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Back to The EGF system
THE EGF RECEPTOR
a.a. 1

in glioblastoma, and has a
deletion of exons
2 to 7 (a.a. 6 to 273)
a.a. 6
a.a. 273
is often found
a.a.621
a.a. 644
a.a. 1210
KRAS*
KRAS mutations can induce
non-response to anti EGFR
monoclonals (panitumumab, cetuximab) or EGFR-TK
inhibitors. Such mutations
trigger the RAS pathway
Mutations of the intracellular portion of EGFR involving exons 17 to 21 (a.a. 712 to 979), and especially exon 19, in Non small Cell Lung Cancer, can facilitate efficacy of oral TK inhibitors (gefitinib and erlotinib)
* KRAS Kirsten rat sarcoma viral oncogen homolog
a.a. = amino acid, followed by its number
Mab 806 (Ludwig Institute)
is a monoclonal specially
built against this deleted
variant of EGFR. A peptide vaccine (CDX 110) is in clinical trials against this variant
Most anti EGFR monoclonals target the extracellular portion of the EGFR
EGF system
EGF receptor
EGF agonists & pathways
Sheddases & ADAMs
VEGF
VISIT OTHER KEY PAGES :
BioTherapies
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exon skipping
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protein kinases
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MONOCLONALS
abatacept
abciximab
adalimumab
alefacept
alemtuzumab
anti KDR
basiliximab
belatacept
bevacizumab
CDP 791
cetuximab
dacluzimab
denosumab
eculizumab
efalizumab
etanercept
IMC 1121
infliximab
ipilimumab
lumiliximab
Mab 806
mapatumumab
matuzumab
natalizumab
nimotuzumab
ocrelizumab
ofatumumab
omalizumab
palivizumab
panitumumab
ranibizumab
rituximab
ticilimumab
trastuzumab
VEGF Trap
zalutumumab
ABOUT MONOCLONALS
what is a monoclonal
chains & fragments
therapeutic fields
what are CDs
types of monoclonals
fusion proteins
cells to build monoclonals
making monoclonals
IgG1/IgG2 differences
F(ab) fragments
Fc fragment
Fc structure
Fc e receptors
DISEASES
bird flu
cancer
diabetes
human growth hormone diseases
lysosomal diseases
mitochondrial diseases
multiple sclerosis
myelodysplastic sd
myopathies
osteoporosis
paroxysmal nocturnal hemoglobinuria
psoriasis
Cells/organelles
cell cycle
cells
chromosomes
DNA repair
exons
hemopoietic prog.
introns
lysosomes
mb. receptors
membrane CDs
mitochondria
proteasomes
stem cells
Pathways
Adams
AKT
amino acids
complement
cancer pathways
cdk
c-Met
DPP IV
EGF
EGFRvIII
GPCR
G proteins
HGF
ILGF
kinome
Kras
mannose P
MET
NFKB
nucleotides
protein kinases
proteins
Ras
RET
sheddases
sunitinib/sorafenib
VEGF
Wnt
The other escape route from the TK inhibitors is the c-MET pathway
These activating mutations of KRAS are met with in :
90% of pancreatic cancers
40% of colorectal cancers
10 to 20% of Non Small Call Lung Cancers
They seem to have no influence on the activity of Avastin
click below to get details