Gallium-68 scans approved in the USA (for imaging of neuroendocrine tumors)

Demonstrating how easy it is to “miss” news that may be important to at least a few members of the prostate cancer community, we have just learned that gallium-68 dotatate ([68Ga]dotatate) PET scanning was approved by the U.S. Food and Drug Administration (FDA) on June 1, 2016 — but not specifically for use in the detection of metastatic or micrometastatic prostate cancer.

What the FDA actually approved is a product called NetSpot. This is a kit for the preparation of an injection of [68Ga]dotatate, which is a radioactive agent for use in combination with PET scanning. [68Ga]dotatate can help to locate tumors in adult and pediatric patients with a rare condition known as somatostatin receptor positive neuroendocrine tumors or NETs.

It is important for readers to understand that this is not a form of gallium-68 imaging agent that is linked to a prostate-specific membrane antigen or PSMA. That type of gallium-68 imaging agent is still in development here in the USA for the detection of progressive forms of prostate cancer, although it is available in several European countries and is also available as an investigational agent at selected centers here in the USA.

However, we know that neuroendocrine tumors can increasingly be identified among patients with advanced forms of metastatic, castration-resistant prostate cancer (mCRPC), and particularly in those patients who have already received treatment with newer drugs like abiraterone acetate (Zytiga) and enzalutamide (Xtandi). What is less clear at present is just how many of those NETs in prostate cancer patients might be somastatin receptor positive.

The FDA, in approving NetSpot has stated that:

NETs are rare noncancerous (benign) or cancerous (malignant) tumors that develop in the hormone-producing cells of the body’s neuroendocrine system. These cells are found throughout the body in organs, such as the stomach, intestines, pancreas, lungs and other locations. NETs have receptors for somatostatin, a hormone that regulates the endocrine system. Ga 68 dotatate, a positron emitting analogue of somatostatin, works by binding to such receptors.

From a prostate cancer-specific perspective, what is important here is that the FDA has approved this agent. It is therefore available for use by specialists in nuclear medicine and appropriately qualified radiologists for imaging of appropriate patients. It may or may not have value in the imaging of selected NETs in some prostate cancer patients. The fact that the FDA has approved this type of gallium-68 imaging agent also heightens the likelihood that we may see some form of PSMA-linked gallium-68 imaging agent approved by the FDA in the not too distant future. The other thing that has yet to become clear is whether Medicare and commercial insurers would cover costs associated with the use of this test to try to detect neuroendocrine forms of metastatic prostate cancer.

4 Responses

  1. This post raises a question that has troubled me for some time, and came up again this week.

    While we know advanced prostate cancer tumors can morph into neuroendocrine and/or small-cell-like forms, and behave like them, are they in fact neuroendocrine/small cell cancers, and will they respond to screening agents the same way?

    They certainly act like neuroendocrine/small cell cancers, but on a molecular and genetic level are they the same?

  2. I was treated with Zytiga + prednisone for 18 months and my PSA went down to < 0.006. Blood tests detected high bone growth and an 18F scan found two metastases at the illium and the C5 vertebra. My oncologist stated these were neurocrine tumors which do not produce PSA. Additional blood tests were for CEA (colon or thyroid cancer), LDH (cellular damage is occurring), chromogranin A (a carcinoid or neuroendocrine tumor marker), Tandem-R Ostase (bone growth).

    My test showed chromogranin A and Tandem R-ostase were off the chart.

    I am now being treated with Xofigo, Zytiga + prednisone, and Firmagon to see what happens.

    I’m wondering if long-term Zytiga caused the de-differentiation of the prostate cancer into neurendocrine tumors.

  3. Dear Stan:

    There is an association between risk for neuroendocrine tumor development and treatment with drugs like Zytiga aand Xtandi, but there is also a simpler risk for neuroendocrine tumor development among patients who survive for long periods of time with castration-resistant prostate cancer (CRPC).

    As far as I am aware (at this time) it is almost impossible to tell exactly why any specific man with CRPC develops a neuroendocrine tumor.

  4. Stan:

    I encourage you to discuss genomic sequencing with your medical team to learn if your tumor has any actionable genes. Feel free to reach out to me at .

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