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Parathyroid Hormone-related Protein in Patients with Primary Breast Cancer and Eucalcemia¹

Department of Molecular Medicine, Endocrine and Diabetes Unit [E. B., H. R., Y. P., B. G.] and Neurogenetic Unit [A-C. S. N.], Department of Oncology-Pathology [E. E., E. v. S.], Karolinska Hospital and Institute, S-171 76 Stockholm, Sweden; St. Vincent's Institute of Medical Research, 3065 Melbourne, Australia [W. R.]; Department of Medicine, Division of Endocrinology and Metabolism, Veterans Affairs Medical Center, West Haven, Connecticut 06516 [W. J. B.]; Department of Oncology, University Hospital of Trondheim, N-7006 Trondheim, Norway [U. G. F.]; and University of California, San Diego and the San Diego Veterans Affairs Medical Center, La Jolla, California 92161 [D. W. B., L. J. D.]

Parathyroid hormone-related protein (PTHrP) is a causative factor of humoral hypercalcemia in breast cancer and other malignancies. We studied circulating PTHrP levels with three different immunoassays directed against different parts of the PTHrP molecule in 48 patients with breast cancer and eucalcemia. The methods used were: (a) a RIA with antibodies directed toward the midregion (63–78); (b) an immunofluorometric assay with two antibodies against 1–34 and 38–67; and (c) an immunoradiometric assay with antibodies against 1–40 and 1–72. Although most patients had PTHrP levels indistinguishable from normal when measured by all three methods, four patients had increased serum levels in the IFMA. PTHrP was detected by immunohistochemistry in tumors from nearly all patients. One patient with elevated PTHrP in plasma measured by IFMA showed intense staining of tumor by immunohistochemistry; the tumor was histologically graded as III (severe) and was the largest of all tumors in this patient group. The IFMA can identify increased serum PTHrP in some patients with breast cancer who are not hypercalcemic. This assay may be especially useful in screening patients for this tumor during a relative early phase of the disease.

¹ This study was supported by Grants 3129 EB and 3921 A-C SN from the Swedish Cancer Society, Grant 5992 EB from the Swedish Medical Research Council, the Funds of the Karolinska Institute, and by the NIH and the Department of Veterans Affairs (to L. J. D.).

² To whom requests for reprints should be addressed, at Department of Molecular Medicine, Endocrine and Diabetes Unit, Karolinska Hospital L1:02, S-171 76 Stockholm, Sweden. Fax: 46 8 30 34 58; E-mail: bucht@enk.ks.se.

Received 4/20/98. Accepted 7/17/98.

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