Avid Bioservices Inc (CDMO)

[biopharm]

David Carbone - Peregrine Pharmaceuticals KOL

Unbelieveable... now many others will begin to see the value of all the KOL's, including David Carbone. Dec 10, 2013 Peregrine made that announcement and a date I don't forget. Pay close to attention to those words = "Notch". I believe another Peregrine KOL was just in Greece this past summer explaining all about Notch signalling and all the happenings that go on within Notch Signaling, that is becoming "new knowledge" based on prior knowledge that the DMC must be made aware of as well.

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"Our findings might explain why erlotinib in clinical trials seems to worsen survival in patients with early-stage lung cancer," says co-corresponding author David Carbone, MD, PhD, professor of medicine, Division of Medical Oncology at the OSUCCC -- James. "They also suggest that combining an EGFR inhibitor with a Notch inhibitor should overcome the effect."

The study was published in the journal Cancer Research.

---------Here is the full publication

Why targeted drug doesn't benefit patients with early-stage lung cancer

Date:
October 27, 2014

Source:
Ohio State University Wexner Medical Center

Summary:
The drug erlotinib is highly effective in treating advanced-stage lung cancer patients whose tumors have a particular gene mutation, but when the same drug is used for patients with early-stage tumors with the same gene change, they fare worse than if they took nothing. This study might explain why.

he drug erlotinib is highly effective in treating advanced-stage lung cancer patients whose tumors have a particular gene change, but when the same drug is used for patients with early-stage tumors with the same gene change, they actually fare worse than if they took nothing. A study by researchers at The Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC -- James) and at Cincinnati Children's Hospital might show why.

Oncologists use erlotinib to treat lung cancers that have a mutation in a gene called epidermal growth factor receptor (EGFR). The gene mutation causes EGFR to run like it has a stuck accelerator, and erlotinib blocks the overactive molecule. The study shows that while erlotinib effectively causes tumors to shrink -- suggesting that the drug is helping -- this drug also increases the aggressiveness of the tumor so that growth is accelerated when therapy ends. This study finds that this is due to a secondary and previously unknown effect of inhibiting EGFR.

The researchers found that when erlotinib blocks EGFR, it activates a second signaling molecule called Notch3. Activation of that pathway leads to increased development of cancer stem cells among the surviving tumor cells and to accelerated tumor growth.

"Our findings might explain why erlotinib in clinical trials seems to worsen survival in patients with early-stage lung cancer," says co-corresponding author David Carbone, MD, PhD, professor of medicine, Division of Medical Oncology at the OSUCCC -- James. "They also suggest that combining an EGFR inhibitor with a Notch inhibitor should overcome the effect."

The study was published in the journal Cancer Research.

Carbone, co-corresponding author Stacey Huppert, of Cincinnati Children's Hospital, and their colleagues conducted the study using several cell lines of non-small-cell lung cancer, the most common form of lung cancer, to learn if inhibiting EGFR enhances the activity of the Notch signaling pathway.

"We found that the activated, mutated EGFR directly inhibits Notch signaling, and that inhibiting EGFR with erlotinib removes this restraint and activates Notch signaling," says Carbone, who is the Barbara J. Bonner Chair in Lung Cancer Research. "It suggests that specific dual targeting might overcome this adverse effect."

The study's key technical findings include:

In two non-small-cell lung cancer cell lines, erlotinib treatment killed 84 percent and 75 percent of cells; of the surviving cells, 23 percent and 70 percent were stem-like cells, respectively (versus 4 percent and 18 percent of control cells);
Erlotinib treatment increased the potential for growth of surviving lung cancer cells;
Erlotinib treatment increased the number of stem-like cells through activation of the Notch3 receptor.


Journal Reference:

R. R. Arasada,
J. M. Amann,
M. A. Rahman,
S. S. Huppert,
D. P. Carbone.

EGFR Blockade Enriches for Lung Cancer Stem-like Cells through Notch3-Dependent Signaling. Cancer Research, 2014; 74 (19): 5572 DOI: 10.1158/0008-5472.CAN-13-3724

http://www.sciencedaily.com/releases/2014/10/141027144854.htm

My landscape equipment has been sold, all of my customer base has been sold and I'm officially all done with the landscaping business and ready for the move back to Cali next year. Where did the landscape money go? PPHM and no Phoenix Rising... I don't buy because of a message board, but do buy based on the wealth of information that comes out of it, which rarely happens on most IHUB boards.

Get the rocket ready Loof...

CJ, thanks for "ALL" the organization in the INTRO section as it is an invaluable piece of work that shows the will and determination of all those at Peregrine.

Now... is it Roche or BMS or Bayer or Allergan or... a little piece of the pie for everyone : )

What better biotech value can one own? A stock that just may profit from every corner of the biotech space, unless someone wants to reach over that conference table and give SK an offer he can't refuse : )

I will have to say though... the strong opposition here resulted in the purchase of more shares over the past 2 years

Good luck to all : ) ...especially the shorts who may not have enough on the long side to offset their short position. Oh my.