Analysis of the Par2 modifier of pulmonary adenoma formation in mice

Min Wang; Yian Wang; Ming You; Theodora R. Devereux

doi:10.1080/01902140490495598

Analysis of the Par2 modifier of pulmonary adenoma formation in mice

Min Wang, Yian Wang, Ming You, Theodora R. Devereux

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

1 Scopus citations

Abstract

Inbred strains of mice show various susceptibilities to spontaneous and chemical-induced lung tumorigenesis. Genetic analyses have revealed that lung tumor susceptibilities of inbred mouse strains are governed by quantitative trait loci (QTLs) located on multiple chromosomes. A major lung tumor resistance QTL, designated pulmonary adenoma resistance 2 (Par2), was mapped to the mouse chromosome 18 independently by several groups and accounted for up to 60% phenotype variance between the susceptible A/J and more resistant BALB/c strains. The authors recently conducted studies to positionally clone the Par2 gene. This review summarizes the effort and progress towards the identification of Par2 candidates.

Original language	English (US)
Pages (from-to)	193-204
Number of pages	12
Journal	Experimental Lung Research
Volume	31
Issue number	2
DOIs	https://doi.org/10.1080/01902140490495598
State	Published - Mar 2005

Keywords

Congenic mice
DNA polymerase iota
Linkage mapping
Mouse lung tumor susceptibility
Par2

ASJC Scopus subject areas

Molecular Biology
Pulmonary and Respiratory Medicine
Clinical Biochemistry

Divisions

Medical Oncology

Access to Document

10.1080/01902140490495598

Cite this

@article{620c7f13fe9a469dad75973c8b9ddbda,

title = "Analysis of the Par2 modifier of pulmonary adenoma formation in mice",

abstract = "Inbred strains of mice show various susceptibilities to spontaneous and chemical-induced lung tumorigenesis. Genetic analyses have revealed that lung tumor susceptibilities of inbred mouse strains are governed by quantitative trait loci (QTLs) located on multiple chromosomes. A major lung tumor resistance QTL, designated pulmonary adenoma resistance 2 (Par2), was mapped to the mouse chromosome 18 independently by several groups and accounted for up to 60\% phenotype variance between the susceptible A/J and more resistant BALB/c strains. The authors recently conducted studies to positionally clone the Par2 gene. This review summarizes the effort and progress towards the identification of Par2 candidates.",

keywords = "Congenic mice, DNA polymerase iota, Linkage mapping, Mouse lung tumor susceptibility, Par2",

author = "Min Wang and Yian Wang and Ming You and Devereux, \{Theodora R.\}",

note = "Funding Information: Received 8 January 2004; accepted 9 February 2004. This work has been supported in part by NIH grants R01CA099147 and R01CA58554. The authors thank Cynthia Kaye for her editing of this manuscript. Address correspondence to Theodora R. Devereux, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, Research Triangle park, NC 27709, USA. E-mail: [email protected]",

year = "2005",

month = mar,

doi = "10.1080/01902140490495598",

language = "English (US)",

volume = "31",

pages = "193--204",

journal = "Experimental Lung Research",

issn = "0190-2148",

publisher = "Taylor and Francis Ltd.",

number = "2",

}

TY - JOUR

T1 - Analysis of the Par2 modifier of pulmonary adenoma formation in mice

AU - Wang, Min

AU - Wang, Yian

AU - You, Ming

AU - Devereux, Theodora R.

N1 - Funding Information: Received 8 January 2004; accepted 9 February 2004. This work has been supported in part by NIH grants R01CA099147 and R01CA58554. The authors thank Cynthia Kaye for her editing of this manuscript. Address correspondence to Theodora R. Devereux, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, Research Triangle park, NC 27709, USA. E-mail: [email protected]

PY - 2005/3

Y1 - 2005/3

N2 - Inbred strains of mice show various susceptibilities to spontaneous and chemical-induced lung tumorigenesis. Genetic analyses have revealed that lung tumor susceptibilities of inbred mouse strains are governed by quantitative trait loci (QTLs) located on multiple chromosomes. A major lung tumor resistance QTL, designated pulmonary adenoma resistance 2 (Par2), was mapped to the mouse chromosome 18 independently by several groups and accounted for up to 60% phenotype variance between the susceptible A/J and more resistant BALB/c strains. The authors recently conducted studies to positionally clone the Par2 gene. This review summarizes the effort and progress towards the identification of Par2 candidates.

AB - Inbred strains of mice show various susceptibilities to spontaneous and chemical-induced lung tumorigenesis. Genetic analyses have revealed that lung tumor susceptibilities of inbred mouse strains are governed by quantitative trait loci (QTLs) located on multiple chromosomes. A major lung tumor resistance QTL, designated pulmonary adenoma resistance 2 (Par2), was mapped to the mouse chromosome 18 independently by several groups and accounted for up to 60% phenotype variance between the susceptible A/J and more resistant BALB/c strains. The authors recently conducted studies to positionally clone the Par2 gene. This review summarizes the effort and progress towards the identification of Par2 candidates.

KW - Congenic mice

KW - DNA polymerase iota

KW - Linkage mapping

KW - Mouse lung tumor susceptibility

KW - Par2

UR - https://www.scopus.com/pages/publications/14644431814

UR - https://www.scopus.com/inward/citedby.url?scp=14644431814&partnerID=8YFLogxK

U2 - 10.1080/01902140490495598

DO - 10.1080/01902140490495598

M3 - Article

C2 - 15828125

AN - SCOPUS:14644431814

SN - 0190-2148

VL - 31

SP - 193

EP - 204

JO - Experimental Lung Research

JF - Experimental Lung Research

IS - 2

ER -

Analysis of the Par2 modifier of pulmonary adenoma formation in mice

Abstract

Keywords

ASJC Scopus subject areas

Divisions

Access to Document

Other files and links

Fingerprint

Cite this