A method for modulating angiogenesis in a cancer or tumor refractory to anti-VEGF, including identifying a cancer cell as being referactory to anti-VEGF, and then contacting the cancer cell refractory to anti-VEGF with an effective amount of an agent that modulates interaction between Gal1 or a Gal1 fragment and the natural binding partner of Gal1 or the Gal1 fragment to thereby modulate angiogenesis.
