Metastatic disease to the parathyroid gland is poorly documented. When performing surgery for primary thyroid cancer, the search for parathyroid gland metastases is often overlooked because of the desire to preserve parathyroid function. Metastatic disease from other cancers to a benign parathyroid gland or to a parathyroid adenoma probably suggests a grave prognosis because it likely indicates widespread metastatic disease; however, isolated metastases to the parathyroid may occur. Although these lesions may be uncommon they may not be as rare as once thought.

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This study investigates the role of tumor nitric oxide (NO) and vascular regulation in tumor ulceration following high-dose tumor necrosis factor-a (TNF) treatment. Using TNF-responsive (MethA) and nonresponsive (LL2) mouse tumors, tumor NO concentration was measured with an electrochemical sensor and tumor blood flow by Doppler ultrasound. Mice were also pretreated with a selective inducible nitric oxide synthase (iNOS) inhibitor, 1400 W. Tumors harvested from TNF-treated mice were cryosectioned and immunostained for murine macrophages, or/and iNOS. MethA tumor-bearing mice were depleted of macrophages. Pre-and post-TNF tumor NO levels were measured continuously, and mice were followed for gross tumor response. In MethA tumors, TNF caused a 96% response rate, and tumor NO concentration doubled. Tumor blood flow decreased to 3% of baseline by 4 hr and was sustained at 24 hr and 10 days post-TNF. Selective NO inhibition with 1400 W blocked NO rise and decreased response rate to 38%. MethA tumors showed tumor infiltration by macrophages post-TNF and the pattern of macrophage immunostaining overlapped with iNOS immunostaining. Depletion of macrophages inhibited tumor NO increase and response to TNF. LL2 tumors had a 0% response rate to TNF and exhibited no change in NO concentration. Blood flow decreased to 2% of baseline by 4 hr, recovered to 56% by 24 hr and increased to 232% by 10 days. LL2 tumors showed no infiltration by macrophages post-TNF. We conclude that TNF causes tumor infiltrating, macrophage-derived iNOS-mediated tumor NO rise and sustained tumor blood flow shutdown, resulting in tumor ulceration in the responsive tumor. ' 2008 Wiley-Liss, Inc.Key words: high-dose TNF; nitric oxide; blood flow; macrophage; tumor The therapeutic potential of targeting the tumor vascular supply is now widely recognized and has led to improvement in survival in patients with advanced cancer. 1-3 Continued investigation into novel strategies of antivascular therapies and further study of the mechanisms of current antivascular therapies will help to advance this field.Regional perfusion with high-dose recombinant human tumor necrosis factor-a (TNF) is an effective antivascular therapy in clinical practice. It achieves an overall response rate of 90-100% and complete response rate of 80-90% when combined with melphalan for extremity melanoma, making this treatment one of the most effective single-administration therapies for solid malignancies. 4-6 TNF in combination with melphalan has demonstrated synergistic antitumor activity in the treatment of melanomas and soft tissue sarcomas that are recurrent, deep-seated or bulky. One of the advantages of this therapeutic is that it is selective to tumor tissue and spares surrounding normal tissue. 7 Despite the tumoricidal potential of TNF, severe toxicity such as hypotension, abnormalities in liver function, leukopenia and thrombus formation has made TNF difficult to be used systemically as an antitumor drug. This problem has been circumvented by using isolated limb perfusion (I...

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