• 哈爾濱醫(yī)科大學(xué)附屬第一醫(yī)院乳腺甲狀腺外科（黑龍江哈爾濱 150001）;

引用本文： 吳小虎,代文杰. Met：有望成為治療三陰型乳腺癌的新靶點. 中國普外基礎(chǔ)與臨床雜志, 2013, 20(7): 812-814. doi: 復(fù)制

1. Prat A， Parker JS， Karginnova O， et al. Phenotypic and molecular characterization of theclaudin-low intrinsic subtype of breast cancer[J]. Breast Cancer Res， 2010， 12(5)：R68.
2. Brenton JD， Carey LA， Ahmed AA， et al. Molecular classification and molecular forecasting of breast cancer： ready for clinical application?[J]. J Clin Oncol， 2005， 23(29)： 7350-7360.
3. Weigelt B， Baehner FL， Reis-Filho JS. The contribution of gene expression profiling to breast cancer classification， prognostication and prediction： a retrospective of the last decate[J]. J Pathol， 2010， 220(2)：263-280.
4. Liedtke C， Mazouni C， Hess KR， et al. Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer[J]. J Clin Oncol， 2008， 26(8)：1275-1281.
5. Dent R， Trudeau M， Pritchard KI， et al. Triple-negative breast cancer：clinical features and patterns of recurrence[J]. Clin Cancer Res， 2007， 13(15 Pt 1)：4429-4434.
6. Ponzo MG， Lesurf R， Petkiewicz S， et al. Met induces mammary tumors with diverse histologies and is associated with poor outcome and human basal breast cancer[J]. Proc Natl Acad Sci USA， 2009， 106(31)：12903-12908.
7. Gonzalez-Angulo AM， Chen H， Karuturi MS， 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[J]. Cancer， 2013， 19(1)：7-15.
8. Turke AB， Zejnullahu K， Wu YL， et al. Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC[J]. Cancer Cell， 2010， 17(1)：77-88.
9. Baselga J， Albanell J， Ruiz A， et al. PhaseⅡand tumor pharma-codynamic study of gefitinib in patients with advanced breast cancer[J]. J Clin Oncol， 2005， 23(23)：5323-5333.
10. Mueller KL， Madden JM， Zoratti GL， et al. Fibroblast-secreted hepatocyte growth factor mediates epidermal growth factor receptortyrosine kinase inhibitor resistance in triple-negative breast cancersthrough paracrine activation of Met[J]. Breast Cancer Res， 2012，.
11. Accornero P， Miretti S， Bersani F， et al. Met receptor acts uniq-uely for survival and morphogenesis of EGFR-dependent normal mammary epithelial and cancer cells[J]. PLoS One， 2012， 7(9)：e44982.
12. Gastaldi S， Sassi F， Accornero P， et al. Met signaling regulates growth， repopulating potential and basal cell-fate commitment of mammary luminal progenitors：implications for basal-like breast cancer[J]. Oncogene， 2012， 32(11)：1428-1440.
13. Shojaei F， Lee JH， Simmons BH， et al. HGF/c-Met acts as an alternative angiogenic pathway in sunitinib-resistant tumors[J]. Cancer Res， 2010， 70(24)：10090-10100.
14. (4)： R104.
15. Gallahan D， Kozak C， Callahan R. A new common integration region (int-3) for mouse mammary tumor virus on mouse chromosome17[J] . J Virol， 1987， 61(1)：218-220.
16. Xu K， Usary J， Kousis PC， et al. Lunatic fringe deficiency coop-erates with the Met/Caveolin gene amplicon to induce basal-like breast cancer[J]. Cancer Cell， 2012， 21(5)：626-641.
17. Burgess T， Coxon A， Meyer S， et al. Fully human monoclonal antibodies to hepatocyte growth factor with therapeutic potentialagainst hepatocyte growth factor/c-Met-dependent human tumors[J]. Cancer Res， 2006， 66(3)： 1721-1729.
18. Peters S， Adjei AA. MET： a promising anticancer therapeutictarget[J]. Nat Rev Clin Oncol， 2012， 9(6)：314-326.
19. US National Library of Medicine. Clinical Trials. gov[online]，2012， http：//clinicaltrials. gov/show/NCT01186991.
20. Munshi N， Jeay S， Li Y， et al. ARQ197， a novel and selective inhibitor of the human c-Met receptor tyrosine kinase with antit-umor activity[J]. Mol Cancer Ther， 2010， 9(6)：1544-1553.
21. US National Library of Medicine. Clinical Trials. gov[online]， 2012， http：//clinicaltrials. gov/ct2/show/NCT01147484.
22. Wu ZS， Wu Q， Wang CQ， et al. miR-340 inhibition of breast cancer cell migration and invasion through targeting of oncoproteinc-Met[J]. Cancer， 2011， 117(13)：2842-2852.
  1. 1. Prat A， Parker JS， Karginnova O， et al. Phenotypic and molecular characterization of theclaudin-low intrinsic subtype of breast cancer[J]. Breast Cancer Res， 2010， 12(5)：R68.
  2. 2. Brenton JD， Carey LA， Ahmed AA， et al. Molecular classification and molecular forecasting of breast cancer： ready for clinical application?[J]. J Clin Oncol， 2005， 23(29)： 7350-7360.
  3. 3. Weigelt B， Baehner FL， Reis-Filho JS. The contribution of gene expression profiling to breast cancer classification， prognostication and prediction： a retrospective of the last decate[J]. J Pathol， 2010， 220(2)：263-280.
  4. 4. Liedtke C， Mazouni C， Hess KR， et al. Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer[J]. J Clin Oncol， 2008， 26(8)：1275-1281.
  5. 5. Dent R， Trudeau M， Pritchard KI， et al. Triple-negative breast cancer：clinical features and patterns of recurrence[J]. Clin Cancer Res， 2007， 13(15 Pt 1)：4429-4434.
  6. 6. Ponzo MG， Lesurf R， Petkiewicz S， et al. Met induces mammary tumors with diverse histologies and is associated with poor outcome and human basal breast cancer[J]. Proc Natl Acad Sci USA， 2009， 106(31)：12903-12908.
  7. 7. Gonzalez-Angulo AM， Chen H， Karuturi MS， 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[J]. Cancer， 2013， 19(1)：7-15.
  8. 8. Turke AB， Zejnullahu K， Wu YL， et al. Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC[J]. Cancer Cell， 2010， 17(1)：77-88.
  9. 9. Baselga J， Albanell J， Ruiz A， et al. PhaseⅡand tumor pharma-codynamic study of gefitinib in patients with advanced breast cancer[J]. J Clin Oncol， 2005， 23(23)：5323-5333.
  10. 10. Mueller KL， Madden JM， Zoratti GL， et al. Fibroblast-secreted hepatocyte growth factor mediates epidermal growth factor receptortyrosine kinase inhibitor resistance in triple-negative breast cancersthrough paracrine activation of Met[J]. Breast Cancer Res， 2012，.
  11. 11. Accornero P， Miretti S， Bersani F， et al. Met receptor acts uniq-uely for survival and morphogenesis of EGFR-dependent normal mammary epithelial and cancer cells[J]. PLoS One， 2012， 7(9)：e44982.
  12. 12. Gastaldi S， Sassi F， Accornero P， et al. Met signaling regulates growth， repopulating potential and basal cell-fate commitment of mammary luminal progenitors：implications for basal-like breast cancer[J]. Oncogene， 2012， 32(11)：1428-1440.
  13. 13. Shojaei F， Lee JH， Simmons BH， et al. HGF/c-Met acts as an alternative angiogenic pathway in sunitinib-resistant tumors[J]. Cancer Res， 2010， 70(24)：10090-10100.
  14. 14. (4)： R104.
  15. 15. Gallahan D， Kozak C， Callahan R. A new common integration region (int-3) for mouse mammary tumor virus on mouse chromosome17[J] . J Virol， 1987， 61(1)：218-220.
  16. 16. Xu K， Usary J， Kousis PC， et al. Lunatic fringe deficiency coop-erates with the Met/Caveolin gene amplicon to induce basal-like breast cancer[J]. Cancer Cell， 2012， 21(5)：626-641.
  17. 17. Burgess T， Coxon A， Meyer S， et al. Fully human monoclonal antibodies to hepatocyte growth factor with therapeutic potentialagainst hepatocyte growth factor/c-Met-dependent human tumors[J]. Cancer Res， 2006， 66(3)： 1721-1729.
  18. 18. Peters S， Adjei AA. MET： a promising anticancer therapeutictarget[J]. Nat Rev Clin Oncol， 2012， 9(6)：314-326.
  19. 19. US National Library of Medicine. Clinical Trials. gov[online]，2012， http：//clinicaltrials. gov/show/NCT01186991.
  20. 20. Munshi N， Jeay S， Li Y， et al. ARQ197， a novel and selective inhibitor of the human c-Met receptor tyrosine kinase with antit-umor activity[J]. Mol Cancer Ther， 2010， 9(6)：1544-1553.
  21. 21. US National Library of Medicine. Clinical Trials. gov[online]， 2012， http：//clinicaltrials. gov/ct2/show/NCT01147484.
  22. 22. Wu ZS， Wu Q， Wang CQ， et al. miR-340 inhibition of breast cancer cell migration and invasion through targeting of oncoproteinc-Met[J]. Cancer， 2011， 117(13)：2842-2852.