her2 breast cancer cured (when transplanted in mice) using triple targetted therapy
 

vs her family:

Combination treatment stymies breast cancer growth [Eureka News Service]
HOUSTON (May 5, 2007)—A combination of three different drugs that block the HER-2 receptor, a critical cellular growth signal for some breast cancers, eradicated aggressive breast tumors in mice and could point the way toward developing better treatments inpatients, said researchers from the Breast Center at Baylor College of Medicine in a report that appears today in the Journal of the National Cancer Institute.
"For the first time, we were able to cure mice of a very aggressive human breast tumor," said Dr. Rachel Schiff, assistant professor in the Breast Center at Baylor College of Medicine and senior author of the report.

In prior such studies, treatment only slowed or delayed the growth of tumors, she said. In this case, the tumors disappear and do not come back, even when treatment is stopped.

The treatment involved is a new approach known as "targeted" therapy because the protein (in this case, HER-2) driving a tumor to grow is first identified in a patient's tumor and then specific drugs are used to block that particular growth pathway in the cells, said Dr. Kent Osborne director of the Breast Center and the Dan L. Duncan Cancer Center with BCM. He is also an investigator on the study.

"When you go after a specific target in a patient's tumor, the treatment is likely to be more effective and less toxic," said Schiff.

The tumors in question - nearly 25 percent of all breast cancers - have high levels of HER-2. While the HER-2 makes the tumors more aggressive, it also provides a target against which new drugs can act.

Previously, treatment for patients with HER-2 positive tumors was less effective.

"Now we have effective treatment, and survival is markedly improved," said Dr. Grazia Arpino, lead investigator of the study and a postdoctoral fellow at BCM.

"These tumors are initially highly sensitive to a drug known as trastuzumab or Herceptin, one of the drugs used in combination in the mouse study and which is approved by the FDA (U.S. Food and Drug Administration) for treatment," said Schiff.

However, the tumor is wily and can sometimes escape the drug's effects, resulting in resistance. Adding two other experimental drugs - gefitinib and pertuzumab — that inhibit HER-2 in different ways can more completely block the growth signals in the tumor, causing it to die.

In one of the tumors studied in this report, blocking the stimulatory effects of estrogen on the tumor was also necessary for optimal treatment, said Schiff. Completely blocking the HER pathway is critical, she said. Leaving out just one of the three drugs was much less effective.

A clinical study using drug combinations in newly diagnosed patients with HER-2 positive breast cancer will start soon under the direction of physicians at BCM's Breast Center, said Osborne.

"We are very excited to see if our laboratory results can be translated to patients with the more aggressive types of breast cancer," he said.

^^^^^^^^^^^^

Treatment of Human Epidermal Growth Factor Receptor 2-Overexpressing Breast Cancer Xenografts With Multiagent HER-Targeted Therapy [Journal of the National Cancer Institute]
Background: Human epidermal growth factor receptor 2 (HER2) is a member of the HER signaling pathway. HER inhibitors partially block HER signaling and tumor growth in preclinical breast cancer models. We investigated whether blockade of all HER homo- and heterodimer pairs by combined treatment with several inhibitors could more effectively inhibit tumor growth in such models.
Methods: Mice carrying xenograft tumors of HER2-overexpressing MCF7/HER2-18 (HER2-transfected) or BT474 (HER2-amplified) cells were treated with estrogen supplementation or estrogen withdrawal, alone or combined with tamoxifen. One to three HER inhibitors (pertuzumab, trastuzumab, or gefitinib) could also be added (n ?8 mice per group). Tumor volumes, HER signaling, and tumor cell proliferation and apoptosis were assessed. Results: were analyzed with the t test or Wilcoxon rank sum test and survival analysis methods. All statistical tests were two-sided.

Results: Median time to tumor progression was 21 days for mice receiving estrogen and 28 days for mice receiving estrogen and pertuzumab (difference = 7 days; P = .001; hazard ratio [HR] of progression in mice receiving estrogen and pertuzumab versus mice receiving estrogen = 0.27, 95% confidence interval [CI] = 0.09 to 0.77). Addition of gefitinib and trastuzumab to estrogen and pertuzumab increased this time to 49 days (difference = 21 days; P = .004; HR of progression = 0.28, 95% CI = 0.10 to 0.76). MCF7/HER2-18 tumors disappeared completely and did not progress (for ?189 days) after combination treatment with pertuzumab, trastuzumab, and gefitinib plus tamoxifen (19 of 20 mice) or plus estrogen withdrawal (14 of 15 mice). Both combination treatments induced apoptosis and blocked HER signaling and proliferation in tumor cells better than any single agent or dual combination. All BT474 tumors treated with pertuzumab, trastuzumab, and gefitinib disappeared rapidly, regardless of endocrine therapy, and no tumor progression was observed for 232 days.

Conclusion: Combined treatment with gefitinib, trastuzumab, and pertuzumab to block signals from all HER homo- and heterodimers inhibited growth of HER2-overexpressing xenografts statistically significantly better than single agents and dual combinations.

Time will tell
 

Good Lord. I was not aware of it. Thank you for sharing with us.

I guess they(lab,docs,pharmaceutical companies,etc) have to wait to see first if it will work with mice..before beginning any clinical trial. In any event, it's always uplifting and brings a lot of hope to all of us.

Again, thanks for sharing, Joe.

Hi, with the use of these three drugs, Her1,2, and 3 are blocked. Many her2+ are positive for all three.

All I can say is HURRY! This is such good news if it indeed translates to humans...

Lani - I adore you! Seriously, I haven't been posting lately, but I truly appreciate your work in sharing new research with us. Thank you! Belindax

I don't quite understand. Another study using the same combination with the same results was released at San Antonio in 2004.

http://www.abstracts2view.com/sabcs/...p?nu=BCS4L_713

Regards
Joe

Joe - it looks to me like the differnce is that they haven't only focussed on E+ cancers (as they did in the initial study), and that the tumours have been shown to die and not to return - all the more evidence that when the HER2 cancer is isolated, it can be treated successfully. And, good news that they are now intending to start human trials of this combo, eh?


B

Truly exciting news. Hope the translation to human will confirm the validity in human cancer treatment. Thanks for the posting

The last line in the abstract suggested clinical trials 3 years ago. I will certainly ask this question at ASCO.

Regards
Joe

Joe, the study your reference is one of my ALL TIME FAVORITES! As I recall, the focus on that one was to restore tamoxifen sensitivity in ER+ cancers. Definitely, do some snoopin and schmoozin around ASCO for news on this!

I agree, finding out if dumb old human BC will also respond can't happen too soon!

Joe (and all)
 

One of the big differences between that abstract and this article is that in the study cited in the ASCO abstract they used not only MCF7 cells transfected with her2 (an artificial construct which may not have any similarity to any naturally occuring tumor) but also BT474
a tumor which naturally occured in the poor person whose cell line was propagated and perpetuated which is her amplified (eg FISH+) and ER+. This human breast cancer cell line was implanted into the rodent,so...

This is as close as it gets to simulating her2+ER+ breast cancer as it occurs in humans.

Estrogen depletion ie, AIs were studied --in the abstract I believe only tamoxifen was studied, which represents a SERM, which blocks the estrogen receptor rather than depleting estrogen.

For all of those (like Jean) wondering what is the best AI, or whether STS and'or 17OH-HSD should also be blocked (aromatase is only one of three enzymes responsible for the formation of estrogen and similar compounds
not only in body fat, muscle and adrenal gland, but also within the breast cancer cells themselves), and worrying about using creams with parabens and other estrogen-like compounds, I thought the following sentence was particularly helpful:

All BT474 tumors treated with pertuzumab, trastuzumab, and gefitinib disappeared rapidly, regardless of endocrine therapy, and no tumor progression was observed for 232 days.

It is the same team of investigators who presented (abstract) and published
(today's article) both. It represents continued work by the lab on the same issue over the years...they have improved the meaningfulness of their study but adding the more representative cancer cell line (BT474), trying to gauge the import of estrogen depletion as well as estrogen receptor blockade (perhaps even addressing ER degradation if I remember correctly and Fulvestrant was addressed--but that might have been another article I read today), and determining that even without removing estrogen or preventing it from having its usual proliferation-inducing effect these three targetted agents sufficed to "cure" this subset of breast cancer which represents about 10% of breast cancers

Genentech makes two of the three drugs and also makes Tarceva, which works similarly to Iressa, but which, unlike Iressa is FDA approved (for another purpose). Let's hope Genentech hops on this bandwagon!

I went again with my friend to this year's Annual Stockholders Meeting (I am not a stockholder). They reported good progress with pertuzumab--
for the passive among us, let's hope and pray...for the activists among us, let's try to use our energies to help push this progress forward!

additional comments
 

1)sorry I typed ASCO rather than SABCS(San Antonio meeting)

2) that study was different in that it was looking to restore tamoxifen efficacy in tumors that became tamoxifen resistant by developing her2 positivity where they did not have it before. That is very different from her2+ER+ TUMORS WHICH are by their nature relatively tamoxifen resistant from the get-go and which have a very different gene expression profile.

Enough for tonight!

Thank you, again Lani. Your article, and now your interperetation of for us, has helped me pull through a dark post-chemo week. This seems to be the best news going at the moment, and I agree, anything we can do to push it we should. I agree that Gentech needs to get on the bandwagon - it is heartening that the initial research is independent, but to get the funding needed to make this thing really move along will need the drug companies to get on board. And getting trials takes soooooo long... Was there anyone involved in the early Herceptin days? What worked then?


Bx

Any idea of cost?
 

I was just wondering how much this combination might cost if it works. Does anyone have any idea?

I saved up for herceptin and would not have gotten it under my circumstances if I had not prepared for it financially, so I always think about this. Ironically, about 1/3 of the way through my treatment, the UK National Health Service decided to fund herceptin, including my herceptin, but I wouldn't have gotten it if I hadn't already been on it.

It might also be useful for people to know so they can be prepared for their copayments.

If I never need this combination then at least I will be well prepared for my old age.

As someone who had to stop Herceptin before 12 months due to heart issues, I will be very interested in any side effects on the heart. Otherwise, this is wonderful news.

Belinda
 

I believe there is a book sometimes available on Amazon about the making of herceptin, which chronicals the history of the discovery, the difficulties finding the right target population to treat (which almost stymied its development) and the parties involved (including Dr. Slamon, of course).

I believe Lily Samuels Tartikoff was terribly helpful in fund-raising (she got Revlon involved) for the early stages of the research.

I haven't read it myself to see how the ideas generated by Dr. Slamon got developed by Genentech into an approvable drug.

Anyone out there who read it?

I read the book and the story is pretty amazing. Scary that Herceptin almost didn't get out of the development phase. One of the take-aways from the book was the power of the advocacy community-- they really rallied to get as many women as possible included in the adjuvent trials, with the well-founded hunch that the drug would be a wonder.

Given the premium that these drugs are commanding, I can imagine that the business development people are all to happy to take bets now on targeted therapy-- at the time Herceptin was developed, it really was out-of-the-box thinking.

Here's a link to the book:
http://www.amazon.com/Her-2-Making-H...8212264&sr=8-1

Jen

I read it (twice) when I began my journey into the world of BC. The name of the book is HER-2: The making of Herceptin, a revolutionary treatment for Breast Cancer, written by Robert Bazell. I found it at my public library. Now with chemo brain in full mode it is hard for me to remember all the specifics but I will try to give a brief summary.

Lily Tartikoff was instrumental in securing the initial funding for Dr. Slamon’s research. He had treated her husband Brandon Tartikoff for Hodgkin’s disease and she was so grateful, that she made it her mission to get him the money he needed to move his research forward (he was having trouble getting funding). She approached the CEO of REVLON and challenged him to do more for women than just make lipstick. The fundraising “Fire & Ice Ball” and the Revlon Run/Walk for Women were a result of this challenge.

The book details the many years of research that went into the discovery of the HER-2 protein and the making of Herceptin. It also tells of how the pharmaceutical companies finally came on board. Most of all, it shows the relentless dedication and passion that Dr. Slamon put into this research, not to mention the brave women who participated in the initial trials.

Geri, Jen and Lani - thank you - am going to order the book. Seems like it's never to early to start organising. It's heartening the researchers are continuing their investigations - would be terrible if it ended ecause a PHD was successfully delivered. It's a pity their media release wasn't picked up properly.I am new to this but it seems a shame the big BC orgs aren't channelling the good news stories to the media (we see a lot of rubbish reported here - a couple of weeks ago their was a nonsense story about Neulasta being a new cure for C!).

Have passed on all of this info to an aussie bc forum - would be good ifus aussies could get involved early, we seem to be years behind you US girls in terms of trials and treatments.

Lets keep talking!

B

Lani and all,

I simply cannot get this post out of my mind! Basically it seems so logical in principle to attack all possible pathways at once. I have always considered a cancer cell to be the equivallent of a 'pest' and the only way to deal with a pest is to go hard on it first time round, as to not allow it to develop resistance.

Anyhow, you said "for the activists among us, let's try to use our energies to help push this progress forward!". How can we push these things forward???? as mentioned in 2004 they had already published about the great results of combinaisons of drugs (either er+ or not the principle was already established) was working but nothing much was done since..<!-- / message -->

I have also noticed that unfortunatly that they may consider trial to take place for herceptin virgin only..does that mean that they would leave all of us behind! [how about lapatinib+gefinitib and pertuzumab]

I think that slowing the growth of cancer enough to allow your immune system to deal with it is the way forward.

I feel a need to get involved here.. So how can we push things forwards???

Genentech makes pertuzumab, herceptin and Tarceva
 

Tarceva is a tyrosine kinase inhibitor of EGFR like IRESSA is. Trying to get different drug companies to cooperate in a clinical trial can be difficult, but perhaps Genentech would be interested in a trial of three of their products.

There is going to be an interesting conference on the biological basis of breast cancer at the end of June with Francisco Esteva, Laszlo Pusztai (sorry about spelling), Carlos Arteaga, Mark Pegram, etc who think deeply about how all the her2 groups interact. It will be held in Santa Monica and will probably be quite
detailed in the molecular biology of breast cancer. These researchers as well as Martine Piccart and Edith Perez as well as George Sledge, Neil Spector and, of course, Dr. Slamon are all truly interested in the multipronged attack necessary in individual breast cancer treatment which is directed and targetted against the molecular "bad actors" driving each particular cancer.

Susan Desmond-Helman(sorry about my spelling--chief scientific officer) and
Pamela Klein (in charge of herceptin) might be good people to ask whether Genentech is interested in starting up such trials

.

Hopefully the length of treatment required with three agents is far shorter than that required with one, or the cost will end up prohibitive.

Am off in the am for Denmark, so may not join back in for a while (until jet lag recovered from and computer setup sorted out)

Hi Full of Beans. I feel like you do about this. I am going to start with a review of the book mentioned in the posts above. You know, we seem to get a report every day of research advances in BC - yesterday there was a local article on Tykerb. I am blown away that this multi-receptor research hasn't made it into the news at all - it really is an important development, and publicity would help to build awareness, and expectations.

Would love to keep chatting about this.

Would seem that in addition to mutual support, a really good function of this forum could be promotion and collective action. Just not sure how to make that happen.

PS - I have a lot of previous career experience as a trade union activist (early career) and more recently a political and policy adviser to State-level Governments, but in industrial relations, social policy and economics, not in Health. I am thinking a lot about how I can make that experience useful, - not a hard prospect in my own State, but most of the decisions that would need to be influenced are private-sector, international and later national here in Australia - it's a challenge but an interesting one. It's important to find people with energy and/or contacts and/or skills prepared to collaborate to build an international campaign. This site is probably a good place to start.

But, women in all walks of life get BC, so surely there are people who can provide complimentary skills and networks - it is just a matter of finding them.

The reason I want to read the book on the history of herceptin, is that I am just not familiar with the processes required to bring new drugs into the marketplace and into the hands of the women that need them. I think that knowledge will be really important.

At least we can tick the "brains trust" box - Lani is already providing us with the knowledge of the science, which is the ight place to start. (Thank you Lani, again!)

PPS Lani - thanks for your most recent post - the conference sounds good and will no doubt be an important professional network-building event for those very important scientists. Have a safe and productive trip to Denmark.

Belindax

Well, I finally got Robert Bazell's book - I think it's a very important book. It seems like Herceptin would not be available to us even now were it not for The passionate obsinance of a number of characters, and a whole lot of happenstance. There were so many points at which the process of developing and bringing the drug to market almost went off the rails.

But I am left wondering if it was a freak. The fact that Genentech was a biotech company not a drug company when Trastuzumab was first being explored meant that risks were taken that may not happen in a big pharmaceutical company.

Hopefully not - I know biotech is seen as an 'industry of the future' and I think to be informed and to be able to advocate in the way that many people did for Herceptin (AIDS advocates seemed to be great allies for BC advocates) we need to understand more about biotech companies, and more about how decisions are made about funding for the development of new treatments.

Still exploring.....

Ditto for me too!
 

What do we do to get it rolling fast!
We as a group (I am sure) would love to help!

Jean

Any news in ASCO regarding the progress on this?

Belinda, just saw your response now and your experience is impressive and you can count me on in term of lobbying! I am French so I am naturally good at this :-)

Jean was kind enough to alert me to this thread. I am replying so that I can hear what all of you bright minds are sharing. Thank-you!

Terri
(spouse of Ruth, dx 5/1, completed 2nd of 6 TCH)

Good to be working together!!!! Full of Beans try and read the book, if you haven't already. The historical account of how Herceptin got out there is just the best - and there are loads of lessons. Especially in relation to how important it is to do this work collaboratively.

The copy I have was from my onc nurse - it was a complimentary copy that says 'with compliments of Roche" (who bought genentech). Anyone got any contacts at Roche? This book is more useful than many of the dead trees I was given in the form of pamphlets.

I need to learn more about how this whole system works - maybe we can do this together? Maybe we can get enough HER2 women to share knowledge about how trials work, how products are commercialised....

I am in, but it isn't something I can do alone - I need to also build a network of supoprt in Australia. Maybe we need to be exploring more how this wonderful site and medium can be used as a powerful tool for activism!!!

Should we start by posting anything we know about anything at all that might help or any ideas for getting started?

(F.O.B - lol - French people have a formidable history for taking action to sort out problems....with you on board heads might well roll!!!!!!!)

Bxxxxx

Promising news. I am worried that all of us who have done Herceptin already won't be able to access the trio, much like 3 years ago where people who had already done chemo had difficulty obtaining Herceptin. BB

Bev - I am doing herceptin now - you know what, most of the activists in the Herceptin story were not bc sufferers. I am not sure how trials would work - perhaps someone who knows about trials could help with this question?

BUT what I can share is the thoughts of a dear friend of my husband and I (he was our Best Man) - he has had n-h lymphoma for well over 10 years and has doggedly sought out trials and experimental treatments. He says

"The longer I live, the longer I am going to live".

He means, the longer he stays alive, the longer it is likely that better treatments or even a cure will come through the work of the scientists and the more likely it is that he will live even longer. His aim is to just keep going!

So Bev - the more we work together to bring on the treatments - the more likely we will be able to have access to them, not only in trials but after the trials have given us new treatments, when our previous treatments no longer matter unless they threaten to harm us.

Belindax

Very cool. Great post. Let's hope it continues to be researched.

reading over and over
 

make me fell happy and with hope reading this post everytime I wish we know something more about the same .....how we can help ???

more info
 

the Breast Center at Baylor College of Medicine
http://www.breastcenter.tmc.edu/graphics/banner.jpg
<!-- InstanceBeginEditable name="content" -->C. Kent Osborne and Rachel Schiff Laboratory

Welcome

Our laboratory is a team effort between C. Kent Osborne, M.D. a clinical scientist and cell biologist, and Rachel Schiff, Ph.D., a molecular biologist, and is one of several basic/translational research laboratories comprising the Breast Center at Baylor College of Medicine and The Methodist Hospital in the Texas Medical Center in Houston, Texas. Both Drs. Osborne and Schiff have Faculty Appointments in the Department of Medicine and in the Department of Molecular and Cellular Biology. Dr. Osborne is the Director of the Breast Center and he has more than 25 years of experience in translational and clinical research in breast cancer. Dr. Schiff has much experience in molecular and cellular biology of breast cancer and is an expert in exploiting breast cancer preclinical models towards the development of novel approaches of targeted therapies.
The research objective of our laboratory is to understand the molecular mechanisms by which breast cancers become resistant to endocrine therapy and then to develop new treatment strategies to block or overcome this resistance. In this research, we combine molecular/genetic analyses with cell biology to answer important clinically relevant questions using cell culture and animal models that we developed two decades ago, along with newly developed ones. Major interests include the crosstalk that we and others have discovered between growth factor receptor and/or other cellular kinase signaling and estrogen receptor signaling pathways, and the role of ER coactivators and corepressors in the development of hormone therapy resistance. We have shown that growth factor receptor signaling such as that initiated by tyrosine kinase receptors of the EGF family play an important role in hormone therapy resistance and that blockade of these pathways represents a new strategy to prevent it. The ER coactivator AIB1 (SRC3) which is often either amplified and/or overexpressed in breast cancer, and the ER corepressor protein FKHR that is often lost in breast cancer are modulated by growth factor signaling and we believe are key to the resistant phenotype.
Various projects include: 1) determine the mechanisms by which receptor tyrosine and serine/ threonine kinases cause resistance to tamoxifen and other endocrine therapies, 2) investigate whether therapies that target these pathways can overcome resistance, 3) identify the role of AIB1 phosphorylation in ER function and hormone therapy resistance, 4) determine if the ER corepressor FKHR functions as a tumor suppressor gene in breast center, and 5) define molecular profiles in human breast cancer specimens that predict selective hormone therapy resistance and, then, identify new therapeutic targets to reverse it.
For more details, please see the research page.
<!-- InstanceEndEditable -->Home | Patient Care | Research | About Us | Contact Us
Privacy Notices
BCM Home | BCM Intranet | BC Intranet
Copyright © 2005 Breast Center, One Baylor Plaza, Houston, Texas 77030. All Rights Reserved.



<FORM action=http://www.google.com/search method=get>
<INPUT maxLength=255 size=18 name=q> <INPUT class=buttonstyle type=submit value=Search name=googleButton> <INPUT type=hidden value=www.breastcenter.tmc.edu name=domains> <INPUT type=hidden value=www.breastcenter.tmc.edu name=sitesearch> </FORM>

<TABLE id=labMenuList cellSpacing=0 cellPadding=0><TBODY><TR><TD noWrap>Lab Home</TD><TD noWrap>Research</TD><TD noWrap>Training</TD><TD noWrap>Lab Members </TD><TD noWrap>Resources</TD><TD noWrap>Opportunities</TD><TD noWrap>Publications</TD><TD noWrap>Links</TD></TR></TBODY></TABLE>

• <LI class=menubar>Home <LI class=menubar>Patient Care
  • Appointments
  • Mammograms
  • Maps & Visitor Info
  • Our Doctors
  • Services >>
    • Prevention
    • Genetic Evaluation
    • Diagnostic Evaluation
    • Treatment
    • Psychosocial Support
  • Clinical Trials
  • Breast Cancer Info
  • Hospital Partners
  • Ben Taub Breast Oncology Clinic
  • Patient Satisfaction
  • Volunteers
  • Donation Information
  <LI class=menubar>Research
  • Faculty
  • Research Facilities
  • Research Labs >>
    • Pathology Lab
    • Powel Brown Lab
    • Eric Chang Lab
    • Suzanne Fuqua Lab
    • Adrian Lee Lab
    • Michael Lewis Lab
    • Yi Li Lab
    • Steffi Oesterreich Lab
    • Kent Osborne Lab
  • Core Facilities >>
    • Animal Handling & Imaging
    • Biostatistics and Informatics
    • Pathology
    • Q-PCR
  • Training
  • Seminars
  • Breast Cancer Symposium
  • SPORE Grant
  • Breast Program Project
  • Recruiting >>
    • Living in Houston
    • Training
    • Resources
  • Donation Info
  <LI class=menubar>Education
  • Clinical Research Training
  • Basic & Translational Research Training
  <LI class=menubar>Recruiting
  • Employment Resources
  • Living in Houston
  <LI class=menubar>About Us
• Contact Us

<SCRIPT src="http://www.google-analytics.com/urchin.js" type=text/javascript></SCRIPT><SCRIPT type=text/javascript>_uacct = "UA-583596-1";urchinTracker();</SCRIPT><!-- InstanceEnd -->

I've been unable to find any trials with this exciting triple combo. Does anyone know why this isn't moving forward faster?
Eric

I wrote to them about a year ago, they answered that they were thinking about it..

There might be the issue of lvf problem i suppose but yes I agree eric it seems to be taking time. I hope Lani sees this as she may have more answer for us.

It seems as if the trial is going to be designed only for those who are newly diagnosed.

I wonder whether anyone will do a trial for women with advanced HER2+ bc.

"A clinical study using drug combinations in newly diagnosed patients with HER-2 positive breast cancer will start soon under the direction of physicians at BCM's Breast Center, said Osborne."

That would be very disappointing.

off trial
 

Our onc told us she and others were giving Herceptin "off-label" before trial was done for early stage. Perhaps some oncs would be willing to give this trio to those that don't qualify for the trial in the the same manner.

Lani,
As always big heartfelt thanks on your recent posting.
Now, dear one what can we do to push this forward?

Jean

TSund and Jean
 

First TSund--the reason herceptin could be given off-label adjuvantly for bc was that herceptin was already approved for metastatic bc. That is the point of the term "off-label" use--it is use of a drug already approved for a different
indication for another disease/affliction for which it is not yet (or ever) approved.

Jean--I thought the way to move this forward was to help the researchers at Baylor get a hold of specimens and histories of her2+ patinets--especially her2+ER+ patients. When I last spoike up about this at an ASCO poster exhibit
I think it was with the Susan Komen people, they offered me a handout regarding how Komen could help with this and what they were already doing.

It had been many many months since I had heard from/tumor repository" and only about 5% or those who read the original post about how many would donate their specimen and give access to their records responded, causing me feel my efforts were better directed elsewhere.

I have been in touch with the Baylor people (saw them at ASCO and the Era of Hope), pointing out to them some interesting work being done by Jose Baselga's group in Spain(poster at ASCO) on how giving herceptin and tykerb "turbs" up the ADCC immune reaction against her2 and am aware that Mark Slikowski at Genentech has been supplying the samples to the Baselga group for their studies and is cooperating with them.

I also attended THE annual AACR meeting and heard Axel Ullrich, whom they
lauded as the true "inventor" of herceptin and provided with a "lifetime achievement award" explaining that her3 will be the key to curing her2 breast cancer.

I have heard Max Wicha at both AACR and ASCO describe how her 2 regulates the percentage of and invasiveness of cancer stem cells in breast tumors and, in general, asked lots of questions and alluded to the fact that
a repositiory of sample awaits interested researchers if the finances, legalities and logisitics could be worked out.

Max Wicha is starting a multicenter trial with a gamma secretase inhibitor (already FDA approved for Alzheimers I believe) trying to eliminate the cancer stem cells and thus the reucrrences of breast cancer.

I posted earlier an article which unfortunately should some increased cardiotoxicity adding pertuzumab (not FDA approved) to herceptin--I am sure Genentech, which has been on a roll with its products, is hesitant to begin a trial with the indication that there may be increased cardiotoxicity of the combination.

Another problem is that Iressa is approved but only for a VERY narrow indication and it is made by a different drug company than the other two drugs (which are made by Genentech). Genentech also makes an oral EGFR inhibiting TKI, Tarceva. It is very diffcult to get different drug companies to cooperate in a clinical trial.

The best hope would be Genentech--but they are about to be bought out by their majority stockholder, Roche --a much less innovative compnay who spend much less of their income on basic research and have a very different corporate "behavior" it would seem.

I don't know what her2 support as a group can do other than write letters to Roche, should they get their way, urging them not to change the governance or modus operandi of Genentech (but money talks, not letters!)

After attending 7 maor meetings in the last 12 months, I may only attend one more before San Antonio. I will continue to try to find out what is
holding up this trial and get back to your on what might be done to speed it up.

re: Roche purchase of Genentech
 

Lani - I'm very thankful for the time you invest with us. The following is an article discussing the company purchase...

http://www.medicalnewstoday.com/articles/118446.php

Roche said that if it acquired Genentech, it would allow Genentech to maintain its creative independence and that patients would benefit from the acquisition. Barbara Brenner, executive director of Breast Cancer Action, said, "Genentech has actually gone out of its way to engage conversations with the activist community." Brenner added, "We rarely agree, but at least we can talk to them. I have trouble imagining that will continue if Roche owns the company" (Chase, Wall Street Journal, 8/14)