象征性的分析和減少超大規(guī)模集成電路技術(shù)

Most cancer morbidity and mortality occurs upon spread of the tumor
from an original localized site. Primary tumors are, by and large, accessible
for surgical removal or radiological elimination. However, once the tumor
extends beyond the physiological borders, these approaches are either
rendered ineffective or engender significant morbidity and mortality in
themselves. Subsequent therapeutics suffer from the need to be globally or
broadly applied with the concomitant toxicities. Limiting this dissemination
would provide palliative benefit, improve physical targeting of cytotoxic
therapies, or just stabilize the tumor in a manageable state. Therefore, such
limitation of tumor dissemination per se is an appropriate goal for new
therapies. However, to realize this in a rational and targeted manner, tumor
cell behaviors that enable dissemination must be defined and their key
molecular controls identified.
Tumor dissemination takes two forms, invasion and metastasis (Table 1).
Localized invasion of unaffected tissue and adnexia compromises normal
homeostatic functions of the organs. This invasion is distinct from noninvasive
but otherwise growing localized tumors in that the invasive tumor
cells breach physiologic boundries and/or organ capsules to interdigitate
with normal cells. That this ability is not simply related to cell proliferation
was evident when it was noted that the growth rate of invasive tumors was
not appreciably greater than encapsulated counterparts (1). A number of cell
properties were examined as the basis for this contiguous spread. Induced
cell motility has come to be recognized as the dominant regulator of tumor
invasion (2), particularly as matrix degradation and remodeling is now
understood to be limited rather than extensive, and a part of or partner to
motility (3, 4) (see Chapter 7).