Despite the potential for gemcitabine-(C4-amide)-[anti-EGFR] and gemcitabine-(C4-amide)-[anti-HER2/neu] to collectively stimulate complement C9 mediated lysis, ADCC responses and promote IgG/complement facilitated opsonization of neoplastic cells in a manner that attains enhanced levels of selective anti-neoplastic cytotoxicity, it continues to be technically difficult to simultaneously simulate and accurately measure each of these three immune-dependent responses utilizing ex-vivo models for neoplastic disease states. Here, EGFR is linked to neoplasm.