Date of Award

Spring 1995

Document Type

Restricted Thesis

Terms of Use

© 1995 Gaël-Christophe G. McGill. All rights reserved. Access to this work is restricted to users within the Swarthmore College network and may only be used for non-commercial, educational, and research purposes. Sharing with users outside of the Swarthmore College network is expressly prohibited. For all other uses, including reproduction and distribution, please contact the copyright holder.

Degree Name

Bachelor of Arts



First Advisor

Robert E. Savage


The control of cell proliferation, differentiation. and death requires the coordinated regulation of specific genes that influence progression through the cell cycle. Pathways leading to growth and differentiation are closely linked to those leading to programmed cell death/apoptosis. An integration of signals from both the soluble (growth factors and hormones) and insoluble (extracellular matrix (ECM) and neighboring cell surfaces) environment of the cell is necessary for entry into anyone of these cell fates, and mutations in these regulatory pathways often results in abberant cell cycling and cancer. While it is well established that many cellular proto-oncogenes which code for growth factors or their receptors are involved in cancer (6 and references therein), only recently has research focused on cell-ECM interactions, the intracellular signaling events they activate. and their significance in cancer. Specifically, decreased requirements for substrate attachment and spreading as well as altered patterns of integrin expression have been observed in transformed cells (124, 146, 82). In addition, transformation has been shown to confer resistance to apoptosis triggered by the loss of anchorage in endothelial and epithelial cell types (137). A better understanding of the mechanisms by which ECM/integrin-transduced signals cooperate with growth factor activated pathways to regulate proliferation, cell cycle arrest, or apoptosis seems crucial in devising new therapies against cancer.