Stress kan kanker veroorzaken*
Volgens een studie door wetenschappers van de Yale Universiteit betekent elke
dag stress op de lange termijn een trigger
voor de ontwikkeling van tumoren. Tot nu toe dachten wetenschappers altijd dat tumoren zich slechts konden ontwikkelen als er verschillende kankerverwekkende mutaties plaatsvonden in één cel. Nu blijkt dat mutaties in verschillende cellen zich ook kunnen ontwikkelen tot een tumor als er een verbinding wordt gemaakt tussen die cellen.
Volgens het onderzoek zorgt de stress van alledag ervoor dat deze verbindingen tussen de verschillende cellen makkelijker gelegd worden.
Volgens Prof. Tian Xu, leider van het onderzoek is het niet alleen emotionele stress door werk of gezin
die kanker kan veroorzaken, maar bijvoorbeeld ook fysieke stress veroorzaakt door lichamelijk trauma."
Stress could cause cancer claim scientists
Stress could be a trigger for some cancers, new research suggests.
Scientists have discovered that everyday emotional stress is a trigger for the growth of tumours
They discovered that any sort of trauma, emotional or physical, can act as a "pathway" between cancerous mutations bringing them together in a potentially deadly mix.
The findings, published in Nature, seemed to show for the first time that the conditions for developing the disease can be affected by your emotional environment including every day work and family stress.
Professor Tian Xu, a geneticist at Yale University who led the study, said: "A lot of different conditions can trigger stress signaling - physical stress, emotional stress, infections, inflammation – all these things.
"Reducing stress or avoiding stress conditions is always good advice."
Until now, scientists believed more than one cancer-causing mutation needed to take place in a single cell in order for tumours to grow.
But Prof Xu and colleagues at Yale University, working with fruit flies, showed mutations can promote cancer even when they are located in different cells. This is because stress opens up "pathways" between them.
He said: "The bad news is that it is much easier for a tissue to accumulate mutations in different cells than in the same cell."
Interaction between RasV12 and scribbled clones induces tumour growth and invasion
Ming Wu1,3, José Carlos Pastor-Pareja1,3 & Tian Xu1,2
1. Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, 295 Congress Avenue, New Haven, Connecticut 06519, USA
2. Fudan-Yale Biomedical Research Center, Institute of Developmental Biology and Molecular Medicine, School of Life Sciences, Fudan University, 220 Han Dan Road, Shanghai 20043, China
3. These authors contributed equally to this work.
Correspondence to: Tian Xu1,2 Correspondence and requests for materials should be addressed to T.X.
(Email: tian.xu@yale.edu).
Abstract
Human tumours have a large degree of cellular and genetic heterogeneity1. Complex cell interactions in the tumour and its microenvironment are thought to have an important role in tumorigenesis and cancer progression2. Furthermore, cooperation between oncogenic genetic lesions is required for tumour development3; however, it is not known how cell interactions contribute to oncogenic cooperation. The genetic techniques available in the fruitfly Drosophila melanogaster allow analysis of the behaviour of cells with distinct mutations4, making this the ideal model organism with which to study cell interactions and oncogenic cooperation. In Drosophila eye-antennal discs, cooperation between the oncogenic protein RasV12 (ref. 5) and loss-of-function mutations in the conserved tumour suppressor scribbled (scrib)6, 7 gives rise to metastatic tumours that display many characteristics observed in human cancers8, 9, 10, 11. Here we show that clones of cells bearing different mutations can cooperate to promote tumour growth and invasion in Drosophila. We found that the RasV12 and scrib- mutations can also cause tumours when they affect different adjacent epithelial cells. We show that this interaction between RasV12 and scrib- clones involves JNK signalling propagation and JNK-induced upregulation of JAK/STAT-activating cytokines, a compensatory growth mechanism for tissue homeostasis. The development of RasV12 tumours can also be triggered by tissue damage, a stress condition that activates JNK signalling. Given the conservation of the pathways examined here, similar cooperative mechanisms could have a role in the development of human
cancers. (Januari 2010)
