Flipping the oncogene switch: Illumination of tumor maintenance and regression

Lynda Chin; Ronald A. DePinho

doi:10.1016/S0168-9525(99)01968-X

Flipping the oncogene switch: Illumination of tumor maintenance and regression

Lynda Chin, Ronald A. DePinho

Genomic Medicine

Research output: Contribution to journal › Short survey › peer-review

28 Scopus citations

Abstract

The genetic construction of cancer-prone mice, combined with the capacity to control transgene expression in vivo, provides new opportunities to study the role of oncogenes in the maintenance of fully formed tumors. These inducible cancer models provide a means to dissect how specific oncogenic signals influence host-tumor symbiosis, to validate the importance of a given oncogenic lesion in established advanced tumors, and to predict the biological response and adaptations to therapies targeted to that cancer-causing genetic alteration. Copyright (C) 2000 Elsevier Science Ltd.

Original language	English (US)
Pages (from-to)	147-150
Number of pages	4
Journal	Trends in Genetics
Volume	16
Issue number	4
DOIs	https://doi.org/10.1016/S0168-9525(99)01968-X
State	Published - Apr 1 2000

ASJC Scopus subject areas

Genetics

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10.1016/S0168-9525(99)01968-X

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title = "Flipping the oncogene switch: Illumination of tumor maintenance and regression",

abstract = "The genetic construction of cancer-prone mice, combined with the capacity to control transgene expression in vivo, provides new opportunities to study the role of oncogenes in the maintenance of fully formed tumors. These inducible cancer models provide a means to dissect how specific oncogenic signals influence host-tumor symbiosis, to validate the importance of a given oncogenic lesion in established advanced tumors, and to predict the biological response and adaptations to therapies targeted to that cancer-causing genetic alteration. Copyright (C) 2000 Elsevier Science Ltd.",

author = "Lynda Chin and DePinho, {Ronald A.}",

note = "Funding Information: We apologize to colleagues whose work was not discussed or cited owing to space constraints. We thank D.G. Tenen and colleagues, D.W. Felsher and J.W. Bishop for communicating data prior to publication, and N. Sharpless for critically reviewing this manuscript. L.C. is supported by NIH Mentored Clinician Scientist Award and the Harvard Skin Disease Center Grant. R.A.D. is supported by grants from the NIH and the ACS. L.C. is a V Foundation Scholar. R.A.D. is an American Cancer Society Research Professor.",

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AU - DePinho, Ronald A.

N1 - Funding Information: We apologize to colleagues whose work was not discussed or cited owing to space constraints. We thank D.G. Tenen and colleagues, D.W. Felsher and J.W. Bishop for communicating data prior to publication, and N. Sharpless for critically reviewing this manuscript. L.C. is supported by NIH Mentored Clinician Scientist Award and the Harvard Skin Disease Center Grant. R.A.D. is supported by grants from the NIH and the ACS. L.C. is a V Foundation Scholar. R.A.D. is an American Cancer Society Research Professor.

PY - 2000/4/1

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N2 - The genetic construction of cancer-prone mice, combined with the capacity to control transgene expression in vivo, provides new opportunities to study the role of oncogenes in the maintenance of fully formed tumors. These inducible cancer models provide a means to dissect how specific oncogenic signals influence host-tumor symbiosis, to validate the importance of a given oncogenic lesion in established advanced tumors, and to predict the biological response and adaptations to therapies targeted to that cancer-causing genetic alteration. Copyright (C) 2000 Elsevier Science Ltd.

AB - The genetic construction of cancer-prone mice, combined with the capacity to control transgene expression in vivo, provides new opportunities to study the role of oncogenes in the maintenance of fully formed tumors. These inducible cancer models provide a means to dissect how specific oncogenic signals influence host-tumor symbiosis, to validate the importance of a given oncogenic lesion in established advanced tumors, and to predict the biological response and adaptations to therapies targeted to that cancer-causing genetic alteration. Copyright (C) 2000 Elsevier Science Ltd.

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Flipping the oncogene switch: Illumination of tumor maintenance and regression

Abstract

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