Abstract: Active acquisition of the established malignant phenotypic traits of primary breast carcinoma is primarily directed by an infiltration of the stroma that concurrently and in turn also acquires an increased vascular density. In such a setting of biologic instability and progressiveness, the mechanics of pathogenesis of the malignant transformation process are primarily dictated by a series of overlapping regions of influence in multiple foci of breast involvement such process evolves in a manner that specifically and deterministically outlines integral lesion pathogenesis as carcinogenesis. Stromal infiltration and increased stromal vascular density, hence are active promoters of the malignancy in terms that do not solely or phenomenally outline such carcinomatous transformation. The stromal phenomena integrally enveloping proliferative foci of ductal and lobular epithelium are the source of the incremental progressiveness in carcinogenesis in a manner that also contributes to potential diversity of the specific morphologic attributes of the primary malignant lesion. Such processes are operatively determined irrespective of subsequent dynamics of spread of the lesion, locally and systemically. In this manner, an integral complexity of evolution of the acquired malignant process primarily originates within potential sites of an apparently initial reactive or proliferative focus that initiates stromal change; this is dominantly characterized by involved infiltrative change as reflected and classically denoted at times by infiltrating epitheliosis or papillomatosis in the first instance. It is in the analysis of such regionally dynamic and overlapping phenomena that the carcinogenesis phenomena are determined biologically beyond simple consideration of the subsequent sequential consequences of local spread and metastasis of the proliferative focus. Such considerations implicate attributed novel phenomena as a redefined malignant transformation series of events through the initiation and maintenance of progression and as further amplified infiltrativeness and spread, locally and systemically. It is in terms of such redefinition of the mechanics of malignant characterization that the proliferative neoplasm is both an original focus for infiltration and spread and also a real consequence of such phenomena in the enhancement of neoplastic malignancy both biologically and pathogenically.