IMR Press / EJGO / Volume 41 / Issue 2 / DOI: 10.31083/j.ejgo.2020.02.5101
Open Access Original Research
Clinical significance of MET receptor protein and mRNA expression in invasive breast cancer
Show Less
1 Department of Pathology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine,Seoul, 03181, South Korea
2 Department of Surgery, Seoul National University Bundang Hospital, Seongnam, Gyeonggi, 13620, South Korea
3 Department of Pathology, Chung-Ang University College of Medicine, Seoul, 06973, South Korea
Eur. J. Gynaecol. Oncol. 2020, 41(2), 240–245;
Published: 15 April 2020

Mesenchymal epithelial transition (MET) receptor factor, the hepatocyte growth factor receptor, is a receptor tyrosine kinase that is overexpressed and activated in a subset of human epithelial malignancies. In this study, the clinical significance of mesenchymal epithelial transition protein and mRNA expression in invasive breast cancer tissues was investigated. A tissue microarray was constructed using tissues from 371 patients with invasive ductal cancer (IDC) who underwent radical tumor excision for breast cancer and were performed. The correlation between mesenchymal epithelial transition mRNA and protein expression were analyzed with mesenchymal epithelial transition immunohistochemistry (IHC) and RNAscope in situ hybridization (ISH). Positive immunohistochemistry results for mesenchymal epithelial transition protein were detected in 46 (13%) patients, and 45 (12%) patients exhibited high mesenchymal epithelial transition mRNA levels. mesenchymal epithelial transition protein and high mesenchymal epithelial transition mRNA levels were significantly associated with high histologic grade, negative estrogen receptor (ER) status, and a high proliferation index in invasive ductal cancer. Kaplan-Meier analysis showed no significant association of either mesenchymal epithelial transition mRNA or protein expression with survival. There was, however, a significant correlation between mesenchymal epithelial transition mRNA expression and mesenchymal epithelial transition protein expression. The present study showed that mesenchymal epithelial transition mRNA and protein expression are significantly correlated and are important prognostic factors in invasive breast cancer.

In situ hybridization
Invasive ductal carcinoma

Breast cancer is the most common cancer among women worldwide [1]. Epidemiological studies have shown that more than 400,000 individuals worldwide die each year from breast cancer [2]. Mesenchymal epithelial transition receptor factor (hereafter, referred to as MET) is a plasma membrane protein that transduces signals from the extracellular matrix to the cytoplasm and is activated by the binding of hepatocyte growth factor (HGF, also known as scatter factor) [3]. The MET proto-oncogene is located on chromosome 7q31 and encodes a receptor tyrosine kinase (RTK) that acts as the receptor for HGF. MET gene mutation, overexpression, and amplification occur in a variety of human tumor types, and these events are closely related to the aberrant activation of the HGF/MET signaling pathway [4]. Overexpression of MET has been shown to contribute to the development of invasive phenotypes during breast cancer progression both in vivo and in vitro. Some studies found MET to act as a negative prognostic biomarker and predict poor survival in breast cancer patients [5-7]. Although some studies suggest that MET is a stronger indicator of poor prognosis than traditional markers, such as Her2/neu and epidermal growth factor receptor (EGFR) [5,8,9], other studies suggest there is no statistically significant relation between MET and breast cancer prognosis [8,10,11]. In recent years, MET was reported to be associated with a favorable prognosis in breast cancer patients [12,13]. However, MET was also found to play a role in the development of herceptin and endocrine therapy-resistance in breast cancer [6,7]. In breast cancer studies, MET protein overexpression determined using immunohistochemistry (IHC) was 3.8-80.0%, MET gene copy number gain determined using quantitative real-time polymerase chain reaction (qPCR) was 44-74.2%, and MET gene amplification determined using fluorescence in situ hybridization (FISH) was 4.7-27.7% [14]. Of these methods, IHC is widely used in clinical practice and is the most common screening method for MET-positive cancers.

In this study, RNA in situ hybridization (ISH) was performed using paired DNA oligonucleotide probes and preamplifier, amplifier-labeled probes for visualization [15]. Quantification of MET protein levels (by IHC) and MET mRNA levels (by RNAscope ISH) was also carried out for 371 invasive breast cancer tissues.

Materials and Methods

Surgically resected breast cancer tissue specimens obtained from 371 patients who underwent mastectomy for invasive ductal carcinoma (IDC) at Kangbuk Samsung Hospital (Seoul, Korea) from March 2003 to December 2007, were collected. The submitted study followed the guidelines of and was approved by the local institutional review board (KBC14077). Patient survival data, including dates and causes of death, were obtained from the Korean Central Cancer Registry, Ministry of Health and Welfare, Korea. Standard histopathological examination included the type of cancer and the pathological tumor stage, assessed according to the criteria reported in the sixth edition of the AJCC Staging Manual [16].

Tissue array blocks were prepared and in situ detection of MET mRNA was performed manually using an RNAscope kit, according to the manufacturer’s instructions. Briefly, formalin-fixed, paraffin-embedded (FFPE) tissue sections (4 μm thick) were pretreated by heating and incubating with proteases prior to hybridization with MET target probes. Positive staining was indicated by brown punctate dots present in the nucleus and/or cytoplasm. MET expression levels were categorized into five grades according to the manufacturer’s scoring guidelines: no staining (score 0), staining that was difficult to see at a 40 × magnification in more than 10% of tumor cells (score 1), staining that was difficult to see at a 20 × magnification but could be visualized at a 40 × magnification in more than 10% of tumor cells (score 2), and staining that could be visualized at 10 × magnification in more than 10% of tumor cells (score 3). Ubiquitin C (UBC) served as the positive control. Samples were considered adequate for analysis when the UBC mRNA signals were easily visible under a 10 × magnification objective lens (Fig. 2).

Immunohistochemical staining was performed using an automatic immunostainer, according to the manufacturer’s instructions. The primary antibody was anti-total MET (SP44; rabbit monoclonal; prediluted, Ventana Medical Systems, Tucson, AZ). Briefly, 4-μm thick whole-tissue sections were transferred to poly-L-lysine-coated adhesive slides and dried for 30 min at 74 °C. After standard heat epitope retrieval in ethylenediaminetetraacetic acid (EDTA, pH 8.0) for 1 h, samples were incubated with antibodies against estrogen receptor (ER; 1:50 dilution, DAKO, Santa Clara, CA), progesterone receptor (PR; 1:200 dilution, DAKO, Santa Clara, CA), human epidermal growth factor receptor 2 (HER2; 1:500 dilution, Ventana Medical Systems, Tucson, AZ), and Ki-67 (clone SP6; 1:50 dilution, DAKO, Santa Clara, CA) using an autostainer. Sections were subsequently incubated with the appropriate reagents from the ultraView Universal DAB Kit (Ventana Medical Systems, Inc.) and counterstained with Harris hematoxylin.

A semiquantitative approach was used to generate a score for each tissue core as follows: no membrane staining or membrane staining in < 10% of tumor cells (score 0), faint/barely perceptible partial membrane staining in < 10% of tumor cells (score 1), weak-to-moderate staining of the entire membrane in > 10% of tumor cells (score 2), and strong staining of the entire membrane in > 10% of tumor cells (score 3). Scores of 0 and 1 were considered negative for MET overexpression, and scores of 2 and 3 were considered positive for MET overexpression (Fig. 1).

Figure 1.

— Representative images for MET immunohistochemistry (IHC). (A) IHC score 0, (B) IHC score 1, (C) IHC score 2, and (D) IHC score 3 (400×).

Figure 2.

— Representative images for MET RNA in situ hybridization (ISH). (A) ISH score 0, (B) ISH score 1, (C) ISH score 2, and (D) ISH score 3 (400×).

A cut-off value of at least 10% positively stained nuclei was used to define ER and PR positivity. Membrane staining for HER2 was classified as follows: membranous staining in 0-10% of cells (score 0), faint incomplete staining in at least 10% of cells (score 1+), weak to moderate complete staining in at least 10% of cells (2+), and strong complete staining in at least 10% of cells (3+). HER2 overexpression was defined as a score of 3+. Cell staining for Ki-67 and p53 was expressed as a percentage. The Ki-67 labeling index was graded as low if the number of positive cells was < 10% and high if the number of positive cells was > 10%. P53 was classified as positive when > 10% of cells were positively stained with a strong intensity.

Statistical analysis was performed using the SPSS software, version 15.0. Pearson’s χ2 test was used to examine the correlation between variables. Survival analyses were performed using a Kaplan-Meier curve and the log-rank test. The Cox proportional hazard model was used for the survival analysis. All p values < 0.05 were considered statistically significant.


The clinical characteristics of the 371 patients included in the present study are summarized in Table 1. Thirty-four patients experienced relapse, and 11 patients died of breast cancer-related causes. The median follow-up period was 48 months (range 7-74). The median recurrence-free survival (RFS) time was 45 months.

Table 1 Patient demographics and characteristics
Characteristics No. of patients (%)
Mean age, years (range) 49 (25-79)
Histologic grade 1 85 (24.6)
2 142 (41)
3 119 (34.4)
T stage T1 203 (54.7)
T2 150 (40.4)
T3 18 (4.9)
N stage N0 231 (62.3)
N1 86 (23.2)
N2 23 (6.2)
N3 31 (8.4)
AJCC stage I 151 (40.7)
II 163 (43.9)
III 57 (15.4)
HR status Negative 131 (35.9)
Positive 234 (64.1)
HER2 Negative 303 (82.8)
Positive 63 (17.2)
Intrinsic type Luminal A 215 (58.9)
Luminal B 19 (5.2)
HER2 overexpression 44 (12.1)
TN 87 (23.8)
Hormone therapy No 62 (25.8)
Yes 178 (74.2)
Adjuvant chemotherapy No 50 (20.8)
Yes 190 (79.2)

Abbreviations: AJCC, American Joint Committee on Cancer; HR, hormone receptor; HER2, human epidermal growth factor receptor 2.

Among the 353 cases for which IHC information was available, the frequency of MET IHC positive cases was 13.0% (46/353); 11.9% (42/353) was the frequency of cases with score 1 and 1.1% (4/353) was the frequency of cases with score 2. There were no score 3 cases. However, there were score 3 areas in the ductal carcinoma in situ (DCIS) portion accompanied by invasive ductal carcinoma (IDC). IHC scores 1 and 2 were categorized as high MET protein expression.

Among the 364 cases for which MET ISH information was available, the frequency of ISH positive cases was 76.1% (277/364). The frequency breakdown by ISH score was as follows: 64.8% (236/364) score 1, 4.9% (18/364) score 2, 6.3% (23/364) score 3, and 1.1% (4/364) score 4. ISH scores 2-4 (45 cases, 12.4%) were categorized as high MET mRNA expression.

MET IHC results showed that high MET expression was significantly associated with high histologic grade, negative ER, negative PR, HER2 overexpression, triple negative tumor, and CK5 and EGFR expression. MET RNAscope in situ hybridization showed that high MET mRNA expression was significantly associated with high histologic grade, negative ER, negative PR, HER2 overexpression, triple negative tumor, p53 overexpression, and EGFR expression. MET mRNA and protein expression were found to be significantly associated with aggressive histologic features and the hormone receptor-negative phenotype in breast cancers (Table 2).

Table 2 Clinicopathologic correlation of MET immunohistochemistry and mRNA in situ hybridization results in invasive breast cancer
Low High Low High
N % N % p value N % N % p value
Total 307 87.0 46 13.0 319 87.6 45 12.4
Age (years) < 50 183 59.6 28 60.9 0.871 185 58.0 30 66.7 0.268
> 50 124 40.4 18 39.1 134 42.0 15 33.3
Histologic grade 1 201 70.3 14 32.6 < 0.001 212 71.1 13 31.0 < 0.001
2 or 3 85 29.7 29 67.4 86 28.9 29 69.0
N stage N0 187 67.5 32 69.6 0.782 192 66.7 33 73.3 0.374
N1 90 32.5 14 30.4 96 33.3 12 26.7
AJCC I 210 68.4 38 82.6 0.049 220 69.0 36 80.0 0.129
II-IV 97 31.6 8 17.4 99 31.0 9 20.0
ER Negative 119 38.9 29 63.0 0.002 120 37.9 33 73.3 < 0.001
Positive 187 61.1 17 37.0 197 62.1 12 26.7
PR Negative 132 43.1 29 63.0 0.012 135 42.6 31 68.9 0.001
Positive 174 56.9 17 37.0 182 57.4 14 31.1
HER2 overexpression Absent 258 84.3 31 67.4 0.005 268 84.5 31 68.9 0.01
Present 48 15.7 15 32.6 49 15.5 14 31.1
Intrinsic type Luminal A 193 63.3 15 32.6 0.001 203 64.2 11 24.4 < 0.001
Luminal B 15 4.9 4 8.7 16 5.1 3 6.7
HER2 overexpression 33 10.8 11 23.9 33 10.4 11 24.4
Triple Negative 64 21.0 16 34.8 64 20.3 20 44.4
Triple Negative vs. non-TN Triple Negative 64 21.0 16 34.8 0.038 64 20.3 20 44.4 < 0.001
Non-TN 241 79.0 30 65.2 252 79.7 25 55.6
p53 Negative 220 74.8 31 67.4 0.286 234 77.0 23 52.3 < 0.001
Positive 74 25.2 15 32.6 70 23.0 21 47.7
CK5 Negative 140 50.9 15 34.1 0.038 142 49.7 17 41.5 0.327
Positive 135 49.1 29 65.9 144 50.3 24 58.5
EGFR Negative 254 88.5 32 72.7 0.004 266 89.0 30 71.4 0.002
Positive 33 11.5 12 27.3 33 11.0 12 28.6

Abbreviations: IHC, immunohistochemistry; ISH, in situ hybridization; AJCC, American Joint Committee on Cancer; ER, estrogen receptor; PR, progesterone receptor; HER2, human epidermal growth factor receptor 2; TN, triple negative; CK, cytokeratin; EGFR, epidermal growth factor receptor.

In the 353 invasive breast cancers studied, there was a positive correlation between MET mRNA and protein expression (r = 0.583, p < 0.001; Table 3). All four cases with an RNA ISH score of 4 showed MET protein expression. Among the 23 cases with an RNA ISH score of 3, 14 cases (75%) showed an IHC score of 2, and two cases (9%) showed an IHC score of 3.

Table 3 Correlation of MET mRNA scores (assessed by RNA in situ hybridization) with MET protein scores (assessed by immunohistochemistry)
MET mRNA scores (ISH) MET protein scores (IHC)
0 (n = 307) 1 (n = 42) 2 (n = 4) p value
0 (n = 76) 76 (100%) 0 (0%) 0 (0%) < 0.001
1 (n = 232) 216 (93%) 16 (7%) 0 (0%)
2 (n = 18) 8 (44%) 9 (50%) 1 (6%)
3 (n = 23) 7 (30%) 14 (61%) 2 (9%)
4 (n = 4) 0 (0%) 3 (75%) 1 (25%)

Abbreviations: IHC, immunohistochemistry; ISH, in situ hybridization.

Kaplan-Meier analyses of MET IHC and ISH data showed no significant correlation with overall survival (OS) or RFS. Subgroup analyses of lymph node metastasis, hormone receptor expression, hormone therapy, and adjuvant chemotherapy showed no significant association of OS or RFS with MET protein or mRNA expression. In the multivariate survival analysis, MET positivity was not an independent prognostic factor for OS or RFS.


The main purpose of this retrospective study was to assess the possible correlation of MET mRNA expression (RNAscope in situ hybridization) and MET protein expression (IHC) in invasive breast cancers; a strong positive correlation was identified. Previously, it was shown that the mRNA expression of HER2 [17] and MET [18], as evaluated by RNA ISH, was well-correlated with protein overexpression and gene amplification, which were evaluated by IHC and FISH, respectively.

High levels of MET expression have been found in a variety of epithelial tumors. Several cancer cell lines exhibiting MET gene amplification, such those from non-small cell lung carcinomas (NSCLCs) and in gastric carcinomas, are dependent on MET for growth and survival, and MET inhibition in these cell lines results in decreased cell proliferation and death [19,20]. The most frequent cause of constitutive MET activation in human cancers is protein overexpression resulting from transcriptional upregulation in the absence of gene aberrations [21]. It is fairly well known that amplification of MET is not a common event in breast cancer, relative to other cancer subtypes (renal, gastric, and lung carcinomas). In breast cancer, it seems that overexpression of MET is not typically caused by the increased gene copy number of MET/polysomy7 [21].

The simplest molecular mechanism of MET activation in tumor cells, which involves HGF-dependent MET activation, also occurs in normal cells. In some cases, tumor cells express both HGF and its receptor, enabling an autocrine loop in which secreted HGF binds to MET, causing constitutive activation of MET and its downstream signaling pathways and thus enhancing tumor growth and invasive behavior. Such HGF-MET autocrine loops have been detected in gliomas, osteosarcomas, and mammary, prostate, breast, lung, and other carcinomas; they are often associated with malignant progression of tumors and correlate with poor prognosis [21].

Among the subtypes of IDC, triple negative breast cancer is more associated with MET expression [10,23]. When expressed in the mammary gland, MET can cause basal-like breast carcinomas [24]. MET was associated with poor OS in lymph node-negative breast cancer and with poor RFS in hormone receptor-positive and triple negative breast cancers, but it was not associated with prognosis in HER2-positive breast cancer [3]. Low protein expression of MET in ER-positive and HER2-positive breast cancer was reported [11]. The MET receptor is also associated with trastuzumab resistance of HER2-overexpressing breast cancer cells [7].

MET overexpression has been reported in 14-53.6% of patients with breast cancer [10,25,26]. In the current study, no statistically significant relationship was found between MET and breast cancer survival. Interestingly, in one meta-analysis of MET expression in breast cancer, MET overexpression was correlated with poor RFS and OS in western patients but not in Asian patients [3].

The present study confirmed that MET protein expression (determined through IHC) correlates with MET mRNA expression (determined through ISH) in invasive breast cancers.

Ethics approval and consent to participate

This study was approved by IRB of the Kangbuk Samsung Hospital (KBC14077) and written informed consent was waived.

Authors’ contributions

SID: writing, data analysis, medical record review; HCS: medical record review; HSK: funding, data analysis, writing

Conflict of Interest

The authors declare no competing interests.


This study was supported by a Superbiochips research grant (C2014072 [1268]).

Ferlay J., Soerjomataram I., Ervik M., Dikshit R., Eser S., Mathers C., et al.: “GLOBOCAN2012 v 1.0, Cancer incidence and mortality worldwide: IARC CancerBase No. 11”. [Internet]. Lyon, France: International Agency for Research on Cancer, 2013. 10.1186/s12885-017-3314-528499365
Kamangar F., Dores G.M., Anderson W.F.: “Patterns of cancer incidence, mortality, and prevalence across five continents: defining priorities to reduce cancer disparities in different geographic regions of the world”. J. Clin. Oncol., 2006,24, 2137. 16682732
Yan S., Jiao X., Zou H., Li K.: “Prognostic significance of c-Met in breast cancer: a meta-analysis of 6010 cases”. Diagn. Pathol., 2015,10, 62. 10.1186/s13000-015-0296-y26047809
Zhang Y., Xia M., Jin K., Wang S., Wei H., Fan C., et al.: “Function of the c-Met receptor tyrosine kinase in carcinogenesis and associated therapeutic opportunities”. Mol. Cancer, 2018,17, 45. 10.1186/s12943-018-0796-y29455668
Ghoussoub R.A., Dillon D.A., D’Aquila T., Rimm E.B., Fearon E.R., Rimm D.L.: “Expression of c-met is a strong independent prognostic factor in breast carcinoma”. Cancer, 1998,82, 1513. 10.1002/(sici)1097-0142(19980415)82:8<1513::aid-cncr13>;2-79554529
Hiscox S., Jordan N.J., Jiang W., Harper M., McClelland R., Smith C., et al.: “Chronic exposure to fulvestrant promotes overexpression of the c-Met receptor in breast cancer cells: implications for tumourstroma interactions”. Endocr. Relat. Cancer, 2006,13, 1085. 10.1677/erc.1.0127017158755
Shattuck D.L., Miller J.K., Carraway K.L., Sweeney C.: “Met receptor contributes to trastuzumab resistance of Her2-overexpressing breast cancer cells”. Cancer Res., 2008,68, 1471. 18316611
Tolgay Ocal I., Dolled-Filhart M., D’Aquila T.G., Camp R.L., Rimm D.L.: “Tissue microarray-based studies of patients with lymph node negative breast carcinoma show that met expression is associated with worse outcome but is not correlated with epidermal growth factor family receptors”. Cancer, 2003,97, 1841. 10.1002/cncr.1133512673709
Lengyel E., Prechtel D., Resau J.H., Gauger K., Welk A., Lindemann K., et al.: “C-Met overexpression in node-positive breast cancer identifies patients with poor clinical outcome independent of Her2/neu”. Int. J. Cancer, 2005,113, 678.
Inanc M Ozkan M., Karaca H., Berk V., Bozkurt O., Duran A.O., et al.: “Cytokeratin 5/6, c-Met expressions, and PTEN loss prognostic indicators in triple-negative breast cancer”. Med. Oncol., 2014,31, 801. 24326984
Zagouri F., Brandstetter A., Moussiolis D., Chrysikos D., Dimitrakakis C., Tsigginou A., et al.: “Low protein expression of MET in ER-positive and HER2-positive breast cancer”. Anticancer Res., 2014,34, 1227.
Gisterek I., Lata E., Halon A., Matkowski R., Szelachowska J., Biecek P., et al.: “Prognostic role of c-met expression in breast cancer patients”. Rep. Pract. Oncol. Radiother., 2011,16, 173.
Koh Y.W., Lee H.J., Ahn J.H., Lee J.W., Gong G.: “MET expression is associated with disease-specific survival in breast cancer patients in the neoadjuvant setting”. Pathol. Res. Pract., 2014,210, 494. 10.1016/j.prp.2014.04.00224814255
Zhao X., Qu J., Hui Y., Zhang H., Sun Y., Liu X., et al.: “Clinico Pathological and prognostic significance of c-Met overexpression in breast cancer”. Oncotarget, 2017,8, 56758.
Wang F., Flanagan J., Su N., Wang L.C., Bui S., Nielson A., et al.: “RNAscope: a novel in situ RNA analysis platform for formalinfixed, paraffin-embedded tissues”. J. Mol. Diagn., 2012,14, 22.
Greene F.L., Page D.L., Fleming I.D., Fritz A., Balch C.M., Haller D.G., et al.: “American Joint Committee on Cancer: AJCC Cancer Staging Manual”. 6th ed, New York, NY, USA: Springer, 2002,157.
Kwak Y., Yun S., Nam S.K., Seo A.N., Lee K.S., Shin E., et al.: “Comparative analysis of the EGFR, HER2, c-MYC, and MET variations in colorectal cancer determined by three different measures: gene copy number gain, amplification status and the 2013 ASCO/CAP guideline criterion for HER2 testing of breast cancer”. J. Transl. Med., 2017,15, 167. 10.1186/s12967-017-1265-x28764718
Choi J., Lee H.E., Kim M.A., Jang B.G., Lee H.S., Kim W.H.: “Analysis of MET mRNA expression in gastric cancers using RNA in situ hybridization assay: its clinical implication and comparison with immunohistochemistry and silver in situ hybridization”. PLoS One, 2014,9, 111658.
Gromoslaw A.S., Raffaella S., Beth M., Gayatry M., Anne B., Heidi A., et al.: “Amplification of MET May Identify a Subset of Cancers with Extreme Sensitivity to the Selective Tyrosine Kinase Inhibitor PHA-665752”. Proc. Natl. Acad. Sci. U S A, 2006,103, 231.
Jeffrey A.E., Kreshnik Z., Tetsuya M., Youngchul S., Courtney H., Joon Oh P., et al.: “MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling”. Science, 2007,316, 1039. 17463250
Danilkovitch-Miagkova A., Zbar B.: “Dysregulation of Met receptor tyrosine kinase activity in invasive tumors”. J. Clin. Invest., 2002,109, 863. 10.1172/JCI1541811927612
Carracedo A., Egervari K., Salido M., Rojo F., Corominas J.M., Arumi M., et al.: “FISH and immunohistochemical status of the hepatocyte growth factor receptor (c-Met) in 184 invasive breast tumors”. Breast Cancer Res., 2009,11, 402. 19439036
Wang M., Liang L., Lei X., Multani A., Meric-Bernstam F., Tripathy D., et al.: “Evaluation of cMET aberration by immunohistochemistry and fluorescence in situ hybridization (FISH) in triple negative breast cancers”. Ann. Diagn. Pathol., 2018,35, 69. 10.1016/j.anndiagpath.2018.04.00429843069
Ponzo M.G., Lesurf R., Petkiewicz S., O'Malley F.P., Pinnaduwage D., Andrulis I.L., et al.: “Met induces mammary tumors with diverse histologies and is associated with poor outcome and human basal breast cancer”. Proc. Natl. Acad. Sci. U S A, 2009,106, 12903. 10.1073/pnas.081040210619617568
Zagouri F., Bago-Horvath Z., Rossler F., Brandstetter A., Bartsch R., Papadimitriou C.A., et al.: “High MET expression is an adverse prognostic factor in patients with triple-negative breast cancer”. Br. J. Cancer, 2013,108, 1100. 10.1038/bjc.2013.3123422757
Gonzalez-Angulo A.M., Chen H., Karuturi M.S., Chavez-MacGregor M., Tsavachidis S., Meric-Bernstam F., et al.: “Frequency of mesenchymal- epithelial transition factor gene (MET) and the catalytic subunit of phosphoinositide-3-kinase (PIK3CA) copy number elevation and correlation with outcome in patients with early stage breast cancer”. Cancer, 2013,119, 7. 10.1002/cncr.2760822736407
Back to top