Hi Giora,

Yup, we can confirm this.  Cheryl-Anne noticed it first and pointed 
it out to me.  Dr. Talpaz was sitting about 4 rows in front of us and 
was dutifully taking notes.  It was good to see.

Regards,
Mark

--- In [EMAIL PROTECTED], "giora1" <[EMAIL PROTECTED]> wrote:
> hallo mark
> thanks so much for your summary. its great.
> i just spoke to one of the israeli representatives who came back 
from the ash and i heard an interesting remark concerning drs at the 
ash.
> he mentioned that he sat next to dr talpaz who was attending many 
of the presentations and was sitting and taking notes from other drs 
presentations like a yound student. he also mentioned that dr talpaz 
was one of the very few to do it.
> it only shows no matter how expert you are you still learn from 
others. the problem is that many drs dont realize it.
> shalom
> giora
>   ----- Original Message ----- 
>   From: mpetersen123 
>   To: [EMAIL PROTECTED] 
>   Sent: Sunday, December 12, 2004 8:13 AM
>   Subject: [CML] Re: Newbie ASH Summary (1/3) - Intro - Gay, Nancy, 
Richard T, Wayne, Allen
> 
> 
> 
> 
>   Thanks everyone for the complements. I hope the summary is useful 
to 
>   some.  Unfortunately it took longer to post than I wanted, so 
much of 
>   what was discussed is probably old hat by now.  Having it 
summarized 
>   might be useful though.
> 
>   Nancy, you brought up a good point about CML being targeted 
because 
>   it's simple and so well understood.  When I was first diagnosed 
my 
>   oncologist said that everyone with CML has the same exact disease 
>   (the ph chromosome).  He said that if you examine 1,000 breast 
cancer 
>   patients you'll see 1,000 different cancers. Another example of 
this 
>   was an AML session that Cheryl-Anne and I sat through (it came 
after 
>   a CML session).  The topic was inhibition targets for AML.  Talk 
>   about a complex disease.  It was easily 10x more complicated than 
>   CML.  There were at least a dozen or so pathways that were 
discussed, 
>   apparently all of which are active in AML.  It's clear that a 
cure 
>   for something like AML will be far more difficult.
> 
>   Also, thanks for bringing up the LLS.  I forgot to mention that 
the 
>   LLS sponsored a lot of the BMS-354825 research.  Very cool!
> 
>   Lastly, as far as Dr. Druker is concerned.  Meeting him was 
really a 
>   high point for me at ASH.  Many of those who presented are 
>   essentially clinicians who see a lot of CML patients and can 
comment 
>   on various studies and the statistics of various things.  Both 
Dr. 
>   Druker and Dr. Sawyers have impressed me because in addition to 
being 
>   clinicians they are both high powered scientists.  In addition, 
Dr. 
>   Druker also struck me as a good person whose work is all about 
>   putting the patients first.  I'm envious now of those of you who 
are 
>   patients who see Dr. Druker. 
> 
>   Regards,
>   Mark
> 
> 
> 
>   --- In [EMAIL PROTECTED], "hey00nanc" <[EMAIL PROTECTED]> wrote:
>   > 
>   > --- In [EMAIL PROTECTED], "mpetersen123" <[EMAIL PROTECTED]> 
>   wrote:
>   > > 
>   > > 
>   > > A few people have asked me to post a newbie ASH summary 
because 
>   of 
>   > my 
>   > > perspective as a 6 month newly diagnosed CML patient.  So I 
>   figured 
>   > > that I would sit down and write about the topics that I found 
>   > > interesting and of the most importance. 
>   > 
>   > ________________
>   > 
>   > Thanks Mark,
>   > You did a really great job with your summary, with the special 
>   little 
>   > bits of info that you gleaned from some of the 'biggies' and 
your 
>   own 
>   > interpretation, based on lots of personal research. And I'm 
glad 
>   that 
>   > you also had fun!
>   > 
>   > My few comments:
>   > There is a reason that there is so much research into CML and 
that 
>   a 
>   > race for the cure is on. It wasn't just 'luck' for us. CML is 
>   probably 
>   > the simplest cancer there is....where almost all cmlers in 
early 
>   > chronic phase have just the same, well understood chromosomal 
>   > abnormality, the ph+ chromosome. Of course, we know it is not 
quite 
>   as 
>   > simple as that...there are those who have what we call the 
standard 
>   > 'garden variety' cml and those who have something a bit 
different, 
>   > like translocations between 3 chromosomes, etc. But in 
comparison 
>   > between what is known about other cancers and what is known 
about 
>   cml, 
>   > there is a huge difference. So, it makes sense to work on the 
>   simplest 
>   > cancer first....this should be the one that is the easiest to 
>   solve, 
>   > the easiest to cure. Curing a cancer would be any researcher's 
>   dream! 
>   > We lucked out! 
>   > 
>   > Here I will add my thanks to all of those on this list who have 
>   been 
>   > fund raisers for the Leuk & Lym Society, with their 
participation 
>   in 
>   > teams in training marathons, etc. This society has funded a lot 
of 
>   the 
>   > research, including the collaboration between Druker and 
Sawyers in 
>   > researching the mollecular pathways and detecting mutations. 
>   > 
>   > Personally, I was interested in your comments about early 
>   resistance 
>   > and the 'wild type'. I will review all the previous notes for 
when 
>   I 
>   > see Dr. Druker in early January and we talk about my next best 
>   option.
>   > 
>   > And lastly I wanted to comment on your impression that Dr. 
Druker 
>   was 
>   > more reserved about the potential of BMS than Dr. 
Sawyers.....Dr. 
>   > Druker always wants statistically significant scientific proof 
>   first, 
>   > but I expect that he is enthusiastic under the surface. I will 
let 
>   you 
>   > know if I see another side when I have my follow-up. 
>   > 
>   > The question with Gleevec has been, why can it get so many to 
CCR 
>   (I 
>   > think maybe about 97% of the newly diagnosed).......but so few 
to 
>   > PCRU (maybe 5-10%)? We hope that these new more potent drugs 
will 
>   take 
>   > people to a higher level of response. 
>   > 
>   > Thanks again Mark for all your sharing.
>   > Maui Nanc
> 
> 
> 
> 
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