The Biology of Cancer - Vibrational Spectroscopy for Tissue Analysis - page 48

the reduced adhesiveness of cancer cells also results in morphological and
cytoskeletal alterations: Many tumour cells are rounder than normal ones, in
part because they are less firmly attached to either the extracellular matrix or
neighboring cells [7]. Cancer cells are capable of creating their own signals
(and reprogram) for growth and division [77].
In a simple description, some of the common characteristics of malignant
cells are as follows [6]:
• The morphology and size of cells are different and more variable
than those of normal cells.
• The nucleus of the cells is larger than in normal cells.
• Large cells with multiple nuclei can be seen.
• Normal tissues are invaded by malignant cells.
Two additional properties of cancer cells affect their interaction with other
tissue components, thereby playing important roles in invasion and metas-
tasis. First, malignant cells generally secrete proteases (e.g., collanenase in
carcinomas), which digest extracellular matrix components, allowing the
cancer cells to invade adjacent normal tissues. Second, cancer cells secrete
growth factors that promote the formation of new blood vessels ( angiogen-
esis ). Angiogenesis is needed to support the growth of a tumour because
blood vessels are required to supply oxygen and nutrients to the proliferat-
ing tumour cells. The formation of such new blood vessels is important not
only in supporting tumour growth, but also in metastasis. These capillaries
provide a ready opportunity for cancer cells to enter the circulatory system
and begin the metastatic process [7].
Another general characteristic of most cancer cells is that they fail to dif-
ferentiate normally. Such effective differentiation is closely coupled to abnor-
mal proliferation, since most fully differentiated cells cease cell division.
Rather than carrying out their normal differentiation program, cancer cells
are usually blocked at an early stage of differentiation, consistent with their
continued active proliferation [7].
Some of the properties and specifications of cancer cells are consequences
of activation of oncogenes or the ablation of the tumour suppressor genes,
which may lead to the fact that the growth arrest process associated with
ageing (senescence) may be overridden. Senescence is usually correlated
with a decrease in the length of telomeres, which are short, tandem repeats
of hexanucleotide 5'-TTAGGG-3' at the ends of each chromosome. Telomeres
are synthesized by telomerase, a ribonucleo-protein DNA polymerase that is
active in many tumours but is not common in normal tissue [78]. In tumour
cell lines, telomerase activity reaches a maximum in the S phase and a vari-
ety of inhibitors of cell cycle progression (e.g., transforming growth factor β1)
inhibit the activity of telomerase [30].