AstraZeneca and rivals on the EGF front lacked this kind of detailed patient-targeting data.
ImClone's Erbitux blocked the EGF receptor in a slightly different way, using an injectable monoclonal antibody.
Lab evidence indicates that an overactive EGF system may help tumors produce more VEGF.
Now, Goddard says, his most important job is to prove that his EGF drug works.
Large amounts of EGF, ten or more times normal production, can trigger a cell to grow uncontrollably.
By 1999 Zeneca had devised a drug, Iressa, that interrupted the pathways between EGF and tyrosine kinase.
When EGF docks on a receptor, it signals to an enzyme called tyrosine kinase to regulate cell growth.
It could be that Iressa simply did not knock EGF out well enough.
When EGF drugs are working strongly, patients usually develop a skin rash because EGF is also over-expressed in the skin.
Because EGF is present in more than half of cancers, trials of Iressa are under way for prostate and breast cancer.
In the 1980s researchers found high levels of EGF receptors in human tumors of the brain, lung, breast, bladder and pancreas.
Large amounts of EGF, as much as 10 to 100 times the normal production, can trigger a cell to grow uncontrollably.
Because EGF is present in more than half of all cancers, Iressa trials are under way for prostate and breast cancer.
Erbitux and Vectibix are antibodies that bind to receptors on the cell surface called EGF and blocks signals that turn kras on.
The accumulating data led researchers at Zeneca Group, now AstraZeneca, to wonder whether blocking EGF receptors with a drug might slow tumor growth.
Both pills inhibit a receptor for a protein called the epidermal growth factor (EGF) that many tumors seem to depend upon to grow.
The researchers also found that EGF levels were lower in groups suffering from CLD or respiratory distress syndrome than in the control group.
Hunting for other targets in the early 1980s, he focused on a protein called epidermal growth factor, or EGF, then a hot area of research.
The unfortunate reality is that it is simply not clear how good a target EGF is, and it won't be until more clinical data is public.
If AstraZeneca is right, then all of the EGF drugs could see their market severely limited until doctors and drugmakers learn to use these compounds in chemotherapy.
Like a key in a lock, EGF binds to a receptor on a cell's surface, sending off a signal to the cell to divide, grow and die.
McKillop insisted on the convenience of an oral drug, but the scientists found it impossible to devise a pill that would block EGF from binding to its receptor.
Separately, Genentech is doing early-stage testing of 2C4, a drug that works by a novel mechanism to simultaneously disrupt both Her-2 and EGF in a variety of tumor types.
Directing a team of 50 scientists at Zeneca's labs in Cheshire, U.K., McKillop collected urine samples from employees to isolate EGF and come up with a compound that could effectively block its activity.
McKillop directed a team of 50 scientists at Zeneca's labs in Cheshire, U.K., that collected urine samples from employees to isolate EGF and come up with a compound that could effectively block its activity.
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