This transcript has been edited for clarity.
Kaniksha Desai, MD: Welcome to the Thyroid Stimulating Pod cast. This pod cast was created in partnership with the American Thyroid Association to discuss up-to-date diagnosis and management of a wide array of thyroid diseases.
I’m your host, Dr Kaniksha Desai. Today, we’re exploring an important and fast-moving topic in thyroid oncology: RET inhibitors for advanced medullary thyroid cancer.
Medullary thyroid cancer (MTC) is a rare and distinct form of thyroid cancer that arises from the parafollicular C cells rather than the typical thyroid follicular cells. It only accounts for a small percentage of thyroid cancers, but it carries its own unique challenges.
For years, treatment options were limited to multikinase inhibitors, which have had modest efficacy and significant side effects, but the discovery of RET inhibitors has been a key driver in many cases of treatments for patients with advanced MTC. We’ve entered a new era of precision therapy that has dramatically changed the outlook for many patients with MTC.
To understand this evolution, I’m thrilled to be joined by Dr Mimi Hu, a professor of endocrine neoplasia and hormonal disorders at the University of Texas MD Anderson Cancer Center. Dr Hu is a national leader in thyroid cancer, hereditary endocrine syndromes, and bone and mineral disorders.
She earned her engineering degree from Rice University and her medical degree from UT Houston, and she completed her residency and endocrine fellowship at Baylor College of Medicine, where she served as chief medical resident. Since joining the staff at MD Anderson in 2007, she’s led multiple clinical trials and published a significant number of papers on medullary thyroid cancer, including RET-targeted therapies.
In today’s episode, we’ll discuss what RET alterations mean in the context of MTC and why they’re actionable targets; the current landscape of RET inhibitors and how they differ; how to approach treatment decisions and management side effects in patients who are on RET inhibitors; and real-world considerations such as resistance, sequencing, and future directions for advanced medullary thyroid cancer.
Welcome to the pod cast, Dr Hu.
Mimi I. Hu, MD: Thank you so much, Dr Desai, for that introduction. I’m happy to be here.
Desai: Let’s take a small step back and talk about medullary thyroid cancer in general for the start, and then we will get into RET inhibitors after that. Can you explain how MTC is different than many of the traditional differentiated thyroid cancers?
Hu: Yes. MTC is a very interesting subtype of thyroid cancer. First of all, it’s a very rare disease. Approximately 1000-1200 cases are diagnosed in a year in the United States. As you indicated earlier, it is a cancer that arises from the C cells in the thyroid gland — C standing for “calcitonin producing.”
Although they arise in the thyroid gland, they’re not the same as the other types of thyroid cancer, which we call differentiated thyroid cancer, which comprises papillary, follicular, oncocytic, and even the more aggressive types of poorly differentiated or anaplastic thyroid cancer. Out of all cases of thyroid cancer, MTC represents about 3%.
Additionally, the MTC is different from the differentiated thyroid cancer cells in that MTC cells produce two molecules, which we use as tumor markers, calcitonin and CEA, or carcinoma embryonic antigen. This is different from the thyroglobulin tumor marker that we use when we’re following patients with differentiated thyroid cancer.
Additionally, MTC has an interesting and unique aspect that 25% of these patients could have a hereditary disorder. That’s associated with this disorder called multiple endocrine neoplasia type 2, and it’s associated with an activating mutation of the RET proto-oncogene. This is a very unique type of thyroid cancer and certainly rare.
Desai: What is the standard of care for MTC currently?
Hu: In our patients, when they are diagnosed with MTC (usually with a biopsy to prove disease), the first thing you want to do is to evaluate if the patient has the hereditary syndrome associated with an activating mutation of the RET proto-oncogene. Even if you probe into the patient’s personal history or their family history and you don’t identify any other indications for the other endocrine neoplasias, such as primary hyperparathyroidism, which leads to hypercalcemia, or pheochromocytoma with high adrenaline levels, if you do their RET genetic tests, about 1%-7% of those patients will have a germline RET mutation. It is important that every patient with MTC undergo genetic testing and counseling with a genetic counselor. Once you get that information, then it could help you even determine what is the best surgery for these patients.
Now, I say surgery because that really is the most targeted way of managing patients with MTC. The tumor arises from the thyroid gland and the hope is to offer a total thyroidectomy so that you could prevent any risk of the disease spreading to other areas. Unfortunately, about 80% of patients at the time of diagnosis already have lymph node metastases.
This is mainly because MTC is typically a very slow-growing disease and may not convey any symptoms to the patients that would’ve led to their earlier evaluation. Lymph node metastases are not uncommon. Unfortunately, once lymph nodes are involved with thyroid cancer, even in the hands of the most experienced surgeon who knows MTC and offers and provides a very comprehensive surgery, in that setting the chance of getting curative intent is still quite low.
Our patients need to be educated that it’s not unexpected that after a really good surgery, which may include lymph node dissection, they may still have evidence of disease by biochemical markers detectable after their surgery. Thus, in patients with MTC, lifelong surveillance is necessary by monitoring their tumor markers, calcitonin and CEA, and with appropriate imaging.
Desai: That is neck ultrasound or would you recommend other imaging?
Hu: Always an ultrasound of the neck, because it doesn’t convey any radiation and it’s a very effective way of distinguishing pathologic-appearing lymph nodes compared with benign lymph nodes or other structures in the neck. Ultrasound of the neck is a very straightforward and reasonable study to do when you’re evaluating your patients either every 6 months for the first couple of years and then potentially annually.
In addition to that, if you see that their tumor markers, calcitonin or CEA, are still present or if they are more importantly progressing, then you might want to add on some other imaging studies for cross-sectional imaging, and also to look and survey for distant metastases.
That could include CT of the neck to provide a better way of imaging the disease up high, above the jawline, that your ultrasound can’t see, or even behind the sternum in the upper mediastinum. Sometimes you want to consider CT of the chest with contrast so that you can look at mediastinal or hilar lymph nodes and also parenchymal lung disease.
You can also do CT of the abdomen with a liver protocol or MRI of the abdomen with a liver protocol because besides the lymph nodes in the neck, the next most common places where MTC would go to outside the neck are lungs or liver. Good cross-sectional imaging of those areas are necessary.
Occasionally, MTC can metastasize to the bones, so a good imaging study of the bones, such as an axial skeleton MRI, would be very effective. Occasionally, you’ll think about functional imaging studies such as gallium-DOTATE PET. FDG PET/CT can be useful in clarifying if lymph node metastases are present in our patients with MTC, but because of the indolent nature of MTC, many times the FDG PET will be negative.
If our cross-sectional imaging with ultrasound, CT, or MRI is non effective in identifying distant metastases in a patient with progressive tumor markers, then you do want to consider maybe a functional imaging study, such as PET/CT, to clarify if there are any other lesions that you’re missing.
Desai: This actually brings me to the topic we’re discussing, a treatment for advanced thyroid cancer today. Can you define that patient population or what you consider advanced MTC?
Hu: Yes. This is always a very common question from our patients and also from my colleagues. Tumor markers progressing certainly is a suggestion that there is disease progression, but that could still just represent microscopic progression, not necessarily radiologic progression. This means that, on a microscopic scale, disease might be progressing but radiologically, we’re not seeing anything change.
In that setting, observation and maybe doing imaging to clarify if there’s any structural progression as necessary, but biochemical progression by itself is not enough to consider systemic therapy or other treatments that might try to get the numbers down lower.
The reason why is that, unfortunately, even in this day and age, we don’t have any treatment that can offer curative intent. For any procedure that is either focal treatment or even systemic therapy, there are some consequences such as side effects or down-the-road complications. We don’t want to implement some treatment unless we really have to. That’s why it’s limited to radiologic progression.
With radiologic progression, sometimes you’ll see millimeter changes in lung nodules or liver metastases over the course of a year or two or three. That is very indolent and doesn’t necessarily require any medical therapy because these patients will be asymptomatic, and any treatment that you offer could convey side effects. Thus, for indolent radiologic progression, we would still recommend active surveillance.
It’s really when disease is growing at a considerable pace. We typically go along with what we have enrolled in our clinical trials, where there’s 20%-30% progressive disease within 6-12 months. That’s when we’re seeing more radiologic progression that could be consequential for our patients. Either disease that’s in a location that, if it continues to grow, it could compress on locoregional structures and threaten their organ function, or even if it were in the bones, it could lead to fractures or even central nervous system compromise.
Radiologic progression is when we will consider systemic therapy. Prior to that, if we can think about those patients who have oligoprogressive metastases. Say the majority of their disease is pretty stable, but it’s really just some lymph nodes in the neck that are progressing, but they’re in important areas like our central compartment and might threaten tracheal or esophageal function, then you might want to consider surgery again.
In patients who might have mediastinal or hilar lymph node progression, but everything else is pretty stable, sometimes you could think about surgery to remove those, or even focal radiation therapy. There are focal treatments that you can consider for oligoprogressive disease.
Desai: Systemic therapy is almost like a last-line resort. Let’s talk about RET inhibitors. What are they and what’s the story behind them?
Hu: As I said earlier, out of all of our patients with MTC, about 25% may have the hereditary syndrome, multiple endocrine neoplasia type 2A. This is due to an activating point mutation of the RET proto-oncogene. All of our patients with hereditary disease will have a RET mutation.
In the nonhereditary patients, approximately 45% of them will have a RET mutation as the driver of their disease. We don’t know why it occurred; it just did. Outside of those RET mutations, in our nonhereditary population, another 15% of these patients may have a RAS mutation. For the remainder, sometimes it could be very bland and we don’t identify any driver mutation. When you take all comers, the hereditary patients and the nonhereditary MTC patients, more than 60% of our MTC patients will harbor a RET activating mutation.
With better next-generation sequencing testing platforms, we’re seeing even some rare RET deletions and also some duplications. Those are much less common, but we are finding those. Additionally, other solid tumors can have RET fusions or RET rearrangements, where a portion of the RET gene is fused to another gene leading to an activated portion of the RET kinase.
Among patients with papillary thyroid cancer, about 10% may harbor a RET fusion. In non-small cell lung cancer, about 1%-2% may harbor a RET fusion. Other solid tumors may also have this as a driver mutation. Because of this understanding as RET as an oncogenic driver of disease, there was a large amount of investigation into whether you can design a drug that would specifically inhibit that kinase, the RET receptor.
Around 2017, there were phase 1/2 clinical trials investigating RET inhibitors. One is now called selpercatinib and the other one is called pralsetinib. These were designed specifically to be highly active RET inhibitors with less or potentially no inhibition of other kinases, where multikinase inhibitors such as vandetanib or cabozantinib, which are kinase inhibitors that are FDA approved for MTC, can target multiple kinases, especially vascular endothelial growth factor receptor, which mediates angiogenesis, but also other kinases.
With the multikinase inhibitors, by having this nonspecific activity on other kinases, you can see a spectrum of more consequential side effects that our patients will experience, and that could be dose-limiting for these patients. RET inhibitors were very promising for our patients because they potentially target the oncogenic driver more effectively and there are potentially less off-target effects on other kinases.
Desai: With this more targeted therapy, we’re kind of briefly talking about how there are maybe fewer side effects than comparatively for the multiple kinase inhibitors. Can you talk about what the side effects of the RET inhibitors are?
Hu: When I started participating in these trials early on and we put patients on these drugs, the most common comment I would receive from them was, “Doc, I think you’re giving me a placebo sugar pill because I feel so good.”
There are some side effects that can be associated with any drugs that we implement. In the RET inhibitors, the more common one would be dry mouth, seen with selpercatinib and to a lesser degree with pralsetinib, but also, we can see hypertension with these patients about 30% of the time.
In addition, we can see elevated liver enzymes in about 20%-30% of the patients. This could be asymptomatic, but very rarely it can even lead to liver failure and jaundice. Additionally, low white blood cell count, especially neutrophils being low or lymphocytes being low, can be seen in these patients. In general, patients tolerate these drugs much better than what we have seen with vandetanib or cabozantinib.
Desai: Dr Hu, can you share a specific patient example of someone that has used these RET inhibitors and how their particular outcomes were?
Hu: I have a patient who, years ago, presented with metastatic disease, and the patient was already initiated on cabozantinib. The patient did have quite a few side effects, especially appetite changing, her taste, and she was losing weight and having diarrhea. Although it did offer control of her disease, after about 2 years or so, she was getting really worn out by this drug, even though we tried to do dose adjustments and reductions of dose.
I actually, at the time, switched her over to vandetanib, which I do consider to be slightly less toxic of a drug compared with cabozantinib. Patients do seem to tolerate a little bit better, and also they tend to be more weight neutral.
With the change to vandetanib, the patient did respond better in terms of tolerance, but there were still issues. She still had the occasional diarrhea that could limit what the patient would be able to tolerate eating. The patient tolerated the drug very well and it controlled her disease for a good long while.
After years of being on vandetanib, and I knew she had a RET alteration, I said, You know, the RET inhibitor selpercatinib is FDA approved now, would you like to try it? She was very resistant because it was more like many of our patients would rather continue with the devil they know than to try another drug that they may not be so certain about its effect on them.
She resisted the change for a little bit but, after some further discussion and counseling, made the decision to halt the vandetanib and to transition over to selpercatinib. It’s been a while now on selpercatinib and the patient tells me, “I’m like a new person. I feel so much better. I’m glad I did it. It was scary at first, but I’m glad I did it.”
This is a reflection of a patient who’s been on all three agents, had radiologic responses, but really side effects led to the drug changes. It does tell us that, over the past 10-14 years, there has been much advancement in this area and it is benefiting our patients.
Desai: Thank you for sharing that great story. This is just a reminder that if your patient is on some of these older medications, you could actually consider switching them, even if they’re having good response if they’re having many side effects.
Hu: Right. If they’re tolerating drug and they’re having oncologic benefit, I wouldn’t change anything. A smooth-running car should not be fixed. If there are some issues that are just leading to a burden of side effects and wearing on the patient’s overall quality of life, it might be worth discussing.
Desai: Thank you. The side effects are better, but is the medication more effective in controlling their disease? I know we have comparisons now. Can you talk a little bit about this?
Hu: With our initial phase 1 and phase 2 studies, we saw very promising results in our selpercatinib previously treated patients, where there was an objective response rate of 73%. In drug-naive patients, it was about 81%. With pralsetinib in the phase 1/2 trial, patients who were previously treated with cabozantinib or vandetanib, the objective response rate was 52%, and with those who were naive to treatment, it was about 71%.
This is what led to accelerated approval in 2020 for both of these agents for RET-mutated MTC, RET fusion-positive non-MTC, and also non-small cell lung cancer. What is really amazing is that there is actually a phase 3 trial comparing selpercatinib with cabozantinib or vandetanib, considered standard-of-care therapy, in a multicenter, international trial.
This is the first phase 3 trial investigating any agent in thyroid cancer compared with other active agents, as different from placebo. Some interim results were published a few years ago in The New England Journal of Medicine and they found that the progression-free survival in patients who were treated with selpercatinib was significantly better than those patients who were treated with standard of care therapy, cabozantinib, or vandetanib, with a hazard ratio of 0.28.
The objective response rate in the selpercatinib-treated group was almost 70%. In the control group with cabozantinib or vandetanib, it was 38%. There were significant responses in these patients and also durable responses. The median progression-free survival was not yet reached at the time of data lock for this publication for selpercatinib, but in the control group, the patients treated with cabozantinib and vandetanib, the median progression-free survival was 16.8 months. There were very durable, long responses.
In addition, we saw that the patients tolerated selpercatinib much better, where dose reduction was needed in about 38% of the patients treated with selpercatinib, but in the patients treated with the control arm, about 77% required a dose reduction. In terms of treatment discontinuation attributed to adverse effects, it was much higher in the control group, at 26%, compared with the selpercatinib group, where it was less than 5%.
Desai: Just to review, this medication has now become first-line treatment? I just wanted to verify,
Hu: Although guidelines have not been updated yet to reflect that, these interim results from this phase 3 study and also our experience from the phase 1/2 study really do support using a RET inhibitor as first-line therapy in patients who have RET-mutated MTC. It’s highly effective and our patients tolerate it much better.
Desai: When we’re talking about getting this medication, is it covered by insurance? How easy is it to get this medication for our patients?
Hu: Yes. Since the accelerated approval in 2020, I have not found any problems with insurance approval, especially since the phase 3 trial with the selpercatinib came about. Since 2020, I have not had any resistance from insurance companies for this agent, at least for my patients who are from the United States.
Desai: That’s actually really good because many newer medications can be more costly or not approved by insurance. This is promising news for our patients.
I know we talked about the side effects, but what do you do to monitor patients that are on RET inhibitors? You would get liver functions tests since you mentioned the liver problems, blood pressure, and what else?
Hu: When my patients first get started on therapy, I definitely tell them to go and get a blood pressure cuff. I recommend that they do a daily log of their blood pressure and their heart rate at least twice a day. In addition, daily side effects; you can never remember your side effects in retrospect, so it’s better to log it on a daily basis. Then I ask them to send their patient logs to us about once a week so that we have an idea of how they’re doing with the drug starting off.
In terms of lab evaluation, I have them do lab check at 2 weeks, 4 weeks, 6 weeks, and 8 weeks after initiating a RET inhibitor. This is predominantly to look at their complete blood cell count — to look out for low white counts or any other anomalies, but mainly low white count — and also liver function tests to see if those alanine aminotransferase and aspartate aminotransferase levels are rising. It can happen very quickly, within 2 weeks.
If you start noticing anything like that changing and it’s really mild, you can continue with drug. If they’re getting into more serious ranges, what we consider grade 2 or grade 3, you might have to implement a drug hold, reduce the dose, or resume at a lower dose.
I always recommend a check of more comprehensive lab testing, including thyroid function test, tumor markers, and EKG at 4 weeks and 8 weeks just to evaluate for other abnormalities that can arise with these drugs.
Then I see them with repeat imaging approximately 3 months after they initiate therapy just to see radiologically what kind of impact we’re having on the tumors. If everything is pretty stable, then maybe just every-3-month evaluations. They know how to reach out to us if they have any issues.
Desai: Speaking of issues, many people get fatigued and this medication can actually affect triiodothyronine (T3) levels. Can you talk a little bit about what you check and what other treatment options you give patients?
Hu: Yes. A very interesting thing that especially us endocrine oncologists started noticing while we were treating our patients on these trials was that their thyroid-stimulating hormone (TSH) started rising, their thyroxine (T4) seemed normal, and yet they were having fatigue. Although we don’t often evaluate T3, I started checking T3 levels and noticed that they were quite low. In these patients, I would start liothyronine and it seemed to help. It would get their TSH closer to normal and their fatigue started getting better.
This was actually investigated more formally by the group at Mass General, Dr Boucai and her colleagues. They published a study a few years ago where they found that the RET inhibitor led to an off-target effect on D2-mediated T3 production, so it actually inhibited the type 2 iodothyronine deiodinase.
This is making sense why we’re seeing T3 levels decrease. This happened more predominantly in our patients who were athyrotic, meaning their thyroid was removed. I actually had a patient who only had a half-thyroid surgery. Prior to knowing it was MTC, they did a lobectomy, and lo and behold, MTC. Eventually, the patient had liver metastases.
Although he never needed any thyroid hormone because his half thyroid was able to maintain his thyroid function, while he was on selpercatinib, I noted the TSH going up, but not nearly as much as my patients who were completely athyroid. His T4 was fine and he didn’t have any fatigue, so I didn’t put him on any medication.
In the population of lung cancer patients, obviously many of them still have an intact thyroid gland and they did not have as many of these issues. It was really the endocrine patients where this was found to be more relevant and prevalent because they were often athyrotic. This is a very interesting phenomenon.
Desai: Do you start all your patients on T3, or do you wait to see labs and symptoms and then select?
Hu: No, I don’t start T3 immediately because it doesn’t happen in everyone. Why that doesn’t happen in everyone, I don’t know. I just monitor them. I check those thyroid labs at 4 weeks, 8 weeks, and every 3 months. If I start to notice TSH rising and it corresponds with symptoms of fatigue, that’s when I give them a trial of T3.
Desai: I know you talked a little bit about checking imaging at 3 months and 6 months, to see how the medication is responding and how the radiographic changes are occurring, presumably to shrink the tumor. Do you ever have cases where you get drug resistance and the tumor that was previously shrinking now expands or progresses?
Hu: Yes. In our trials, certainly the majority of our patients did have durable responses, but there was a small percentage of patients who did have progressive disease either 1 year, 2 years, or even 3 years after initiating drug therapy. Actually, in the interim results that were published for the phase 3 trial, progressive disease was seen in about 2% of the patients treated with selpercatinib. It’s a low percentage of patients.
Unfortunately, when they progress, we have identified emergent mutations that have led to resistance to the drug therapy. We always knew that the RET V804M or V804L gatekeeper mutation is a known resistance mechanism for patients when they’re on vandetanib or cabozantinib.
The reason why is that the RET receptor on the intracellular portion has an adenine binding pocket on the kinase portions of this receptor. Adenosine triphosphatase ATP binds into that pocket, it activates and phosphorylates the kinase, and that is what leads to the receptor to be activated, leading to cell division, proliferation, and growth.
When there is a gatekeeper RET 804 mutation, it’s actually leading to some structural change where the kinase inhibitor cannot fit into that binding pocket and prevents the ATP binding to that receptor. Thus, it’s leading to resistance to vandetanib and cabozantinib.
What we also have found is that, when the patients are on this RET inhibitor, selpercatinib or pralsetinib, it led to control of their disease because this drug can still bind into that ATP binding pocket despite the gatekeeper mutation.
While patients were on these RET inhibitors, we did find that with time, there were these new mutations such as solvent front RET mutations, such as 810, or even other mutations — what we call bypass mechanisms. Basically these bypass mechanisms are allowing the cancer cell to still proliferate and grow despite the RET inhibitor still may be binding and inhibiting the RET receptor.
Yes, progression can be seen. It is a small population, but when it does develop, it tends to be associated with these emergent resistance mechanisms, which get to be very problematic because we don’t have good drugs to target these emergent mutations at this time.
Desai: If you have progression on one medication, you can’t switch to another RET inhibitor, correct?
Hu: That’s a great question. What I always recommend is, at the time of progression, try to biopsy the progressive lesion if it’s accessible for the biopsy, and do mutational testing to see if there is a resistance mutation. If there isn’t, then you might consider a change to another RET inhibitor or a different drug. That being said, if there is a resistance mutation, then we are thinking about either clinical trials, if there is a drug that can target it, or you have to start getting very creative in exploring other options.
Desai: Is there any way to resensitize patients once they’ve had this gateway mutation or a different mutation where they’ve gotten resistance? Is that something that’s being investigated or we’re just going down a different route?
Hu: No. Unfortunately, once MTC tumors develop these additional resistance mutations, it’s almost like they’re acting like a poorly differentiated thyroid cancer or an anaplastic thyroid cancer. It’s similar to those situations where there are many mutations driving disease. My hypothesis is that no single agent will be effective in managing these patients when they have additional mutations.
It used to be thought that MTC is a pretty low tumor mutation burden cancer. Usually, it’s just one driver mutation, if we find it at all. Once they develop more mutations, I just don’t think a single agent will be effective. I’m always optimistic and hope that there are smarter people out there than me who are looking into this in the lab.
Desai: In the world of RET inhibitors, is there anything new on the horizon? Is there anything else coming out?
Hu: There have been some phase 1 trials looking at other RET inhibitors and even next-generation RET inhibitors, which were designed to also target those emergent RET solvent front mutations. So far, until I see more published data, we’re not seeing much durable activity in those agents.
What I would say, though, is there are some possible areas of exploration. We know that, with MTC, there is overexpression of DLL3, which is delta-like ligand type 3. This typically is associated with patients with a little more aggressive MTC and lymph node metastases. It’s not unusual to find that our patients with advanced disease have DLL3 overexpression. There are agents being explored in clinical trials and even FDA approved for small cell lung cancer, which is also a neuroendocrine cell in lineage, where they’re targeting DLL3 in those tumors.
This is an area that warrants some investigation. Could immunotherapy be considered in patients with MTC? At this time, I don’t think we have enough data to support that, as we know that MTC typically has a very cold microenvironment for immune cells. Who knows what might develop in the future.
Desai: What would you, for our listeners today, say are the top 3 things that they should remember about RET inhibitors?
Hu: First of all, I think that RET inhibitors have been a game changer for our patients with MTC. They’re effective, they offer prolonged control in the majority of our patients, and they are much better tolerated than the older multikinase inhibitors vandetanib and cabozantinib. However, I would say there’s still a role for vandetanib and cabozantinib because obviously about 15% or more of our patients do not harbor a RET mutation. For those patients who have progressive disease, standard of care is still vandetanib and cabozantinib.
The RET inhibitors, although very effective in the majority of our patients, they’re still not the holy grail. Unfortunately, we still see progression in some of our patients. When that happens, it’s associated with these really bad players, these resistance mutations, that at this time we don’t have good drug therapy to combat.
I’m always very optimistic about continued investigation development in the lab and also clinically to see if we can get a hold of this in the future.
Desai: Thank you so much for joining us today. This was a great discussion. For our listeners, I just had one more piece of information to add. I know Dr Hu said it earlier, but make sure all your patients with MTC do get RET gene testing because there are options available.
Thank you again for joining me. For our listeners, stay tuned to our next episode where we’re going to shift our focus to a growing area of interest, which is active surveillance for small thyroid cancers. Thank you so much.
Hu: Thank you so much, Dr Desai, for your time.
Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.
Cite this: RET Inhibitors in Medullary Thyroid Cancer - Medscape - Nov 24, 2025.
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