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targeted therapies emerge, and more antibodies
are commercialized. At the same time, there is
increasing demand to shift from large specimens
to small-core needle samples. Consequently, the
sample size will continue to shrink and the
complexity of the analyte repertoire will expand.
Thus, the future will bring greater demands on
the sensitivity, precision, and versatility of
RPMA technology. RPMA technology will
evolve
shift, and this may be the best predictor of resis-
tance or ef
cacy. The knowledge we gain from
the ongoing clinical research trials will shape
how signal pathway pro
ling will be done in
the clinical practice of the future.
References
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cyclin b1 as a classi
generation ampli
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'
s perspective. We can
imagine a time in which readout is fully elec-
tronic or embodied in a bead array chip that
can be read on a DNA sequencer type instru-
ment. It may even be possible to achieve a multi-
plex assay with high sensitivity in a homogenous
(solution phase) format.
Genomic sequencing reveals dozens to
hundreds of mutations or chromosome aberra-
tions in an individual patient
'
ling with antibody microarrays. Genome
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analysis from formalin-
expression pro
s tumor. Presently,
there is no way to determine which of these
genetic changes are functionally important and
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The key utility of RPMA is to
'
xed tissues: implications for
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reporter deposition, a novel method of signal ampli-
fill this missing
functional gap. We believe that going forward
genomic clinical research protocols will increas-
ingly combine whole genome sequencing/tar-
geted resequencing with RNA Seq and RPMA
of tumor versus blood together with measure-
ment of circulating nucleic acids. RPMA
provides direct functional information about
which activated protein signal pathways have
hijacked the neoplastic cells, or the host microen-
vironment, and are the drivers of the disease.
Ongoing clinical trials employing RPMA may
reveal unexpected endpoints, pathway intercon-
nections, and activated pathways that correlate,
or do not correlate, with outcome or with
genomic or genetic data. We may
fication. II. Application to membrane immunoassays.
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'
find that acti-
vated proteins we expect to decrease following
therapy may do the opposite because of compen-
satory feedback or adaption to therapy or clonal
Armi C, et al. Selec-
tivity and promiscuity in the interaction network
mediated by protein recognition modules. FEBS Lett
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'
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