what you are describing is a cancer between the hormonal and nervous system. Below are some treatment therapies:
[edit] Surgery and chemotherapy
Surgery is the only therapy that can cure GEP-NETs. However, the typical delay in diagnosis, giving the tumor the opportunity to metastasize, makes most GEP-NETs ineligible for surgery (non-resectable).
There is "no established standard therapy for the liver metastasis of pancreatic endocrine tumors" (Sato et al. 2000, [12]). The most common nonsurgical therapy for all GEP-NETs is chemotherapy, although chemotherapy is reported to be largely ineffective for carcinoids, not particularly durable (long-lasting) for PETs, and inappropriate for PETs of nonpancreatic origin.
When chemotherapy fails, the most common therapy, in the United States, is more chemotherapy, with a different set of agents. Some studies have shown that the benefit from one agent is not highly predictive of the benefit from another agent, except that the long-term benefit of any agent is likely to be low.
Strong uptake of somatostatin analogs is a negative indication for chemo.
[edit] Symptomatic relief
There are two major somatostatin-analog-based targeted therapies. The first of the two therapies provides symptomatic relief for patients with secretory tumors. In effect, somatostatin given subcutaneously or intramuscularly "clogs up" the receptors, blocking the secretion of hormones from the tumor cells. Thus a patient who might otherwise die from severe diarrhea caused by a secretory tumor can gain additional years of life.
Specific counter-hormones or other hormone-blocking medications are sometimes also used to provide symptomatic relief.
[edit] Hormone-delivered radiotherapy
The second of the two major somatostatin-analog-based targeted therapies is called peptide receptor radionuclide therapy (PRRT), though we might simply call it hormone-delivered radiotherapy. In this form of radioisotope therapy (RIT), radioactive substances (called radionuclides or radioligands) are chemically conjugated with hormones (peptides or neuroamines); the combination is given intravenously to a patient who has good uptake of the chosen hormone. The tumor cells pull the hormone to them, and the attached radiation kills nearby cells. In patients with strongly overexpressing tumor cells, nearly all the radiation either sticks to the tumors or is excreted in urine. As Rufini et alia say, GEP-NETs "are characterized by the presence of neuroamine uptake mechanisms and/or peptide receptors at the cell membrane, and these features constitute the basis of the clinical use of specific radiolabeled ligands, both for imaging and therapy" (Rufini, Calcagni, and Baum 2006, [13]).
The use of PRRT for GEP-NETs is similar to the use of iodine-131 as a standard therapy (in use since 1943) for nonmedullary thyroid tumors (which are not GEP-NETs). Thyroid cells (whether normal or neoplastic) tend to be avid for iodine, and nearby cells are killed when iodine-131 is infused into the bloodstream and is soon attracted to thyroid cells. Similarly, overexpressing GEP-NET cells (neoplastic cells only) are avid for somatostatin analogs, and nearby cells are killed when radionuclides attached to somatostatin analogs are infused into the bloodstream and are soon attracted to the tumor cells. In both therapies, hormonal targeting delivers a much higher dose of radiation than external beam radiation could safely deliver.
As of 2006, PRRT is available in at least dozen medical centers in Europe. In the USA it is FDA-approved, and available at the MD Anderson Cancer Center, but using a radionuclide, indium-111, that is vastly weaker than the lutetium-177 and the even stronger yttrium-90 used on the European continent. In the UK, only the radionuclide metaiodobenzylguanidine (I-MIBG) is licensed (but GEP-NETs are rarely avid for MIBG). PRRT with lutetium or yttrium is nowhere an "approved" therapy, but the German health insurance system, for example, covers the cost for German citizens.
MIBG therapy was developed in the 1980s and PRRT in the 1990s, and practitioners continue to refine their choices of radionuclides to maximize damage to tumors, of somatostatin analogs to maximize delivery, of chelators to bind the radionuclides with the hormones (and chelators can also increase uptake), and of protective mechanisms to minimize damage to healthy tissues (especially the kidneys).
[edit] Hepatic artery-delivered therapies
One therapy for liver metastases of GEP-NETs is hepatic artery embolization (HAE). Larry Kvols, of the Moffitt Cancer Center and Research Institute in Tampa, Florida, says that "hepatic artery embolization has been quite successful. During that procedure a catheter is placed in the groin and then threaded up to the hepatic artery that supplies the tumors in the liver. We inject a material called embospheres [tiny spheres of glass or resin, also called microspheres] into the artery and it occludes the blood flow to the tumors, and in more than 80% of patients the tumors will show significant tumor shrinkage" (Kvols 2002, [14]). HAE is based on the observation that tumor cells get nearly all their nutrients from the hepatic artery, while the normal cells of the liver get about 75 percent of their nutrients (and about half of their oxygen) from the portal vein, and thus can survive with the hepatic artery effectively blocked. [9]
Another therapy is hepatic artery chemoinfusion, the injection of chemotherapy agents into the hepatic artery. Compared with systemic chemotherapy, a higher proportion of the chemotherapy agents are (in theory) delivered to the lesions in the liver. [10]
Hepatic artery chemoembolization (HACE), sometimes called transarterial chemoembolization (TACE), combines hepatic artery embolization with hepatic artery chemoinfusion: embospheres bound with chemotherapy agents, injected into the hepatic artery, lodge in downstream capillaries. The spheres not only block blood flow to the lesions, but by halting the chemotherapy agents in the neighborhood of the lesions, they provide a much better targeting leverage than chemoinfusion provides.
Radioactive microsphere therapy (RMT) combines hepatic artery embolization with radiation therapy: microspheres bound with radionuclides, injected into the hepatic artery, lodge (as with HAE and HACE) in downstream capillaries. In contrast with PRRT, the lesions need not overexpress peptide receptors. (But PRRT can attack all lesions in the body, not just liver metastases.) Due to the mechanical targeting, the yttrium-labeled microspheres "are selectively taken up by the tumors, thus preserving normal liver" (Salem et al. 2002, [15]).
[edit] Other therapies
Radiofrequency ablation (RFA) is used when a patient has relatively few metastases. In RFA, a needle is inserted into the center of the lesion and is vibrated at high frequency to generate heat; the tumor cells are killed by cooking.
Cryoablation is similar to RFA; a endothermic substance is injected into the tumors to kill by freezing. Cryoablation has been considerably less successful for GEP-NETs than RFA.
Interferon is sometimes used to treat GEP-NETs; its use was pioneered by Dr. Kjell Öberg at Uppsala. For GEP-NETs, Interferon is often used at low doses and in combination with other agents (especially somatostatin analogs such as octreotide). But some researchers claim that Interferon provides little value aside from symptom control.
As described above, somatostatin analogs have been used for about two decades to alleviate symptoms by blocking the production of hormones from secretory tumors. They are also integral to PRRT. In addition, some doctors claim that, even without radiolabeling, even patients with nonsecretory tumors can benefit from somatostatin analogs, which purportedly can shrink or stabilize GEP-NETs. But some researchers claim that this "cold" octreotide provides little value aside from symptom control.
Finally, therapies based on growth factor inhibitors are in the experimental stage. These inhibitors of epidermal growth factor receptors (EGFRs), of vascular endothelial growth factor receptors (VEGFRs), and of angiopoietin-related growth factor (AGF) include imatinib, sunitinib, temozolide, thalidomide, sorafenib, and panitumumab.
remember that therapies and treatments do not work for all and have different effects on different people. for more information I suggest you talk to your oncologist. good luck!
2006-11-06 13:31:14
·
answer #1
·
answered by The cuter 3
·
1⤊
0⤋
How carcinoma of unknown primary is treated
Many different treatments are used either alone or in combination to treat CUP. Some of the treatments that are used are:
Surgery (taking out the cancer in an operation)
Radiation therapy (using high-dose x-rays to kill cancer cells)
Chemotherapy (using drugs to kill cancer cells)
Hormone therapy (using hormones to stop the cancer cells from growing)
Surgery is a common treatment for CUP. A doctor may remove the cancer and some of the healthy tissue around it. Different operations are used depending on where the cancer is found. If the cancer has spread to lymph nodes, the lymph nodes may be removed (lymph node dissection). If the nodes involved are in the groin, this operation is called a superficial groin dissection. If the cancer has spread to lymph nodes and also to some surrounding areas, the doctor may have to remove a larger portion of tissue around the nodes. When muscles, nerves, and other tissue in the neck are removed, this is called a radical neck dissection.
Radiation therapy uses x-rays or other high-energy rays to kill cancer cells and shrink tumors. Radiation may be used alone or before or after surgery.
Chemotherapy uses drugs to kill cancer cells. Chemotherapy may be taken by mouth or it may be put into the body by a needle in a vein or muscle. Chemotherapy is called a systemic treatment because the drugs enter the bloodstream, travel through the body, and can kill cancer cells throughout the body. Chemotherapy may be used alone or after surgery. Therapy given after an operation when there are no cancer cells that can be seen is called adjuvant therapy.
Hormone therapy is used to stop the hormones in the body that help cancer cells grow. This may be done by using drugs that change the way hormones work or by surgery that takes out organs that make hormones, such as the testicles (orchiectomy).
Treatment by stage
Treatment of CUP depends on where the doctor thinks the cancer started, what the cancer cells look like under a microscope, and other factors. Surgery and tests may be done to find where the cancer started.
Standard treatment may be considered because of its effectiveness in patients in past studies, or participation in a clinical trial may be considered. Not all patients are cured with standard therapy and some standard treatments may have more side effects than are desired. For these reasons, clinical trials are designed to find better ways to treat cancer patients and are based on the most up-to-date information. Clinical trials are ongoing in most parts of the country for CUP. To learn more about clinical trials, call the Cancer Information Service at 1-800-4-CANCER (1-800-422-6237); TTY at 1-800-332-8615.
(Yahoo Health)
2006-11-06 13:19:39
·
answer #4
·
answered by cubbi_bear21 2
·
0⤊
1⤋