الفهرس 
Cancer biology
DC as a potential anticancer immunotherapeutic approachOnly 14 pages are availabe for public view
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Abstract
Cancer accounts for a significant proportion of deaths worldwide. Cancer patients are most likely to be treated successfully when they are diagnosed at the early stages of the disease through traditional treatments such as surgery,chemotherapy and radiotherapy. However, many cancer patients are diagnosed at late stages where the cancer has become progressive and metastasized to other organs. Even if the cancer is treated at the early stages, minimal residual cells could remain dormant post-treatment and may cause tumor relapse later on where the cancer became more aggressive and eventually metastasized to other organs.
Cancer is one of the leading causes of morbidity and mortality
worldwide. According to the GLOBOCAN estimates of cancer incidence and
mortality which is generated by the International Agency for Research on
Cancer, there are an estimated 18.1 million new cancer cases in the year 2018.
(Bray et al., 2018).
The common therapeutic strategies used mainly in the treatment of
cancer patients are surgery, radiotherapy, and chemotherapy. Cancer
heterogeneity is one of the reasons of poor prognosis in cancer patients treated
by these strategies (Pandya et al., 2016). Cancer is caused by the
accumulation of genetic alterations, which lead to the activation or increase
of proteins that promote cell growth and survival and the loss or inactivation
of proteins that promote cell cycle arrest or cell death (Bruttel and
Wischhusen, 2014).
Many molecular lesions occur every day, most of these are repaired
instantly which means that highly effective control mechanisms must be
present to prevent tumors formation by mutant cells. This comprises both cellintrinsic
mechanisms, such as tumor suppressor genes and DNA repair
enzymes and the cell-extrinsic mechanisms of the immune system (Bruttel
and Wischhusen, 2014).
Tumor progression involves complicated cellular and molecular
processes that are preceded by genetic or epigenetic changes leading to the
transformation to cancer cells. Theoretically, carcinogenesis can be divided
Chapter II Review of Literature
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into the following stages: initiation, promotion, progression and metastasis.
These stages are associated with many complex and dynamic cellular events
as summarized in Figure 2.1 (Ayob and Ramasamy, 2018).
Initiation encompasses the alteration or mutation of genes generated
spontaneously or induced by the exposure to a carcinogen. Genetic alterations
can lead to dysregulation of many biochemical signaling pathways that are
associated with proliferation, differentiation, and survival. This can be
affected by many factors, including the type and rate of carcinogen
metabolism and the DNA repair responses (Siddiqui et al., 2015).
The promotion stage is regarded as a relatively long and reversible
process in which the accumulation of actively proliferating pre-neoplastic
cells occur. During this period, this stage could be altered by chemopreventive
agents which could affect the tumor growth rate (Ayob and
Ramasamy, 2018).
Progression is the stage between a pre-malignant lesion and the
development of an invasive cancer (Moolgavkar and Luebeck, 2003). It is
the last stage of neoplastic transformation in which genetic and phenotypic
modifications as well as cellular proliferation occur. During this stage, a fast
increase in the tumor size, where cells may undergo additional mutations with
metastatic potential. Chemo-preventive agents act preferentially within both
initiation and promotion stages of carcinogenesis (Siddiqui et al., 2015). The
metastatic stage of carcinogenesis involves the migration of cancer cells
from the primary tumor site to other body sites through the bloodstream or
the lymphatic system (Bregenzer et al., 2019).