Biomedical Engineering Reference
In-Depth Information
which is the principle point at which cell size and nutrient availability are
monitored. In animals, the primary example of cell cycle control in G 2 is
provided by oocytes . Vertebrate oocytes can remain arrested in G 2 for long
periods of time (several decades in humans) until their progression to the M
phase is triggered by hormonal stimulation.
Properties of Cancerous Cells
Much evidence shows that cancer develops by a multistep process [3], and
the uncontrolled growth of cancer cells results from accumulated abnormali-
ties affecting many of the cell regulatory mechanisms. This relationship is
reflected in several aspects of cell behaviour that distinguishes cancer cells
from their normal counterparts. Cancer cells typically display abnormalities
in the mechanisms that regulate normal cell proliferation, differentiation,
and survival [7].
The general features of neoplastic cells result in specific changes in nucleic
acid, protein, lipid, carbohydrate quantities, and/or conformations. For exam-
ple, neoplastic cells are known to produce more lactate than normal cells.
The DNA protein interaction is also disturbed in malignant transformations
resulting in repeated duplication and amplification of DNA sequences [1].
Neoplastic cells are characterized by increased nuclear material, an increased
nuclear-to-cytoplasmic ratio, increased mitotic activity, abnormal chromatin
distribution, and decreased differentiation. There is a progressive loss of cell
maturation, and proliferation of these undifferentiated cells results in increased
metabolic activity. Histologically, neoplasms are characterized by cellular
crowding and disorganization. The increased metabolic activity induces rapid
angiogenesis and results in the formation of leaky vessels [1].
It has been demonstrated that the total lipid and phospholipid content of
cancerous tissue are more than that of the normal tissue [70]. The total cho-
lesterol content of malignant tissues is also reported to be higher than that of
normal tissue [70]. Membranes of lung cancer tissue are reported to be more
fluid than the corresponding normal tissues. Furthermore, high plasma
membrane fluidity of lung tumours is associated with poor prognosis [71,72].
Cell membrane fluidization is linked with multidrug resistance [73]. Not only
the lipid levels, but also the protein levels are altered due to carcinogenesis
[74-76]. Wong et al. studied seven different proteins in normal and cancer-
ous cervical tissues [75]. The structure of the proteins of the cytoskeleton and
extracellular matrix (ECM) are transformed by cancer [77]. Altered protein
structures also change the ability of the cancer cells to contract or stretch,
by influencing their deformation. As a result, the motility of cancer cells can
be very different from that of normal cells [24], causing them to migrate to
different sites in the human body and induce metastasis [77]. In addition,
 
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