FYI AACR conference in colorado till April 22nd
 

http://www.aacr.org/home/scientists/...ting-2009.aspx

Hopefully good news will come out of this!

am there
 

lots of her2 agents, mTor inhibitors, HSP 90 inhibitors in trials with really hopeful results.

Her2 bc felt to have been changed from worse prognosis than her2- to better prognosis for many (those who respond and don't develop resistance) New agents for those who don't respond or develop resistance and usually to be ADDED to herceptin or lapatinib.

Herceptin/lapatinib combo felt to be promising as well.

More later!

Lani

Lani,

I am thankful you are there, but I had to laugh because when I read the title to your post I thought that you are like a secret agent. Good thing you "work" for us.

And really glad to hear that tykerb/herceptin = good combo

Flori

Thanks again for information Lani. Looking forward to further update.Thanks to info on this board I now have the confidence to challenge oncs about synergy between herceptin and other chemo combinations even when they are very negative!!
Praying for us all on this journey. Love Ellie

"New agents for those who don't respond or develop resistance and usually to be ADDED to herceptin or lapatinib."

Talking about Hsp-90 inhibitor, sheddase inhibitor?

Lani is right on. We HER2 types seem to be deemed "the chosen ones" these days. I saw a poster on the Lapatinib/Herceptin combo and spoke with the presenter for a bit. Will try to post some abstracts when I get home - unless Lani beats me to it ...

Lani and StephN,
Thanks for your posts and hopeful news.
karen z

Lani and Stephanine,

I am so glad both of you are there. Thanks for posting and letting us know what is going on.

Amelia

am pooped
 

Attend from 7am -630 everyday without even lunch breaks and view/glance over 1900 posters Sunday, 900 posters Monday, 1900 posters today and will view/glance over 900 posters tomorrow before leaving!!!!

Best talks today by Neal Rosen explaining what "oncogene addiction" means--although this term is used a lot in the literature he feels mostly it is by authors who don't really understand it. Dr. Rosen has done seminal work on Hsp90 inhibitors and feels they are best suited for her2+ breast cancer. He feels PI3K inhibitors will best be used with other targeted agents which block further down the pathway or another pathway altogether.

Also superb was Dr. Max Wicha's talk on breast cancer stem cells and the funniest moment was the playing of a video of Hugh Laurie as Dr. House proclaiming that cancer stem cells ARE for REAL and are truly responsible for everything!!!! Dr. Wicha loved that!

Spoke again with Dr. Scaltriti who works with Dr. Baselga and did the work I reported on last year on how wonderfully herceptin/lapatinib synergize.

Lots of people working on ways to reverse herceptin resistance, new anti her2 agents--all agree to continue on herceptin past resistance, just add things to it!

Interesting posters on topical agents vs. EGFR inhibitor rashes, hand-foot syndrome, how to avoid hair loss with chemo.

I spoke with an investigator re how you ladies have reported losing the outer part of your eyebrows and eyelash length with herceptin. He is doing studies on EGFR inhibitors actions by studying patient's hair follicles from
plucked hairs. I suggested you might be willing to pluck your eyebrows and contribute to medical research??????

I also attended lectures on brain tumors, leukemias, myeloma, neuroendocrine tumors of gut, pancreas, so I was one busy propellerhead!

Gotta go!

StephN here
 

We have broken down the booth, shipped the leftover materials, retrived our luggage, had some lunch and are waiting for the airport shuttle.

Coming from a minimally science-educated background, just speaking with the few people I picked out to discuss their posters was strain enough on the old chembrain. Lani's mention of the work on new targets is truly boggling. There are literally thousands of people working on bits of DNA and cell components, and we know that only a small percentage of that work will bear fruit.

I am being rushed off the hotel computer by others, so there will be more soon!

I wasn't paying attention so I have started another thread where I will post what I learned at the AACR. We all attended as many posters and as many talks as we could and met many passionate researchers at the booth as well. There was so much information that it became overwhelming. One statement I heard from the researchers was that it was so complex, with so many pathways and targets that it was impossible for them to wrap their minds around the whole picture. One even said that they need a genius, that the ordinary human brain cannot comprehend the sheer complexity of all of this research. I will post more on what I was able to learn as I am sure everyone else will as well.

Leslie

There does seem to be an ever evolving number of pathways. What seems pivotal to me is whether cancer stem cells are the critical target. I wonder if that might explain why there can be shrinkage of tumors without overall survival benefit. Especially if some chemos, while killing the majority of cancer cells, leave cancer stem cells behind. Figuring out which chemos attack the "right" target might be a big step. In other words, is there a paradigm shift.
Another part of the cancer stem cell issue, if it holds water, is whether that could mean benefit from local therapy (lung RFA, spheres etc) even when multiple met sites are involved. i.e. does local therapy kill more cancer stem cells than produced by any rescue response. I've never understood why local therapies (with systemic) that you would think would reduce the tumor burden aren't considered beneficial after a certain point.

Rich -
A partial answer to your question about determining the right target does go to the stem cell problem. I had several researchers tell me that in their preclinical models, the stem cells were NOT killed and this is one reason for the prevelance of brain mets and a reason that we can appear to have an early stage cure and then have a switch flipped on new tumors many years later.

I am glad Faux mentioned the "genius" part. Makes me feel better that so much of the science was over my head. Those are some very smart researchers and they say things like "the more we find out, the less we KNOW."

That was a little disconcerting, but on the other hand others were feeling that since our DNA is decoded the research is moving quite rapidly. In what direction is the 64,000 dollar question.

Any further highlights now that the recon team has had a chance to rest?
I would like to have handy whatever articles there are about continuing Herceptin post progression. Anything further on circulating Her2 and CTCs?

Rich, I found this conference to be more about basic research. What I saw was more about why Herceptin doesn't work for some HER2+ patients. One of the explanations I saw was that Herceptin works better for patients whose receptors are homodimers rather heterodimers. In other words the receptor is made up of two Her2 proteins rather than a Her2 and a Her3 protein. Most of what I saw was nowhere near clinical trials. Maybe Stephanie has more insight into this than I do.

Several of the researchers that I talked to felt like we were very close to breast cancer being a manageable chronic disease, much more so than many of the other cancers. I will post more later. I have been catching up on my yard and garden this week end.

Leslie