Antioncogenes and human cancer

David P. Carbone; John D. Minna

doi:10.1146/annurev.me.44.020193.002315

Antioncogenes and human cancer

David P. Carbone, John D. Minna

Research output: Contribution to journal › Review article › peer-review

10 Scopus citations

Abstract

Multiple genetic lesions are thought to transform a normal cell into a malignant one, and both dominant and recessive genetic effects have been identified in this process. Antioncogenes (or tumor suppressor genes) act in a recessive manner, in which both maternal and paternal alleles need to be inactivated to abrogate normal function. The identification of these lesions is giving us insight into the regulatory pathways in the cell and may translate into future improvements in prevention, diagnosis, prognosis, and therapy of human cancer.

Original language	English (US)
Pages (from-to)	451-464
Number of pages	14
Journal	Annual review of medicine
Volume	44
DOIs	https://doi.org/10.1146/annurev.me.44.020193.002315
State	Published - 1993

Keywords

chromosomes
mutation
oncogenes
tumor suppressor genes

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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10.1146/annurev.me.44.020193.002315

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AU - Minna, John D.

PY - 1993

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N2 - Multiple genetic lesions are thought to transform a normal cell into a malignant one, and both dominant and recessive genetic effects have been identified in this process. Antioncogenes (or tumor suppressor genes) act in a recessive manner, in which both maternal and paternal alleles need to be inactivated to abrogate normal function. The identification of these lesions is giving us insight into the regulatory pathways in the cell and may translate into future improvements in prevention, diagnosis, prognosis, and therapy of human cancer.

AB - Multiple genetic lesions are thought to transform a normal cell into a malignant one, and both dominant and recessive genetic effects have been identified in this process. Antioncogenes (or tumor suppressor genes) act in a recessive manner, in which both maternal and paternal alleles need to be inactivated to abrogate normal function. The identification of these lesions is giving us insight into the regulatory pathways in the cell and may translate into future improvements in prevention, diagnosis, prognosis, and therapy of human cancer.

KW - chromosomes

KW - mutation

KW - oncogenes

KW - tumor suppressor genes

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JO - Annual review of medicine

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ER -

Antioncogenes and human cancer

Abstract

Keywords

ASJC Scopus subject areas

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