Cancer and
Inflammations
Basics
of cancer development
Cancer results from the outgrowth of a
clonal population of cells from tissue. The development of cancer, referred to
as carcinogenesis, can be modeled and characterized in many ways. Cancer
development requires the acquisition of six fundamental properties:
self-sufficient proliferation, insensitivity to anti-proliferative signals,
evasion of apoptosis, unlimited replicative potential, the maintenance of
vascularization, and, for malignancy, tissue invasion and metastasis.
Cancer can also be considered regarding
a step-wise development functionally grouped into three phases: initiation,
promotion, and progression. Initiation is characterized by genomic changes
within the “cancer cell,” such as point mutations, gene deletion and
amplification, and chromosomal rearrangements leading to irreversible cellular
changes. Tumour development is promoted by the survival and clonal expansion of
these “initiated” cells. Progression encompasses a substantial growth in tumour
size and either growth-related or mutually exclusive metastasis.
Relation
between Cancer and inflammation: -
v Chronic infection in immunocompetent hosts such
as human papilloma virus or hepatitis B and C virus infection leads to
cervical and hepatocellular carcinoma, respectively.
v Microbes may cause
cancer due to opportunistic infection such as in Kaposi’s sarcoma (a result
of human herpes virus (HHV)-8 infection) or inappropriate immune
responses to microbes in certain individuals, which may occur in
gastric cancer, secondary to Helicobacter pylori colonization or cancer because
of long-standing inflammatory bowel disease precipitated by the intestinal
microflora.
v Conditions associated
with chronic irritation and subsequent inflammation predispose to cancer, such as
the long-term exposure to cigarette smoke, asbestos, and silica.
v However, the tumour
associated stroma may undergo selective pressure, as there have been recent
reports of genetic changes in tumour associated stroma [51] and even loss of
p53 in tumour-associated fibroblasts.
v The cell death and
tissue injury that may occur right after initiation may induce tissue repair
and homeostatic responses leading to tumour progression. In addition, signals
derived from microbes also might activate innate microbial recognition pathways
enhancing the development of tumours.
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