Teleconference Notes Part One

[Guest guest]

Hi Everyone,

For those of you who weren't able to listen to today's teleconference

given by the L & L Society with Dr. Druker as speaker, I've taken down

a few notes. I'll post it in two posts since it's quite long. This

post will recap what he said in the first 30 mins and the next post

will go over the questions that people asked in the second half of

the talk.

He started with a recap of the history of CML.

It was in 1845 when pathologists first documented a case of CML.

Then in 1960 the Philadelphia chromosome was discovered but it wasn't

until 1973 that they recognized which genes were involved. In the

1980's they realized that a new gene resulted from the translocation

(BCR/ABL). Dr. Druker then started to work on a way of inhibiting

this cancerous gene in 1993. Once they understood what was causing

the cancer, he could work on developing a targeted therapy to stop

the cancer.

June 1998 was when the first trial of Gleevec started.

Survival rates for a newly diagnosed patient starting on Gleevec is

95%.

Progression to accelerated or blast phase is just 7% in 6 years.

Loss of response is seen in about 16-17% of patients (this is

strictly a loss of response, not progression of disease). These

response losses are mainly in the first couple of years of treatment.

In the 6th year of follow up, no progression was seen at all and less

than 1% lost their response.

There is a consistent trend now that makes Dr. Druker confident to

say that people treated with Gleevec today will have the prospect of

living out a normal life span.

He said that achieving CCR in one year is the main goal of therapy.

Maintaining a CCR is more important than a 3 log reduction (although

a 3 log reduction is better, it's just that it's not significant

enough to warrant a change in treatment in order to achieve it). So

there's no reason to change drugs or increase Gleevec dosage just to

achieve a 3 log reduction as long as a person is in a good solid

CCR.

He recommends a BMB every 6 months until CCR and a PCR every 3

months. After CCR, he will do BMB's only once every 18-24 months

unless there's an increasing trend in PCR then he'll do it earlier.

70% of patients will get CCR in one year. If someone is close to CCR

after a year, he recommends continuing Gleevec. If the person is no

where near CCR after a year, then he increases the dose or starts a

new drug.

People usually relapse because the target is mutated which doesn't

allow the drug to bind. Sprycel and Tasigna work well for many of

the mutations that occur. People with the mutation T315i should go

to transplant though as none of the drugs currently available work

well for this particular mutation.

There have been no long term consequences for patients after 6 years

of using Gleevec (no one has grown a third eye yet).

Trials are going on to compare the new drugs with Gleevec for front

line treatment but right now he doesn't recommend new patients start

with anything other than Gleevec because of the long term safety data

of Gleevec being well tolerated and very effective.

Combining Gleevec with one of the other newer drugs could potentially

prevent mutations but this must only be done in a clinical trial so

right now, he's not recommending this treatment for patients outside

of trials.

Quality of life issues are important. Since we know now that CCR is

what is important and there isn't a need to push patients to getting

a 3 log reduction, he is dropping patients who take 600mg and 800mg

to 500mg or 600mg to improve their quality of life. He doesn't

recommend any doses below 400mg unless there's supporting data to do

so such as drug levels.

Part two coming up.........

[Guest guest]

Hi Tracey,

Thank you for an excellent summary.

I also listened to the teleconference and always earn something new from

them.

The most important thing I came back from on his talk was that achieving CCR

is good enough to keep you from disease advancement. It always has bothered

me that many doctors advocate a dose increase so that their patients can

achieve PCRU or MMR without and data to say that this is more important than

just CCR.

Zavie

Zavie (age 69)

67 Shoreham Avenue

Ottawa, Canada, K2G 3X3

CCR SEP/01. #102 in Zero Club

e-mail: zmiller@...

Tel: 613-726-1117

Fax: 309-296-0807

Cell: 613-202-0204

ID: zaviem

YM: zaviemiller

Skype: Zavie

_____

From: [mailto: ] On Behalf Of Tracey

Sent: March 26, 2008 4:34 PM

Subject: [ ] Teleconference Notes Part One

Hi Everyone,

For those of you who weren't able to listen to today's teleconference

given by the L & L Society with Dr. Druker as speaker, I've taken down

a few notes. I'll post it in two posts since it's quite long. This

post will recap what he said in the first 30 mins and the next post

will go over the questions that people asked in the second half of

the talk.

He started with a recap of the history of CML.

It was in 1845 when pathologists first documented a case of CML.

Then in 1960 the Philadelphia chromosome was discovered but it wasn't

until 1973 that they recognized which genes were involved. In the

1980's they realized that a new gene resulted from the translocation

(BCR/ABL). Dr. Druker then started to work on a way of inhibiting

this cancerous gene in 1993. Once they understood what was causing

the cancer, he could work on developing a targeted therapy to stop

the cancer.

June 1998 was when the first trial of Gleevec started.

Survival rates for a newly diagnosed patient starting on Gleevec is

95%.

Progression to accelerated or blast phase is just 7% in 6 years.

Loss of response is seen in about 16-17% of patients (this is

strictly a loss of response, not progression of disease). These

response losses are mainly in the first couple of years of treatment.

In the 6th year of follow up, no progression was seen at all and less

than 1% lost their response.

There is a consistent trend now that makes Dr. Druker confident to

say that people treated with Gleevec today will have the prospect of

living out a normal life span.

He said that achieving CCR in one year is the main goal of therapy.

Maintaining a CCR is more important than a 3 log reduction (although

a 3 log reduction is better, it's just that it's not significant

enough to warrant a change in treatment in order to achieve it). So

there's no reason to change drugs or increase Gleevec dosage just to

achieve a 3 log reduction as long as a person is in a good solid

CCR.

He recommends a BMB every 6 months until CCR and a PCR every 3

months. After CCR, he will do BMB's only once every 18-24 months

unless there's an increasing trend in PCR then he'll do it earlier.

70% of patients will get CCR in one year. If someone is close to CCR

after a year, he recommends continuing Gleevec. If the person is no

where near CCR after a year, then he increases the dose or starts a

new drug.

People usually relapse because the target is mutated which doesn't

allow the drug to bind. Sprycel and Tasigna work well for many of

the mutations that occur. People with the mutation T315i should go

to transplant though as none of the drugs currently available work

well for this particular mutation.

There have been no long term consequences for patients after 6 years

of using Gleevec (no one has grown a third eye yet).

Trials are going on to compare the new drugs with Gleevec for front

line treatment but right now he doesn't recommend new patients start

with anything other than Gleevec because of the long term safety data

of Gleevec being well tolerated and very effective.

Combining Gleevec with one of the other newer drugs could potentially

prevent mutations but this must only be done in a clinical trial so

right now, he's not recommending this treatment for patients outside

of trials.

Quality of life issues are important. Since we know now that CCR is

what is important and there isn't a need to push patients to getting

a 3 log reduction, he is dropping patients who take 600mg and 800mg

to 500mg or 600mg to improve their quality of life. He doesn't

recommend any doses below 400mg unless there's supporting data to do

so such as drug levels.

Part two coming up.........

[Guest guest]

Hi Tracey,

You are such an excellent note taker! Hats off to you! I needed you

in college! lol

I heard from my hubby that you got through on the phone lines and

asked Dr. Druker about female issues.

I had to leave the teleconference for a short while to pick my

daughter up from the bus stop. I missed YOUR question!! wahhhhh.

It's so cool when someone comes on the phone for questions and you

know who they are!

Thanks for all you do! Lynn

>

> Hi Everyone,

>

> For those of you who weren't able to listen to today's

teleconference

> given by the L & L Society with Dr. Druker as speaker, I've taken

down

> a few notes. I'll post it in two posts since it's quite long.

This

> post will recap what he said in the first 30 mins and the next post

> will go over the questions that people asked in the second half of

> the talk.

>

> He started with a recap of the history of CML.

>

> It was in 1845 when pathologists first documented a case of CML.

> Then in 1960 the Philadelphia chromosome was discovered but it

wasn't

> until 1973 that they recognized which genes were involved. In the

> 1980's they realized that a new gene resulted from the

translocation

> (BCR/ABL). Dr. Druker then started to work on a way of inhibiting

> this cancerous gene in 1993. Once they understood what was causing

> the cancer, he could work on developing a targeted therapy to stop

> the cancer.

>

> June 1998 was when the first trial of Gleevec started.

>

> Survival rates for a newly diagnosed patient starting on Gleevec is

> 95%.

>

> Progression to accelerated or blast phase is just 7% in 6 years.

>

> Loss of response is seen in about 16-17% of patients (this is

> strictly a loss of response, not progression of disease). These

> response losses are mainly in the first couple of years of

treatment.

>

> In the 6th year of follow up, no progression was seen at all and

less

> than 1% lost their response.

>

> There is a consistent trend now that makes Dr. Druker confident to

> say that people treated with Gleevec today will have the prospect

of

> living out a normal life span.

>

> He said that achieving CCR in one year is the main goal of

therapy.

> Maintaining a CCR is more important than a 3 log reduction

(although

> a 3 log reduction is better, it's just that it's not significant

> enough to warrant a change in treatment in order to achieve it). So

> there's no reason to change drugs or increase Gleevec dosage just

to

> achieve a 3 log reduction as long as a person is in a good solid

> CCR.

>

> He recommends a BMB every 6 months until CCR and a PCR every 3

> months. After CCR, he will do BMB's only once every 18-24 months

> unless there's an increasing trend in PCR then he'll do it earlier.

>

> 70% of patients will get CCR in one year. If someone is close to

CCR

> after a year, he recommends continuing Gleevec. If the person is

no

> where near CCR after a year, then he increases the dose or starts a

> new drug.

>

> People usually relapse because the target is mutated which doesn't

> allow the drug to bind. Sprycel and Tasigna work well for many of

> the mutations that occur. People with the mutation T315i should

go

> to transplant though as none of the drugs currently available work

> well for this particular mutation.

>

> There have been no long term consequences for patients after 6

years

> of using Gleevec (no one has grown a third eye yet).

>

> Trials are going on to compare the new drugs with Gleevec for front

> line treatment but right now he doesn't recommend new patients

start

> with anything other than Gleevec because of the long term safety

data

> of Gleevec being well tolerated and very effective.

>

> Combining Gleevec with one of the other newer drugs could

potentially

> prevent mutations but this must only be done in a clinical trial so

> right now, he's not recommending this treatment for patients

outside

> of trials.

>

> Quality of life issues are important. Since we know now that CCR

is

> what is important and there isn't a need to push patients to

getting

> a 3 log reduction, he is dropping patients who take 600mg and

800mg

> to 500mg or 600mg to improve their quality of life. He doesn't

> recommend any doses below 400mg unless there's supporting data to

do

> so such as drug levels.

>

> Part two coming up.........

>