
  • wos:000286433300005
  • pmid:20862743
  • scopus:79251529557
ISSN
1097-0142
DOI
10.1002/cncr.25440
language
English
LU publication?
yes
id
45168b5d-858c-4e6f-a82a-f21f7f07475d (old id 1687945)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20862743?dopt=Abstract
date added to LUP
2010-10-06 08:27:09
date last changed
2017-07-23 04:55:33
@article{45168b5d-858c-4e6f-a82a-f21f7f07475d,
  abstract     = {The focus of cancer research is on cancer-specific mutations, with most clinical trials involving targeted drugs. Huge numbers of DNA lesions and tumor resistance events, in each of the >10(13) cells of a human individual, form a striking contrast to the low, and also very narrow, cancer incidence window (10(-1)-10(0)). A detailed consideration of these quantitative observations seems to question the present paradigm, while suggesting that a systemic regulatory network mechanism is a stronger determinant for overt cancer disease, as compared with cancer-specific gene products. If we shall ever achieve major improvements in survival, we must gain understanding of this systemic network, rather than targeting therapy to a limited set of molecules or mutations. This may give us new opportunities for development of highly potent therapeutic tools. Cancer 2010. © 2010 American Cancer Society.},
  author       = {Bredberg, Anders},
  issn         = {1097-0142},
  language     = {eng},
  pages        = {440--445},
  publisher    = {John Wiley & Sons},
  series       = {Cancer},
  title        = {Cancer: More of polygenic disease and less of multiple mutations? A quantitative viewpoint.},
  url          = {http://dx.doi.org/10.1002/cncr.25440},
  volume       = {Okt},
  year         = {2011},
}