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Regression in renal cell carcinoma as re-expression of cell death in kidney development

Article Abstract:

A significantly higher percentage of Renal Cell Carcinomas (RCC) undergo spontaneous regression. A new hypothesis for this phenomenon states that spontaneous regression of RCCs is a re-expression of cell death which normally occurs during the embryonic formation of the kidneys. Nephrogenesis is characterized by regressive events wherein certain intermediate structures are programmed to appear and disappear. Cancer cells resemble embryonic cells in some respects, a resemblance that could be carried as far as reverting back to the regression of tissues seen in embryonic kidney tissues.

Author: Pansera, Francesco
Publisher: Johns Hopkins University Press
Publication Name: Perspectives in Biology and Medicine
Subject: Health
ISSN: 0031-5982
Year: 1992
Research, Carcinoma, Renal cell, Renal cell carcinoma, Cancer regression

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Could atherosclerosis originate from defective smooth muscle cell death (apoptosis)?

Article Abstract:

Research into the origin of atherosclerosis contradicts the monoclonal approach which identifies the condition as an oligoclonal disorder. The pivotal role of polyclonal response in vascular smooth muscle growth is now being advanced as a likely hypothesis. Analysts, however, advocate that subject to certain assumptions, atherosclerosis may have a growth path similar to that obtained in human follicular B-cell lymphoma. This is upheld by recent findings in non-transformed smooth muscle cells. This thesis also helps explore other lesser known aspects of atherosclerosis.

Author: Rembold, Christopher
Publisher: Johns Hopkins University Press
Publication Name: Perspectives in Biology and Medicine
Subject: Health
ISSN: 0031-5982
Year: 1996
Analysis, Growth, B cells, Atherosclerosis, Vascular smooth muscle

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Form and cause in multiple sclerosis

Article Abstract:

A molecular model is developed to explain the presence of sharp plaqueedges and the possible etiology and pathogenesis of demyelination in multiple sclerosis. The model shows that the sharpness of the lesion edge is an inverse function of the width. The width (W) is represented by the equation, W = DuV, where Du is the diameter of the target unit of tissue affected by the pathologic agent while V is the number of units of pathologically involved borders.

Author: Pansera, Francesco
Publisher: Johns Hopkins University Press
Publication Name: Perspectives in Biology and Medicine
Subject: Health
ISSN: 0031-5982
Year: 1993
Models, Multiple sclerosis, Demyelination, Demyelinating diseases

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