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Mol. Cells 2009; 28(4): 315-320

Published online September 30, 2009

https://doi.org/10.1007/s10059-009-0143-7

© The Korean Society for Molecular and Cellular Biology

Non-Redundancy within the RAS Oncogene Family: Insights into Mutational Disparities inCancer

Ken S. Lau, and Kevin M. Haigis

Received: September 8, 2009; Accepted: September 11, 2009

Abstract

The RAS family of oncoproteins has been studied exten-sively for almost three decades. While we know that activation of RAS represents a key feature of malignant transformation for many cancers, we are only now beginning to understand the complex underpinnings of RAS biology. Here, we will discuss emerging cancer genome sequencing data in the context of what is currently known about RAS function. Taken together, retrospective studies of primary human tissues and prospective studies of experimental models support the notion that the variable mutation frequencies exhibited by the RAS oncogenes reflect unique functions of the RAS oncoproteins.

Keywords cancer, mutation, RAS, signaling

Article

Minireview

Mol. Cells 2009; 28(4): 315-320

Published online October 31, 2009 https://doi.org/10.1007/s10059-009-0143-7

Copyright © The Korean Society for Molecular and Cellular Biology.

Non-Redundancy within the RAS Oncogene Family: Insights into Mutational Disparities inCancer

Ken S. Lau, and Kevin M. Haigis

Received: September 8, 2009; Accepted: September 11, 2009

Abstract

The RAS family of oncoproteins has been studied exten-sively for almost three decades. While we know that activation of RAS represents a key feature of malignant transformation for many cancers, we are only now beginning to understand the complex underpinnings of RAS biology. Here, we will discuss emerging cancer genome sequencing data in the context of what is currently known about RAS function. Taken together, retrospective studies of primary human tissues and prospective studies of experimental models support the notion that the variable mutation frequencies exhibited by the RAS oncogenes reflect unique functions of the RAS oncoproteins.

Keywords: cancer, mutation, RAS, signaling

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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