I have to agree with Gina's take on this, and it is not clear to me why your oncologist views the thyroid carcinoma as something of a clinical sidelight, nor why treatment cannot proceed sanely in a parallel but certainly coordinated track, and it is opaque to me how potential surgical intervention would dislodge the deployment of trastuzumab (Herceptin) for any clinically significant time.
Of course, I have no issue with the convening of a tumor board for coordinated analysis, although I must say I am not a fan of tumor boards that do not include the major player, and ultimate decider, for most if not all of the key discussion - the patient should be privy to, and able to query, all aspects of the deliberations and how fundamental components of her care are being weighed and decided.
But on the central question, although stemming I hope from good intentions rather than territorial turf establishment, your oncologist may perhaps - no fault of his own given his breast carcinoma specialization - be insufficiently aware of the real concerns and issues on the thyroid side. The concern is obviously - at least to me - of a very rare papillary carcinoma arising in a struma ovarii of the complex teratoma, and I'd be astonished if any serious proportion of thyroid carcinoma experts would disagree. So let me explain this:
Struma ovarii is a very rare disease; it's considered a (complex) ovarian teratoma - a type of germ cell tumor that may contain several different types of tissue, but in which thyroid tissue is usually the predominant or sometimes exclusive element - that can be malignant in a low, indeterminate percentage of cases, and struma ovarii can mimic other malignancies, but it typically occurs as a part of a benign cystic teratoma. Its etiology, natural history, and optimal treatment regimen are not wholly determined because of the small number of published cases, so its precise pathogenesis remains somewhat controversial. But as to what the best evidence says about such pathogenesis, since estrogens can regulate thyrotropin (TSH) release, hormone replacement therapy (HRT) is thought to play a role in the growth of struma ovarii. So in essence, as Gina shrewdly considers, there may very well be an important estrogen component.
As to diagnosis, cystic type strumas are quite challenging to diagnose, and non-malignant proliferative changes within struma can be misdiagnosed as cancer. In general, positive IHC staining for thyroglobulin, T3 and T4 is taken to confirm the diagnosis of struma ovarii. However, because of its rarity, there is no complete consensus on struma ovarii treatment, although there has emerged some considerable agreement due to recent research data. Certainly, each case must be managed individually and definitive therapy would depend on the extent of the disease or involvement.
The most important complications of struma ovarii - although again, quite rare - are malignant transformation and thyrotoxicosis, but especially the former, so the fear would be of a rare papillary carcinoma arising in a struma ovarii of a mature cystic teratoma, since although extremely rare, malignant transformation is known to occur, usually as classical papillary thyroid carcinoma (PTC), and so raises the possibility of malignancy arising in these struma ovarii. Given that, surgical removal of any ovarian neoplasm is a prudent recommendation.
Although papillary carcinoma is the most commonly occurring thyroid-type carcinoma in ovarian struma, it's been decisively established by my compatriot, Christos Papanikolaou at Hippokration General Hospital that histological malignancy in struma does not necessarily equate with biological malignancy - a rather subtle point - so the majority of thyroid-type carcinomas do not spread beyond the ovary. For this reason of localization to the ovary, simple oophororectomy is indeed the therapy of choice for the vast majority of patients, as agreed upon by leading thyroid experts Lawrence Roth at Indiana University and Aleksander Talerman at Thomas Jefferson University, and Mehrangiz Hatamia and colleagues Albert Einstein College of Medicine, among innumerable others.
I uncovered a telling case of this whole scenario in the literature much like yours. French researcher Ghander and colleagues described the case of as woman who presented with a papillary thyroid carcinoma. After 131I administration for thyroid remnant ablation, a whole-body scan showed a thyroid bed uptake and a pelvic uptake corresponding to an ovarian cyst on ultrasonography, with normal PET scan and with preablation thyroglobulin more elevated than usually found after total thyroidectomy, and in which the histopathological analysis revealed a benign struma ovarii. In this case, serum-stimulated Tg returned to undetectable value and diagnostic WBS was negative at 6 months after oophorectomy. This treatment procedure follows the consensus that surgery should be scheduled as soon as safely possible because of the concern of malignant transformation. Of course, every case is individual but this suggests how mainstream the agreement would be to proceed to oophorectomy as a prophylactic maneuver, something perhaps your oncologist is not folding into the broader perspective of joint carcinomas, if of course he is at all aware of these somewhat arcane considerations and findings.
So in any integrated treatment plan coming out of tumor board considerations, the thyroid "voice" or perspective must be weighed and given ful respect, preferably during such proceedings, but afterwards if necessary, before final settlement of your plan of care, and there should be an avenue in which anti-HER2 therapy can be timed in coordination with any surgical intervention to not impose any excessive delay in the initiation of Herceptin therapy. And of course, even low levels of hormone positivity as in your case still represent potential beneficial therapeutic targets of an endocrine therapy like an unilateral oophorectomy, and may confer some extra measure of anti-estrogen protection that is not generally trivial.
Breast Cancer Watch