Lead Target Mig7, a pan cancer-specific target

•  This oncofetal gene expression is induced by multiple growth factors and is localized at multiple types of primary tumors, metastatic niche as well as in circulation.

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•  Mig7 is not expressed by normal cells and is primate-specific.

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•  This cysteine- and lysine-rich protein is embryonic, trophoblast cell- and solid tumor cancer cell-specific.

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•  Functional studies demonstrate that it causes epithelial to mesenchyme transition through inducing TWIST expression, carcinoma cell invasion of extracellular matrix, and formation of vessel-like structures in 3D cultures.

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•  Mig7 increases membrane type 1 matrix metalloproteases enzyme (MT1-MMP) activity, sustains activity of ERK 1/2, AKT as well as S6 kinase signaling, and increases cleavage to form pro-invasion laminin-332 γ2 chain fragments. These events are required for cancer progression and metastasis.

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•  Mig7 polyclonal and monoclonal antibodies significantly inhibit cancer cell invasion and peptide vaccine induces ex vivo cancer cell killing.

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•  Novel Mig7 monoclonal antibodies reduce primary tumor size to that of control in endometrial carcinoma nude mouse pilot studies.

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Mig7 targeted therapies would likely reduce:

 

1.  or eliminate unwanted current therapies side effects due because Mig7 expression is specific to cancer cells. 

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2.  R&D, regulatory and approval costs because Mig7 is expressed by many types of cancers, 96% of malignant cancers at primary and metastatic sites as well as in circulating cancer cells.

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3.  or prevent resistance because Mig7 expression is induced by several key promoters of cancer such as c-Met (HGF), EGF, IGF-1 and Cox-2 activation of their respective tyrosine kinase receptors. It is known that  cancer cells can become resistant to one receptor targeting therapy by using another receptor for growth and invasion.

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