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PubMed1994

Parathyroid hormone-related protein expression in gynecic squamous carcinoma cells.

BACKGROUND: The regulation of parathyroid hormone-related protein (PTH-rP) mRNA levels and immunoreactive (ir)PTH-rP formation by peptide growth factors, particularly transforming growth factor-beta (TGF-beta) and epidermal growth factor (EGF), in squamous cell carcinomas of gynecologic origin is largely unknown. METHODS: PTH-rP mRNA levels were evaluated by Northern analysis in A431 cells (derived from a human vulvar epidermoid carcinoma) and ME-180 cells (derived from a human papillomavirus-infected squamous cell carcinoma of the cervix). PTH-rP protein levels in cell culture media were evaluated using both radioimmunoassay and immunoradiometric assay techniques. These results were compared with those from a lung carcinoid cell line known to produce PTH-rP, namely, NCI-H727 cells. RESULTS: TGF-beta 1 or EGF treatment caused an increase in the levels of PTH-rP mRNA in A431 cells; these increases in PTH-rP mRNA were detectable after 60 minutes of treatment, were maximal at approximately 4-8 hours, and were approximately additive. Immunoreactive PTH-rP was not detectable (using two different PTH-rP immunoassays) in the culture medium or cell sonicates of A431 cells before or after treatment with TGF-beta 1, EGF, or TGF-beta 1 plus EGF. ME-180 cells responded to EGF (but not to TGF-beta 1) with an increase in the level of PTH-rP mRNA as early as 2 hours; irPTH-rP was present (by use of either immunoassay) in the medium of these cells at 8 and 24 hours. In NCI-H727 (human lung carcinoid) cells, TGF-beta 1 and EGF acted alone and synergistically to effect increases in PTH-rP mRNA and the accumulation of irPTH-rP. CONCLUSIONS: TGF-beta 1 and EGF regulation of PTH-rP gene expression in squamous cell carcinomas of gynecologic origin is unique for each cell line studied and different from that in human lung carcinoid cells.

Base Sequence↗
PubMed2005

Immunohistochemical localization of parathyroid hormone-related protein (PTHrP) and serum PTHrP in normocalcemic patients with oral squamous cell carcinoma.

Cancer cells produce parathyroid hormone-related protein (PTHrP) in the early phase of malignancy development, before hypercalcemia occurs. The relationship between PTHrP and the clinicopathologic features of oral squamous cell carcinoma is poorly understood. We studied 60 patients (43 men, 17 women; mean age, 64.8 +/- 11.2 years) with primary oral squamous cell carcinoma, from whom pretreatment biopsy specimens were obtained. We examined the relationship among immunohistochemical PTHrP expression, serum PTHrP levels, clinical characteristics of the tumor, and histopathologic aspects of the tumor. The mean calcium concentration for the 60 patients was 9.1 +/- 0.4 mg/dl. No patients had laboratory evidence of hypercalcemia before treatment. Six patients had serum levels of C-terminal (C)-PTHrP higher than the normal level of 55.3 pmol/l. There were no significant differences in serum C-PTHrP levels according to TNM stages. Abundant positive immunoreactivity for anti-PTHrP (1-34) antibody was recognized diffusely in the whole cytoplasm of many tumor cells. Anti-PTHrP (38-64) antibody staining tended to localize as small granules in the cytoplasm, especially close to the nuclear periphery. There was no correlation between the serum C-PTHrP concentration and the intensity of either immunostain. The intensity of PTHrP was proportionally related to the degree of differentiation or extent of keratinization (P < 0.05) and the histologic malignancy grade of the tumor (P < 0.05), when using antibody against PTHrP (1-34), but not when using antibody against PTHrP (38-64). Serum C-PTHrP levels did not correlate with the intensity of cellular PTHrP expression and characteristics of the tumor at the initial patient visit. The fragment that includes PTHrP (1-34) may be involved in the differentiation of oral squamous cell carcinoma. The differences between immunoreactivities may have been due to differing tissue malignancies and the use of different antibodies. The results suggest the need for caution when interpreting immunoreactivities of PTHrP in malignancies.

Antibodies, Monoclonal↗
PubMed1995

Parathyroid hormone-related peptide is expressed and rapidly inducible in human liver cell cultures that have a bile duct phenotype.

Parathyroid hormone-related peptide is the major factor responsible for hypercalcemia of malignancy. There is increasing evidence that parathyroid hormone-related peptide also plays an important role in the growth and differentiation of both neoplastic and non-neoplastic cells. Recently we found that reactive human bile ductules and cholangiocarcinomas, but not normal bile ducts, human hepatocytes nor hepatocellular carcinomas, express parathyroid hormone-related peptide and we speculated that parathyroid hormone-related peptide may function as a growth and differentiation factor for bile ductular epithelial cells. Using a specific polyclonal antibody for immunostaining and a digoxigenin-random prime-labeled probe for in situ hybridization assay, we found that only cell lines with a bile duct phenotype expressed parathyroid hormone-related peptide and its mRNA. HepG2 cells with hepatocellular phenotype (CK19-, CK7-, CK8+, CK18+, albumin+) do not express parathyroid hormone-related peptide. However, A16 (HepG2 derived cell line) expressing bile duct marker CK19, also expressed parathyroid hormone-related peptide, while hepatocyte markers CK8, CK18, CALLA and albumin were negative. In addition, the H1 cell line (adult human hepatocytes immortalized in our laboratory by SV40 DNA transfection, passaged at least 40 times and cultured for 13 months) expressed bile duct marker CK7 and parathyroid hormone-related peptide, while hepatocyte markers CK8, CK18, CALLA and albumin were negative. Previous studies demonstrated that parathyroid hormone-related peptide gene expression in keratinocytes can be modulated by serum, growth factors and cycloheximide although there is a species and cellular specificity.(ABSTRACT TRUNCATED AT 250 WORDS)

Bile Ducts↗
PubMed2004

Autopsy case of prostate cancer with multiple endocrine neoplasia 2A.

We describe an autopsy case of a 65-year-old man with prostate cancer accompanied by multiple endocrine neoplasia 2A (MEN 2A), including malignant pheochromocytomas, thyroid medullary carcinomas and parathyroid hyperplasia. Metastatic lesions from the prostate primary were identified using immunohistochemistry for prostate specific antigen within both primary and metastatic pheochromocytomas in the liver. To investigate the affinity of prostate cancer for pheochromocytoma cells, immunohistochemistry was carried out using a number of antibodies and both tumors were positive for N-cadherin. Interestingly, pheochromocytomas, thyroid medullary carcinomas and prostate cancer were all positive for the anti-RET antibody. The immunohistochemical results suggest that the cell affinity may, in part, result from cell-cell adhesion via N-cadherin. Although prostate cancer is rarely associated with MEN, RET activation may have participated in the tumorigenesis of this case.

Aged↗
PubMed1983

[Diagnostic and surgical tactics in primary hyperparathyroidism].

Fifty seven patients with primary hyperparathyroidism are reported to be successfully operated. The pneumomodiastinography and hypotensive esophagoscopy, according to Reimberg--Semzov, were used for preoperation localization of the pathologically changed para thyroid glands. Operation technique applied in adenoma, hyperplasia and carcinoma of parathyroid glands is described. The lethality of the operations performed is 0 per cent. The early and late postoperative results are analyzed as well as the favourable effect on the alterations in the osseous, gastrointestinal and excretory system. The necessity of early diagnosis of the disease is stressed upon as well as the timely performance of the operation.

Adenoma↗
PubMed1987

Parathyroid adenoma in patient with prostatic carcinoma and hypercalcemia.

A sixty-seven-year-old white man with prostatic carcinoma was noted to be hypercalcemic and was subsequently found to have a parathyroid adenoma. Review of the literature revealed only 13 prior cases of hypercalcemia in patients with prostate malignancy. In none of those recorded cases was a parathyroid abnormality found, although a complete evaluation was not made in most of the patients. Because of the infrequent occurrence of hypercalcemia and prostatic carcinoma, it is suggested that patients with both disorders be evaluated for causes of hypercalcemia other than those generally associated with malignancy.

Adenocarcinoma↗
PubMed1996

Ectopic production of intact parathyroid hormone by a squamous cell lung carcinoma in vivo and in vitro.

Ectopic tumoral production of intact parathyroid hormone (PTH) is rare. The PTH-related protein is the common cause of hypercalcemia in most solid tumors, particularly squamous and renal carcinomas. We report the case of a 71-yr-old man with a PTH-producing squamous cell lung carcinoma. Immunocytochemical analysis of the tumor tissue as well as of cultured tumor cells revealed PTH positive staining. Cultured tumor cells released PTH and were calcium sensitive, producing 122 +/- 16 pg/microgram DNA of intact PTH (mean +/- SEM) at 0.5 mmol/L calcium compared with 26 +/- 2 pg/microgram DNA at 3.0 mmol/L calcium. Somatostatin analogues have been used in the treatment of humoral hypercalcemia of malignancy (HHM). However, we found that somatostatin (0.1 microgram/L) in cultured tumor cells increased the release of intact PTH (123 +/- 19 versus 82 +/- 1 pg/microgram DNA, P < 0.05) and thus might have a negative effect on the HHM. This report is the first to describe a true ectopic PTH-producing squamous cell lung carcinoma associated with HHM.

Aged↗
PubMed1996

Molecular genetics of primary and secondary hyperparathyroidism.

Hyperparathyroidism (HPT) can be caused by solitary parathyroid adenomas and carcinomas, and primary and secondary multiglandular parathyroid disease. Primary HPT is also a feature of several hereditary diseases e.g. multiple endocrine neoplasia type 1 and type 2A (MEN1 and 2A), familial hypocalciuric hyperparathyroidism (FHH), the HPT-jaw tumor syndrome (HPT-JT), and familial isolated HPT. Summarizing data from the literature and our own observations, various genetic abnormalities are observed in the pathogenesis of HPT. These include chromosomal deletions of the MEN1 locus on 11q in sporadic and MEN1 associated primary HPT, of RB1 on 13q in carcinomas, and of the FHH gene located on 3q in sporadic primary and secondary HPT. Genetic material is also lost from chromosomes 1p, 6q, 15q and X suggesting loss of yet unidentified tumor suppressor genes in these regions. In addition the HRPT2 gene on 1q, as well as the proto-oncogenes RET on 10q and PRAD1 on 11q are associated with a subset of parathyroid tumors.

Gene Deletion↗
PubMed1977

Successful autotransplantation of the parathyroid glands during total thyroidectomy for carcinoma.

In a consecutive series of 118 total thyroidectomies during a period of 11 years, autotransplantation of one or more parathyroid glands was used in 64 patients. During the first nine years of this series, autotransplantation was used in only 25 per cent of the total thyroidectomies, with a 3 per cent incidence of permanent hypoparathyroidism. During the last two years, autotransplantation of the parathyroid was used in 89 per cent of 54 total thyroidectomies, with a zero incidence of hypoparathyroidism.

Adolescent↗
PubMed1995

Osteoporosis-like changes in Walker carcinoma 256-bearing rats, not accompanied with hypercalcemia or parathyroid hormone-related protein production.

Walker carcinoma 256 (W256) was reported to induce hypercalcemia dependent on bone metastasis and/or parathyroid hormone-related protein (PTHrP) in the rat, providing a model of the humoral hypercalcemia of malignancy. In this study, after the subcutaneous inoculation of cells of the W256/S line, which is maintained in this laboratory, into young female Wistar Imamichi rats (6 weeks old), serum calcium and phosphorus levels changed only within the control range, whereas serum alkaline phosphatase activity and urinary calcium level significantly increased and urinary phosphorus decreased during the tumor growth, resulting in hypercalciuria and hypophosphaturia. W256/S did not express PTHrP-mRNA, whereas LLC-W256 cells did express it. Serum PTHrP level was not changed in W256/S-bearing rats. Osteoporosis-like changes, bone weight loss, low contents of bone calcium and phosphorus, and a decrease in the bone mineral density (BMD), were observed in the femur 14 days after the tumor inoculation. There was a pronounced decrease in the serum 17 beta-estradiol level during the tumor growth. The reduction of BMD of femurs in W256/S-bearing rats was significantly inhibited by treatment with salmon calcitonin or 17 beta-estradiol. On the basis of these results, W256/S carcinoma-bearing rats seem to be a useful model for osteoporosis of hypoovarianism.

Animals↗
PubMed1980

Thyrotropin receptors in normal human thyroid. Nonclassical binding kinetics not explained by the negative cooperativity model.

Saturation analysis of equilibrium binding of iodinated thyrotropin (125I-TSH) to normal human thyroid preparations yielded linear Scatchard plots under non-physiological conditions of pH 6.0 or 20 mM Tris/acetate buffer, pH 7.4. The apparent equilibrium dissociation constant of this binding was approximately 10(-8) M. By contrast, nonlinear plots were obtained under standard conditions of pH 7.4 and 40 mM Tris/acetate buffer. Resolution of the components of these curves by computer analysis revealed the presence of at least two classes of binding sites, one of which is of a low capacity and high affinity (approximately 10(-10) M) consistent with receptor binding. The other component is of a high capacity and lower affinity. Binding to non-target tissues of muscle, parathyroid, mammary carcinoma, and placenta was only demonstrable at pH 6.0 or in 20 mM Tris/acetate buffer, pH 7.4, yielding linear Scatchard plots with similar binding affinity (approximately 10(-8)M) to normal thyroid but much reduced capacity. Preincubation of thyroid tissue at 50 degrees C resulted in an apparent selective loss of the high affinity component of binding measured under standard conditions. Kinetic experiments on the dissociation of bound 125I-TSH were undertaken to determine whether the non-linearity of Scatchard plots was due to two or more classes of binding sites or negative cooperativity. It was found that the experimental determinant that is presently ascribed to a negative cooperativity phenomenon regulating receptor affinity (i.e. an enhanced dilution-induced dissociation rate in the presence of excess native hormone), although apparently hormone-specific, was demonstrated under nonphysiological binding conditions and in non-target tissue. Significantly, the phenomenon was found under conditions of pH 6.0 or 20 mM Tris where a linear Scatchard plot was obtained. The evidence thus suggests that 125I-TSH binds to heterogeneous binding sites (of which the high affinity is probably the receptor for TSH) and that the enhanced dilution-induced dissociation of bound hormone by native hormone for this system, is only a characteristic of the low affinity binding site (maybe gangliosides).

Breast Neoplasms↗
PubMed1995

Undifferentiated carcinoma in the cardioesophageal junction which produces parathyroid hormone related protein.

A 68-year-old man with undifferentiated carcinoma occurring in the cardioesophageal junction accompanied by hypercalcemia is reported. The serum level of parathyroid hormone-related protein (PTHrP) was remarkably elevated. Serum calcium and PTHrP levels decreased following chemotherapy, but this amelioration was temporary. He died of hypercalcemia. On autopsy, a significant amount of immunoreactive PTHrP was detected in the tumor tissue extract, and the tumor cells were stained strongly positive for PTHrP by immunohistochemistry. This is the first case of undifferentiated carcinoma in the gastrointestinal tract which demonstrated hypercalcemia due to PTHrP produced by the malignant tumor.

Aged↗
PubMed1985

Recurrent hyperparathyroidism due to implantation of parathyroid tissue.

Recurrence of hyperparathyroidism after initially successful primary operation is usually caused by inadequate resection of diseased tissue or recurrent carcinoma. Since it is known that normal parathyroid tissue may be autotransplanted into a muscle bed, it is plausible that inadvertent implantation of parathyroid tissue spilled at operation may occur. In four of 23 reoperations for hyperparathyroidism in an 11 year period, we found evidence that iatrogenic parathyroid implantation had occurred. Two of the four patients had multiple parathyroid implants in the previous operative field, and one of these patients had documented spillage of a cystic adenoma during the original operation. Another two of the four patients were found to have recurrent adenomas containing suture material at sites of previous excision of the adenomas. No patient had gross or histologic evidence of parathyroid carcinoma. We conclude that inadvertently spilled parathyroid tissue may implant in the neck or mediastinum and cause persistent or recurrent hypercalcemia. Therefore, all efforts should be made to handle the parathyroid glands only by their pedicles and not to crush, suture, or violate the capsule. Needle aspiration of parathyroid cysts could lead to implantation along the needle tract.

Adenoma↗
PubMed2005

Parathyroid hormone-related protein and serum calcium in patients with renal cell carcinoma.

OBJECTIVE: To evaluate serum parathyroid hormone-related protein (PTHrP) in relation to serum calcium and clinical outcome of patients with renal cell carcinoma. METHODS: Sera from 243 patients with renal cell carcinoma were collected prior to therapy. Serum PTHrP was analyzed using an immunoradiometric assay. Tumour stage, nuclear grade, corrected serum calcium, and survival were assessed. RESULTS: Serum PTHrP was detectable in 37/243 sera (15%) and hypercalcaemia (> or =2.60 mmol/l) in 32/220 (15%). A positive correlation between serum PTHrP and serum calcium was found (r = 0.326; p < 0.01). Following subdivision of the material, based on storage time, the frequency of detectable serum PTHrP seemed to decrease with time. Serum calcium, but not serum PTHrP, was correlated to tumour stage (p < 0.001). Survival was similar for patients with detectable and undetectable PTHrP, but those with hypercalcaemia had a significantly shorter survival time compared to those with normal serum calcium (p < 0.001). A multivariate analysis showed that tumour stage and serum calcium were independent prognostic factors, but not grade or PTHrP. CONCLUSIONS: A positive relation of serum PTHrP to serum calcium was demonstrated in patients with renal cell carcinoma. Hypercalcaemia but not serum PTHrP predicted a worse prognosis.

Adult↗
PubMed1998

Coexpression of parathyroid hormone-related protein and its receptor in breast carcinoma: a potential autocrine effector system.

Parathyroid hormone-related protein (PTHrP), the pathogenic factor in most cases of humoral hypercalcemia of malignancy, is also expressed by many normal tissues. Its diverse biologic activities in these tissues are mediated by the PTH/PTHrP receptor through autocrine and paracrine mechanisms. Recent data suggest that PTHrP and its receptor might also influence the growth and metastatic spread of some cancers through similar local actions. Accordingly, immunohistochemical studies using murine monoclonal antibodies to detect coexpression of PTHrP and the PTH/PTHrP receptor were performed on 52 invasive breast carcinomas to assess the existence of this potential autocrine effector system. All of the 52 invasive breast carcinomas expressed reactivity for PTHrP, and 50 (96%) of these tumors also expressed reactivity for the receptor. Although additional investigations are necessary for evaluation of the role of PTHrP and PTH/PTHrP receptor in tumor pathogenesis, our current study demonstrates the presence of this potential autocrine effector system in the great majority of invasive breast carcinomas.

Adult↗
PubMed2005

Ghrelin localization in rat and human thyroid and parathyroid glands and tumours.

Ghrelin, the endogenous ligand of the growth hormone secretagogue receptor (GHS-R), is a 28 amino acid peptide originally isolated from rat stomach that has been primarily involved in the central neuroregulation of GH secretion and food intake. Previous studies demonstrated that ghrelin has a widespread expression in different normal cells and tissues, as well as in gastric, thyroid, testicular, breast and lung neoplasias. In the current study, we use molecular biology to detect ghrelin transcripts expression in rats, and immunohistochemical techniques to investigate the cellular distribution of this peptide in rat and human thyroid and parathyroid glands and tumours. Ghrelin was localized in thyroid C cells and in parathyroid cells. Thyroid carcinomas (medullar, follicular and papillary) and parathyroid adenomas also showed intense and diffuse immunostaining for ghrelin. These data provide direct morphological evidence that ghrelin may well be acting in a paracrine fashion in the regulation of thyroid follicular cell function. The diffuse ghrelin immunostaining found in the parathyroid gland opens up the possibility of its secretion to the bloodstream or its involvement in the regulation of the parathyroid function. Overall, expression of ghrelin in human and rat thyroid and parathyroid glands is highly suggestive of a conserved role of this molecule in the regulation of thyroid and parathyroid cell function.

Animals↗