Collectively, these data suggest that although the failure to express α(II) PH and to deposit angiostatic collagen fragments (e.g. endostatin, arresten) in the ECM might account for the faster growth and more vigorous angiogenesis observed in p53(-/-) tumors, changes in endostatin or arresten levels are not a factor in the development of sunitinib resistance in p53-WT RCC nor in the enhanced suppression of angiogenesis and tumor growth resulting from the concurrent administration of MI-319 with sunitinib. Here, TP53 is linked to neoplasm.