Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis

Charles E. Patek; Mark J. Arends; William A.H. Wallace; Feijun Luo; Suzanne Hagan; David G. Brownstein; Lorraine Rose; Paul S. Devenney; Walter Kolch; Owen J. Sansom

doi:10.1016/j.yexcr.2007.11.004

Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis

Charles E. Patek, Mark J. Arends, William A.H. Wallace, Feijun Luo, Suzanne Hagan, David G. Brownstein, Lorraine Rose, Paul S. Devenney, Walter Kolch, Owen J. Sansom

Vision Sciences

Research output: Contribution to journal › Article › peer-review

28 Citations (Scopus)

Abstract

To examine the roles of endogenous K-ras 4A and K-ras 4B splice variants in tumorigenesis, murine lung carcinogenesis was induced by N-methyl-N-nitrosourea (MNU), which causes a K-ras mutation (G12D) that jointly affects both isoforms. Compared with age-matched K-rastm¿4A/- mice (where tumours can express mutationally activated K-ras 4B only), tumour number and size were significantly higher in K-ras+/- mice (where tumours can also express mutationally activated K-ras 4A), and significantly lower in K-rastm¿4A/tm¿4A mice (where tumours can express both wild-type and activated K-ras 4B).

Original language	English
Pages (from-to)	1105-1114
Number of pages	10
Journal	Experimental Cell Research
Volume	314
Issue number	5
DOIs	https://doi.org/10.1016/j.yexcr.2007.11.004
Publication status	Published - 1 Mar 2008

Keywords

K-ras 4B
lung cancer
K-ras 4A
tumorigenesis

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Documents and Links

10.1016/j.yexcr.2007.11.004

Cite this

@article{3b32b3d348a64b5da9a9e8bba46b16d0,

title = "Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis",

abstract = "To examine the roles of endogenous K-ras 4A and K-ras 4B splice variants in tumorigenesis, murine lung carcinogenesis was induced by N-methyl-N-nitrosourea (MNU), which causes a K-ras mutation (G12D) that jointly affects both isoforms. Compared with age-matched K-rastm¿4A/- mice (where tumours can express mutationally activated K-ras 4B only), tumour number and size were significantly higher in K-ras+/- mice (where tumours can also express mutationally activated K-ras 4A), and significantly lower in K-rastm¿4A/tm¿4A mice (where tumours can express both wild-type and activated K-ras 4B).",

keywords = "K-ras 4B, lung cancer, K-ras 4A, tumorigenesis",

author = "Patek, {Charles E.} and Arends, {Mark J.} and Wallace, {William A.H.} and Feijun Luo and Suzanne Hagan and Brownstein, {David G.} and Lorraine Rose and Devenney, {Paul S.} and Walter Kolch and Sansom, {Owen J.}",

note = "<p>Originally published in: Experimental Cell Research (2008), 314 (5), pp.1105-1114</p>",

year = "2008",

month = mar,

day = "1",

doi = "10.1016/j.yexcr.2007.11.004",

language = "English",

volume = "314",

pages = "1105--1114",

journal = "Experimental Cell Research",

issn = "1090-2422",

publisher = "Elsevier Inc.",

number = "5",

}

TY - JOUR

T1 - Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis

AU - Patek, Charles E.

AU - Arends, Mark J.

AU - Wallace, William A.H.

AU - Luo, Feijun

AU - Hagan, Suzanne

AU - Brownstein, David G.

AU - Rose, Lorraine

AU - Devenney, Paul S.

AU - Kolch, Walter

AU - Sansom, Owen J.

N1 - <p>Originally published in: Experimental Cell Research (2008), 314 (5), pp.1105-1114</p>

PY - 2008/3/1

Y1 - 2008/3/1

N2 - To examine the roles of endogenous K-ras 4A and K-ras 4B splice variants in tumorigenesis, murine lung carcinogenesis was induced by N-methyl-N-nitrosourea (MNU), which causes a K-ras mutation (G12D) that jointly affects both isoforms. Compared with age-matched K-rastm¿4A/- mice (where tumours can express mutationally activated K-ras 4B only), tumour number and size were significantly higher in K-ras+/- mice (where tumours can also express mutationally activated K-ras 4A), and significantly lower in K-rastm¿4A/tm¿4A mice (where tumours can express both wild-type and activated K-ras 4B).

AB - To examine the roles of endogenous K-ras 4A and K-ras 4B splice variants in tumorigenesis, murine lung carcinogenesis was induced by N-methyl-N-nitrosourea (MNU), which causes a K-ras mutation (G12D) that jointly affects both isoforms. Compared with age-matched K-rastm¿4A/- mice (where tumours can express mutationally activated K-ras 4B only), tumour number and size were significantly higher in K-ras+/- mice (where tumours can also express mutationally activated K-ras 4A), and significantly lower in K-rastm¿4A/tm¿4A mice (where tumours can express both wild-type and activated K-ras 4B).

KW - K-ras 4B

KW - lung cancer

KW - K-ras 4A

KW - tumorigenesis

U2 - 10.1016/j.yexcr.2007.11.004

DO - 10.1016/j.yexcr.2007.11.004

M3 - Article

SN - 1090-2422

VL - 314

SP - 1105

EP - 1114

JO - Experimental Cell Research

JF - Experimental Cell Research

IS - 5

ER -

Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis

Abstract

Keywords

UN SDGs

Documents and Links

Fingerprint

Cite this