ILC - The Odd One Out?

daisylover- So you could have done an AI with either Lupron shots OR oophorectomy? I have no idea why MDA doesn't consider this an option. Out of curiousity, I should ask (along with why an AI is even needed if you don't have your ovaries at all... isn't that enough to stop the hormones?? Anyone know?)

Gemini, I get that your onc doesn't do TMs, but don't they do any bloodwork at all? Mine does TMs, but they also check blood counts, liver function, cholesterol etc. at each visit. The first year they also checked something to do with clotting, to make sure I didn't have damage that way from the chemo (I think).

I have not had blood work showing tumor markers at Dana Farber. I had a lot of blood work done for the Palbociclib trial that I was on, but none at my visit today - I am off the trial. I did have one round of blood work at Emerson by my second opinion doctor (part of Mass General). She did check a tumor marker... She's a hematologist, though... She also scheduled me for a bone scan which the DF oncologist told me to cancel. At Dana Farber, they try to avoid procedures that will lead to false positives. (So my oncologist says.) They want you to have symptoms that persist before doing tests and scans. I would guess that we have similar protocols?

I don't know anything about either the endo biopsy or D&C - hoping someone knowledgeable will share their thoughts.

It was interesting at my appointment today. My oncologist indirectly referred to me as "high risk for recurrence". I was surprised because my OncotypeDX is 9 (relatively low)... maybe not really predictive for ILC?

Texas, yes, my oncologist said that I could continue on Lupron with the AI, but it would have to be monthly. She preferred me to have the oophorectomy with the AI. If I do not tolerate the AI's well, I can resume Tamoxifen. Had my last Lupron shot today! MsPharoah has explained as much as I know about other sources of Estrogen.

Gemini, I didn't ask her for an explanation of the "high risk". She was sharing a lot of information, and towards the end, she began talking about oophorectomy and AI being for high risk of recurrence. She did not actually indicate that she was talking about me. I am embarrassed to admit that I was confused. I asked if her if I was actually switching to the AI or staying on Tamoxifen. Then, it was her turn to be confused. She was sure that I had agreed to try the AI, which I had. We moved on to discuss which one. I think that my risk factors are the positive lymph node(s) and cancer in both breasts. ( Are you a twin? I have a twin brother )

IllinoisNancy- I'm sorry you're having to wait for results! I've also had BC twice now, and I'm sure the fear in having tests done only increases after the 2nd round.

MsPharoah- Thanks for the info- I think I remember hearing something about "other" estrogen now that you mention it!

daisylover- So confusing! Hopefully you'll tolerate the AI, and so glad you're done with Lupron for now. I had the shots years ago for endometriosis and had a really hard time on them.

hi Daisy, no need to apologize! I find the quarterly oncologist check-ups to be frustrating at times -- I often feel rushed, and it's hard to pack in all the info in the short time that they allot for the appointments. I had a great checkup, though, with my breast surgeon's nurse practitioner. They called me and ask kind of sheepishly if I wouldn't mind seeing her instead of the BS due to schedule conflicts. It turned out to be one of the most comprehensive follow-ups I've had since my active treatment ended nearly two years ago. The Nurse practitioner was very knowledgeable, informative, and spent a long time answering all my questions.

Also, I'm not a twin -- just astrologically! But being a Gemini, I've always felt a longing for a twin. :-)

good question. I'd also like to hear from others about Femara.

On a slightly different topic, I found newer info discussing drug resistance between ILC vs. IDC and thought I'd summarize that info below.

Hopefully this isn't too technical:
There is generally a good response for the vast majority who receive endocrine-based therapy; however, de novo (or acquired resistance) is an inevitable problem for some.
The somatic mutation profile of a tumor may contribute to this; for example, tumors harboring or acquiring driver mutations in ESR1 or ERBB2 or amplifications at 8p12 (FGFR1) or 11q13 (CCND1) may be less responsive to targeted endocrine therapy. In support of this, the ER-positive ILC cell line model MDA-MB-134VI was found to be de novo tamoxifen resistant, yet cells were sensitized to anti-estrogen therapy when in combination with FGFR1 inhibitors. See: http://www.ncbi.nlm.nih.gov/pubmed/24425047 {University of Pittsburgh research from 2014}.

Estrogen-related receptor gamma/AP1 signalling may also mediate Tamoxifen resistance in the SUM44 cell model system. See: http://www.ncbi.nlm.nih.gov/pubmed/18974135/ {Georgetown University research from 2008}.

Recent research has also shown that PIK3CA mutations are selected during progression from the primary ILC tumor to a local recurrence but not through to dissemination of distant metastases.
While links between PIK3CA mutation and endocrine therapy resistance have been investigated in some breast cancers, this mechanism has not been specifically studied in ILC; however, it is reasonable to hypothesize that this may be the case in some endocrine-resistant ILCs.

Recent data (based on subset analysis of the BIG 1-98 clinical trial) suggest there may be an improved response to the AI "Femara" (Letrozole) compared to Tamoxifen in ILCs, but the biological mechanisms driving the differences in response need to be further investigated.
As the understanding of the biological mechanisms that underpin response and resistance to anti-estrogen therapies improve, researchers will be able to better predict which treatment regime would be most effective (endocrine therapy or in combination with other targeted therapies).

Did I confuse everyone and ruin this thread with technical mumbo jumbo? Sorry...

Haha John no you didn't ruin the thread and I look forward to your posts. Just wish I could understand them. About the Femara, I couldn't tolerate it at all. Started off really well but ended up feeling like an old lady, could hardly get up out of my car my joints were so painful. However I could have tolerated that. It was what it did to my heart that has upset me. I am now on medication for high blood pressure and palpitations. Not to mention the numb fingers and feet which I am sure are from Femara (I didn't have chemo). I'm sure it poisoned me. I think it has affected my kidneys as well.

Femara/letrozole has been ok for me, and I am glad to be on it because it appears to be a good drug for ILC. I had early-stage premenopausal ILC and tamoxifen failed me. It turns out that the reported SOFT results would not have changed the recommendation for me (based on my age and the tumor characteristics etc.) that I just take tamoxifen. BUT, they did not report anything with ILC analyzed separately.

I also take chodroitin/glucosamine tabs. My MO told me to do this. I use fresh ginger in my smoothies also a joint help, and ceylon cinnamon. Liquid B vitamins, liquid D3, coral calcium. I am surviving. Yes, Femara is the better drug for ILC.

Hmm, reading this thread has made me really wonder why tamoxifen was the only option presented to me by my MO. I am an ILC survivor, now 7 months into my tamoxifen treatment and fairly miserable with SEs. I thought I was asking all the right questions and educating myself pretty well, but wonder if one of the other hormonal therapies mentioned here might be better for me. Interested to hear more...thanks!

I am taking Arimidex for my pleomorphic invasive lobular carcinoma and my pleomorphic lobular carcinoma in situ. (My my invasive tubular carcinoma just gets the benefit from the AI's.)  I had a double lumpectomy and whole breast radiation.  No chemo.  I had a low oncotype score. 

Why is Femara the best Aromatase Inhibitor?

I am a DES daughter. 

I had an oophorectomy because I was not in menopause and I needed to be medically induced into menopause so that I could take the Arimidex.  I took monthy Zoladex (Goserelin) shots for 3 months prior to the oophorectomy.  I cannot metabolize Tamoxifen but AI's are more beneficial for invasive lobular carcinoma anyway.

ILC is scary because it is hard to detect and is frequently missed on mammograms and sonograms.  I don't know the data for MRI's detecting ILC or LCIS.  Does anyone know? 

How do you stop worrying that ILC or LCIS might be present but missed on imaging?  Am I just neurotic?  (I worry because this has happened to me already.)  Actually, I am SO LUCKY that my ILC was diagnosed.  It was really a miracle.  I am so thankful for my team of doctors.  They really saved my life.

I finished my radiation in October 2014.  Nothing was found on my mammo or sono at my 6 month follow up.  However, I have extremely dense breasts and my doctors refer to my breasts as "busy breasts".  Because I could feel lumps, I was referred for an MRI.  2 suspicious areas were found on my MRI in May 2015.  One lump was biopsied and was benign - 7 benign findings in the lump but luckily, no atypias.  I did have moderate epithelial hyperplasia and prominent sclerosing adenosis though. The second suspicious area (BI-RAD 4B) is a 1.5 cm linear non-mass enhancement with rapid washin washout kinetics.  I must wait and watch for 6 months. Both of these suspicious areas were detected in the breast that was radiated.  As I said, I am taking Arimidex.  Does anyone know why suspicious areas might occur so soon after treatment in a breast that was radiated?  I am hoping that the linear non-mass with rapid washin washout kinetics is scar tissue because it is located near my lumpectomy site.

Of course, now I have a giant hematoma from my MRI guided biopsy that was done in May. 

Thanks for listening/reading.  It helps to have this site to rant.

I will know the outcome in November 2015.  I am keeping the faith that this will be benign.

Good luck to all of you.

614, it IS unfortunately pretty unsettling to wait and watch with ILC. In my case I had a BMX, which helps a bit. At least I don't have to worry about my boobs. I could still have a tiny bit of breast tissue left behind somewhere, so I am not 100% in the clear as far as breasts are concerned, but at least it is much easier to monitor a flat chest wall for any bumps or irregularities.

As for how you could have "stuff" so soon after rads, there are roughly 3 answers: 1. scar tissue, 2. benign something or other, 3. more bad stuff that they didn't detect the first time around. 1 and 2 are far more likely than 3, but you asked.

614, i also made the decision to do BMX. I didn't want to be in constant fear of it going to the other side or not getting it all. I was told for best outcome a BMX was in the best interest. I found my lump that a mammo had missed. I am grateful that the Lord helped me find it and got me through this. I get my 3D nipple tattoos today! The last step.

Robin