Although, Avastin and Kadcyla areboth targeting processes and they block specific protein receptors, the twodiffer in the mechanism of action inside the cells.
Avastin lessens the developmentof new blood vessels as well as tumour growth. It works by only blocking solubleVEGF-A. When VEGF-A signalling is congested in an extremely vascularisedtumour, it results in inhibition of blood flow, ‘endothelial cell apoptosis,pericyte migration and empty basement membrane sleeves’ (Google Books 2018). Nevertheless, if avastin treatment is ceased,the VEGF proteins are accessible to stimulate the residual endothelial cells,which ‘uses the empty basement membrane sleeves as a scaffold for rapidrevascularization of the tumours as new blood vessels begin to form again’ (Google Books 2018). Overexpression ofVEGF causes edema which is ‘an accumulation of fluid around the tumour due toincreased endothelial cell permeability; thereby compromising the blood-brainbarrier’ (Google Books 2018). Withavastin, when VEGF reduce in number, the permeability of endothelial cells alsodecreases. As a result, the veracity of the blood brain barrier is reinstated.When the vascular system is reinstated it allows better functioning.
Consequently, with functional blood vessels, chemotherapy agents can beallotted successfully which in turn destroys tumour cells thereby decreasingthe growth rate of the tumour. (GoogleBooks 2018)