Therapy

Advances in Nuclear Oncology:: Diagnosis and Therapy by Emilio Bombardieri, John Buscombe, Giovanni Lucignani, Otmar

By Emilio Bombardieri, John Buscombe, Giovanni Lucignani, Otmar Schober

The diagnostic and healing achievements in radiopharmaceuticals and nuclear drugs instrumentation ? puppy, SPECT, MR, CT and their hypbrids PET-CT and SPECT-CT

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In adults, about two-thirds of brain tumors arise from supratentorial structures, while in children about twothirds of brain tumors are infratentorial. Over one-half of brain neoplasms are metastases from tumors outside the CNS, and involve the skull or any intracranial structure. 1 Their incidence is 5–10 per 100 000 in the general population. Gliomas are divided histologically into astrocytomas, oligodendrogliomas, mixed gliomas, ependymal tumors, and tumors of the choroid plexus. Grading is performed according to World 9781841846149-Ch03 24 8/21/07 4:33 PM Page 24 Advances in Nuclear Oncology Health Organization (WHO) criteria, taking into account the presence of nuclear changes, mitotic activity, endothelial proliferation, and necrosis.

Endothelial cadherins and tumor angiogenesis. Exp Cell Res 2006; 312: 659–67. 18. Baluk P, Hashizume H, McDonald DM. Cellular abnormalities of blood vessels as targets in cancer. Curr Opin Genet Dev 2005; 15: 102–11. 19. Brasch RC, Li KC, Husband JE et al. In vivo monitoring of tumor angiogenesis with MR imaging. Acad Radiol 2000; 7: 812–23. 9781841846149-Ch02 8/21/07 4:05 PM Page 21 Targets 20. Bremer C, Mustafa M, Bogdanov A Jr et al. Steady-state blood volume measurements in experimental tumors with different angiogenic burdens – a study in mice.

FDHT-PET is feasible in patients with advanced prostate cancer with testosterone levels that are in the castrate range. 32,33 There are more than 90 known protein kinase genes in the human genome: 58 encode transmembrane receptor TKs distributed into 20 subfamilies, and 32 encode cytoplasmatic, non-receptor TKs in ten subfamilies. 35 Apoptosis also plays a significant role in cancer response to therapy. Programmed cell death pathways, many of which are p53 dependent, are triggered when tumor cells detect damaged DNA.

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