RGD Reference Report - Mutant KRAS, chromosomal instability and prognosis in colorectal cancer. - Rat Genome Database

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Mutant KRAS, chromosomal instability and prognosis in colorectal cancer.

Authors: Castagnola, P  Giaretti, W 
Citation: Castagnola P and Giaretti W, Biochim Biophys Acta. 2005 Nov 25;1756(2):115-25. Epub 2005 Jul 13.
RGD ID: 2306732
Pubmed: PMID:16112461   (View Abstract at PubMed)
DOI: DOI:10.1016/j.bbcan.2005.06.003   (Journal Full-text)

The RAS gene family provides a global effect on gene expression by encoding small GTP-binding proteins which act as molecular switches connecting extracellular signals with nuclear transcription factors. While wild type RAS proteins are switched off shortly after activation, mutant RAS proteins remain constitutively activated leading to complex interactions among their downstream effectors. For some human tumor types, these interactions were shown to contribute to cancer genesis and progression by inducing changes in cell survival, apoptosis, angiogenesis, invasion and metastasis. This review addresses the controversial link of KRAS mutations in colorectal cancer with chromosomal instability and patient prognosis.

Molecular Pathway Annotations    Click to see Annotation Detail View

RGD Manual Annotations

TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
altered extracellular signal-regulated Raf/Mek/Erk signaling pathway  TAS 2306732; 2306732; 2306732 RGD 
colorectal cancer pathway   TAS 2306732; 2306732; 2306732 RGD 
Objects Annotated

Genes (Rattus norvegicus)
Kras  (KRAS proto-oncogene, GTPase)

Genes (Mus musculus)
Kras  (Kirsten rat sarcoma viral oncogene homolog)

Genes (Homo sapiens)
KRAS  (KRAS proto-oncogene, GTPase)


Additional Information