A cohort of approximately one hundred participants recently diagnosed and not yet treated for neuroendocrine tumors will eventually be selected for this study, providing an adequate sample size to produce significant validity, reliability, and generalizability (Gabriel et al., 2007). A control group of approximately twenty-five individuals recently given negative results on conventional scintigraphy and/or dedicated CT diagnostic measures for neuroendocrine tumors will also be included in this study. All study participants will undergo imaging/diagnostic testing for neuroendocrine tumors using each of the three target methodologies -- [68Ga]-DOTATOC-based PET imaging, conventional scintigraphy, and dedicated CT (111ln-octreotide scintigraphy), with all tests completed on each patient within a four-day timeframe and all testing for the study completed in a three-month period. Follow-up documentation of treatments, neuroendocrine tumor diagnosis confirmation or rejection using histopathology, CT and MRI, and an ultimate determination of neuroendocrine tumor at the time of initial testing will also be conducted in order to validate the findings of initial diagnostic outcomes from the methodologies employed in the research, with follow-up examinations occurring at three weeks and again at six weeks after initial testing (Buchmann et al., 2007; Gabriel et al., 2007). Several local facilities have the capabilities to perform all necessary tests as described herein, and will be selected based on cost, availability, and proximity to participants (to reduce rates of attrition). Images...
Comparisons of outcomes in the primary research group will serve as the base measure for the accuracy and efficacy of the various diagnostic measures investigated. The control group will be used to provide greater potential evidence of false positive emergence in the tests utilized, and could also demonstrate inaccuracy in previous clinical diagnostics.Ga DOTA TOC Radio Pharmaceutical Neuroendocrine tumors (NET) are neoplasms characterized by tissue immunoreactivity for neuroendocrine differentiation markers, appearance as a small mass that can be off white to yellow often in submucosa and prevalence throughout the body but typically found in the intestine or lungs (Oberg2011). The tumors can be malignant and are typically detected through hormone markers in a first diagnosis (Arnold 2003). Because of the diffuse nature of
Magnetic Resonance Imaging History of MRI The Magnetic Resonance Imaging (MRI) was first tested in Budapest Hungry in 1882. Later in 1937, Professor Isidor Rabi of Columbia University assembled a Nuclear Magnetic Resonance. This tool was effective because it could absorb and emit radio waves after exposure to a strong magnetic field. Professor Carr Herman produced one-dimensional MRI imaging processor in 1952. The nuclear powered NMR was instrumental in experiments developed to
Certainly, it must be stated that more study is needed and worth pursuing in this diagnostic method in forensics. References Bisset, R. et al. (2002) Postmortem examinations using magnetic resonance imaging: four-year review of a working service BMJ 2002;324:1423-1424 (15 June) Online available: http://bmj.bmjjournals.com/cgi/content/full/324/7351/1423 Post Mortem Magnetic Resonance Imaging (MRI) (2005) http://www.forensicmed.co.uk/developments.htm Alderstein M.E., Peringa J., van der Hulst V.P.M, Blaauwgeers H.L.G., van Lith J.M.M. (2003), 'Perinatal mortality: clinical value of post-mortem magnetic
Tumor Invasion and Metastasis Tumor Invasion This is a paper that concentrates on tumor invasion and metastasis. There are five references used for this paper. Cancer is one of the deadliest diseases faced by mankind today. It is important to look at tumor invasion and metastasis to understand how cancer can spread and ways in which the progress of cancer can be arrested. Tumor Invasion A substantial problem in the treatment of carcinoma patients is
Tumor Suppression Protein 53 and Effects on Cellular Function and Aging Tumor Suppression Protein 53 (P53) was originally linked to tumor proliferation and thought to be an oncogene. Research led to an understanding that P53 was in actuality a tumor suppression protein and suppression of the P52 gene is the most widely genetic defect found in tumors (Levine 1991). Further study of p53 and the family of tumor suppression genes led
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