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Download e-book for kindle: Diagnostic and Therapeutic Nuclear Medicine for by Karel Pacak, David Taïeb

By Karel Pacak, David Taïeb

ISBN-10: 3319460366

ISBN-13: 9783319460369

ISBN-10: 3319460382

ISBN-13: 9783319460383

Based at the so much novel methods and state of the art medical and medical information about radionuclide imaging and treatments for neuroendocrine tumors, this medical guidebook represents a special collaborative attempt among endocrinologists, nuclear physicians, oncologists, surgeons, physicists, radio-pharmacists and geneticists. It starts off with the embryology, category and molecular genetics of gastroenteropancreatic neuroendocrine tumors and carcinoids, chromaffin telephone tumors, and MEN1- and MEN2-related tumors. Following a bankruptcy on radiopharmaceuticals in neuroendocrine imaging, it turns to the physics and know-how of present and state of the art radiology, together with SPECT/CT and PET/CT and PET/MR. Discussing of radionuclide imaging covers the tumors pointed out above, in addition to pulmonary and thymic neuroendocrine tumors and medullary thyroid carcinoma. A presentation of radionuclide treatments follows, together with 131I-MIBG treatment, somatostatin receptor-based treatment, and alpha radionuclide remedy, in addition to the function of nanoparticles.
Comprehensive and up to date, Diagnostic and healing Nuclear medication for Neuroendocrine Tumors will help and consultant physicians who come across sufferers with those stipulations, both from a diagnostic or healing point of view, and especially emphasizes the present and rising clinical units and imaging and healing options.

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Additional info for Diagnostic and Therapeutic Nuclear Medicine for Neuroendocrine Tumors

Sample text

Although molecular technology is now available to detect most mutations in NF1 [57], it is typically not required because in 95 % of cases a diagnosis of NF1 can be made by age 11 years on the basis of clinical findings alone. NF1 has one of the highest rates of spontaneous mutation of any gene in the human genome. This in part explains why between 30 and 50 % of patients have de novo mutations, which if they occur post-­zygotically, can give rise to mosaic phenotypes [58]. Events of germline mosaicism are very rare in this condition [59].

Mutations in this gene are usually associated with the presence at diagnosis of a single retroperitoneal tumor [100]. In fact, only 25–40 % of all carriers will ever develop a tumor [101, 102]. This explains why most patients have no family history of disease at the time of their diagnosis. This fact, along with the frequent appearance of a single tumor in affected individuals, makes it very difficult to identify potentially hereditary cases. Although the underlying cause of reduced penetrance is unknown, possible genetic explanations include inhibition of cell proliferation due to secondary loss of vital genetic material in the proximity of the remaining normal allele or that additional loss of chromosome 11 is required (Hensen model) [63].

It is recommended that screening for PCC begins between ages 5 and 16 for carriers of highest-, high-, and moderate-risk mutations [24, 27]. 2 VHL VHL (OMIM 193300), with an incidence of 1 in 36,000 live births, is a dominantly inherited familial cancer syndrome caused by germline mutations in the VHL tumor suppressor gene [28, 29]. This gene encodes three gene products: a protein comprising 213 amino acids and two shorter isoforms, one produced by alternative splicing (excluding exon 2) and the other by alternative initiation.

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Diagnostic and Therapeutic Nuclear Medicine for Neuroendocrine Tumors by Karel Pacak, David Taïeb


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