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In the post human-genome project era, cancer specific genomic maps
are redesigning tumor taxonomy by evolving from histopathology to
molecular pathology. The success of a cancer drug today is
fundamentally based on the success in identifying target genes that
control beneficial pathways. The overwhelming power of genomics and
proteomics has enlightened researchers about the fact that the
PI3K-mTOR pathway is the most commonly up-regulated signal
transduction pathway in various cancers, either by virtue of its
activation downstream of many cell surface growth factor receptors
or by virtue of its collateral and compensatory circuitry with
RAS-MAPK pathway. Oncogenic signaling in the majority of solid
tumors is sustained via the PI3K-AKT-mTOR pathway. Because of its
prominent role in many cancer types, the PI3K-mTOR pathway has
become a major therapeutic target. The volume includes two
complementary parts which address the problem of etiology and
disease progression and is intended to portray the very basic
mechanisms of the PI3K-AKT-mTOR signaling pathway's involvement in
various facets of the cancer, including stem cell renewal, cell
metabolism, angiogenesis, genetic instability, and drug resistance.
Significant progress has been made in recent years elucidating the
molecular mechanism of cancer cell proliferation, angiogenesis, and
drug-resistance in relation to the PI3K-mTOR pathway and this
volume provides an in-depth overview of recent developments made in
this area.
In the post human-genome project era, cancer specific genomic maps
are redesigning tumor taxonomy by evolving from histopathology to
molecular pathology. The success of a cancer drug today is
fundamentally based on the success in identifying target genes that
control beneficial pathways. The overwhelming power of genomics and
proteomics has enlightened researchers about the fact that the
PI3K-mTOR pathway is the most commonly up-regulated signal
transduction pathway in various cancers, either by virtue of its
activation downstream of many cell surface growth factor receptors
or by virtue of its collateral and compensatory circuitry with
RAS-MAPK pathway. Oncogenic signaling in the majority of solid
tumors is sustained via the PI3K-AKT-mTOR pathway. Because of its
prominent role in many cancer types, the PI3K-mTOR pathway has
become a major therapeutic target. The volume includes two
complementary parts which address the problem of etiology and
disease progression and is intended to portray the very basic
mechanisms of the PI3K-AKT-mTOR signaling pathway's involvement in
various facets of the cancer, including stem cell renewal, cell
metabolism, angiogenesis, genetic instability, and drug resistance.
Significant progress has been made in recent years elucidating the
molecular mechanism of cancer cell proliferation, angiogenesis, and
drug-resistance in relation to the PI3K-mTOR pathway and this
volume provides an in-depth overview of recent developments made in
this area.
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