High K-ras mutation rates in goblet-cell-type adenocarcinomas of the lungs

Tsuchiya, Eiju; Furuta, Reiko; Wada, Naomi; Nakagawa, Ken; Ishikawa, Yuichi; Kawabuchi, Beniyo; Nakamura, Yusuke; Sugano, Haruo

doi:10.1007/bf01197773

Cited by 34 publications

(25 citation statements)

References 13 publications

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“…In contrast, K-ras status was associated with maspin expression in lung adenocarcinoma. It has been reported that mucinous bronchioloalveolar carcinoma (BAC) preferentially harbors a K-ras mutation (Tsuchiya et al, 1995;Marchetti et al, 1996). Mucinous BAC is composed of neoplastic cells resembling goblet cells, which are present in the proximal airway tracts in the normal tissue.…”

Section: Discussionmentioning

confidence: 99%

Maspin expression in normal lung and non-small-cell lung cancers: cellular property-associated expression under the control of promoter DNA methylation

2004

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Maspin has been demonstrated to be a suppressor of invasion and cell motility in vitro, whereas in vivo analyses have reported that increased expression of maspin is associated with malignant behavior. The present study examined maspin expression in normal lung and nonsmall-cell lung cancers. Only proximal airway cells in the normal lung expressed maspin, and the expression was associated with decreased methylation. This association was also observed in non-small-cell lung cancers, but the expression was quite different among histologic subtypes; 20 of 21 squamous cell carcinomas showed intense, uniform expression, whereas the expression status varied among adenocarcinomas. Of the 119 adenocarcinomas, 60 were negative, 23 positive and 36 showed a heterogeneous expression pattern. The expression was inversely correlated with markers of peripheral airway cells. Taken together, the results suggest that maspin may be expressed in association with the proximal airway cell type. It is of note that the heterogeneous expression pattern of maspin is quite distinctive, showing geographic positivity in the individual tumors. Separate analysis of methylation status in positive and negative portions of individual tumors provided an instance of intratumor diversity associated with promoter DNA methylation.

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Section: Discussionmentioning

confidence: 99%

Maspin expression in normal lung and non-small-cell lung cancers: cellular property-associated expression under the control of promoter DNA methylation

2004

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“…KRAS mutations have been shown to be significantly associated with a shortened survival in surgically treated patients . The KRAS mutations occur almost exclusively in adenocarcinoma, showing a strong association with a cytologic subtype of adenocarcnima, goblet cell type (Tsuchiya et al, 1995). The reason for the histologic type-specific involvement of RAS mutations in adenocarcinoma has not yet been elucidated.…”

Section: The Ras Gene Familymentioning

confidence: 99%

Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer

2002

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“…Since NSCLC, including pulmonary adenocarcinoma, arises from bronchopulmonary epithelium (Tsuchiya et al, 1995;Cooper et al, 1997), we targeted pulmonary epithelial cells by administering recombinant AdCre [adenoCrevirus] of sucient high titer (up to 4610 9 pfu/ml) intratracheally. In order to suppress perioperative infections, mice were treated with cotrimoxazole 1 week before and after AdCre administration.…”

Section: Introductionmentioning

confidence: 99%

Mouse model for lung tumorigenesis through Cre/lox controlled sporadic activation of the K-Ras oncogene

et al. 2001

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The onset of human lung cancer occurs through sequential mutations in oncogenes and tumor suppressor genes. Mutations in K-Ras play a prominent role in human non-small cell lung cancer. We have developed a mouse lung tumor model in which K-Ras can be sporadically activated through Cre-lox mediated somatic recombination. Adenoviral mediated delivery of Cre recombinase in lung epithelial cells gave rise to rapid onset of tumorigenesis, yielding pulmonary adenocarcinomas with 100% incidence after a short latency. The lung tumor lesions shared many features with human non-small cell lung cancer. Our data show that sporadic expression of the K-Ras oncogene is sucient to elicit lung tumorigenesis. Therefore this model has many advantages over conventional transgenic models used thus far. Oncogene (2001) 20, 6551 ± 6558.

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High K-ras mutation rates in goblet-cell-type adenocarcinomas of the lungs

Cited by 34 publications

References 13 publications

Maspin expression in normal lung and non-small-cell lung cancers: cellular property-associated expression under the control of promoter DNA methylation

Maspin expression in normal lung and non-small-cell lung cancers: cellular property-associated expression under the control of promoter DNA methylation

Genetic alterations of multiple tumor suppressors and oncogenes in the carcinogenesis and progression of lung cancer

Mouse model for lung tumorigenesis through Cre/lox controlled sporadic activation of the K-Ras oncogene

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