Essentially stable disease

So I received a copy of the letter that goes to my doctors after my clinic appointment today. I don’t know why I bother reading it as I always get a little bit flustered by it. It states that I am on palliative care… I have mentioned this before but I must be feeling a bit sensitive as I really hate the fact that it means treatment without a cure. Palliative care leading to end of life care….. Grrrrr…..

I simply cannot be dying from this disease.  It’s not acceptable and I don’t believe for one minute that the pulmonary nodules in my lungs have had little change in size since last time. The words written in the letter state ‘essentially stable disease’. Essentially? So the fact there are now none in my lymph nodes doesn’t show that there is a regression of it?

I am unsure why I get ruffled by the stupid comments in the letters. I wish they would be more positive. Other than stating I am tolerating the capecitibine incredibly well there isn’t much else that reads positively. I don’t know why I would expect them to feel the same as I. I expect they have seen many more like me die. They expect me to be the same. I simply won’t have it.

I’m tired again today. I had a hot bath with olbas oil last night before bed then had quite good sleep until my throat started to get all tickly. I spent a few hours coughing. My voice is a bit hoarse but it hasn’t gone completely. I’m hoping it will pass by quickly….


Maybe something has changed in me and that is why I’m fighting off this illness. I wish I could see inside myself and know what is happening with the canSer in my lungs. I could visualise better if I knew what they looked like. I must spend more time visualising…


Pete came across some more news about triple negative that sounds really promising;

Metastatic breast cancer cells are even more adaptable and able to evade targeted treatment than researchers suspected as recently as a few months ago, which means they present a heightened treatment challenge that in many cases may be overcome only with multiple targeted therapies delivered at the same time.

The findings were discussed at IMPAKT 2013 Breast Cancer Conference, sponsored by the European Society for Medical Oncology.


The new wrinkle in drug resistance has been dubbed reprogramming, a way that metastatic breast cancer cells (but presumably a property shared by other advanced solid tumours’ as well) quickly respond to a drug that shuts down an essential cell protein, a kinase, by turning on other, alternative kinases within days of drug exposure. Many of the new, targeted therapies that have successfully treated advanced-stage breast cancer and other solid tumours are kinase inhibitors, such as trastuzumab (Herceptin) and lapatinib (Tykerb).

Using a newly-developed technique for assessing many different kinases within a cell at once, Gary Johnson, Ph.D., reported that treatment of isolated, advanced breast cancer cells in vitro with a kinase inhibitor drug produced within a week a dramatic shift in the cell’s overall kinase profile, something he calls the cell’s “kinome.” Part of this reprogramming response probably occurs because of new genes that the cancer cell turns on or up regulates, and part is probably driven by epigenetic changes in the cell, said Dr. Johnson, professor and chairman of pharmacology at the University of North Carolina in Chapel Hill.

Clinicians familiar with this finding quickly recognized that the phenomenon is an important, new barrier to successful treatment in patients that will require creative solutions using rational, multidrug, or multi-sequence regimens.


Dr. Lisa A. Carey, an oncologist who collaborates with Dr. Johnson, said she believes that reprogramming may explain her recent, frustrating results treating metastatic breast cancer patients with an investigational inhibitor of the epidermal growth factor receptor (EGFR), a tyrosine kinase.

“We gave the inhibitor to patients with triple-negative breast cancer, where the EGFR is clearly unregulated, a big, juicy target, and yet only 25% of the patients responded. Most of the time, the cancers had alternative mechanisms to keep the EGFR pathway active,” Dr. Carey hypothesized based on Dr. Johnson’s recent findings. “The good news was that 25% of the time the treatment worked,” said Dr. Carey, professor of haematology oncology at the University of North Carolina and medical director of the university’s Breast Centre.

The new finding on breast-cancer cell reprogramming “helps us understand why the EGFR inhibitor didn’t work in most patients, it helps us understand what cancer cells do, and it helps us design our next approach. Most cancer drug development right now targets kinases,” she said in an interview.

“One way to approach this is to use multiple agents at once, but if you add drugs you also add toxicity and expense. And in some patients the cell doesn’t reprogram. We need to understand how reprogramming works,” with the potential to develop agents that block reprogramming instead of trying to deal with the changes that reprogramming causes. “This is an explanation of why patients don’t respond to even targeted treatments, and it gives us a way forward to potentially prevent it. Reprogramming is reproducible and potentially targetable. I think we can get around it.”


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