Complex effects of Ras proto-oncogenes in tumorigenesis

Roberto Diaz, Lluis Lopez-Barcons, Daniel Ahn, Antonio Garcia-Espana, Andrew C. Yoon, Jeremy Matthews, Ramon Mangues, Roman Perez-Soler, Angel Pellicer

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Ras proteins have been found mutated in about one-third of human tumors. In vitro, Ras has been shown to regulate distinct and contradictory effects, such as cellular proliferation and apoptosis. Nonetheless, the effects that the wild-type protein elicits in tumorigenesis are poorly understood. Depending on the type of tissue, Ras proto-oncogenes appear to either promote or inhibit the tumor phenotype. In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice. After injecting different doses of a tumorigenic cell line, the wild-type mice exhibited a shorter latency of tumor development than the knockouts, indicating that there are N-ras-dependent differences in the stromal cells. Likewise, we have analyzed B-cell lymphomas induced by either N-methylnitrosourea or by the N-ras oncogene in mice that over-express the N-ras proto-oncogene and found that the over-expression of wild-type N-ras is able to increase the incidence of these lymphomas. Considered together, our results indicate that Ras proto-oncogenes can enhance or inhibit the malignant phenotype in vivo in different systems.

Original languageEnglish (US)
Pages (from-to)535-539
Number of pages5
JournalCarcinogenesis
Volume25
Issue number4
DOIs
StatePublished - Apr 2004

Fingerprint

ras Genes
Proto-Oncogenes
Carcinogenesis
Methylcholanthrene
Knockout Mice
Phenotype
Methylnitrosourea
ras Proteins
Neoplasms
Fibrosarcoma
B-Cell Lymphoma
Stromal Cells
Lymphoma
Cell Proliferation
Apoptosis
Cell Line
Incidence
Proteins

ASJC Scopus subject areas

  • Cancer Research

Cite this

Diaz, R., Lopez-Barcons, L., Ahn, D., Garcia-Espana, A., Yoon, A. C., Matthews, J., ... Pellicer, A. (2004). Complex effects of Ras proto-oncogenes in tumorigenesis. Carcinogenesis, 25(4), 535-539. https://doi.org/10.1093/carcin/bgh026

Complex effects of Ras proto-oncogenes in tumorigenesis. / Diaz, Roberto; Lopez-Barcons, Lluis; Ahn, Daniel; Garcia-Espana, Antonio; Yoon, Andrew C.; Matthews, Jeremy; Mangues, Ramon; Perez-Soler, Roman; Pellicer, Angel.

In: Carcinogenesis, Vol. 25, No. 4, 04.2004, p. 535-539.

Research output: Contribution to journalArticle

Diaz, R, Lopez-Barcons, L, Ahn, D, Garcia-Espana, A, Yoon, AC, Matthews, J, Mangues, R, Perez-Soler, R & Pellicer, A 2004, 'Complex effects of Ras proto-oncogenes in tumorigenesis', Carcinogenesis, vol. 25, no. 4, pp. 535-539. https://doi.org/10.1093/carcin/bgh026
Diaz R, Lopez-Barcons L, Ahn D, Garcia-Espana A, Yoon AC, Matthews J et al. Complex effects of Ras proto-oncogenes in tumorigenesis. Carcinogenesis. 2004 Apr;25(4):535-539. https://doi.org/10.1093/carcin/bgh026
Diaz, Roberto ; Lopez-Barcons, Lluis ; Ahn, Daniel ; Garcia-Espana, Antonio ; Yoon, Andrew C. ; Matthews, Jeremy ; Mangues, Ramon ; Perez-Soler, Roman ; Pellicer, Angel. / Complex effects of Ras proto-oncogenes in tumorigenesis. In: Carcinogenesis. 2004 ; Vol. 25, No. 4. pp. 535-539.
@article{35d132bfc37d4a0198a5e495da436685,
title = "Complex effects of Ras proto-oncogenes in tumorigenesis",
abstract = "Ras proteins have been found mutated in about one-third of human tumors. In vitro, Ras has been shown to regulate distinct and contradictory effects, such as cellular proliferation and apoptosis. Nonetheless, the effects that the wild-type protein elicits in tumorigenesis are poorly understood. Depending on the type of tissue, Ras proto-oncogenes appear to either promote or inhibit the tumor phenotype. In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice. After injecting different doses of a tumorigenic cell line, the wild-type mice exhibited a shorter latency of tumor development than the knockouts, indicating that there are N-ras-dependent differences in the stromal cells. Likewise, we have analyzed B-cell lymphomas induced by either N-methylnitrosourea or by the N-ras oncogene in mice that over-express the N-ras proto-oncogene and found that the over-expression of wild-type N-ras is able to increase the incidence of these lymphomas. Considered together, our results indicate that Ras proto-oncogenes can enhance or inhibit the malignant phenotype in vivo in different systems.",
author = "Roberto Diaz and Lluis Lopez-Barcons and Daniel Ahn and Antonio Garcia-Espana and Yoon, {Andrew C.} and Jeremy Matthews and Ramon Mangues and Roman Perez-Soler and Angel Pellicer",
year = "2004",
month = "4",
doi = "10.1093/carcin/bgh026",
language = "English (US)",
volume = "25",
pages = "535--539",
journal = "Carcinogenesis",
issn = "0143-3334",
publisher = "Oxford University Press",
number = "4",

}

TY - JOUR

T1 - Complex effects of Ras proto-oncogenes in tumorigenesis

AU - Diaz, Roberto

AU - Lopez-Barcons, Lluis

AU - Ahn, Daniel

AU - Garcia-Espana, Antonio

AU - Yoon, Andrew C.

AU - Matthews, Jeremy

AU - Mangues, Ramon

AU - Perez-Soler, Roman

AU - Pellicer, Angel

PY - 2004/4

Y1 - 2004/4

N2 - Ras proteins have been found mutated in about one-third of human tumors. In vitro, Ras has been shown to regulate distinct and contradictory effects, such as cellular proliferation and apoptosis. Nonetheless, the effects that the wild-type protein elicits in tumorigenesis are poorly understood. Depending on the type of tissue, Ras proto-oncogenes appear to either promote or inhibit the tumor phenotype. In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice. After injecting different doses of a tumorigenic cell line, the wild-type mice exhibited a shorter latency of tumor development than the knockouts, indicating that there are N-ras-dependent differences in the stromal cells. Likewise, we have analyzed B-cell lymphomas induced by either N-methylnitrosourea or by the N-ras oncogene in mice that over-express the N-ras proto-oncogene and found that the over-expression of wild-type N-ras is able to increase the incidence of these lymphomas. Considered together, our results indicate that Ras proto-oncogenes can enhance or inhibit the malignant phenotype in vivo in different systems.

AB - Ras proteins have been found mutated in about one-third of human tumors. In vitro, Ras has been shown to regulate distinct and contradictory effects, such as cellular proliferation and apoptosis. Nonetheless, the effects that the wild-type protein elicits in tumorigenesis are poorly understood. Depending on the type of tissue, Ras proto-oncogenes appear to either promote or inhibit the tumor phenotype. In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice. After injecting different doses of a tumorigenic cell line, the wild-type mice exhibited a shorter latency of tumor development than the knockouts, indicating that there are N-ras-dependent differences in the stromal cells. Likewise, we have analyzed B-cell lymphomas induced by either N-methylnitrosourea or by the N-ras oncogene in mice that over-express the N-ras proto-oncogene and found that the over-expression of wild-type N-ras is able to increase the incidence of these lymphomas. Considered together, our results indicate that Ras proto-oncogenes can enhance or inhibit the malignant phenotype in vivo in different systems.

UR - http://www.scopus.com/inward/record.url?scp=1942436234&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1942436234&partnerID=8YFLogxK

U2 - 10.1093/carcin/bgh026

DO - 10.1093/carcin/bgh026

M3 - Article

C2 - 14633661

AN - SCOPUS:1942436234

VL - 25

SP - 535

EP - 539

JO - Carcinogenesis

JF - Carcinogenesis

SN - 0143-3334

IS - 4

ER -