Cancer: More of polygenic disease and less of multiple mutations? A quantitative viewpoint.
(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:
https://lup.lub.lu.se/record/1687945
- author
- Bredberg, Anders LU
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Cancer
- volume
- Okt
- pages
- 440 - 445
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000286433300005
- pmid:20862743
- scopus:79251529557
- pmid:20862743
- 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
- 2016-04-04 08:56:24
- date last changed
- 2022-01-29 07:55:48
@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 Inc.}}, 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}}, doi = {{10.1002/cncr.25440}}, volume = {{Okt}}, year = {{2011}}, }