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Tumorigenesis: RAF/RAS oncogenes and mismatch-repair status.

TLDR
The results not only provide genetic support for the idea that mutations in BRAF and KRAS exert equivalent effects in tumorigenesis, but also emphasize the role of repair processes in establishing the mutation spectra that underpin human cancer.
Abstract
Genes of the RAF family encode kinases that are regulated by Ras and mediate cellular responses to growth signals. Activating mutations in one RAF gene, BRAF, have been found in a high proportion of melanomas and in a small fraction of other cancers. Here we show that BRAF mutations in colorectal cancers occur only in tumours that do not carry mutations in a RAS gene known as KRAS, and that BRAF mutation is linked to the proficiency of these tumours in repairing mismatched bases in DNA. Our results not only provide genetic support for the idea that mutations in BRAF and KRAS exert equivalent effects in tumorigenesis, but also emphasize the role of repair processes in establishing the mutation spectra that underpin human cancer.

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Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer.

TL;DR: The current status of the different approaches and targets that are under evaluation and development for the therapeutic intervention of this key signaling pathway in human disease are summarized.
Journal ArticleDOI

Mechanism of Activation of the Raf-Erk Signaling Pathway by Oncogenic Mutations of B-Raf

TL;DR: The high activity mutants signal to ERK by directly phosphorylating MEK, whereas the impaired activity mutants stimulate MEK by activating endogenous C-RAF, possibly via an allosteric or transphosphorylation mechanism.
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Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability.

TL;DR: This work surmises that CRI represents the seventh hallmark of cancer, and suggests that an additional mechanism involved in cancer-related inflammation (CRI) is induction of genetic instability by inflammatory mediators, leading to accumulation of random genetic alterations in cancer cells.
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Roles of the raf/mek/erk pathway in cell growth, malignant transformation and drug resistance

TL;DR: The Raf/MEK/ERK pathway has different effects on growth, prevention of apoptosis, cell cycle arrest and induction of drug resistance in cells of various lineages which may be due to the presence of functional p53 and PTEN and the expression of lineage specific factors.
References
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Journal ArticleDOI

Lessons from Hereditary Colorectal Cancer

TL;DR: The authors are grateful to the members of their laboratories for their contributions to the reviewed studies and to F. Giardiello and S. Hamilton for photographs of colorectal lesions.
Journal ArticleDOI

Stabilization of β-Catenin by Genetic Defects in Melanoma Cell Lines

TL;DR: Genetic defects that result in up-regulation of β-catenin may play a role in melanoma progression.
Journal Article

Mutational Analysis of the APC/β-Catenin/Tcf Pathway in Colorectal Cancer

TL;DR: It is suggested that CTNNB1 mutations can uniquely substitute for APC mutations in CR tumors and that β-catenin signaling plays a critical role in CR tumorigenesis.
Journal ArticleDOI

Differential Regulation of Raf-1, A-Raf, and B-Raf by Oncogenic Ras and Tyrosine Kinases

TL;DR: Results show that maximal activation of B-Raf merely requires signals that generate Ras-GTP, whereas activation of Raf-1 and A-Rafa requires Ras- GTP together with signals that lead to their tyrosine phosphorylation, and B-raf may be the primary target of oncogenic Ras.
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