2012
DOI: 10.2217/crc.12.40
|View full text |Cite
|
Sign up to set email alerts
|

Role of the MET–HGF axis in colorectal cancer: precepts and prospects

Abstract: SUMMARY Colorectal cancer (CRC) accounts for 10% of all cancer-related mortality globally. Despite significant therapeutic advances, overall survival is limited. The restricted repertoire of therapies necessitates investigation into novel pathways of colorectal carcinogenesis. The proto-oncogene MET encodes a receptor tyrosine kinase that acts as a receptor for the HGF. Dysregulation of this MET–HGF axis has been implicated in proliferation, survival and metastasis in various tumor types including CRC. Increas… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

0
14
0

Year Published

2013
2013
2024
2024

Publication Types

Select...
5
1
1

Relationship

1
6

Authors

Journals

citations
Cited by 14 publications
(14 citation statements)
references
References 75 publications
0
14
0
Order By: Relevance
“…However, HGF/cMET activation has been implicated as an important mechanism of metastatic progression and treatment resistance. Future studies should address the need to biopsy the most recent site of metastatic progression, since targeted therapy directed against HGF/cMET may be of considerable value in surmounting both primary and acquired resistance in selected CRC populations [110]. …”
Section: Discussionmentioning
confidence: 99%
“…However, HGF/cMET activation has been implicated as an important mechanism of metastatic progression and treatment resistance. Future studies should address the need to biopsy the most recent site of metastatic progression, since targeted therapy directed against HGF/cMET may be of considerable value in surmounting both primary and acquired resistance in selected CRC populations [110]. …”
Section: Discussionmentioning
confidence: 99%
“…[1, 2] Due to its critical role in cancer biology, inhibition of the MET pathway is being actively investigated in numerous clinical trials. [14] MET amplification appears to identify a subset of cancers, uniquely sensitive to MET inhibitors, both in vitro and in vivo .…”
Section: Introductionmentioning
confidence: 99%
“…MET (mesenchymal-epithelial transition factor) proto-oncogene on chromosome 7q31 encodes for a receptor tyrosine kinase (RTK) and regulates a variety of downstream signaling pathways that initiate gene expression involved in promoting tumor growth, survival, angiogenesis, invasion and metastases. [ 1 , 2 ] Due to its critical role in cancer biology, inhibition of the MET pathway is being actively investigated in numerous clinical trials. [ 1 4 ] MET amplification appears to identify a subset of cancers, uniquely sensitive to MET inhibitors, both in vitro and in vivo .…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Terminal effectors of this pathway consist of extracellular signal-regulated kinases, c-Jun N-terminal kinases, and p38s. These factors further translocate into the nucleus and modulate activity of several transcription factors (Jung et al, 2012;Raghav & Eng, 2012). In other pathway PI3K activate by MET.…”
Section: Central Signaling Pathways Regulated By Metmentioning
confidence: 99%