EGFR Positive UPSC and Clear Cell Patients
I had my original tumor from surgery sent in for a tumor assay/profiling to be done. I was staged as a stage 1B (on the old FIGO chart). My doctor gave me a promising prognosis (70-80%)with treatment. After that prognosis I received the reports from the tumor profiling. I took the printed report in to the doctors office. I don't think that he actually even read this report since he never commmented to me about it. I was given carbo/taxetere for chemo. The PA looked at the report and said she thought I was on the right track. After reading recently on the post "Moving up a new post on funtional profiling posted on the long long long UPSC post that loads so slow", it mentions EGFR. Stating that in a medical report it says that EGFR in UPSC and Clear cell positively decrease survival from 86 to 27%. I checked my profiling report and I am positive for EGFR. This is an alarming finding!! My doctor made no comments to me about EGFR, therefore I don't think he read my reports or doesn't know that it is a significant marker.
My question is how many ladies here have had profiling done? If you have had profiling done, what was your result/finding for EGFR? Positive or negative? How has your UPSC behaved so far? Recurrances? Over how long a time frame?
I read this discussion board several times per week. I have gained an immense amount of knowledge from the ladies on this board. I do not post often because I am still learning about UPSC and I am not as knowledgeable as others here. I have recently finsihed 6 rounds of carbo/taxetere (neither of which attack EGFR cells) and 3 brachy therapy treatments. I thought that I had a good chance at beating UPSC because of the early stage and aggressive treatment but I am not so sure now. My doctor did not order any follow up tests after I was finished with treatment...not even a chest x-ray. He told me that I would have a CT a year from my original CT, which was the first part of Feb., 2011. I know that I am in a better situation than many of the later staged ladies that are battling this terrible disease. I am just nervous about the future, as is everyone of us here. I am hoping that someone else has had the profiling done and is farther along the cancer journey so that they can answer some of my questions. I would like to know how many are EGFR positive. I am alarmed by the information about EGFR. I know that nothing has changed for me since last week or last month. It is realization of this information that is just hitting me hard emotionally. I probably just need time to process this and prepare. After a UPSC diagnosis everything relating to the cancer seems to alarm me!
I say continual prayers that some advancement will be made in the treatment/cure of this horrible disease.
Pat
Comments
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I am so sorry that something I posted long ago haunts you now.
I hate to see someone who was feeling hopeful read something that shakes their faith in the wisdom of that hope. Knowledge is power, but not if it haunts you in the darkest part of the night. (((Pat))) I was really focused on EGRF when I was first diagnosed in 2008 with UPSC (stage 3-c) since it scared me because it is so prevalent in papillary serous cancers. In fact I SAVED an article all this time, plus some notes from Greg ("gdpawel" is the handle I think he posts under here), which is now somewhat dated (2007), on that subject. I want to paste it in here, because it does offer treatment suggestions for those with EGFR and there is HOPE when there are targeted treatments to try. You might want to post on the Ovarian Cancer Board here and ask for those women's experiences with PARP1 inhibitors, which look promising for EGFR.
Here you go:
Findings presented at the 41st Annual Meeting of the European Society for Clinical Investigation in Uppsala, Sweden, April 18, 2007, concluded that "functional profiling" with cell culture assays is relevant for the study of both "conventional" and "targeted" anti-neoplastic drug agents (anti-tumor and anti-angiogenic activity of Iressa, Tarceva, Sutent, Nexavar, and Avastin in primary cultures of "fresh" human tumors).
Cell Culture Assays with "cell-death" endpoints can show disease-specific drug activity, are useful clinical and research tools for "conventional" and "targeted" drugs, and provide unique information complementary to that provided by "molecular" tests. There have been more than 25 peer-reviewed publications showing significant correlations between cell-death assay results and patient response and survival.
Many patients are treated not only with a "targeted" therapy drug like Tarceva, Avastin, or Iressa, but with a combination of chemotherapy drugs. Therefore, existing DNA or RNA sequences or expression of individual proteins often examine only one component of a much larger, interactive process. The oncologist might need to administer several chemotherapy drugs at varying doses because tumor cells express survival factors with a wide degree of individual cell variability.
There is a tactic of using biopsied cells to predict which cancer treatments will work best for the patient, by taking pieces of live "fresh" tumor tissue, applying different chemotherapy treatments to it, and examining the results to see which drug or combination of drugs does the best job killing the tumor cells. A cell culture assay test with "functional profiling," using a cell-death endpoint, can help see what treatments will not have the best opportunity of being successful (resistant) and identify drugs that have the best opportunity of being successful (sensitive).
"Functional profiling" measures the response of the tumor cells to drug exposure. Following this exposure, they measure both cell metabolism and cell morphology. The integrated effect of the drugs on the whole cell, resulting in a cellular response to the drug, measuring the interaction of the entire genome. No matter which genes are being affected, "functional profiling" is measuring them through the surrogate of measuring if the cell is alive or dead.
For example, the epidermal growth factor receptor (EGFR) is a protein on the surface of a cell. EGFR-inhibiting drugs certainly do target specific genes, but even knowing what genes the drugs target doesn't tell you the whole story. Both Iressa and Tarceva target EGFR protein-tyrosine kinases. But all the EGFR mutation or amplificaton studies can tell us is whether or not the cells are potentially susceptible to this mechanism of attack. They don't tell you if Iressa is better or worse than Tarceva or other drugs which may target this. There are differences. The drugs have to get inside the cells in order to target anything. So, in different tumors, either Iressa or Tarceva might get in better or worse than the other. And the drugs may also be inactivated at different rates, also contributing to sensitivity versus resistance.
As an example of this testing, researchers have tested how well a pancreatic cancer patient can be treated successfully with a combination of drugs commonly used to fight lung, pancreatic, breast, and colorectal cancers. The pre-test can report prospectively to a physician specifically which chemotherapy agent would benefit a cancer patient. Drug sensitivity profiles differ significantly among cancer patients even when diagnosed with the same cancer.
The "functional profiling" technique makes the statistically significant association between prospectively reported test results and patient survival. It can correlate test results that are obtained in the lab and reported to physicians prior to patient treatment, with significantly longer or shorter overall patient survival depending upon whether the drug was found to be effective or ineffective at killing the patient's tumor cells in the laboratory.
This could help solve the problem of knowing which patients can tolerate costly new treatments and their harmful side effects. These "smart" drugs are a really exciting element of cancer medicine, but do not work for everyone, and a test to determine the efficacy of these drugs in a patient could be the first crucial step in personalizing treatment to the individual.
Author/Speaker/Performer :Larry Weisenthal, M.D., Ph.D.; Contact information: phone: (714) 596-2100.
The 102 page pdf on this is still available at this Link: http://weisenthal.org/Weisenthal_ESCIa.pdf Source : Eur J Clin Invest 37 (suppl. 1):60, 2007
and here's something more from the Komen Fdn:
Cetuximab. Triple-negative tumors are known to overexpress EGFR,[20] and 2 studies presented at SABCS 2007 explored the role of cetuximab, a humanized monoclonal antibody directed against EGFR, in this tumor type. Both of the trials included a platinum agent because preclinical data suggested that triple-negative tumors may have defects in BRCA1-mediated DNA repair and thus may be sensitive to DNA-damaging agents such as platinums.[21]
An ongoing study in metastatic triple-negative breast cancer is evaluating the role of sunitinib antiangiogenesis monotherapy compared with best available chemotherapy.[27] Other emerging targets for treatment incorporate components of cellular proliferative pathways, including the phosphoinositide 3-OH kinase pathway and the mitogen-activated protein kinase pathway, DNA repair, and growth-factor receptors such as EGFR and c-kit. Agents currently in phase 1/2 evaluation for triple-negative disease include dasatinib and PARP1 inhibitors. It is hoped that further advances in targeted treatment and optimization of chemotherapy will provide more effective treatment and improved outcomes for this aggressive subclass of breast cancer.0 -
Linda-Thank youlindaprocopio said:I am so sorry that something I posted long ago haunts you now.
I hate to see someone who was feeling hopeful read something that shakes their faith in the wisdom of that hope. Knowledge is power, but not if it haunts you in the darkest part of the night. (((Pat))) I was really focused on EGRF when I was first diagnosed in 2008 with UPSC (stage 3-c) since it scared me because it is so prevalent in papillary serous cancers. In fact I SAVED an article all this time, plus some notes from Greg ("gdpawel" is the handle I think he posts under here), which is now somewhat dated (2007), on that subject. I want to paste it in here, because it does offer treatment suggestions for those with EGFR and there is HOPE when there are targeted treatments to try. You might want to post on the Ovarian Cancer Board here and ask for those women's experiences with PARP1 inhibitors, which look promising for EGFR.
Here you go:
Findings presented at the 41st Annual Meeting of the European Society for Clinical Investigation in Uppsala, Sweden, April 18, 2007, concluded that "functional profiling" with cell culture assays is relevant for the study of both "conventional" and "targeted" anti-neoplastic drug agents (anti-tumor and anti-angiogenic activity of Iressa, Tarceva, Sutent, Nexavar, and Avastin in primary cultures of "fresh" human tumors).
Cell Culture Assays with "cell-death" endpoints can show disease-specific drug activity, are useful clinical and research tools for "conventional" and "targeted" drugs, and provide unique information complementary to that provided by "molecular" tests. There have been more than 25 peer-reviewed publications showing significant correlations between cell-death assay results and patient response and survival.
Many patients are treated not only with a "targeted" therapy drug like Tarceva, Avastin, or Iressa, but with a combination of chemotherapy drugs. Therefore, existing DNA or RNA sequences or expression of individual proteins often examine only one component of a much larger, interactive process. The oncologist might need to administer several chemotherapy drugs at varying doses because tumor cells express survival factors with a wide degree of individual cell variability.
There is a tactic of using biopsied cells to predict which cancer treatments will work best for the patient, by taking pieces of live "fresh" tumor tissue, applying different chemotherapy treatments to it, and examining the results to see which drug or combination of drugs does the best job killing the tumor cells. A cell culture assay test with "functional profiling," using a cell-death endpoint, can help see what treatments will not have the best opportunity of being successful (resistant) and identify drugs that have the best opportunity of being successful (sensitive).
"Functional profiling" measures the response of the tumor cells to drug exposure. Following this exposure, they measure both cell metabolism and cell morphology. The integrated effect of the drugs on the whole cell, resulting in a cellular response to the drug, measuring the interaction of the entire genome. No matter which genes are being affected, "functional profiling" is measuring them through the surrogate of measuring if the cell is alive or dead.
For example, the epidermal growth factor receptor (EGFR) is a protein on the surface of a cell. EGFR-inhibiting drugs certainly do target specific genes, but even knowing what genes the drugs target doesn't tell you the whole story. Both Iressa and Tarceva target EGFR protein-tyrosine kinases. But all the EGFR mutation or amplificaton studies can tell us is whether or not the cells are potentially susceptible to this mechanism of attack. They don't tell you if Iressa is better or worse than Tarceva or other drugs which may target this. There are differences. The drugs have to get inside the cells in order to target anything. So, in different tumors, either Iressa or Tarceva might get in better or worse than the other. And the drugs may also be inactivated at different rates, also contributing to sensitivity versus resistance.
As an example of this testing, researchers have tested how well a pancreatic cancer patient can be treated successfully with a combination of drugs commonly used to fight lung, pancreatic, breast, and colorectal cancers. The pre-test can report prospectively to a physician specifically which chemotherapy agent would benefit a cancer patient. Drug sensitivity profiles differ significantly among cancer patients even when diagnosed with the same cancer.
The "functional profiling" technique makes the statistically significant association between prospectively reported test results and patient survival. It can correlate test results that are obtained in the lab and reported to physicians prior to patient treatment, with significantly longer or shorter overall patient survival depending upon whether the drug was found to be effective or ineffective at killing the patient's tumor cells in the laboratory.
This could help solve the problem of knowing which patients can tolerate costly new treatments and their harmful side effects. These "smart" drugs are a really exciting element of cancer medicine, but do not work for everyone, and a test to determine the efficacy of these drugs in a patient could be the first crucial step in personalizing treatment to the individual.
Author/Speaker/Performer :Larry Weisenthal, M.D., Ph.D.; Contact information: phone: (714) 596-2100.
The 102 page pdf on this is still available at this Link: http://weisenthal.org/Weisenthal_ESCIa.pdf Source : Eur J Clin Invest 37 (suppl. 1):60, 2007
and here's something more from the Komen Fdn:
Cetuximab. Triple-negative tumors are known to overexpress EGFR,[20] and 2 studies presented at SABCS 2007 explored the role of cetuximab, a humanized monoclonal antibody directed against EGFR, in this tumor type. Both of the trials included a platinum agent because preclinical data suggested that triple-negative tumors may have defects in BRCA1-mediated DNA repair and thus may be sensitive to DNA-damaging agents such as platinums.[21]
An ongoing study in metastatic triple-negative breast cancer is evaluating the role of sunitinib antiangiogenesis monotherapy compared with best available chemotherapy.[27] Other emerging targets for treatment incorporate components of cellular proliferative pathways, including the phosphoinositide 3-OH kinase pathway and the mitogen-activated protein kinase pathway, DNA repair, and growth-factor receptors such as EGFR and c-kit. Agents currently in phase 1/2 evaluation for triple-negative disease include dasatinib and PARP1 inhibitors. It is hoped that further advances in targeted treatment and optimization of chemotherapy will provide more effective treatment and improved outcomes for this aggressive subclass of breast cancer.
Linda,
Thank you for the reply. Knowledge is power. I am glad that you posted this EGFR information again. I had not seen it before. This information is valuable to me even though it does scare me. Ignoring the information does not change the fact that I am EGFR positive. I just need to find a way to deal with this better....everything scares me.
You are an inspiration to me. You are so knowledgeable and are fighting this disease so hard. Keep fighting.
Pat0 -
PatPat51 said:Linda-Thank you
Linda,
Thank you for the reply. Knowledge is power. I am glad that you posted this EGFR information again. I had not seen it before. This information is valuable to me even though it does scare me. Ignoring the information does not change the fact that I am EGFR positive. I just need to find a way to deal with this better....everything scares me.
You are an inspiration to me. You are so knowledgeable and are fighting this disease so hard. Keep fighting.
Pat
Where are you being treated and is your doctor a gyn onc?
JoAnn0 -
Hi PatJoAnnDK said:Pat
Where are you being treated and is your doctor a gyn onc?
JoAnn
I had to look EGFR up and did find an artical that said it could be valuable in future research .
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745284/
I did not have the finances to have mine tested outside of the standard of care. I believe I asked if it was tested and if it could be. I don't remember the answer. That was over two years ago.
It has taken me a while to trust doctors that they are doing the best job. In hindsight , I put my oncologist through alot .
Grace0 -
thanksGracegoi said:Hi Pat
I had to look EGFR up and did find an artical that said it could be valuable in future research .
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745284/
I did not have the finances to have mine tested outside of the standard of care. I believe I asked if it was tested and if it could be. I don't remember the answer. That was over two years ago.
It has taken me a while to trust doctors that they are doing the best job. In hindsight , I put my oncologist through alot .
Grace
Grace, thanks for posting the LINK to that interesting article about EGFR. Not that I understood all of it, but I am going to talk to people who do!
We were talking about early stage treatment the other day, and here is what I had read previously in another article:
"There is currently no consensus on the optimal adjuvant therapy after a surgical staging procedure for USC; however, it is generally believed that aggressive adjuvant therapy is warranted even in early stage disease given the high recurrence rates with surgical resection alone. "0 -
pathologyFayard said:I was reading my biopsy
I was reading my biopsy again, and I could not find results for EGFR.
Am I missing something?
Is this standard?
Fayard, I think that the pathology report is done in-house immediately after (and even during) surgery, whereas the tissue for assay/profiling is sent to a specialized lab.0 -
JoAnnJoAnnDK said:Pat
Where are you being treated and is your doctor a gyn onc?
JoAnn
I am located in Wisconsin. I wanted a GYN/ONC but there is none in our area. There was an "in network" Gyn/Onc that I went to soon after my surgery (before treatment was started). When we met he said "You have UPSC. You have known for a couple of weeks now and should be use to the idea. What do you want me to do about it? You don't need to know any details. Just do the treatment." I was so stunned by this that I couldn't even answer him and never went back to him again!!! My OB/GYN sent me to a regular medical oncologist who consulted with a gyn/onc from an "out of network" facility. I cannot go to any other major hospital in Wisconsin since they are not "in network". The oncologist that I see is located about 50 miles from my home and one of the closest to me.
Did you have tumor assay/profiling done?
Pat0 -
GraceGracegoi said:Hi Pat
I had to look EGFR up and did find an artical that said it could be valuable in future research .
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745284/
I did not have the finances to have mine tested outside of the standard of care. I believe I asked if it was tested and if it could be. I don't remember the answer. That was over two years ago.
It has taken me a while to trust doctors that they are doing the best job. In hindsight , I put my oncologist through alot .
Grace
Thank you for posting the link for the article about EGFR.
Pat0
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