International Journal of Molecular Medicine and Advance Sciences

Year: 2005
Volume: 1
Issue: 4
Page No. 317 - 323

Paracrine Transformation to Autocrine Autonomy in Tumor Cell Proliferation and Spread. Is the Neoplastic Blood Supply a Functional Determinant of Clonality In Inducing Biologic Tumor Progressiveness?

Authors : Lawrence M. Agius

Abstract: A theory of selectivity in terms of clonal progression of neoplasms might directly implicate a primary susceptibility of blood supply systems in transformation of paracrine responsiveness to autocrine autonomy. Subsequent neoplastic evolution might constitute forms of establishment of aberrant vascularity in inducing a clonality of tumor cell subpopulations that are integrally a single system of progression through transformation. In various ways, the active processes of tumor cell proliferation and spread through infiltration and metastases would paradoxically constitute systems of operative autonomy within a context of evolving influence. Indeed, clonality of neoplastic progression might involve a transformation that integrally evolves simply as patterns of aberrant blood supply both in initial establishment and in subsequent evolution towards higher tumor grades. In simple terms, perhaps, one might speak of different modes of evolving transformation of tumor cells as clonally derived cells centered on aberrant blood supply that is inherently a point of reference in terms even of basic malignant transformation as a carcinogenic event. Beyond even considerations of strict initial malignant transformation, however, aberrant blood supply systems would constitute a persistent source of transformation in establishing neoplastic progression in terms largely of biologic attributes of clonality towards transformation of paracrine responsiveness to autocrine autonomy.

How to cite this article:

Lawrence M. Agius , 2005. Paracrine Transformation to Autocrine Autonomy in Tumor Cell Proliferation and Spread. Is the Neoplastic Blood Supply a Functional Determinant of Clonality In Inducing Biologic Tumor Progressiveness? . International Journal of Molecular Medicine and Advance Sciences, 1: 317-323.

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