A blog by Ronny Allan

HRT and Neuroendocrine Tumours (NETs): What Patients Need to Know

HRT and Neuroendocrine Tumours (NETs): What Patients Need to Know

Before you read this…

This article discusses hormone replacement therapy (HRT) in the context of general health, menopause, and neuroendocrine tumours (NETs). It is provided for educational purposes only and does not recommend starting, stopping, or changing any form of HRT.

The suitability of HRT depends on many individual factors, including tumour type, grade, hormone sensitivity, medical history, and personal risk–benefit considerations. These vary widely between people with NETs.

Only your own specialist team can advise on whether HRT is appropriate for you. No treatment decisions should be made based on this article alone.

 

Hormones and cancer often get mentioned together, so it’s understandable that people with neuroendocrine tumours (NETs) worry about whether Hormone Replacement Therapy (HRT) could “feed” their tumour. The reassuring news is that current evidence does not show that standard HRT causes NETs or accelerates their growth. Many NET patients safely use HRT under medical supervision.  This is one of the most frequently asked questions in my large private Facebook group.  

So why does this topic cause so much confusion?  Let’s break it down clearly and accurately.

 

Hormone‑Dependent Cancers: Where the Worry Comes From

Some cancers genuinely are driven by hormones. These tumours have receptors for specific hormones, and when those hormones bind, they can stimulate tumour growth. These are known as hormone‑dependent cancers.

Examples include:

  • Breast cancer Many breast cancers are estrogen‑ or progesterone‑receptor positive. Neuroendocrine breast cancers tend to be less ER/PR‑positive, but it can occur.
  • Prostate cancer These cancers can be driven by androgens (male hormones).

In these cancers, hormones act like fuel. Blocking or reducing those hormones is a key part of treatment.

This is not how NETs behave.

 

NETs and Hormones: A Completely Different Biology

NETs are unique because some of them can produce hormones, sometimes in excess. This can lead to clinical syndromes such as:

  • Carcinoid syndrome
  • Insulinoma
  • Gastrinoma
  • VIPoma
  • Glucagonom
  • Somatostatinoma
  • Other much less common ‘omas’
  • Cushing’s

But here’s the crucial distinction…….

In NETs, hormones are an output, not an input.

Functional NETs release hormones, but they are not driven by estrogen, progesterone, or testosterone in the way breast or prostate cancers can be. The metabolic pathways, receptor biology, and tumour‑growth mechanisms are entirely different.

NETs are primarily influenced by:

  • Genetic and epigenetic changes
  • Signalling‑pathway alterations
  • Somatostatin receptor expression
  • Tumour grade and proliferation rate
  • Microenvironmental factors

Not sex hormones.

This is why anti‑estrogen or anti‑androgen therapies are not used in NET treatment — there’s no evidence they would help.

 

The One Exception in hormone dependency: Type I Gastric NETs

There is one NET subtype where hormones play a role — but it has nothing to do with HRT or sex hormones.

Type I gastric NETs (gNETs) can develop through a gastrin‑driven pathway:

  1. Autoimmune atrophic gastritis damages the acid‑producing parietal cells.
  2. Low stomach acid triggers chronically high levels of gastrin.
  3. Gastrin overstimulates enterochromaffin‑like (ECL) cells.
  4. Over many years, this can progress from ECL hyperplasia → dysplasia → small gastric NETs.

This is a local stomach‑specific feedback loop, driven by gastrin, not estrogen, progesterone, testosterone, or HRT.

Type I gastric NETs are the one exception where a hormone (gastrin) drives tumour development — but this mechanism is unique to the stomach and has nothing to do with HRT or sex hormones.

A Rare Side Note: Breast Neuroendocrine Tumours

A small number of people develop primary breast neuroendocrine neoplasms (breast NENs). Because these arise in the breast, they can sometimes express:

  • ER (estrogen receptor)
  • PR (progesterone receptor)
  • HER2 (Human Epidermal Growth Factor Receptor 2)

This can include rare cases of HER2‑positive breast NENs.

These tumours follow breast cancer biology, not classical NET biology. They are treated according to breast cancer protocols, and their receptor status reflects breast‑specific pathways — not NET pathways.

This breast‑specific phenomenon has no relevance to HRT safety in other NETs. i.e. It does not apply to midgut, hindgut or foregut NETs.

Another Rare Side Note: Prostate Neuroendocrine Neoplasms

A very small number of people develop prostate neuroendocrine neoplasms (prostate NENs). These tumours are biologically closer to aggressive prostate cancer variants than to classical gastroenteropancreatic or lung NETs.

Prostate NENs can include:

  • Small‑cell neuroendocrine carcinoma of the prostate
  • Large‑cell neuroendocrine carcinoma
  • Mixed adenocarcinoma–neuroendocrine tumours

These tumours often arise after long‑term androgen‑deprivation therapy (ADT) for prostate adenocarcinoma. In other words: ✔ They are not driven by testosterone

Another Rare Side Note: Testicular NETs and Testosterone Replacement in Men

Testicular neuroendocrine tumours are extremely rare. They behave like classical NETs, not like hormone‑dependent cancers. Whether they arise in the testis or represent metastases from another NET site, they do not rely on testosterone for growth and do not use androgen‑driven signalling pathways. They also do not respond to androgen‑deprivation therapy (ADT), which is why lowering testosterone has no therapeutic effect on these tumours.

Some men receive hormone replacement in the form of testosterone replacement therapy (TRT) to treat low testosterone. TRT improves energy, bone health, libido, and wellbeing — but it does not stimulate NETs, including testicular NETs or prostate neuroendocrine neoplasms. NETs are not driven by testosterone, and increasing or decreasing testosterone levels does not influence their behaviour.

In short: testicular NETs are not testosterone‑dependent, and TRT has no relevance to NET growth or progression.

This phenomenon is unique to the testis and does not apply to other NETs.

So, Does HRT Cause NETs or Make Them Grow?

There is no strong evidence that HRT causes NETs or accelerates their growth.

This position is supported by:

✔ NET Specialist Guidelines

  • ENETS: NETs are not considered hormone‑dependent tumours; sex hormones are not recognised growth drivers.
  • NANETS: No recommendation to avoid HRT in NET patients; sex hormones are not listed as proliferative factors.

✔ Endocrinology and Menopause Experts

  • Endocrine Society and British Menopause Society: HRT is contraindicated in hormone‑dependent cancers (breast, endometrial), but NETs are not classified as hormone‑dependent.

✔ Peer‑Reviewed Literature

  • NET biology studies consistently show no clinically meaningful estrogen or progesterone receptor expression in typical NETs.
  • NET growth is driven by pathways such as mTOR, PI3K/AKT, and somatostatin receptor signalling, not sex‑hormone signalling.
  • No evidence links HRT to NET recurrence or progression.

✔ Clinical Practice

Many NET patients safely use HRT for:

  • Menopause symptom relief
  • Bone protection
  • Surgical menopause
  • Androgen deficiency

Clinicians typically approve HRT unless there is another unrelated contraindication.

 

Why People Still Worry

It’s completely understandable. When you hear the word “hormone” and you have a tumour, your brain jumps to:

“Will this feed the cancer?”

That fear is valid. But in NETs, the biology simply doesn’t support that mechanism.

Unless new science emerges, there is no established pathway by which standard HRT would stimulate NET growth.

 

Key Takeaways

  • HRT is not known to cause or accelerate NETs.
  • NETs are not hormone‑dependent tumours.
  • Functional NETs produce hormones but are not driven by them.
  • The only hormone‑driven NET pathway involves gastrin in Type I gastric NETs — unrelated to HRT.
  • Breast NENs can occasionally express ER/PR/HER2, but this reflects breast cancer biology, not NET biology.
  • Many NET patients in my large private group safely use HRT under medical supervision.
  • Always follow personalised medical advice.


If you are concerned about any interaction between the two, you should seek professional advice from your specialist. 

Disclaimer

I am not a doctor or any form of medical professional, practitioner or counsellor. None of the information on my website, or linked to my website(s), or conveyed by me on any social media or presentation, should be interpreted as medical advice given or advised by me. 

Neither should any post or comment made by a follower or member of my private group be assumed to be medical advice, even if that person is a healthcare professional.   

Please also note that mention of a clinical service, trial/study or therapy does not constitute an endorsement of that service, trial/study or therapy by Ronny Allan, the information is provided for education and awareness purposes and/or related to Ronny Allan’s own patient experience. This element of the disclaimer includes any complementary medicine, non-prescription over the counter drugs and supplements such as vitamins and minerals.

Thanks for reading.

Ronny

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By Ronny Allan

Ronny Allan is a 3 x award-winning accredited patient leader advocating internationally for Neuroendocrine Cancer and all other cancer patients generally. Check out his Social Media accounts including Facebook, BlueSky, WhatsApp, Instagram and and X.

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