Hormonal imbalances are quite common in many conditions including day to day stuff. With Neuroendocrine Cancer, it can be a real challenge both at diagnostic and maintenance phases. In addition to the cancer angle, there’s some strange stuff going on, inexplicable, frightening for the patient, an unwanted ingredient causing chaos!
Until I was diagnosed with metastatic Neuroendocrine Cancer, I didn’t have a clue about hormones – it’s one of those things you just take for granted. However, hormones are vital to human health (male and female) and it’s only when things go wrong you suddenly appreciate how important they are. Hormones are involved in many conditions, not just an issue with Neuroendocrine Tumours (NETs) but the presence of over-secreting hormones (often called peptides throughout) is useful to aid a diagnosis, albeit it often (but not always) means the tumours have metastasized. It’s also a frequent indication that the person may have an associated NET syndrome.
This is a really complex area and to understand the hormone problems associated with Neuroendocrine Cancer, you need to have a basic knowledge of the endocrine and neuroendocrine systems. I’ve no intention of explaining that (!) – other than the following high level summary:
Hormones are involved in just about every aspect of a human body and it’s all about balance. One of the diagnostic and maintenance challenges for NET doctors is the fact that many people have hormonal imbalances regardless of if they have a NET or not. This could be before, during or after diagnosis. There can be issues taking them out of balance and functional NETs are just one thing that can have an adverse effect.
Working out wherther you have a regular hormonal issue or a NET related hormonal problem can often be difficult but the important thing is to get attention to address the hormonal imbalance to maintain quality of life. Well-known essentially hormonal imbalance issues include (but are not limited to) diabetes, hypothyroidism, anxiety, and depression – these illnesses are much more common than NETs but I accept there can be confusion in whether the connection is NETs or not. I also accept there are known linkages to each of these conditions.
Other common conditions caused by hormonal imbalance include (but are not limited to) hair loss, night sweats, irritability, weight gain, fatigue, eyebrow thinning, migraines, and forgetfulness, although some of these could be connected to the common conditions mentioned previously and I accept some of this could be caused by cancer treatment. Working out whether this is a comorbidity or a side effect of cancer can be a jigsaw.
At least one or more hormones will be involved at various sites and even within certain syndromes, the dominant and offending hormone may differ between anatomical tumour sites. For example, NETs of the small intestine may overproduce serotonin and other hormones which can cause a characteristic collection of symptoms currently called carcinoid syndrome. The key symptoms are flushing, diarrhea and general abdominal pain, loss of appetite, fast heart rate, shortness of breath, and wheezing. The main symptom for me was facial flushing and this was instrumental in my eventual diagnosis. The fact that I was syndromic at the point of diagnosis made it easier to discover, albeit the trigger for the investigation was a fairly innocuous event.
Pancreatic NETs are also affected by the overproduction of hormones including (but not limited to) Insulinomas, Gastrinomas, Glucagonomas, VIPomas, Somatostatinomas, and others. These can cause their own syndromes and are not part of carcinoid syndrome as some organisations incorrectly state. For more on NET syndromes – Read Here.
Absolutely not ……. unless they get out of hand! Hormones are essential to the normal function of the human body. For example, if you didn’t have any of the hormone Serotonin in your system, you would become extremely ill.
In fact, if your glands start secreting too much of certain hormones, your body could become dysfunctional and, in some scenarios, this situation could become life-threatening. Some regular diseases are due to high and low levels of certain hormones. So, hormones are good as long as the balance is correct.
NET patients with an over-secreting tumour causing symptoms may be classed as “functional”.
It’s accurate to say that the type and amount of hormone secretion differs between locations or sites of the functional tumour and this can also create different effects. The division of NETs into larger anatomical regions appears to differ depending on where you look but they all look something like this:
I used the example of Serotonin above because it is the most cited problem with NET although it does tend to be most prevalent in midgut tumours. Serotonin is a monoamine neurotransmitter synthesized from Tryptophan, one of the eight essential amino acids defined as those that cannot be made in the body and therefore must be obtained from food or supplements. About 90% of serotonin produced in the body is found in the enterochromaffin cells of the gastrointestinal (GI) tract where it is used mainly to regulate intestinal movements amongst other functions. The remainder is synthesized in the central nervous system where it mainly regulates mood, appetite, and sleep. Please note there is no transfer of serotonin across the blood-brain barrier.
Alterations in tryptophan metabolism may account for many symptoms that accompany carcinoid syndrome. Serotonin in particular is the most likely cause of many features of carcinoid syndrome as it stimulates intestinal motility and secretion and inhibits intestinal absorption. Serotonin may also stimulate fibroblast growth and fibrogenesis and may thus account for peritoneal and valvular fibrosis encountered in such tumours; serotonin, however, it is said not to be associated with flushing. The diversion of tryptophan to serotonin may lead to tryptophan deficiency as it becomes unavailable for Niacin (B3) synthesis, and is associated with reduced protein synthesis and hypoalbuminaemia; this may lead to the development of pellagra (skin rash, glossitis, stomatitis, confusion/dementia). The latter is rare nowadays due to the improvements in diagnosis, education and the use of somatostatin analogues.
Serotonin is also said to be responsible for ‘right sided’ heart disease (Carcinoid Heart Disease). It is thought that high levels of serotonin in the blood stream damages the heart, leading to lesions which cause fibrosis, particularly of the heart valves. This generally affects the right side of the heart when liver metastases are present. The left side of the heart is usually not affected because the lungs can break down serotonin. Right sided heart failure symptoms include swelling (edema) in the extremities and enlargement of the heart.
Whilst serotonin can be measured directly in the blood, it’s said to be more accurate to measure 5HIAA (the metabolic output of serotonin) via blood or urine, the latter is said to be the most accurate and both have dietary restrictions. Serotonin is said to fluctuate throughout the day, so the serotonin test is just a snapshot.
I wanted to clarify what I said above because this is a confusing subject in patient groups. About 90-95% of serotonin produced in the body is found in the enterochromaffin cells of the gastrointestinal (GI) tract where it is used mainly to regulate intestinal movements amongst other functions. The remainder is synthesized in the central nervous system where it mainly regulates mood, appetite, and sleep. Please note there is no transfer of serotonin across the blood-brain barrier. If you wanted to dig deeper into this, please see my Serotonin overview and a second post mostly covering brain serotonin.
Tackykinins include Substance P, Neurokinin A, Neuropeptide K and others. They are active in the enterochromaffin cells of the GI tract but can also be found in lung, appendiceal and ovarian NETs, and also in Medullary Thyroid Carcinoma and Pheochromocytomas. They are thought to be involved in flushing and diarrhea in midgut NETs. The most common tachykinin is Substance P, which is a potent vasodilator (substances which open up blood vessels). Telangiectasias are collections of tiny blood vessels which can develop superficially on the faces of people who have had NETs for several years. They are most commonly found on the nose or upper lip and are purplish in colour. They are thought to be due to chronic vasodilatation. They are not regularly tested in most countries.
Histamine is a hormone that is chemically similar to the hormones serotonin, epinephrine, and norepinephrine. After being made, the hormone is stored in a number of cells (e.g., mast cells, basophils, enterochromaffin cells). Normally, there is a low level of histamine circulating in the body. However (and as we all know!), the release of histamine can be triggered by an event such as an insect bite. Histamine causes the inconvenient redness, swelling and itching associated with the bite. For those with severe allergies, the sudden and more generalized release of histamine can be fatal (e.g., anaphylactic shock). Mast cell histamine has an important role in the reaction of the immune system to the presence of a compound to which the body has developed an allergy. When released from mast cells in a reaction to a material to which the immune system is allergic, the hormone causes blood vessels to increase in diameter (e.g., vasodilation) and to become more permeable to the passage of fluid across the vessel wall. These effects are apparent as a runny nose, sneezing, and watery eyes. Other symptoms can include itching, burning and swelling in the skin, headaches, plugged sinuses, stomach cramps, and diarrhea. Histamine can also be released into the lungs, where it causes the air passages to become constricted rather than dilated. This response occurs in an attempt to keep the offending allergenic particles from being inhaled. Unfortunately, this also makes breathing difficult. An example of such an effect of histamine occurs in asthma. Histamine has also been shown to function as a neurotransmitter (a chemical that facilitates the transmission of impulses from one neural cell to an adjacent neural cell).
In cases of an extreme allergic reaction, adrenaline is administered to eliminate histamine from the body. For minor allergic reactions, symptoms can sometimes be lessened by the use of antihistamines that block the binding of histamine to a receptor molecule.
In the respiratory tract, thymus, stomach, duodenum, and pancreas (i,e. Foregut NETs), tumours in these areas mostly lack the enzyme aromatic amino decarboxylase that converts 5-HTP (5-Hydroxytryptophan – a precursor to serotonin) to serotonin (technical name = 5-HT); such tumours tend to produce 5-HTP and/or histamine instead of serotonin (but not always). And they may be associated with an atypical flushing and pruritus; increased histamine production may also account for the increased frequency of duodenal ulcers observed in these tumours.
Histamine is thought to be involved with certain types and locations of NET, including Lung and foregut NETs where they can cause pulmonary obstruction, atypical flush and hormone syndromes. However, this involvement has been challenged in 2023 by a study from The Netherlands who claim there is insufficient evidence to label Histamine as a carcinoid syndrome mediator. Read more here.
Kallikrein is a potent vasodilator and “may” account for the flushing and increased intestinal mobility. However, this involvement has been challenged in 2023 by a study from The Netherlands who claim there is insufficient evidence to label Kallikrein as a carcinoid syndrome mediator. Read more here.
Although prostaglandins are overproduced in midgut tumours, their role in the development of the symptoms of carcinoid syndrome is not well established but triggering peristalsis is mentioned in some texts. However, this involvement has been challenged in 2023 by a study from The Netherlands who claim there is insufficient evidence to label Prostaglandins as a carcinoid syndrome mediator. Read more here.
Bradykinin acts as a blood vessel dilator. Dilation of blood vessels can lead to a rapid heartbeat (tachycardia) and a drop in blood pressure (hypotension). Dilation of blood vessels may also be partly responsible for the flushing associated with carcinoid syndrome. However, this involvement has been challenged in 2023 by a study from The Netherlands who claim there is insufficient evidence to label Bradykinin as a carcinoid syndrome mediator. Read more here.
I’ve intentionally put Gastrin in between the Carcinoid Syndrome (serotonin secreting NETs) section and pancreatic NET hormone section. This is because in NETs of the stomach (Gastric NETs – gNETs) (or Gastrinomas of the pancreas or duodenum – see below), elevated Gastrin is almost always related to autoimmune fundic atrophic gastritis (type I gNETs), high gastrin levels due to a gastrinoma (i.e. type II gNETs secondary to a gastrinoma). More recently, general atrophy in chronic H. pylori associated gastritis, functional failure of parietal cells due to mutations or proton pump inhibitor (PPI) use have also been reported to be associated with NETs, some with a background of ECL cell hyperplasia but in cases of PPI also associated with parietal cell hyperplasia.
During a meal, gastrin stimulates the stomach to release gastric acid. This allows the stomach to break down proteins swallowed as food and absorb certain vitamins. It also acts as a disinfectant and kills most of the bacteria that enter the stomach with food, minimising the risk of infection within the gut. Gastrin also stimulates growth of the stomach lining and increases the muscle contractions of the gut to aid digestion. Excess gastrin could indicate a NET known as a Gastric NET (stomach) or a pNET/dNET known as Gastrinoma (see pancreatic hormones below). Many are situated in the Duodenum but the symptoms are similar to the pancreatic Gastrinoma, and most texts I read include in the coverage of “pancreatic NET syndromes”. See Pancreatic Hormones (Gastrinoma) below.
It follows that Gastrin is not within the boundaries of carcinoid syndrome because the causal factors are related to gastritis or Gastrinoma as above, the latter is a syndrome in its own right (see below).
Pancreatic neuroendocrine tumors form in hormone-making cells of the pancreas. You may see these described as ‘Islet Cells’ or ‘Islets of Langerhans’ after the scientist who discovered them. Pancreatic NETs may also be functional or non-functional:
There are different kinds of functional pancreatic NETs. Pancreatic NETs make different kinds of hormones such as gastrin, insulin, and glucagon. Functional pancreatic NETs include the following:
Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn’t mean that you will not get cancer. Talk with your doctor if you think you may be at risk. Multiple endocrine neoplasia type 1 (MEN1) syndrome is a risk factor for pancreatic NETs. Von Hippel-Landau (VHL) is another.
Signs or symptoms can be caused by the growth of the tumor and/or by hormones the tumor makes or by other conditions. Some tumors may not cause signs or symptoms. Check with your doctor if you have any of these problems.
Signs and symptoms of a non-functional pancreatic NET
A non-functional pancreatic NET may grow for a long time without causing signs or symptoms. It may grow large or spread to other parts of the body before it causes signs or symptoms, such as:
Signs and symptoms of a functional pancreatic NET
The signs and symptoms of a functional pancreatic NET depend on the type of hormone being made.
e.g. Gastrinoma – too much gastrin may cause:
Too much gastrin causes a condition known as Zollinger-Ellison syndrome, in which the stomach makes too much acid. In addition to Gastroesophageal reflux, this leads to stomach ulcers, which can cause pain, nausea, and loss of appetite. These ulcers can be recurring. If the ulcers are prone to bleeding, it has the potential to lead to anemia (too few red blood cells), which can cause symptoms like feeling tired and being short of breath. Diarrhea if often a gastrinoma symptom.
e.g. Insulinoma – too much insulin may cause:
e.g. Glucagonoma – too much glucagon may cause:
e.g. VIPoma – too much vasoactive intestinal peptide (VIP) may cause:
e.g. Somatostatinoma – too much somatostatin may cause:
e.g. PPoma – too much pancreatic polypeptide may cause:
Read more by clicking here.
Parathyroid hormone (PTH) is secreted from four parathyroid glands, which are small glands in the neck, located behind the thyroid gland. Parathyroid hormone regulates calcium levels in the blood, largely by increasing the levels when they are too low. A primary problem in the parathyroid glands, producing too much parathyroid hormone causes raised calcium levels in the blood (hypercalcaemia – primary hyperparathyroidism). You may also be offered an additional test called Parathyroid Hormone-Related Peptide (PTHrP). They would probably also measure Serum Calcium in combination with these types of tests. The parathyroid is one of the ‘3 p’ locations often connected to Multiple Endocrine Neoplasia – MEN 1
HPA AXIS – It’s important to note something called the HPA axis when discussing pituitary hormones as there is a natural and important connection and rhythm between the Hypothalamus, Pituitary and the Adrenal glands. However, I’m only covering the pituitary and adrenal due to their strong connection with NETs.
Adrenocorticotropic hormone (ATCH) is made in the corticotroph cells of the anterior pituitary gland. It’s production is stimulated by receiving corticotrophin releasing hormone (CRH) from the Hypothalamus. ATCH is secreted in several intermittent pulses during the day into the bloodstream and transported around the body. Like cortisol (see below), levels of ATCH are generally high in the morning when we wake up and fall throughout the day. This is called a diurnal rhythm. Once ACTH reaches the adrenal glands, it binds on to receptors causing the adrenal glands to secrete more cortisol, resulting in higher levels of cortisol in the blood. It also increases production of the chemical compounds that trigger an increase in other hormones such as adrenaline and noradrenaline. If too much is released, The effects of too much ATCH are mainly due to the increase in cortisol levels which result. Higher than normal levels of ATCH may be due to:
Cushing’s disease – this is the most common cause of increased ATCH. It is caused by a tumour in the pituitary gland (PitNET), which produces excess amounts of ATCH. (Please note, Cushing’s disease is just one of the numerous causes of Cushing’s syndrome). It is likely that a Cortisol test will also be ordered if Cushing’s is suspected.
A tumour outside the pituitary gland, producing ATCH is known as an ectopic ATCH. With NETs, this is most commonly a Thymus, Lung or pNET, Lung/Bronchial/Pulmonary NET.
Calcitonin is a hormone that is produced in humans by the parafollicular cells (commonly known as C-cells) of the thyroid gland. Calcitonin is involved in helping to regulate levels of calcium and phosphate in the blood, opposing the action of parathyroid hormone. This means that it acts to reduce calcium levels in the blood. This hormone tends to involve Medullary Thyroid Carcinoma and Hyperparathyroidism in connection to those with Multiple Endocrine Neoplasia. Worth also pointing out the existence of Calcitonin Gene-Related Peptide (CGRP) which is a member of the calcitonin family of peptides and a potent vasodilator. Please note that hypothyroidism is often a side effect of NETs or treatment for NETs – please click here to read about the connection.
These are two separate but related hormones and neurotransmitters, known as ‘Catecholamines’. They are produced in the medulla of the adrenal glands and in some neurons of the central nervous system. They are released into the bloodstream and serve as chemical mediators, and also convey nerve impulses to various organs. Adrenaline has many different actions depending on the type of cells it is acting upon. However, the overall effect of adrenaline is to prepare the body for the ‘fight or flight’ response in times of stress, i.e. for vigorous and/or sudden action. Key actions of adrenaline include increasing the heart rate, increasing blood pressure, expanding the air passages of the lungs, enlarging the pupil in the eye, redistributing blood to the muscles and altering the body’s metabolism, so as to maximise blood glucose levels (primarily for the brain). A closely related hormone, noradrenaline, is released mainly from the nerve endings of the sympathetic nervous system (as well as in relatively small amounts from the adrenal medulla). There is a continuous low level of activity of the sympathetic nervous system resulting in the release of noradrenaline into the circulation, but adrenaline release is only increased at times of acute stress. These hormones are normally related to adrenal and extra-adrenal NETs such as Pheochromocytoma and Paraganglioma. Like serotonin secreting tumours, adrenal secreting tumours convert the offending hormone into something which comes out in urine. In fact, this is measured (amongst other tests) by 24-hour urine test very similar to 5HIAA (with its own diet and drug restrictions). It’s known as 24-hour urinary catecholamines and metanephrines. Worth noting that adrenaline is also known as Epinephrine (one of the 5 E’s of Carcinoid Syndrome, clearly Pheo/Para have their symptoms but these are not classified as carcinoid syndrome).
This is a steroid hormone, one of the glucocorticoids, made in the cortex of the adrenal glands and then released into the blood, which transports it all around the body. Almost every cell contains receptors for cortisol and so cortisol can have lots of different actions depending on which sort of cells it is acting upon. These effects include controlling the body’s blood sugar levels and thus regulating metabolism acting as an anti-inflammatory, influencing memory formation, controlling salt and water balance, influencing blood pressure. Blood levels of cortisol vary dramatically, but generally are high in the morning when we wake up, and then fall throughout the day. This is called a diurnal rhythm. In people who work at night, this pattern is reversed, so the timing of cortisol release is clearly linked to daily activity patterns. In addition, in response to stress, extra cortisol is released to help the body to respond appropriately. Too much cortisol over a prolonged period of time can lead to Cushing’s syndrome. Cortisol oversecretion can be associated with Adrenal Cortical Carcinoma (ACC) which can sometimes be grouped within the NET family.
Other hormones related to ACC include:
Androgens (e.g. Testosterone) – increased facial and body hair, particularly females. Deepened voice in females.
Estrogen – early signs of puberty in children, enlarged breast tissue in males.
Aldosterone – weight gain, high blood pressure.
Adrenal Insufficiency (Addison’s Disease) occurs when the adrenal glands do not produce enough of the hormone cortisol and in some cases, the hormone aldosterone. For this reason, the disease is sometimes called chronic adrenal insufficiency, or hypocortisolism.
Read more by clicking here.
Clearly the presenting symptoms will give doctors a clue to the oversecreting hormone (see list above). Excessive secretions or high levels of hormones and other substances can be measured in a number of ways. For example:
Well known tests for the most common types of NET include 5-Hydroxyindoleacetic Acid (5-HIAA) 24 hour urine test which is also measured by a blood draw. Note: – tumour markers can be measured simultaneously e.g. Chromogranin A (CgA) blood test and/or Pancreastatin as there can very often be a correlation between tumour mass and tumour secreting activity. CgA / Pancreastatin is a blood test which measures a protein found in many NET tumour cells. These marker tests are normally associated with tumour mass rather than tumour functionality.
By measuring the level of 5-HIAA in the urine or blood, healthcare providers can calculate the amount of serotonin in the body (5-HIAA is a by-product of serotonin). 5-HIAA test is the most common biochemical test for carcinoid syndrome or the degree of how ‘functional’ tumours are. If you’ve understood the text above, you can now see why there are dietary and drug restrictions in place prior to the test.
Pancreatic Hormone testing. There are other tests for other hormones and there is a common test which measured the main hormones seen in NETs. It may be called different things in different countries, but in UK, it’s known as a ‘Fasting Gut Hormone Profile‘.
Scratching the surface here so for a comprehensive list of marker tests for NETs, have a read here.
Of course, reducing tumour bulk through surgery and other treatment modalities should technically reduce over-secretion (I suspect that doesn’t work for all). Other treatments may have the dual effect of reducing tumour burden and the effects of hormone oversecretions.
One of the key treatment breakthroughs for many NET patients is the use of ‘Somatostatin Analogues‘ mainly branded as Octreotide (Sandostatin) or Lanreotide (Somatuline). People tend to associate these drugs with serotonin-related secretions and tumours but they are in actual fact useful for many others including the pancreatic NETs listed above. Patients will normally be prescribed these drugs if they are displaying these symptoms, but some people may be more avid to the drug than others and this may influence future use and dosages. This is another complex area, but I’ll try to describe the importance here in basic terms. Somatostatin is a naturally occurring protein in the human body. It is an inhibitor of various hormones secreted from the endocrine system (some of which were listed above) and it binds with high affinity to the five somatostatin receptors found on secretory endocrine cells. NETs have membranes covered with receptors for somatostatin. However, the naturally occurring Somatostatin has limited clinical use due to its short half-life (<3 min). Therefore, specific somatostatin analogues (synthetic versions) have been developed that bind to tumours and block hormone release. Thus why Octreotide and Lanreotide do a good job of slowing down hormone production, including many of the gut hormones controlling emptying of the stomach and bowel. It also slows down the release of hormones made by the pancreas, including insulin and digestive enzymes – so there can be side effects including fat malabsorption.
The recent introduction of Telotristat Ethyl (XERMELO) is interesting as that inhibits a precursor to serotonin and reduces diarrhea in those patients where it is not adequately controlled by somatostatin analogues.
Other than the effects of curative or cytoreductive surgery, some NETs may have very specialist drugs for inhibiting the less common hormone types. This is not an exhaustive list.
Worth also noting that oversecreting hormones can contribute to a phenomenon (currently) known as Carcinoid Crisis, technically a type of cardiopulmonary hemodynamic instability, and more aptly should be named ‘Hormonal Crisis’ – read more here. For catecholamine secreting tumours (Pheochromocytoma/Paraganglioma), this may be known as Intraoperative Hypertensive Crisis.
A general treatment overview for Neuroendocrine Cancer can be found by clicking here or on the picture.
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. Some content may be generated by AI which can sometimes be misinterpreted. Please check any references attached.
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.
Blog Facebook. Like this page please.
Personal Facebook. Like this page please.
Awareness Facebook Like this page please.
Follow me on X (formerly twitter)
Check out my online presentations
Check out my WEGO Health Awards
A Global first for NET. Omni 128cm Total Body PET at the Peter MacCallum Cancer Centre in Melbourne Australia. According to Professor Michael Hofman, they
My diagnosis came with many strange words including, “carcinoid” and “neuroendocrine” ……… can you spell that please, I said to the doctor. I had a
Ronny Allan’s ‘PoNETry’ © series can be shared with poetry credit to: RonnyAllan.NET Thanks for reading Ronny I also have one about Lanreotide (or “butt
When I was diagnosed, I didn’t even feel ill. It was therefore a bit of a shock being told I had metastatic cancer, advanced enough to
I was assessing performance of the awareness period in November 2025 on Facebook and was astonished to find the size of my reach on that
Here is the monthly summary of November 2025 on RonnyAllan.NET – Every share helps someone understand or even work towards a diagnosis, discovery of the
Discover more from Ronny Allan – Living with Neuroendocrine Cancer Subscribe to get the latest posts sent to your email. Type your email… Subscribe
Bone metastases in Neuroendocrine Tumours (NET) Many of you will know that I am a stage IV small intestine NET and I have one bone
What is Radioligand Therapy? When you browse the internet, you may see the term “Radioligand Therapy (RLT)” and wondered what it was. There’s a simple
Buy me a cup of tea or two? Change the number below to increment. i.e insert 2 = £8, 3 = £12, etc
Overheads to run this site, e.g. software packages, domain registration fees, software tools, misc items. Donate £4 or more so I have the fuel to keep on providing great content!
£4.00
Subscribe to get the latest posts sent to your email.
