AGA Forum > Neuroendocrine tumors: timely diagnosis and optimal intervention

  

Answers from Thomas O'Dorisio MD

 

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The question: What are the current biotherapies for the management of neuroendocrine tumors?
  		   
The biotherapies that I'm aware of are predominantly the congeners of native somatostatin, and those include octreotide acetate, which was clinically approved in the United States in January of 1989, and in Europe slightly before that. Another two synthetic somatostatin congeners are in development. One of them is somatuline, or lanreotide, and the other is vapreotide, which tends to be a little longer half-lifed congener of native somatostatin.

Those are the primary biotherapies for neuroendocrine tumor. The one we're most familiar with in the United States, and we have done some work with the lanreotide, not the vapreotide, is the octreotide acetate. When it's given subcutaneously, it has a half-life of 90 to 120 minutes. When it's given intravenously, the only route, it has a half-life of 60 minutes.

There's the long-acting release form of octreotide acetate. It exists in a degradable polymer, and that's given usually once a month. You can also give it in shorter intervals than that if the tumor is very symptomatic and large, and that has to be intramuscular. It's very safe. Almost all the congeners that I'm aware of, especially octreotide acetate, are very safe drugs.

The other biotherapy that I'm aware of is interferon-alpha, which crosses different fields, because it's used by hepatologists and oncologists. It makes a great deal of sense, because its action, from what I understand, is not one that works within the mechanism of a rapid turnover cell. The nature of neuroendocrine tumors is very slow-going, a rather stable cell population that differentiate fairly close to what they really are.

Those are the two biotherapies that I'm most familiar with. I feel that a first-line biotherapy for neuroendocrine tumors specifically, are native somatostatin and its congeners, both for the rationale that they are replete with somatostatin receptor subtype 2, and for the rationale that the action has been shown to be anti-proliferation, differentiation-not dedifferentiation, but differentiation. The next biotherapies would be those that have receptor 1, subtype 1 agonism, and 2 and maybe 5. We have said before that 2, 3 and 5 are the most important subtypes, but the much more common tumors-colon cancer, for instance-do not have receptor subtype 2 on them. Maybe 20% of breast cancers do. However,they all seem to possess somatostatin receptor subtype 1, so that that agonism, the development of the second generation, will be maybe with an SST, hopefully, 1 subtype agonism.

 

  


Thomas O'Dorisio MD


 

 

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Last updated 10.01.04