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PMID: 29986520 Seiwerth, S., et al

[PubMed: 581875] 247

Gene expression analysis indicated that these suboptimal results were likely due to lower endogenous Nodal signaling and elevated BMP signal activities [1]

Met activation has been extensively shown to drive proliferation, migration, invasion, and angiogenesis in HNSCC and other tumor types (16) and HGF/Met activation is a known mechanism of resistance to anti-EGFR therapy (17)

This boosted tendon cell proliferation and serves as evidence toward the possibility of this peptides healing abilities

ACMG recommendations for reporting of incidental findings in clinical exome and genome sequencing