Taxotere, Carboplatin and Herceptin
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5 years is wayyyyyy toooooo long!
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Ashla, thanks - very encouraging news!
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ashla,
Thanks for sharing the latest progress on the HER2 vaccine. I live in San Antonio and didn't realize that the research was being done here.
It's amazing to watch the progress on the HER2 treatment. I tell people that the identifcation and targeted treatment with Herceptin that was introduced over ten years ago is probably saving my life. I think a HER2 condition prior to the introduction of Herceptin would have been a death sentence. My ONC told me that not treating the HER2 condition would probably result in a 35%-45% recurrence of my cancer. Those are pretty high odds of a recurrence!
Even if it's five yeas until the vaccine becomes available, it's great to see that they're looking for an easier road (no chemo) for any future breast cancer patients with the HER2 condition.
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racerdeb - the phase I portion of this trial was only open to military and their dependents as this trial was initiated by the military. In order to qualify for the phase II portion, which has now become available to civilians and is in two international locations, you have to be between 1-6 months post treatment. I believe that this is 1-6 months post Herceptin, and is for those who have already had chemo. Here is the link to the phase II trial:
http://clinicaltrials.gov/show/NCT00524277
I believe that Fluff is going to North Carolina, and I am looking at going to Washington, D.C. for this.
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Ashla, thanks for sharing the Her2 vaccine information. I had not heard of this before. It brought tears to my eyes.
SpecialK, I hope you and Fluff get to participate. Assuming this will eventually be approved, do you think it will become available to anyone who is her2 positive or only those who are within that 6 month window?
Kellogs I agree...5 years is wayyyyyy toooo long!!!
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brax - I think like Herceptin, which in trials was available to stage IV women but not early stage Her2+, it would eventually become incorporated into regular treatment if it is shown to be safe and viable. For those of us in between, I am not sure. They may find that it is effective even further out from active treatment but it is still in the information gathering phase. Hard to say at this point.
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I find for the most part if you are a year out from surgery (NED for 1 year) no one is interested in you anymore.
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MOre on BC progress....
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Treatment of breast cancer is becoming “horrendously complicated,” according to Brian Leyland-Jones, MD, PhD, director, Winship Cancer Institute at Emory University in Atlanta, Georgia. Leyland-Jones, who spoke at the 9th Annual Northern New Jersey Breast Cancer Conference, held at the John Theurer Cancer Center in February, explained that as research progresses, optimal treatment of breast cancer will involve individualization of therapy to focus on specific targets driving each patient’s cancer. “It is becoming clear that breast cancer has 50 to 80 targetable drivers,” he said.
“This is a time of massive knowledge change in the entire field,” said Leyland-Jones, noting that research is progressing so rapidly that it’s almost becoming impossible to remember all the targeted areas. Advances in both basic research and translational research are producing a plethora of new targets. “The number of targets is shooting up, but fortunately we are getting the drugs to handle those targets,” said Leyland-Jones.
One promising advancement is the development of T-DM1 (also called trastuzumab emtansine, Roche) for HER2-positive disease. T-DM1 is an antibody-drug conjugate (ADC) in which trastuzumab (Herceptin, Genentech) is attached to the chemotherapy DM1 using a stable linker. Results of a phase II trial, presented at the San Antonio Breast Cancer Symposium (SABCS) in December, evaluated first-line therapy with either trastuzumab/docetaxel or T-DM1 in patients with HER2-positive metastatic breast cancer. Compared with trastuzumab/docetaxel, T-DM1 significantly improved progression-free survival (PFS) (median PFS for trastuzumab/docetaxel 9.2 months vs 14.2 months for T-DM1; HR = 0.594; 95% CI, 0.364-0.068; P = .0353). There was significantly less toxicity with T-DM1. At least two ongoing trials (EMILIA and MARIANNE) are continuing to evaluate use of T-DM1 in HER2-positive metastatic breast cancer.
The pivotal phase III CLEOPATRA trial, also presented at SABCS, demonstrated a significant improvement in PFS for dual HER2 inhibition using trastuzumab and pertuzumab. The survival impact demonstrated in the study will be “practice-changing,” said Leyland-Jones.
Many additional targets are under development for breast cancer therapies, including PARP inhibitors, which may have efficacy in BRCA-associated cancer. In a phase III trial published in January 2011, the PARP inhibitor iniparib (BiParSciences/sanofi-aventis), did not meet the primary dual endpoints of overall survival (OS) and PFS in metastatic triple-negative breast cancer. However, a pre-specified subgroup analysis suggested improvements in OS and PFS in the second- and third-line settings, and research on iniparib continues. Iniparib is considered a relatively weak PARP inhibitor, said Leyland-Jones, but it “works in terms of helping DNA repair. The driving force of cancer is DNA repair.”
Other PARP inhibitors under development include rucaparib (Clovis), for BRCA-positive, post-neoadjuvant triple-negative breast cancer; olaparib (AstraZeneca), for BRCA-positive breast cancer; and veliparib (Abbott), for BRCA-positive, triple-negative breast cancer.
Advances in basic research are leading to a greater understanding of the tumor microenvironment, noted Leyland-Jones. New therapeutic targets as a result of these advances include metabolic pathways (serine, glycine synthesis), JAK2 in triple-negative and potentially other breast cancers, androgen receptors in HER2- positive breast cancer; SRC in trastuzumab resistance; and use of large-scale siRNA screens to identify and validate targets.
Advances in translational research have recently led to work on overcoming endocrine therapy resistance, overcoming HER2-targeted therapy resistance, and classification and prognosis in triple-negative breast cancer.
Over the next five years, therapy will increasingly be based on genome sequencing, said Leyland-Jones. The cost of sequencing is also expected to drop, along with the time it takes to see results, he said, with results available within two weeks.
The impact of emerging new therapies will be significant, according to Leyland-Jones. “Breast cancer will be transformed in our lifetimes.”
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Lago I don't understand the NED when there are no tests being done. What I got out of the conversation with my onc was that it all basically falls on me. If at an exam I complain of pain in my leg, arm, chest, etc., it could mean something is going on and they may look more into it. I'm going to revisit this next week with my onc.
Whatever I know abut Her2+ status, I know from this site or my own research. I think I walked out of the hospital thinking I was in a better place with Her2+ status. I was told that if I had to have breast cancer mine was not a bad one to have.
Diagnosis: 2011, IDC, 2cm, Stage I, Grade 3, 0/2 nodes, ER+/PR+, HER2+0 -
Re the very promising vaccine...I called my BS and volunteered for the trial but he didn't seem to want me to do it. Either that or he knew I wasn't eligible. I had just started chemo at the time.
I am already in what he considers a very forward looking study through Mammaprint. For those who haven't had one..Mammpaprint is a 70 gene RNA test done at the time of the biopsy. They will be following us and our treatments to search for RNA links to protocols and prognoses.
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ashla - I also had Mammaprint done at the time of my biopsy - my BS is participating in the study. The vaccine trial is ongoing and still recruiting - it may be available to you when you complete Herceptin.
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MOre on BC progress....
"
Treatment of breast cancer is becoming “horrendously complicated,” according to Brian Leyland-Jones, MD, PhD, director, Winship Cancer Institute at Emory University in Atlanta, Georgia. Leyland-Jones, who spoke at the 9th Annual Northern New Jersey Breast Cancer Conference, held at the John Theurer Cancer Center in February, explained that as research progresses, optimal treatment of breast cancer will involve individualization of therapy to focus on specific targets driving each patient’s cancer. “It is becoming clear that breast cancer has 50 to 80 targetable drivers,” he said.
“This is a time of massive knowledge change in the entire field,” said Leyland-Jones, noting that research is progressing so rapidly that it’s almost becoming impossible to remember all the targeted areas. Advances in both basic research and translational research are producing a plethora of new targets. “The number of targets is shooting up, but fortunately we are getting the drugs to handle those targets,” said Leyland-Jones.
One promising advancement is the development of T-DM1 (also called trastuzumab emtansine, Roche) for HER2-positive disease. T-DM1 is an antibody-drug conjugate (ADC) in which trastuzumab (Herceptin, Genentech) is attached to the chemotherapy DM1 using a stable linker. Results of a phase II trial, presented at the San Antonio Breast Cancer Symposium (SABCS) in December, evaluated first-line therapy with either trastuzumab/docetaxel or T-DM1 in patients with HER2-positive metastatic breast cancer. Compared with trastuzumab/docetaxel, T-DM1 significantly improved progression-free survival (PFS) (median PFS for trastuzumab/docetaxel 9.2 months vs 14.2 months for T-DM1; HR = 0.594; 95% CI, 0.364-0.068; P = .0353). There was significantly less toxicity with T-DM1. At least two ongoing trials (EMILIA and MARIANNE) are continuing to evaluate use of T-DM1 in HER2-positive metastatic breast cancer.
The pivotal phase III CLEOPATRA trial, also presented at SABCS, demonstrated a significant improvement in PFS for dual HER2 inhibition using trastuzumab and pertuzumab. The survival impact demonstrated in the study will be “practice-changing,” said Leyland-Jones.
Many additional targets are under development for breast cancer therapies, including PARP inhibitors, which may have efficacy in BRCA-associated cancer. In a phase III trial published in January 2011, the PARP inhibitor iniparib (BiParSciences/sanofi-aventis), did not meet the primary dual endpoints of overall survival (OS) and PFS in metastatic triple-negative breast cancer. However, a pre-specified subgroup analysis suggested improvements in OS and PFS in the second- and third-line settings, and research on iniparib continues. Iniparib is considered a relatively weak PARP inhibitor, said Leyland-Jones, but it “works in terms of helping DNA repair. The driving force of cancer is DNA repair.”
Other PARP inhibitors under development include rucaparib (Clovis), for BRCA-positive, post-neoadjuvant triple-negative breast cancer; olaparib (AstraZeneca), for BRCA-positive breast cancer; and veliparib (Abbott), for BRCA-positive, triple-negative breast cancer.
Advances in basic research are leading to a greater understanding of the tumor microenvironment, noted Leyland-Jones. New therapeutic targets as a result of these advances include metabolic pathways (serine, glycine synthesis), JAK2 in triple-negative and potentially other breast cancers, androgen receptors in HER2- positive breast cancer; SRC in trastuzumab resistance; and use of large-scale siRNA screens to identify and validate targets.
Advances in translational research have recently led to work on overcoming endocrine therapy resistance, overcoming HER2-targeted therapy resistance, and classification and prognosis in triple-negative breast cancer.
Over the next five years, therapy will increasingly be based on genome sequencing, said Leyland-Jones. The cost of sequencing is also expected to drop, along with the time it takes to see results, he said, with results available within two weeks.
The impact of emerging new therapies will be significant, according to Leyland-Jones. “Breast cancer will be transformed in our lifetimes.”
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MOre on BC progress....
"
Treatment of breast cancer is becoming “horrendously complicated,” according to Brian Leyland-Jones, MD, PhD, director, Winship Cancer Institute at Emory University in Atlanta, Georgia. Leyland-Jones, who spoke at the 9th Annual Northern New Jersey Breast Cancer Conference, held at the John Theurer Cancer Center in February, explained that as research progresses, optimal treatment of breast cancer will involve individualization of therapy to focus on specific targets driving each patient’s cancer. “It is becoming clear that breast cancer has 50 to 80 targetable drivers,” he said.
“This is a time of massive knowledge change in the entire field,” said Leyland-Jones, noting that research is progressing so rapidly that it’s almost becoming impossible to remember all the targeted areas. Advances in both basic research and translational research are producing a plethora of new targets. “The number of targets is shooting up, but fortunately we are getting the drugs to handle those targets,” said Leyland-Jones.
One promising advancement is the development of T-DM1 (also called trastuzumab emtansine, Roche) for HER2-positive disease. T-DM1 is an antibody-drug conjugate (ADC) in which trastuzumab (Herceptin, Genentech) is attached to the chemotherapy DM1 using a stable linker. Results of a phase II trial, presented at the San Antonio Breast Cancer Symposium (SABCS) in December, evaluated first-line therapy with either trastuzumab/docetaxel or T-DM1 in patients with HER2-positive metastatic breast cancer. Compared with trastuzumab/docetaxel, T-DM1 significantly improved progression-free survival (PFS) (median PFS for trastuzumab/docetaxel 9.2 months vs 14.2 months for T-DM1; HR = 0.594; 95% CI, 0.364-0.068; P = .0353). There was significantly less toxicity with T-DM1. At least two ongoing trials (EMILIA and MARIANNE) are continuing to evaluate use of T-DM1 in HER2-positive metastatic breast cancer.
The pivotal phase III CLEOPATRA trial, also presented at SABCS, demonstrated a significant improvement in PFS for dual HER2 inhibition using trastuzumab and pertuzumab. The survival impact demonstrated in the study will be “practice-changing,” said Leyland-Jones.
Many additional targets are under development for breast cancer therapies, including PARP inhibitors, which may have efficacy in BRCA-associated cancer. In a phase III trial published in January 2011, the PARP inhibitor iniparib (BiParSciences/sanofi-aventis), did not meet the primary dual endpoints of overall survival (OS) and PFS in metastatic triple-negative breast cancer. However, a pre-specified subgroup analysis suggested improvements in OS and PFS in the second- and third-line settings, and research on iniparib continues. Iniparib is considered a relatively weak PARP inhibitor, said Leyland-Jones, but it “works in terms of helping DNA repair. The driving force of cancer is DNA repair.”
Other PARP inhibitors under development include rucaparib (Clovis), for BRCA-positive, post-neoadjuvant triple-negative breast cancer; olaparib (AstraZeneca), for BRCA-positive breast cancer; and veliparib (Abbott), for BRCA-positive, triple-negative breast cancer.
Advances in basic research are leading to a greater understanding of the tumor microenvironment, noted Leyland-Jones. New therapeutic targets as a result of these advances include metabolic pathways (serine, glycine synthesis), JAK2 in triple-negative and potentially other breast cancers, androgen receptors in HER2- positive breast cancer; SRC in trastuzumab resistance; and use of large-scale siRNA screens to identify and validate targets.
Advances in translational research have recently led to work on overcoming endocrine therapy resistance, overcoming HER2-targeted therapy resistance, and classification and prognosis in triple-negative breast cancer.
Over the next five years, therapy will increasingly be based on genome sequencing, said Leyland-Jones. The cost of sequencing is also expected to drop, along with the time it takes to see results, he said, with results available within two weeks.
The impact of emerging new therapies will be significant, according to Leyland-Jones. “Breast cancer will be transformed in our lifetimes.”
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Speciak K,
I think you and I are the only ones who appear to have had the Mammaprint. My bs thinks this type of testing will speed up targeted, personalized therapy treatments as the above post shows is needed .
I'll bring up the subject of the vaccine again with my bs and also with my mo. I'll bug them.
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SpecialK,
I saw that the trial was also being done in San Antonio, and I sent an inquiry. Here's the response I received:
Thank you for inquiring about our vaccine clinical trials. Assuming you meet all inclusion criteria, you would not be eligible to enroll for participation until you complete your Herceptin. For the study you reference in the subject line, you must be between 1-6 months from completion of all standard of care treatments (i.e. surgery, chemotherapy, radiation, and Herceptin, if appropriate).
To be seen at my facility (San Antonio Military Medical Center) you must have military benefits, but we are running this study at START/STOH in the medical center if you are a civilian.
Since I won't be finished with my Herceptin until November, I'm not sure if I would be eligible for the trial at that time. I do plan to send an inquiry on the STOH trial to see if the recruiting will continue past November.
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racerdeb - this is what I was referencing in the above post - but it is great that civilians can be seen at the San Antonio location. From what I have seen it seems that recruiting is ongoing in many of these trials for a fairly long period so I would think you have a good chance that you could still get in when you are done with Herceptin in November. It is interesting that Bethesda/Walter Reed is listed as recruiting. When I contacted them they said the testing is actually being done at Sibley in Washington, D.C. - I am a military spouse so I have access, but because Sibley is a civilian hospital I assume anyone can participate if they meet the criteria. Wake Forest where fluff is going is civilian also.
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MD Anderson is also recruiting for the trial (civilian). I discussed it with them when I went there for a consult.
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dance - did they tell you to check with them when you are done with Herceptin?
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I think she said once I am on maintenance Herceptin (I think she meant once I'm done with chemo) to contact them and the nurse will look at my info to see if I qualify. I didn't pay too close attention b/c I knew I couldn't do it right away and figured I'd follow up later to get more details. Perhaps she said once I'm done with Herceptin? I'm not sure now.
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dance - I think the 1-6 months of eligibility is once Herceptin is completely done. They were probably wanting you to contact them while on maintenance Herceptin to see if you meet the other criteria so they could snag you right when you are done. Getting patients withn that 6 month window is why I think they will enroll in this trial for a while - not everyone will be willing to take this on right when they finish active treatment.
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Aha! That is indeed probably what the scoop is. I do understand why people may not want to enroll after surgery, rads, chemo, and a year of Herceptin...especially if they have to travel once a month for 6 months...whew - it's a lot to consider! We'll see how I feel about it as the time gets closer. Right now I'm feeling pretty wiped, so not feeling too motivated, LOL!
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Brax NED (no evidence of disease) means just that. There is no evidence unless you have symptoms and they need to check on them. It doesn't mean cured (although we may be) but right now there is nothing that shows any disease.
If you are not getting the proper answers ask to speak with your onc. s/he can also call you.
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Dougieswife. I am on protonix twice a day, carafate 4 times a day, and maalox inbetween for heartburn. Hope this helps.
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slgarcia I see I wasn't the only one on protonix AND carafate as well during chemo. I actually was the one to suggest the carafate to my onc since I had been on it before.0
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Any suggestions on a good calcium supplement? Every female friend I have who did anything at all about calcium other than a healthy diet has run into some sort of trouble that has been attributed to calcium supplements. From kidney stones, to impossible digestive problems . THe only friend I had who was able to take Fosamax for several years actually broke two different legs in less than two years!
I understand that calcium is supposed to be hard to absorb from many of these sources.
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Ashla,
My urologist told me to take Citracal. I have had several kidney stones and he said Citracal was okay to take.
My MO told me to stop calcium when I was diagnosed and I have not started taking it again.
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Hi All!
I just entered cycle 4 of weekly TCH (actually Abraxane CH), and I am now experiencing hot flashes multiple times per day. I am on weekly Decadron (so that could be the culprit), but also suspecting early menopause. I'm 37, no uterus (that's a whole other story), but I do have my ovaries, so menopause will be a bit of a mystery when it comes around.
Any thoughts? Anyone else go into early menopause or see the hot flashes drop off after chemo?
Lots of hugs,
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Jlaroujo I did have hot flashes in the evening during chemo although not so bad (but I was 49 at the time). After chemo they did subside for a while. I am on Anastrozole (generic Arimidex) so I do get an occasional light flash in the am hours. You won't be on that so maybe after chemo yours will get better too.
I know my mom went through menopause in her early 50's. She only had one ovary. Her flashes were mild as well. My sister just went through it and she had bad hot flashes. I think it's a very individual thing. Also I have read the younger you are going though chemo-pause the more intense it can be.
I know I feel pretty lucky. My friends who went through regular menopause had a 300 times rougher time than I did.
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Julie,
Decadron is probably contributing to them. I had hot flashes for a week during each treatment with steroids. Then they would pass. I went into menopause with chemo (not early because I am 53), and have minimal power surges since chemo. It is hard to know for sure, as Lago said, everyone is different.
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Hi all,
I met with the onc and chemo nurse yesterday to make the final plans for starting my TCH. I will start next Tuesday. TC on Tuesday, H on Wed. My onc likes to break it into two days to allow time for additional fluids and also to infuse more slowly if needed due to possible allergic reactions.
First question: Can you all share what you had in your IV premeds? I have been told I will have the following: Lasix, benadryl, dexamethasone, Aloxi (same family as Zofran), and Emend.
I have not heard others say they received Lasix. The nurse told me it is to make me empty my bladder more and get the Carbo out of my system as fast as possible (to minimize risk of kidney/bladder damage). I did a little reading last night and saw that giving Lasix with Carbo can increase the risk of hearing loss. I am going to discuss this further with my onc, but am curious if any of you have any comments/thoughts/insights on this.
2nd question: I've heard some of you say your blood is drawn prior to chemo and the labs are run and results checked prior to chemo being given, for safety reasons. Is this always done the morning of chemo, aka immediately prior to chemo? I ask this b/c I wonder how they would do this since my onc's office sends bloodwork out. (It's a question I didn't think to ask, but will.) If they say they plan to do bloodwork the day before, do you all think that is safe enough?
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