Table 1

Summary of HGF/Met alterations in breast cancer

Reference

Observations/lesions

Clinical/biological aspects


Yao and colleagues [21]

High levels of HGF in breast tumor tissue

Invasive ductal carcinomas

Tuck and colleagues [16]

HGF/Met autocrine loop in tumor cells

Co-localization at the advancing margins of the tumors

Jin and colleagues [22]

High levels of HGF and c-Met overexpression in breast tissue

Invasive ductal carcinomas

Camp and colleagues [24]

Met overexpression

Reduced survival, relapse and metastatic dissemination

Edakuni and colleagues [23]

Met overexpression

High histological grade, proliferative index, advancing margins

Kang and colleagues [82]

High levels of Met and HGF in node-negative breast cancer

Tumor progression and poor patient outcome

Lengyel and colleagues [83]

Met overexpression in node-positive breast cancer

Disease progression and decrease in disease-free survival

Charafe-Jauffre and colleagues [43]

Met overexpression in breast cancer cell lines

Basal-like phenotype

Lindemann and colleagues [84]

Imbalance in Met expression between tumor and normal tissue

Aggressive ductal carcinoma in situ

Eichbaum and colleagues [85]

High HGF serum levels

Liver metastatic colonization from breast cancer

Garcia and colleagues [45]

Met overexpression in tissue microarrays

Poor prognosis, basal-like phenotype

Finkbeiner and colleagues [49]

Transcriptional upregulation of Met

Anchorage-independent growth of basal-like breast cancer cells

Smolen and colleagues [65]

Met amplification in a Brca1-p53 mouse model of breast cancer

Mouse mammary tumor progression

Ponzo and colleagues [53]

MMTV-Met mutant transgenic mice

Heterogeneous mammary tumors, basal-like phenotype

Graveel and colleagues [52]

Met mutant knock-in mice

Mammary tumors associated with basal-like phenotype


HGF, hepatocyte growth factor; MMTV, mouse mammary tumor virus promoter.

Gastaldi et al. Breast Cancer Research 2010 12:208   doi:10.1186/bcr2617