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With that warning, we note that there are sometimes clinic trials against pancreatic cancer involving unconventional alternative therapies. There are a number of researchers who are in support of these trials. Some perhaps because they think they will succeed.

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Others, who strongly feel that applying the scientific method to these kind of treatments will expose their weaknesses. Only time can tell us what the outcome of these studies will finally demonstrate. We would advise being careful.

There are many sites on the Internet about alternative, complementary, or holistic treatment practices. In our attempt to suggest tempering faith and hope with rationality and care, we would advise being careful. Neuroendocrine tumors of the pancreas islet cell tumors are much less common than tumors arising from the exocrine pancreas. Reports often indicate that there are about two to three thousand cases diagnosed in the U. These different areas of the pancreas are somewhat jumbled up together anatomically — so rather than being like neighbors, the endocrine and exocrine areas of the pancreas are more like ethnicities all living together in the city known as the pancreas.

About one quarter of islet cell tumors do not produce symptoms related to hormone secretion and thus are termed non-functioning. The predominant hormone peptide being secreted gives the functioning islet cell tumor its name. There are a surprising number of these hormonal peptides that islet cell tumors have been found to secrete; some are not even related to the pancreas.

Some of these are very rare. The most common functioning pancreatic endocrine tumors are insulinomas followed by gastrinomas, glucagonomas and VIPomas, respectively. Typically, the symptoms produced by the excess secretion of the predominant hormone in a given functioning endocrine tumor, drives the eventual diagnosis. With the exception of insulinomas, most of the islet cell tumors have fairly similar characteristics, belying the apparent differences caused by the large range of symptom effects related to the secretion of such different hormones.

Histologically under the microscope they tend to be quite similar. It is not possible to ascertain malignancy from the histological appearance; malignancy is seen primarily as a function of finding additional metastatic sites.

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The sites of metastasis of islet cell tumors most commonly are the liver and the lymph nodes in the vicinity of the pancreas. Insulinomas are islet cell tumors which secrete an excess of predominantly insulin. These tumors will typically first present symptoms between the ages of 40 and 50, are more common among women and tend to be small, solitary tumors located in the pancreas itself.

The clinical features of this tumor are related to the effects of insulin-and thus primarily demonstrate symptoms related to hypoglycemia which are relieved by food intake. Other general symptoms include episodic sweating, tremor and rapid heart rate, as well as hunger, nausea, weight gain, and sometimes even central nervous system symptoms including rarely, seizures. Gastrinomas over-secrete the hormone gastrin. The clinical effect of this circumstance is what has come to be called the Zollinger-Ellison syndrome, a triad of signs and symptoms including atypical peptic ulcer disease, gastric hyperacidity and hyper-secretion, and an associated islet cell pancreatic tumor.

Patients with glucagonomas tend to present with mild diabetes and a severe dermatitis. These tumors are frequently fairly large by the time of diagnosis, sometimes greater than two inches in diameter. Over-secretion of this vasoactive intestinal peptide causes watery diarrhea, and low serum potassium and chloride levels. Only about cases of this kind of tumor have been described in the medical literature; the majority are malignant by the time of diagnosis. Carcinoid cancer is the most common of the neuroendocrine tumors, with one-and-a-half diagnosed cases per , of population, although anatomy at autopsy demonstrates about times those that are diagnosed clinically.

They tend to be slow growing. The symptoms and signs of carcinoid tumors range widely, and depend on the location and size of the tumor, on the presence of metastases, and secretions. They can appear to the surgeon as firm nodules bulging into the intestinal lumen can originate from pancreas, lungs, thymus, appendix, and ovaries, etc.

Carcinoid tumors can secrete any number of hormonal, growth and other factors.

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Symptoms related to the tumor and its factors may be intermittent and vague, but the most common presentation is periodic abdominal pain sometimes accompanied by malignant carcinoid syndrome, characterized by flushing of the face, severe diarrhea, and an asthma episode.

The initial evaluation of patients often includes measurement of such factors as serotonin, 5-HT, catecholamines and histamine, and especially urinary 5-HIAA levels. In general, survival rates for patients with carcinoid cancers are related to the size of the primary tumor — and the degree of metastasis. The natural history of islet cell and carcinoid tumors tends to be favorable as compared with pancreatic adenocarcinoma.

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For example, the median survival duration from the time of diagnosis for patients with non-functioning metastatic islet cell tumors approaches five years. The diagnosis of islet cell tumors is aided by the different abnormal biochemical profiles that they may present, which often leads to radiographic means to try and locate the tumor. It would be a mistake to generalize too much about attempts to locate these tumors. But generally, dynamic CT scans with radio-contrast dye, octreotide scintigraphy, transabdominal ultrasound, and selective visceral angiography are all methods employed to elicit radiographic information about the cancer, depending on individual circumstance.

Although they arise from similar cells, these different types of neuroendocrine cancers all behave somewhat differently. The standard treatments tend to be tumor-type specific, but some general observations can be made. Immediate treatment of the symptomatic conditions created by the over-secretion of the hormone s may be appropriate. For example, the use of H2-blockers, omeprazole and even octreotide in gastrinomas. The treatment of choice for localized islet cell tumors is generally curative surgery.

The treatment of metastatic islet cell cancer disease, depending on the tumor type, will often include chemotherapy involving such agents as streptozocin, everolimus, sunitinib, temozolomide, capecitabine, 5-FU, doxorubicin, dacarbazine and octreotide. Recently, there have been published in the medical literature promising studies of aggressive surgery benefiting select cases of metastatic neuroendocrine tumors.

Apparently isolated liver metastases have been treated with such creative approaches as hepatic artery embolization. This may reduce the nutrient blood supply to the metastatic liver tumor which tend to be rather vascular , but this approach remains controversial. Currently, there are studies employing techniques of radioimmunotherapy to selected patients with metastatic islet cell cancer, wherein radioactive elements have been conjugated together with specific compounds sometimes hormonal elements which are chosen for their properties that tend to selectively target islet cell tissue.

These are very interesting early studies which hold the virtue of biologic plausibility, but the final results of the efficacy of this approach is not yet fully known. Pancreatic cancer clinical trials are offered in many parts of the word. These studies seek to establish the validity of new and possibly improved treatment options. Clinical trials are, ideally, a part of a system in which a series of scientifically-controlled experiments shepherd a plausible medical agent, combination of agents or procedure through a process whereby the efficacy of the medical agent or procedure is established or not.

Until more recently, when fast-tracking has become more possible, the process of taking a potential agent from the biochemical stage through clinical trials to final FDA approval could take as long as 15 years. This process begins long before human testing.

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Generally, moving the process into human testing is predicated on successful animal results. It is then that the three primary phases of human testing begins.

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A phase I clinical trial with human subjects seeks to answer questions about whether a drug-agent is reasonably safe for use by humans. It also may seek to learn something of the biokinetics of the drug. And finally tries to establish what the maximum tolerated dose of the drug is. These are the only real aims of a phase I clinical trial, although researchers will, of course, be looking for subtle indications that the drug may show future promise.

Some fraction of phase I clinical trials will move on to the phase II, which seeks to answer the question as to whether the drug has, in fact, an apparent effect against the cancer in question in our case pancreatic cancer. Many potential drug therapies go no further than phase II — as they show no real effect against pancreatic cancer. Successful phase II candidates move on to phase III clinical trials which seek to determine how the new therapy compares to existing standard therapies.

Phase III clinical trials are the core measure of a potential new drug. Phase III clinical trials are controlled experiments whereby patients with similar characteristics are assigned to receive either the existing therapy or to receive the new therapy. After a time, the results of the arms of test are then compared. If the new agent shows similar or improved results as compared to existing therapy, after another step or two it is often approved for release by the FDA. There is even a phase IV to this process which has to do with after-approval monitoring of the new drug for side-effects, etc.

The decision to participate in a clinical trial for pancreatic cancer is a big one and should not be taken lightly. At its very heart a clinical trial is an experiment. Consequently, clinical trials contain inherent risk-both active risks and passive risks. An example of an active risk might be encountering an unexpected side-effect of the drug. An example of a passive risk might include the clinical trial protocol which may call for being off all standard medical treatment for 28 days which is not uncommon before beginning the clinical trial.

More many diseases, this may not patter much. But with pancreatic cancer, this kind of a rule may matter a great deal.