There may be multiple causes of the carcinoma, neuroendocrine type. There is no doubt that it is mainly due to exposure to certain hormones and chemicals. And hormonal agents may also influence the risk of carcinoma, neuroendocrine type by altering the body's metabolic activity.
The average U.S. population in 1995-96 had 47,000 new diagnosis cases of carcinoma (13,000 women), and 34,000 new diagnosis cases were neuroendocrine (9,000 women). The number of new diagnosis cases with carcinoma increased for all ages, regardless of sex.
Signs include weight loss, loss of appetite, malaise, fatigue, blood-stained urine, and a firm enlargement of the cervical lymph nodes that are usually on the left under the arm. Also found are the symptoms of neuroendocrine cancer: Cushing's syndrome, and thyroid dysfunction.
There are various forms of carcinoma with different mechanisms of formation. In most cases, carcinomas formed are benign tumors or malignant tumors in early stage. Carcinoma, neuroendocrine tumors is a tumor formed or made by cells of endocrine apparatus, it is thought to originate from embryonic remnants (brain or other organs) or endocrine malfunction.\n
Radiation therapy is the sole treatment commonly used for carcinoma of neuroendocrine origin, but it is not always helpful. Other treatments commonly used are chemotherapy or combined therapies. Survival depends on the exact type of thyroid cancer and the staging of the disorder.\n
The most conclusive result was achieved in a curative group with limited disease. However, the cure rate was less than 50% in this group, and treatment failures occurred in most patients. Although some patients with advanced PNETs received curative resection, the overall good response rate suggests that a cure is achievable in some patients. Because patients with limited disease achieved a cure rate of 50%, the treatment approach should be changed to focus on this group of patients.
Clinical trials are the best opportunity for patients with neuroendocrine cell cancers for treatment innovation, but clinical eligibility criteria are ambiguous and are poorly implemented by clinical oncologists.
No reliable information is yet available on the efficacy of Tas-102-treated patients. Based on the experience with Tas-102 of different European and American centers, the clinical management plan of Tas-102, that we present, should help clinicians to make rational treatment decisions in most of the patients with Tas-102 treated carcinoid or neuroendocrine tumors.
Based on our clinical survey, we recommend that all patients receive the tas-102 infusion with a gradual increase in dose; at first, the patients receive two doses every three weeks, and then, in one week, they are transferred from two to six doses every three weeks. In general, patients experienced no symptoms, and the therapeutic effect was acceptable. After some patients complained of adverse reactions, we found that the patients who had been taking tas-102 more often exhibited higher BCLT scores when they stopped their treatments. We believe that the BCLT should be monitored continuously when tas-102 is given to patients, especially those who had been taking tas-102 at a high dose.
It was concluded that carcinoma, neuroendocrine families appear to have a different phenotype than noncarinoma, neuroendocrine families, but this difference was not reflected in an increased rate of family members with multiple neoplasms.
All patients in this trial showed excellent safety. Adverse events were experienced by several in the control group, all of which were Grade 1 or 2, and none of these patients had serious adverse events. There were four patients in the tas-102 group who required no further interventions, and all had Grade 1 adverse events. There were 20 patients in the tas-102 group who required treatment, and 14 had a serious adverse event. None of these events was fatal or required interventional treatment. There were no unexpected serious adverse events experienced. [Patient-tas-102 is not medically dangerous]. This trial has proven patients' safety.
It is not known if there have been other trials which use all patient populations and the results from these other studies have been applied to the design of NEPE. We have used the study sample size and result from our tas-102 study to predict if we would detect this effect from our current study design. We believe that the study is under powered and more work is required to investigate the exact effect size for the design we used.