Several (6), which involved scoring the formation of lung metastases after i.v. injection of melanoma cells into immunodeficient mice (7). These studies showed that human melanoma cell lines expressing high levels of TF, which can initiate coagulation in murine as well as in human plasma, were strongly metastatic and that the metastatic potential of the cell lines could be inhibited by treatment with an anti-TF monoclonal antibody that blocks its procoagulant activity. The conclusion drawn from those results was that one or more products of the coagulation cascade mediate the metastatic effect of TF. In this report we have used a different approach to study the role of TF in promoting metastasis. Four matched sets of cloned human melanoma cell lines expressing either normal or mutant TF molecules were generated by retroviral-mediated transfections, and the metastatic potential of the transfected cells was tested in the SCID mouse model of melanoma metastasis (6 8205The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

This report describes two patients with mucinous syringometaplasia whose findings expand the microscopic and clinical spectrum of the entity. The first patient had an eroded nodule that exhibited multiple epidermal invaginations that penetrated deeply into the dermis. In addition to mucinous metaplasia, there was also exuberant papillary epithelial hyperplasia. Expanded eccrine ducts with similar changes appeared as lobules isolated in the dermis but were shown to connect with the invaginations. In the second patient, a clinical "cyst" drained serous fluid. Multiple papillary-cystic epithelial lobules similar to those seen in the first case were located in the dermis. A few approached the epidermis, but epidermal connections were not identified. The epithelium in these lesions was identical to that previously described in mucinous syringometaplasia. The tumors differed from prior cases by virtue of the number of eccrine apparatus involved, the extent and depth of involvement, and the presence of prominent papillary epithelial hyperplasia.

Hypersensitivity reactions (HSR) to oxaliplatin in patients with colorectal cancer include facial flushing, erythema, pruritis, fever, tachycardia, dyspnea, tongue swelling, rash/hives, headache, chills, weakness, vomiting, burning sensations, dizziness, and edema. We report a patient with fever as the sole manifestation of initial HSR, review the literature and discuss the management of HSR. A 57-year-old female with T3N2M0 rectal adenocarcinoma received modified FOLFOX-6. She tolerated the first 8 cycles without any toxicities except grade 1 peripheral neuropathy and nausea. During 9 th and 10 th infusions, she developed fever to a maximum of 38.3℃ with stable hemodynamic status despite medications. During 11 th infusion, she developed grade 3 HSR consisting of symptomatic bronchospasm, hypotension, nausea, vomiting, cough, and fever. On examination, she was pale, cyanotic, with a temperature of 38.8℃, BP dropped to 95/43 mm Hg, pulse of 116/min and O2 saturation of 88%-91%. She was hospitalized for management and recovered in 24 h. Fever alone is not a usual symptom of oxaliplatin HSR. It may be indicative that the patient may develop serious reactions subsequently, as did our patient who developed hypotension with the third challenge. Treatment and prevention consists of slowing the infusion rate, use of steroids and antagonists of Type 1 and 2 histamine receptor antagonists, whereas desensitization could help to provide the small number of patients who experience severe HSR with the ability to further receive an effective therapy for their colorectal cancer.

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Early achievement of maximum analgesia improved hospitalization outcomes and warrant further investigation in prospective studies of individualized pain plans.