I know this sounds a really stupid ignorant question, but Ive tried asking so many medical people and havent had an answer that I can understand.
In the case of ER+ tumours for example, if you remove the oestrogen that they need to grow, by having ovaries removed and taking AI’s which stop the aromatase enzyme converting into oestrogen, in theory shouldnt we be oestrogen free and therefore cancer free?
Obviously, this is not the case as sadly people do go on to get recurrences of their original cancers despite removing their ‘fuel’.
I understand that people can go on to get other tumours that are not connected to the initial one and can therefore be hormone negative and nothing to do with spread from the first tumour, but why does a ER+ cancer spread?
Is it because the hormone treatment failed because the cancer cells become immune to it or start growing in a different way?
I hope I havent upset anyone with my question or my ignorance, but if anyone knows or has been told anything by their oncs, I’d be really grateful to hear from you.
SS
you are not ignorant, that is just the question that cancer researchers are trying to answer. They don’t really know why some cancers continue to grow with all the cells theoretically removed, and the hormones stopped.
They do know that if the cancer has spread to lymph nodes at the time of the primary diagnosis it is more likely to have spread elsewhere in the body and to recur and that the more lymph nodes with cancer and the larger the tumour at diagnosis the more likely you are to have a recurrence. However, breast cancer doesn’t always follow the norm, and sometimes people with small tumours and no lymph node involvement go on to get recurrences and / or secondary breast cancer.
I hope that research will show what is happening. It was interesting to read today of a chance breakthrough in prostate cancer treatment which is helping men with secondaries, but it may have been hyped up so I’ll have to reserve judgement on it until I’ve seen a critique of the study. I’m hoping one day someone will solve some of the riddles that have kept me wondering as you do why it does come back
Mole
Hi,
can I just add to Mole’s post that tumours have different ER+ and PR+ levels, also some are just Er+ or just PR+. So some people will have 8 out of 8 or 100 % hormone sensitive and others will have less. This must affect how well the hormones work. In my area they count them out of 300 and only about one third of mine were hormone sensitive, not sure what the rest would be getting up to but hopefully have been annialated by 12 doses of chemo and rads.
Don’t forget that stats are based on previous years’ figures so every time the treatments change as they discover more successful treatments from the trials and new drugs, those figures can be out of date. They are searching for the cure in our area - on donations!!
lots of luck to you both
Lily x
Mole I read that article on the guys at the Mayo clinic, wouldnt it be wonderful if they found something similar for us?
x
Thanks for taking the time to reply and your input.
It does become a little clearer when as you say Lily, everyone’s tumours are so different and individual to each of us, after all they are our own cells that have just gone wrong in a manner of speaking.
I guess I am very naive to think I would find out why we get secondaries if the most esteemed scientists in the world dont know, its just my way of trying to get my head around it all.
like when I was first diagnosed I took on kind of take on a ‘battle plan’ and thought, ok, my cancer feeds on hormones so I’ll eradicate all oestrogen, that’ll stop the b****er in its tracks, then you hear about others who despite having the same dx and prognosis, taking the same steps, go on to have spread.
I guess the only real explanation is that there isnt one, and there’s no rhyme or reason why our own particular cells behave in a certain way whatever we do to influence them.That Cancer cells cannot be treated as a generic disease but rather the individual’s body make up ‘gone awry’, would that be too simplistic?
As you both say, there is so much research going on in the background as we speak and maybe one day,please God, they will find the answer to the question we all ask, thanks again, lots of food for thought.
SS
Hi SS
I’d love to know as well although it’s a bit late for me as I’ve now developed secondaries. I was highly hormone sensitive at primary dx, had Zoladex and Tamoxifen after WLE and rads (no chemo because my prognosis was so good) I had early stage BC, no node involvement and an 80% (or higher) likelihood of no return. So stats mean diddly squat to me! Since then I have learnt that Tamoxifen doesn’t work for everyone by the very nature of the way it works itself. Obviously it stopped (or never) worked for me. I also think when I stopped Zoladex after 2 years and didn’t stay in the menopause, as my onc kept telling me I would, that the recurrence and spread started - I must have been fairly awash with hormones by then! However I’m now on AI’s which work in a totally different way to Tam and hope they continue to do their job until the next best thing comes along - as we all do. It is so difficult to say this or that will happen as all of us react differently and at the moment no chemotherapy regime is targeted to an individual case. BCC ran a very informative day for us secondaries ladies last year and the oncologist who spoke to us explained all the why’s and wherefore’s so I do understand more now but I doubt if any of my treatments or outcome would have changed.
Nicky