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Table 1 Mechanisms of aberrant c-Met signalling in invasive breast cancer

From: The clinical and functional significance of c-Met in breast cancer: a review

Mechanism Frequency/prognostic significance in breast cancer Reference
Gene mutation MET mutations are uncommon; HGF promoter region mutations occur in 15 to 51% of breast cancers [30,31]
Gene amplification MET amplification is uncommon, occurring in 0 to 8% of breast cancers; MET copy number is positively correlated with TN tumours [32,33]
  Patients with trastuzumab-treated Her2-positive metastatic breast cancer show MET amplification in 27.7% of cases and HGF amplification in 39.3% of cases; patients with MET-amplified Her2-positive tumours have a shorter time to progression [34]
Autocrine signalling HGF and MET mRNA detected in tumour cells in all breast cancers analysed, with strongest positivity at the advancing edge of the tumour [35]
  On IHC, autocrine pattern of staining seen in 46.6% of tumours [37]
Paracrine signalling On IHC, paracrine pattern seen in 59.1% of tumours; paracrine signalling is associated with a worse outcome when c-Met staining is more intense at the tumour front [68]
C-Met activity (phosphorylation) Using RPPA, 47.9% of tumours showed high phospho-c-Met expression; inconsistent relationship with molecular subtype; high phospho-c-Met associated with an increased risk of tumour recurrence [43,44]
  1. Frequency and prognostic significance of the different mechanisms of aberrant c-Met signalling in invasive breast cancer, identified in studies using human tissue samples. HGF, hepatocyte growth factor, IHC, immunohistochemistry, RPPA, reverse-phase protein arrays; TN, triple negative.