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Cancer, type 2 diabetes, and ageing: news from flies and worms.


Hafen, E (2004). Cancer, type 2 diabetes, and ageing: news from flies and worms. Swiss Medical Weekly, 134(49-50):711-719.

Abstract

The tumour suppressor gene PTEN is, next to p53, the second most frequently mutated gene in human cancers. The genes TSC1 and TSC2 are mutated in the severe human syndrome called Tuberous Sclerosis. Patients with this disease have large benign tumours composed of large cells in the brain. The genetic dissection of pathways controlling the growth of cells, organs, and the entire organism in Drosophila has contributed to the understanding of the signalling pathways that are controlled by these two tumour suppressors. Together with studies on nutrient regulation of growth and ageing in the nematode Caenorhabditis elegans, evidence from these model organisms has moved the Insulin/IGF (IIS) and the Target Rapamycin (TOR) signalling pathway onto the centre stage of cellular growth control and made them attractive novel targets for cancer therapy. In this review, I will outline the contributions of model organism genetics to the understanding of these disease relevant pathways and highlight the evolutionary conservation of nutrient-dependent growth regulation.

Abstract

The tumour suppressor gene PTEN is, next to p53, the second most frequently mutated gene in human cancers. The genes TSC1 and TSC2 are mutated in the severe human syndrome called Tuberous Sclerosis. Patients with this disease have large benign tumours composed of large cells in the brain. The genetic dissection of pathways controlling the growth of cells, organs, and the entire organism in Drosophila has contributed to the understanding of the signalling pathways that are controlled by these two tumour suppressors. Together with studies on nutrient regulation of growth and ageing in the nematode Caenorhabditis elegans, evidence from these model organisms has moved the Insulin/IGF (IIS) and the Target Rapamycin (TOR) signalling pathway onto the centre stage of cellular growth control and made them attractive novel targets for cancer therapy. In this review, I will outline the contributions of model organism genetics to the understanding of these disease relevant pathways and highlight the evolutionary conservation of nutrient-dependent growth regulation.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:07 Faculty of Science > Institute of Zoology (former)
Dewey Decimal Classification:570 Life sciences; biology
590 Animals (Zoology)
Language:English
Date:18 December 2004
Deposited On:11 Feb 2008 12:17
Last Modified:26 Mar 2017 05:02
Publisher:EMH Swiss Medical Publishers
ISSN:0036-7672
Free access at:Official URL. An embargo period may apply.
Official URL:https://smw.ch/en/archives/article/?tx_ezmjournal_articledetail[identifier]=smw.2004.09885
PubMed ID:15635489

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