Etiology and development. The mutation in the one of

Etiology and
Molecular Basis of Cancer  

As we know that the alteration in the certain types
of genes lead to change in the normal physiology of the cell functioning and
may be converted into the cancer cells. More than 90% of the cancers are due to
the mutation in genes and only some percentage (5 to 10%) of the cancer may be
present due to hereditary or by the environmental factors. Usually, there are
two genes are responsible for the normal cell division and development
processes. The cell growth by the mitosis are under the control of
proto-oncogene, while the tumor suppressor genes are responsible for the
inhibition of the process (Gronbaek and Guldberg, 2006). Thus the balance
between the both types of genes leads to normal cell growth and development. The
mutation in the one of the both genes enhances the risk of the incidence of
cancer. If the mutation is present in the proto-oncogene the mutated genes are
called oncogenes, that causes excessive cell division and proliferation and may
lead to cancerous cells. The mutation in tumor suppressor genes also causes the
cancer and occurs mostly. But, usually there are most of the cancerous genes
are the tumor inhibition genes, for example, retinoblastoma (Rb) gene p53 gene (Corney  et al., 2008). The main function of the
p53 gene is to controlling the cell division process by checking the DNA repairement
and if the damaged DNA present causes the apoptosis (programmed cell death) (Whibley
et al, 2009). Hence, these genes are participating in the inhibition of
cell division process, are known as tumor suppressor genes.  If, there is any changes or mutation present
in these genes then they may be responsible for the formation of malignant
cells. The mutation causes the loss of the functional ability of the suppressor
genes and enhances the cell division and proliferation which changes in the
cancer cells. As the mutation in the genes increases the malignancy may also
increase in the proportionate manner and spreading the tumor cells throughout
the whole body. Other than the these two types of oncogenes and tumor
suppressor genes, some other types of genes like, apoptosis genes,
anti-apoptosis genes, are also responsible for the generation of cancer.
Mutations in the Insulin like Growth Factors (IGF), Akt genes, Bcl-2 and Bcl-XL
genes are the examples of these types of genes in the formation cancer (Denley
et al., 2008; Zhang et al., 2008; Kim  et
al., 2009).

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The proto-oncogenes and tumor suppressor genes are helpful
in the normal growth of the cells by regulation of protein formation into the
cytoplasm. The proteins stimulate the signals inside the cells for the proper
growth and development. The mutations in these types of gene affect the normal
cell cycle process by the formation of stimulatory proteins and activate the
critical growth stimulatory pathway. These signals are transferred in the form
of growth factors from one cell to another cell. The factors are attached on to
the receptors present on the cell surface and regulate the cell division
process by controlling the cell cycle in nucleus of the cell. The cell cycle
consists of mainly four phases;

1. In the first phase of cycle (G1 phase), the size
and mass of cell increases and replicate the DNA.

2. The second phase is S phase, in which the DNA replication
continues (synthesis) and cell forms all the essential components of the
genetic materials in duplicate.

3. In the next phase, G2 phase, cell ready to the
division and goes into the mitosis phase (M phase). The parent cell divides into
two daughter cells with the equal set chromosomes.

4. Then the daughter cells go either into the G1
phase and the cycle continues or into the G0 phase, resting stage of the cells.

Cyclin, cyclin dependent kinases (CDKs)
and inhibitors (CDIs) are the necessary components for the initiation and
regulation of the phases of the cell cycle. The kinases are phosphorylated with
the help of various cyclins and mediate the progression of cells from previous
phase to next one. The relationship between the cell cycle, cyclins and CDKs is
shown below in Fig. 1. CDIs are responsible for the dephosphorylation of the
CDK proteins and thus inhibit progression of cell phases. These are associated
with the tumor suppressor proteins like, p53 and pRB. The most of the cancers
show the variability in functioning or inability of one or more of these
components or proteins. Impairments in the functioning of these components
involved in the regulation of cell cycle leads to increased proliferation of
cells, the basis of tumor formation. For example, the cyclin D and E level
increases in breast cancer, while in skin cancer cells show the decreased level
of tumor suppressor proteins (p15) (Hanahan and Weinberg, 2000). The unpredictable microenvironment of the cancerous cells in all
of its existing forms i.e. solid tumors, leukemic cells, and sarcomas is well
documented. This phenomenon expressed by cancerous sites in the body poses
various obstacles towards drug’s efficacy. Thus, it becomes necessary to
develop effective delivery module in anticancer drug delivery.