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ASCO Breast Cancer Symposium

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I am so excited to be leaving tomorrow morning for San Francisco to attend the annual ASCO(American Society of Clinical Oncologists) Breast Cancer Symposium. The focus of this meeting will be integrating Emerging Science into Clinical Practice and the most recent clinical study results and findings will be presented. Additionally, I am attending San Antonio Breast Cancer Symposium December 8-13 as a breast cancer advocate. To attend as an patient advocate, one has to have completed the Project LEAD scientific training seminar through the National Breast Cancer Coalition then apply to ASCO or San Antonio. My goal is to report to all of you the highlights and hot topics from both of these symposiums. Google these organizations for daily updates. I strongly recommend pursuing the NBCC advocacy training and then consider applying to attend either of these breast cancer symposiums next year. These symposiums are organized for researchers, investigators, oncologists and clinicians. But, they are also making spots available to patient advocates. Through training, we can all advocate more effectively in support of the recurrent breast cancer community. Check out www.stopbreastcancer.org for information on this advocacy organization and the educational opportunities. I will try to update you as more information becomes available. If any of you are interested in following the updates out of San Antonio in December, www.cancercare.org is sponsoring a free connect workshop titled, "The Latest Developments Reported at the 32nd Annual San Antonio Breast Cancer Symposium". You can listen to the workshop over the telephone or online. To register:
call 1-800-813-4673 or online at www.cancercare.org/connect This is another way to hear the most recent research and innovations in breast cancer investigations.

12 replies

Thank YOU for being our eyes and ears at all of these important events. Please continue to share with us each exciting new piece of information. I'm going to look into being a Super Advocate, though I hesitate because I question if I have the energy to do so. Aw heck, might as well go for it!

Peace~

One question: are you going as a fellow patient, or are you affiliated with one of these organizations? I checked your profile to see HOW you were doing all of this healthwise, but couldn't figure out where you are in treatment. Thanks again for the important info!

Thank you!

Hi,

I want to also add my Thank You!

I have also been thinking of becoming an advocate and I will look into it further.

Thanks again,

ATCD

Yes, please keep us posted on what you learn at these meetings. Thank you for lending your support on behalf of all the rest of us!

Hi Saraj,
Without being intrusive, I would also be interested in knowing a bit more about your current medical status. I've read most of your comments and they are very informative and professional.
Do you have advanced breast cancer, or have you been in treatment for the original bc for 8 years - a really long time, and I do admire you for that.
My interim onco in WI was also affiliated with Mayo Clinic in Rochester, MN but I was never treated there. Thank you for sharing a bit more about yourself, if you're open to that. It helps me to relate to you as well as to the obviously well researched information.
Thanks!

When in San Antonio please visit our exhibit in the exhibition area.
We will also be at the Alamo bc Foundation's welcoming dinner as our HER2 support group donates money for 2 advocates to attend the Symposium each year.

You will really enjoy the experience, the evening mentor sessions are extremely rewarding.

Hugs
Christine
HER2 Support Group

At the 2009 American Society of Clinical Oncology (ASCO) breast cancer symposium, in San Francisco, the Keynote Address (by Martine PIccart-Gebhart of the Jules Bordet Institute) was very relevant to Individualized Tumor Response Testing.

The speaker made the point that only 8% of new drugs entering Phase I trials ever make it to marketing and that this percentage is even lower for cancer drugs, because current drug testing is inefficient, with many drugs failing late in development, with these expensive failures owing, in large measure, to ineffective drugs and poor patient selection (i.e, lack of prognostic and predictive markers for response to therapy).

The speaker went on to note that little progress has been made in identifying which therapeutic strategies are likely to be effective for individual patients. The speaker concluded that identifying markers that can predict response to a particular drug remains a great challenge.

Why was nothing being presented at this meeting which reports any progress at all in drug selection through the use of molecular profiling? When microarrays and high throughput RT-PCR emerged some years back, you'd think that there would be quite a bit of progress by now. Sad to say, there has not.

http://theoncologist.alphamedpress.org/cgi/content/full/12/3/301

A study was presented at the symposium about progress in drug selection through the use of cell-based functional profiling. It delt with the so-called "triple negative" breast cancer (TNBC), which is estrogen receptor negative (ER-), progesterone receptor negative (RP-), and Her2 negative (H2-).

When breast cancer presents as locally advanced disease, it is customarily treated with neoadjuvant (preoperative) chemotherapy, followed by definitive surgery. At the time of surgery, the specimen is assessed to determine if all visible tumor has been destroyed by chemotherapy. When this happens, it is said to be a “pathological complete response” (pCR).

Data shows that obtaining a pCR is everything. Get a pCR, and the survival is excellent. Don’t get a pCR and the survival, especially for TNBC patients, is very poor. How can the pCR rate be improved in TNBC?

The speaker went through all the database of breast cancer cell culture assays (using cell death endpoints) and tried to see if there were any drugs which appeared to be uniquely active in TNBC vs non-TNBC.

There were no major differences between the activity of most drugs in TNBC vs non-TNBC, with one glaring exception: cisplatin, which was dramatically more active in TNBC than in non-TNBC.
The speaker went on to present a lot of data further dissecting which specific markers were most associated with TNBC sensitivity to cisplatin. The data will shortly appear on the ASCO website. When they post slide presentations from the 2009 Breast Cancer Symposium, I'll post it here.

But, essentially, the major markers for platinum sensitivity in breast cancer were estrogen receptor negativity and very poorly differentiated tumors. The minor markers for platinum sensitivity in breast cancer were Her2 negativity and progesterone receptor negativity.

The data compared TNBC to other types of tumors. It’s known that renal cell carcinomas are very resistant to cisplatin (less than 10% response rate), and that is reflected by the cell culture (cell death endpoint) data. It’s known that previously-untreated, poorly differentiated ovarian cancers tend to be very sensitive to cisplatin (70% response rate), and that’s also reflected by the cell culture data. When ovarian cancer patients relapse soon (0 to 6 months) after discontinuation of chemotherapy, they have only a 25% response rate to re-treatment with platinum. When ovarian cancer patients relapse greater than 6 months following discontinuation of chemotherapy, they have a 50% response rate to re-treatment with platinum. These clinical findings are also nicely recapitulated by the cell culture assay data.

Now, breast cancers which are either estrogen receptor positive and/or more than very poortly differentiated (Bloom Richardson score of 4 to eight) tend to be even more resistant to cisplatin than are previously treated ovarian cancer which relapse soon (0 to 6 months) after discontinuation of chemotherapy. In contrast, Triple Negative Breast Cancers tend to be as sensitive or more sensitive (especially when also Bloom Richardson 9/9) to cisplatin than are previously-untreated, poorly-differentiated ovarian cancers.

The data clearly showed the utility of cell culture assays in “targeting” chemotherapy to patient sub-groups who are most likely to benefit from treatment with given individual drugs. It is hard to see how molecular profiling tests could have produced similar insights.

Genomics is far too limited in scope to encompass the vagaries and complexities of human cancer biology when it comes to drug selection. Efforts to administer targeted therapies in randomly selected patients often result in low response rates at significant toxicity and cost.

While researchers continue to develop molecular probes to select candidates, the cell culture analysis platform serves as a functional profile capable of examining the nuances of cellular response to drugs. To exploit the full potential of targeted anticancer therapies, physicians will need laboratory tests that match patients to specific drugs.

Cell culture assays are able to accurately predict how an individual patient's cancer cells will respond to an array of drug combinations. It is able to quantify synergistic drug combinations and individually tailor treatment.

Thanks so much for your detailed explanation gpawelski. I think that I actually understand what you're saying because my oncologist has tried to explain his research in triple negative breast cancer even though I am triple positive.

Keep us informed please. And, I hope you eventually get a free meal!!

Free meal!? LOL!!! I'm not counting on one!

Activity of cisplatin in triple-negative breast cancer in comparison to other cancer types in fresh tumor cell culture assay using a cell death endpoint

http://www.asco.org/ASCOv2/Meetings/Abstracts?&vmview=abst_detail_view&conf ID=70&abstractID=40486

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