Assignment of a locus for mouse lung tumor susceptibility to proximal Chromosome 19

1994 ◽  
Vol 5 (12) ◽  
pp. 749-755 ◽  
Author(s):  
T. R. Devereux ◽  
R. W. Wiseman ◽  
N. Kaplan ◽  
S. Garren ◽  
J. F. Foley ◽  
...  
Keyword(s):  
Lung Tumor ◽  
Mouse Lung ◽  
Chromosome 19 ◽  
Tumor Susceptibility ◽  
Mouse Lung Tumor

scholarly journals Identification of Las2, a Major Modifier Gene Affecting the Pas1 Mouse Lung Tumor Susceptibility Locus

2009 ◽  
Vol 69 (15) ◽  
pp. 6290-6298 ◽  
Author(s):  
Peng-Yuan Liu ◽  
Haris Vikis ◽  
Michael James ◽  
Yan Lu ◽  
Dao-Long Wang ◽  
...  
Keyword(s):  
Lung Tumor ◽  
Modifier Gene ◽  
Susceptibility Locus ◽  
Mouse Lung ◽  
Tumor Susceptibility ◽  
Mouse Lung Tumor

scholarly journals The second intron of the K-ras gene contains regulatory elements associated with mouse lung tumor susceptibility.

1994 ◽  
Vol 91 (4) ◽  
pp. 1589-1593 ◽  
Author(s):  
B. Chen ◽  
L. Johanson ◽  
J. S. Wiest ◽  
M. W. Anderson ◽  
M. You
Keyword(s):  
Lung Tumor ◽  
Regulatory Elements ◽  
Mouse Lung ◽  
Ras Gene ◽  
Tumor Susceptibility ◽  
Mouse Lung Tumor

Effects of Adrenalectomy and Corticosterone Administration on Mouse Lung Tumor Susceptibility and Histogenesis

1988 ◽  
Vol 80 (5) ◽  
pp. 365-369 ◽  
Author(s):  
K. A. Droms ◽  
C. A. Fernandez ◽  
L. G. Thaete ◽  
A. M. Malkinson
Keyword(s):  
Lung Tumor ◽  
Mouse Lung ◽  
Tumor Susceptibility ◽  
Mouse Lung Tumor

Activities of four glycolytic enzymes (HK, PFK, PK, and LDH) and isozymic pattern of LDH in mouse lung tumor induced by urethan

1979 ◽  
Vol 95 (3) ◽  
pp. 287-289 ◽  
Author(s):  
P. R�dy ◽  
I. Arany ◽  
F. Boj�n ◽  
P. Kertai
Keyword(s):  
Lung Tumor ◽  
Glycolytic Enzymes ◽  
Mouse Lung ◽  
Isozymic Pattern ◽  
Mouse Lung Tumor

Failure of the cultivated mushroom (Agaricus bisporus) to induce tumors in the A/J mouse lung tumor model

1997 ◽  
Vol 120 (1) ◽  
pp. 79-85 ◽  
Author(s):  
Kirsten Pilegaard ◽  
Eva Kristiansen ◽  
Otto A Meyer ◽  
Jørn Gry
Keyword(s):  
Agaricus Bisporus ◽  
Lung Tumor ◽  
Tumor Model ◽  
Mouse Lung ◽  
Cultivated Mushroom ◽  
Mouse Lung Tumor

scholarly journals No Involvement of Lysophosphatidic Acid Receptor-3 in Cell Migration of Mouse Lung Tumor Cells Stimulated by 12-O-Tetradecanoylphorbol-13-acetate

2011 ◽  
Vol 24 (3) ◽  
pp. 183-186 ◽  
Author(s):  
Mai Okumura ◽  
Kohei Kato ◽  
Rie Fukui ◽  
Nobuyuki Fukushima ◽  
Toshifumi Tsujiuchi
Keyword(s):  
Cell Migration ◽  
Tumor Cells ◽  
Lysophosphatidic Acid ◽  
Lung Tumor ◽  
Mouse Lung ◽  
Acid Receptor ◽  
Lysophosphatidic Acid Receptor ◽  
Mouse Lung Tumor

scholarly journals A Mouse Lung Tumor Model of Tobacco Smoke Carcinogenesis

2002 ◽  
Vol 68 (2) ◽  
pp. 322-330 ◽  
Author(s):  
H. Witschi
Keyword(s):  
Tobacco Smoke ◽  
Lung Tumor ◽  
Tumor Model ◽  
Mouse Lung ◽  
Mouse Lung Tumor

scholarly journals Chromatin remodeling by the histone methyltransferase EZH2 drives lung pre-malignancy and is a target for cancer prevention

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Carmen S. Tellez ◽  
Maria A. Picchi ◽  
Daniel Juri ◽  
Kieu Do ◽  
Dhimant H. Desai ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cancer Prevention ◽  
Histone Modifications ◽  
Lung Tumor ◽  
Critical Role ◽  
Tumor Model ◽  
Mouse Lung ◽  
Lung Carcinogenesis ◽  
Tobacco Carcinogen ◽  
Mouse Lung Tumor

Abstract Background Trimethylation of lysine 27 and dimethylation of lysine 9 of histone-H3 catalyzed by the histone methyltransferases EZH2 and G9a impede gene transcription in cancer. Our human bronchial epithelial (HBEC) pre-malignancy model studied the role of these histone modifications in transformation. Tobacco carcinogen transformed HBEC lines were characterized for cytosine DNA methylation, transcriptome reprogramming, and the effect of inhibiting EZH2 and G9a on the transformed phenotype. The effects of targeting EZH2 and G9a on lung cancer prevention was assessed in the A/J mouse lung tumor model. Results Carcinogen exposure induced transformation and DNA methylation of 12–96 genes in the four HBEC transformed (T) lines that was perpetuated in malignant tumors. In contrast, 506 unmethylated genes showed reduced expression in one or more HBECTs with many becoming methylated in tumors. ChIP-on-chip for HBEC2T identified 327 and 143 genes enriched for H3K27me3 and H3K9me2. Treatment of HBEC2T and HBEC13T with DZNep, a lysine methyltransferase inhibitor depleted EZH2, reversed transformation, and induced transcriptional reprogramming. The EZH2 small molecule inhibitor EPZ6438 also affected transformation and expression in HBEC2T, while a G9a inhibitor, UNC0642 was ineffective. Genetic knock down of EZH2 dramatically reduced carcinogen-induced transformation of HBEC2. Only DZNep treatment prevented progression of hyperplasia to adenomas in the NNK mouse lung tumor model through reducing EZH2 and affecting the expression of genes regulating cell growth and invasion. Conclusion These studies demonstrate a critical role for EZH2 catalyzed histone modifications for premalignancy and its potential as a target for chemoprevention of lung carcinogenesis.

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