Not exact matches
Once activated, T
cells can home in on a
tumor and target it for
destruction.
At the same time, other switches get flipped throughout the body, modifying everything from metabolism to
cell growth, via other cytokines, such as IL - 6 and
tumor necrosis factor — a, and things like CRP, which mark bacteria for
destruction.
The selective pressure of the competent immune system «edits» the
tumor by selecting for
cells that can avoid immune
destruction.
In effect, Affigen uses cancer's «Achille's Heel»: the proteins which distinguish
tumor cells from normal
cells, that can target
tumor cells for
destruction with extreme sensitivity and precision.
Longitudinal confocal microscopy imaging of solid
tumor destruction following adoptive T
cell transfer.
Interestingly, when parental d42m1 sarcoma
cells were transplanted into wild - type mice, around 20 % of recipients developed «escape»
tumors which evaded immune
destruction and progressed (escape clones).
They are important especially for the
destruction of
cells infected by a virus or of
tumor cells.
Central to the concept of immunoediting is the idea that T -
cell recognition of
tumor - specific antigens drives the
destruction of early
tumors, and later the antigenic «sculpting» of persistent
tumor cells.
In other words, T -
cell destruction of
cells bearing mutant spectrin - B2 «sculpted» the
tumor cells into poorly immunogenic
cells lacking the antigen, which progressed and grew out.
Through its various targets, MMP1 promotes not only
tumor invasion but also breast cancer colonization to bone by mechanisms that include the release of membrane - bound EGF - like growth factors from
tumor cells, leading to activation of EGF receptor signaling and suppression of OPG expression in osteoblasts, which in turn promotes the differentiation and activation of osteoclasts required for bone
destruction and enhanced
tumor growth in the bone microenvironment (32).
Tumors» mutations can encode the seeds of their own
destruction, in the form of immunogenic peptides recognized by T
cells.
They found that
destruction of the cancer was mediated by killer T
cells residing in the
tumor rather than newly infiltrating killer T
cells.
Specifically, some
tumor cells appeared to express PD - L1, essentially «wrapping» themselves in it to avoid immune recognition and
destruction.
A primary function of CTLs is the selective recognition and
destruction of
tumor cells.
Experiments in mice lacking CTLA - 4 and use of CTLA - 4 antibodies demonstrated that absence of CTLA - 4 or blocking its activity could lead to T
cell activation and
tumor destruction.
Duntas (2015) articulates, «In susceptible individuals, iodine excess increases intra-thyroid infiltrating Th17
cells and inhibits T regulatory (Treg)
cells development, while it triggers an abnormal expression of
tumor necrosis factor - related apoptosis - inducing ligand (TRAIL) in thyrocytes, thus inducing apoptosis and parenchymal
destruction» (31, p. 721).
When they do, the symptoms that we see are due to the physical
destruction of these organs as the
tumor grows and crowds out healthy
cells.
M032 kills
tumor cells directly through oncolytic replication and then proceeds to infect
tumor cells in proximity, continuing the process of
tumor destruction.