Walter Kolch

Prof. Walter Kolch

University College Dublin, Systems Biology Ireland, School fo Medicine, Belfield Dublin 4, Ireland
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Research Focus & Metrics

Academic Career Length

39Years (1988-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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14 May 2007 in Oncogene
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Journal Article
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ADA S Dhillon
A S Dhillon
SHS Hagan
S Hagan
ORO Rath
O Rath
Walter KolchWalter Kolch
Walter Kolch
Cancer can be perceived as a disease of communication between and within cells. The aberrations are pleiotropic, but mitogen-activated protein kinase (MAPK) pathways feature prominently. Here, we discuss recent findings and hypotheses on the role of MAPK pathways in cancer. Cancerous mutations in MAPK pathways are frequently mostly affecting Ras and B-Raf in the extracellular signal-regulated kinase pathway. Stress-activated pathways, such as Jun N-terminal kinase and p38, largely seem to counteract malignant transformation. The balance and integration between these signals may widely vary in different tumours, but are important for the outcome and the sensitivity to drug therapy.

1 July 1993 in Nature
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Journal Article
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Walter KolchWalter Kolch
Walter Kolch
GHGisela Heidecker
Gisela Heidecker
GKGeorg Kochs
Georg Kochs
RHRichard Hummel
Richard Hummel
HVHaleh Vahidi
Haleh Vahidi
URUlf R. Rapp
Ulf R. Rapp

14 October 2005 in Nature Reviews Molecular Cell Biology
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Journal Article
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Walter KolchWalter Kolch
Walter Kolch

1 September 1999 in Nature
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KYKam Yeung
Kam Yeung
TSThomas Seitz
Thomas Seitz
SLShengfeng Li
Shengfeng Li
PJPetra Janosch
Petra Janosch
BMBrian McFerran
Brian McFerran
Walter KolchWalter Kolch
Walter Kolch

Verified
Journal Article
Open access
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SLShannon Lee
Shannon Lee
JRJens Rauch
Jens Rauch
Walter KolchWalter Kolch
Walter Kolch
Mitogen-activated protein kinase (MAPK) pathways represent ubiquitous signal transduction pathways that regulate all aspects of life and are frequently altered in disease. Here, we focus on the role of MAPK pathways in modulating drug sensitivity and resistance in cancer. We briefly discuss new findings in the extracellular signaling-regulated kinase (ERK) pathway, but mainly focus on the mechanisms how stress activated MAPK pathways, such as p38 MAPK and the Jun N-terminal kinases (JNK), impact the response of cancer cells to chemotherapies and targeted therapies. In this context, we also discuss the role of metabolic and epigenetic aberrations and new therapeutic opportunities arising from these changes.

1 June 2010 in Nature Reviews Molecular Cell Biology
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BKBoris N. Kholodenko
Boris N. Kholodenko
JHJohn F Hancock
John F Hancock
Walter KolchWalter Kolch
Walter Kolch