A major problem that cancer therapeutics faces today is
coping with a diversity of cancer diseases. Hanahan and Weinberg [1,2] reasoned
that since all mammalian cells express the same molecular mechanisms for proliferation,
differentiation and death, cancers should share a limited number of systems
that govern their behavior. This is insightful because cancers represent an
array of diseases. To develop cancer research into a more logical science and
to provide a focused characterization of cancer, Hanahan et al. [1] defined six
major hallmarks of cancer that control cell homeostasis and proliferation.
These include self-sufficiency in growth signals, insensitivity to
growth-inhibitory (antigrowth) signals, evasion of apoptosis, limitless
replicative potential, sustained angiogenesis, and tissue invasion and
metastasis. Progress made in the last decade has added two emerging hallmarks
including reprogramming of energy metabolism and evading immune destruction
[2]. More recently Vogelstein et al. [3] defined a cancer genome landscape,
finding that cancers are “pathway diseases” with two to eight “driver gene”
mutations from a class of 12 signaling pathways that
regulate three core cellular processes: cell fate, cell survival
and genome maintenance. With an evolving understanding of molecular mechanisms
of cancer, treatment strategies using mutation-specific small molecule drugs or
monoclonal antibodies have been developed to specifically target some cancers
in the perspective of defined cancer hallmarks. One example is the treatment of
B-RAF oncoprotein in melanoma, which provides sufficiency of growth signals
[4]. However, tumors treated with B-RAF inhibitors nearly always develop
resistance after about six to nine months of treatment, and the tumors return
or begin growing again. Thus, new treatment modalities to treat cancer are
needed. When these new modalities are introduced it should be of interest to
determine which of the hallmarks of cancer are targeted. Furthermore,
increasing evidence indicates that it is important to know mechanisms of cell
death.
During developmental and homeostatic cell death, apoptosis
is anti-inflammatory and immunologically silent. However, a number of recent
studies indicate that caspase-dependent processes are important for
immunogenicity [5]. In chemotherapy-induced cell death, some (anthracyclins),
but not all (mitomycin C) caspase-inducing stimuli initiates’ immunogenic cell
death [6], thus immunogenicity depends on factors other than caspase
activation.
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