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Mechanism of Gallium-67 Accumulation in Tumors

Research Service, Veterans Administration Medical Center, Departments of Physiology and Medicine, Albany Medical College of Union University, Albany, New York
Divisions of Nuclear Medicine and Radiation Health Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland

Correspondence: For reprints contact: Min-Fu Tsan, MD, Research Service, V.A. Medical Center, Albany, NY 12208.

ABSTRACT

Neoplasms are characterized by increased perfusion, increased permeability of their capillary beds to macromolecules, and a delay in new lymphatic vessel growth. These lead to the increased entry and residency time of macromolecules in the interstitial space of tumors. Multiple factors contribute to the localization of ⁶⁷Ga in tumors. Adequate blood supply is essential; at areas with no blood supply such as the necrotic center of a large tumor, there is no ⁶⁷Ga accumulation. Gallium-67, mainly in the form of transferin-⁶⁷Ga complex, is delivered to the tumor through capillaries with increased permeability. In tumors, some ⁶⁷Ga is taken up by tumor cells; some may also be taken up by inflammatory cells when they are present. Gallium-67 binding proteins, such as lactoferrin or ferritin, may also contribute to the accumulation and retention of ⁶⁷Ga in tumors; however, their roles are less clear. The intensity of these various factors determine their relative contribution and the degree of ⁶⁷Ga accumulation in tumors.

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