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Wang J, Goetsch L, Tucker L, et al. Anti-c-Met monoclonal antibody ABT-700 breaks oncogene addiction in tumors with MET amplification. BMC Cancer. 2016;16:105doi: 10.1186/s12885-016-2138-z.
Wang, J., Goetsch, L., Tucker, L., Zhang, Q., Gonzalez, A., Vaidya, K. S., Oleksijew, A., Boghaert, E., Song, M., Sokolova, I., Pestova, E., Anderson, M., Pappano, W. N., Ansell, P., Bhathena, A., Naumovski, L., Corvaia, N., & Reilly, E. B. (2016). Anti-c-Met monoclonal antibody ABT-700 breaks oncogene addiction in tumors with MET amplification. BMC cancer, 16105. https://doi.org/10.1186/s12885-016-2138-z
Wang, Jieyi, et al. "Anti-c-Met monoclonal antibody ABT-700 breaks oncogene addiction in tumors with MET amplification." BMC cancer vol. 16 (2016): 105. doi: https://doi.org/10.1186/s12885-016-2138-z
Wang J, Goetsch L, Tucker L, Zhang Q, Gonzalez A, Vaidya KS, Oleksijew A, Boghaert E, Song M, Sokolova I, Pestova E, Anderson M, Pappano WN, Ansell P, Bhathena A, Naumovski L, Corvaia N, Reilly EB. Anti-c-Met monoclonal antibody ABT-700 breaks oncogene addiction in tumors with MET amplification. BMC Cancer. 2016 Feb 16;16:105. doi: 10.1186/s12885-016-2138-z. PMID: 26879245; PMCID: PMC4755020.
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BMC Cancer. 2016 Feb 16;16:105. doi: 10.1186/s12885-016-2138-z.

Anti-c-Met monoclonal antibody ABT-700 breaks oncogene addiction in tumors with MET amplification.

BMC cancer

Jieyi Wang, Liliane Goetsch, Lora Tucker, Qian Zhang, Alexandra Gonzalez, Kedar S Vaidya, Anatol Oleksijew, Erwin Boghaert, Minghao Song, Irina Sokolova, Ekaterina Pestova, Mark Anderson, William N Pappano, Peter Ansell, Anahita Bhathena, Louie Naumovski, Nathalie Corvaia, Edward B Reilly

Affiliations

  1. AbbVie, North Chicago, IL, USA. [email protected].
  2. AbbVie Biotherapeutics, 1500 Seaport Blvd., Redwood City, CA, 94063, USA. [email protected].
  3. IRPF, Centre d'Immunologie Pierre Fabre 5, Av Napoléon III, F-74164, Saint-Julien-en-Genevois, France. [email protected].
  4. AbbVie, North Chicago, IL, USA. [email protected].
  5. AbbVie, North Chicago, IL, USA. [email protected].
  6. IRPF, Centre d'Immunologie Pierre Fabre 5, Av Napoléon III, F-74164, Saint-Julien-en-Genevois, France. [email protected].
  7. AbbVie, North Chicago, IL, USA. [email protected].
  8. AbbVie, North Chicago, IL, USA. [email protected].
  9. AbbVie, North Chicago, IL, USA. [email protected].
  10. Abbott Molecular, Des Plaines, IL, USA. [email protected].
  11. Abbott Molecular, Des Plaines, IL, USA. [email protected].
  12. Abbott Molecular, Des Plaines, IL, USA. [email protected].
  13. AbbVie, North Chicago, IL, USA. [email protected].
  14. AbbVie, North Chicago, IL, USA. [email protected].
  15. AbbVie, North Chicago, IL, USA. [email protected].
  16. AbbVie, North Chicago, IL, USA. [email protected].
  17. AbbVie Biotherapeutics, 1500 Seaport Blvd., Redwood City, CA, 94063, USA. [email protected].
  18. IRPF, Centre d'Immunologie Pierre Fabre 5, Av Napoléon III, F-74164, Saint-Julien-en-Genevois, France. [email protected].
  19. AbbVie, North Chicago, IL, USA. [email protected].

PMID: 26879245 PMCID: PMC4755020 DOI: 10.1186/s12885-016-2138-z

Abstract

BACKGROUND: c-Met is the receptor tyrosine kinase for hepatocyte growth factor (HGF) encoded by the MET proto-oncogene. Aberrant activation of c-Met resulting from MET amplification and c-Met overexpression is associated with poor clinical outcome in multiple malignancies underscoring the importance of c-Met signaling in cancer progression. Several c-Met inhibitors have advanced to the clinic; however, the development of inhibitory c-Met-directed therapeutic antibodies has been hampered by inherent agonistic activity.

METHOD: We generated and tested a bivalent anti-c-Met monoclonal antibody ABT-700 in vitro for binding potency and antagonistic activity and in vivo for antitumor efficacy in human tumor xenografts. Human cancer cell lines and gastric cancer tissue microarrays were examined for MET amplification by fluorescence in situ hybridization (FISH).

RESULTS: ABT-700 exhibits a distinctive ability to block both HGF-independent constitutive c-Met signaling and HGF-dependent activation of c-Met. Cancer cells addicted to the constitutively activated c-Met signaling driven by MET amplification undergo apoptosis upon exposure to ABT-700. ABT-700 induces tumor regression and tumor growth delay in preclinical tumor models of gastric and lung cancers harboring amplified MET. ABT-700 in combination with chemotherapeutics also shows additive antitumor effect. Amplification of MET in human cancer tissues can be identified by FISH.

CONCLUSIONS: The preclinical attributes of ABT-700 in blocking c-Met signaling, inducing apoptosis and suppressing tumor growth in cancers with amplified MET provide rationale for examining its potential clinical utility for the treatment of cancers harboring MET amplification.

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