Annoyed

So my appointment was at 2pm. Kathy drove me out there and then they said there wouldn’t be enough time to have it because I have to wait hour after the parp is given to make sure that I don't have a bad reaction – so annoyed. They had already hooked up my port AND given me the freakin decadron which is almost as bad as the chemo. Anyway, I’m home now, wired, can’t think straight, bad headache –all from the decadron. I have to go back tomorrow at 9:30.

I’m on the Special Access Program for Iniparib (parp) with Gemcitibine and Carboplatin. I was on Gem and Cisplatin before and everything I’ve read said Carbo is easier on you but apparently the nurses there don’t know that – they say it’s worse and I’ve got 5 didn’t anti-nausea drugs to take - ridiculous – I can’t even imagine what all the side effects of those will be.

 I have to go there twice a week for treatments day Day 1 and 8 is  Gem and Carbo and  parp on then days 4 and 11 is just the parp. Then one week off. (three week cycles)  This is the exact protocol I was looking into with the clinical trial in Seattle.

I’ve been on the Triple Negative Foundation discussion forums (very informative) and it seems this does work really well for some people. One woman started in this trial last year and has been on it ever since! It cleared everything up and her dr doesn’t think she should come off until it stops working. CANNOT even IMAGINE!

oh well. I guess I just have to be thankful there is something to try.

Dr. Klimo said the idea is that you do it for a few months and if it works then you continue with just the parps. From reading what others in my situation are going through it seems if you find something that works that you don’t stop until it stops working. There are many people on the discussion boards who have tried the parps and they didn’t work. Anyway, I am really hoping that it works and FAST- having lots of body aches and pain – taking Advils round the clock and my skin mets are getting really bad and uncomfortable. These are the first "symptoms" I've ever had from my cancer and it seems to be getting worse by the day.

F%@K!!

Last week I went to see Dr. Klimo because of a rash I've had under my arm for about a month. In the past week it had become much worse and didn't look like just a "rash" anymore. Dr. Klimo said it looked like cancer and sent me off for a biopsy. I asked him to book me into the private PET scan clinic; I didn't want to be waiting any longer for the BCCA.

I had the biopsy done the next day at Lion's Gate Hospital. The surgeon who did the biopsy also said it looked like cancer.

I came home, phoned the PET clinic and they said they could get me in the next day, which was Friday. I came home Friday after the scan with the disk and looked at it on my computer.

It was really, really bad; much worse than my original scan back in December.

I saw Dr. Klimo this morning. He said the scan was "shitty". The written report confirmed that it was much worse than in December and the skin biopsy confirmed that the cancer had spread to my skin and it too, was triple negative. We are going to start on the Parp Inhibitors that just came available here. They are given through IV with both Gemcitibine and Cisplatin - the chemo drugs I just came off. I will start sometime in the next month.  I will stop the Avastin and Xeoloda pills but continue with the Zometa infusions.

New Hope for the Cure
Drug combination targets aggressive triple-negative breast cancer

With currently available early-detection methods for breast cancer, many people can be treated successfully. But for the 20 percent of patients with so-called triple-negative breast cancer, the outcome is bleak. Now, however, researchers from Harvard Medical School (HMS) and Baylor College of Medicine have identified a critical molecular component to the disease, one that suggests potential therapies involving combinations of FDA-approved, readily available drugs.

“Whereas many basic discoveries have the potential to impact patients’ lives within 10, 20 or 30 years, this has the potential to impact patients’ lives within one year,” says Thomas Westbrook, formerly a postdoctoral fellow at Harvard Medical School and an assistant professor of biochemistry and molecular biology at Baylor College of Medicine since 2007.

The research was published on March 4 in the journal Cell.

Triple-negative breast cancer is an aggressive disease with few therapeutic options. Patients with such tumors can be treated only with chemotherapy. If the cancer spreads, the median survival rate is one year.

The complexity of triple-negative breast cancer renders it so difficult to treat. The disease is extremely heterogeneous, characterized by hundreds of genetic mutations. Without knowing the critical molecular switches that power this type of breast cancer, researchers have no way to develop targeted therapies.

The HMS-Baylor College of Medicine team reports that an enzyme called tyrosine phosphatase PTPN12 is knocked out in 60 percent of nearly 200 triple-negative breast cancers tested. This phosphatase belongs to a class of enzymes that keeps cell-growth pathways in check and cancer at bay.

The team identified the critical enzyme by looking in petri dishes for proteins whose absence caused normal breast cells to become cancerous.

“We were looking for genes that pushed the cells over the edge,” explains Steve Elledge, the Gregor Mendel Professor of Genetics and a professor of medicine at HMS.

One of tyrosine phosphatases’ primary jobs is to turn off another group of enzymes critical for growth called receptor tyrosine kinases. The researchers reasoned that, if they could identify the enzymes that were switched on in the absence of PTPN12, they could pinpoint critical drug targets that might be used to develop therapies for patients with triple-negative breast cancer.

To identify these proteins, the team turned to HMS Associate Professor of Cell Biology Steve Gygi. By taking a look at all proteins activated in cells lacking PTPN12, the researchers found two enzymes crucial for breast cancer’s progression, or metastasis, EGFR and HER2.

In addition, the team used biochemical methods to identify a third receptor enzyme, called PDGFR-b , that was also regulated by PTPN12.

These results collectively suggest that the improper activation of these three tyrosine kinases could be the major cause of triple-negative breast cancer.

“We’ve grabbed a molecular foothold in triple-negative breast cancer,” says Westbrook, who discovered PTPN12 as a postdoctoral fellow in Elledge’s laboratory. “We are now starting to understand the disease better. Even more important, we have a rationale for a combined drug therapy for the disease.”

Their idea: to treat the disease, turn off the trio of enzymes with drugs.

To test their strategy, the team took advantage of two drugs already being used to battle other types of cancer: laptanib (Tykerb), which turns off EGFR and HER2, and sunitinib (Sutent), which turns off PDGFR-b.

The team treated mice with triple-negative breast cancers with either sunitinib or laptanib, or both. In mice treated with sunitinib alone, tumors shrank by nearly 80 percent. But in mice treated with both drugs, tumors shrank by more than 90 percent — and life expectancy more than doubled.

These results suggest that sunitinib and laptanib (or similar drugs) together may be a promising therapy for people with triple-negative breast cancer. And because both drugs are already FDA-approved and sitting on pharmacy shelves, they can be tested immediately in these patients.

“This research underscores the relation of basic bench science to human health,” says Elledge. “If you know what’s driving the cancer, you can think about targeting that for therapy.”

The team hopes to launch a phase II trial for triple-negative breast cancer by the beginning of 2012.


Sutent was one of the drugs we did chemo-sensistivity testing on in Germany and my test came back at 60% which was the highest of all my chemo-sensitivity testing.