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1. Eurelings M, Frijns CJ, Jeurissen FJ: Painful ophthalmoplegia from metastatic nonproducing parathyroid carcinoma: case study and review of the literature. Neuro Oncol; 2002 01;4(1):44-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Painful ophthalmoplegia from metastatic nonproducing parathyroid carcinoma: case study and review of the literature.
  • Parathyroid carcinoma is an uncommon malignancy.
  • Of the fewer than 400 cases reported, most have been cases of producing parathyroid carcinoma with accompanying hypercalcemia.
  • Only 13 patients with nonproducing parathyroid carcinoma have been described.
  • Nine of these 13 patients had metastatic disease.
  • Distal metastases of producing parathyroid carcinoma are treated surgically to prolong survival and prevent complications of hyperparathyroidism and hypercalcemia.
  • One half of the patients with producing parathyroid carcinoma die within 5 years, mostly because of the complications of hypercalcemia.
  • Nonproducing parathyroid carcinoma compares unfavorably with producing parathyroid carcinoma in terms of tumor progression and prognosis.
  • Few data on choice of therapy in nonproducing parathyroid carcinoma are available.
  • We treated our patient with a combination of radiotherapy and chemotherapy.
  • Treatment was followed by an unexpectedly prolonged survival of 31 months after diagnosis of metastatic disease.
  • [MeSH-major] Brain Neoplasms / complications. Carcinoma / complications. Carcinoma / secondary. Ophthalmoplegia / etiology. Ophthalmoplegia / physiopathology. Parathyroid Neoplasms / pathology
  • [MeSH-minor] Combined Modality Therapy. Fatal Outcome. Female. Humans. Middle Aged. Pain / physiopathology. Treatment Outcome

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  • (PMID = 11772432.001).
  • [ISSN] 1522-8517
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 27
  • [Other-IDs] NLM/ PMC1920631
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2. Sharretts JM, Kebebew E, Simonds WF: Parathyroid cancer. Semin Oncol; 2010 Dec;37(6):580-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Parathyroid cancer.
  • Parathyroid cancer is an uncommon malignancy and rare cause of primary hyperparathyroidism (HPT) with a high morbidity and patient death in advanced cases usually resulting from intractable hypercalcemia.
  • Inactivation of the HRPT2/CDC73 gene, encoding the putative tumor-suppressor protein parafibromin and discovered in the context of the hyperparathyroidism-jaw tumor (HPT-JT) syndrome, is a common, somatic event in most parathyroid cancers.
  • Approximately 25% of patients with apparently sporadic parathyroid cancer carry germline HRPT2/CDC73 mutation.
  • Germline DNA analysis for HRPT2/CDC73 mutation is recommended in all patients with parathyroid cancer because of the potential benefit for first-degree relatives, who should nevertheless undergo serum calcium screening.
  • The histopathologic diagnosis of parathyroid cancer is nonspecific unless vascular, lymphatic, capsular, or soft tissue invasion is seen, or metastases are clinically evident.
  • Immunohistochemical analysis of parathyroid tumors for loss of parafibromin expression offers promise as a diagnostic tool.
  • En bloc tumor resection offers the highest chance of cure in patients with suspected parathyroid carcinoma.
  • No adjuvant chemotherapy regimen has yet proven effective, and the role of local adjuvant radiotherapy is being evaluated.
  • Metastatic disease can be palliated with surgical debulking.
  • Medical therapy with the calcimimetic cinacalcet and bisphosphonates can ameliorate hypercalcemia in patients with inoperable disease.
  • [MeSH-major] Parathyroid Neoplasms / pathology. Parathyroid Neoplasms / therapy

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  • [Copyright] Published by Elsevier Inc.
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  • (PMID = 21167377.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 DK043012-06; United States / Intramural NIH HHS / / Z01 DK043320-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDC73 protein, human; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ NIHMS245489; NLM/ PMC3059245
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3. Montenegro FL, Chammas MC, Juliano AG, Cernea CR, Cordeiro AC: Ethanol injection under ultrasound guidance to palliate unresectable parathyroid carcinoma. Arq Bras Endocrinol Metabol; 2008 Jun;52(4):707-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ethanol injection under ultrasound guidance to palliate unresectable parathyroid carcinoma.
  • BACKGROUND: Severe hypercalcemia is the leading cause of death in patients with parathyroid carcinoma.
  • Non-curative resection and pharmacological measures may be useful for palliation in cases with recurrent and metastatic disease.
  • Palliative treatment with intra-neoplastic ethanol injection has not been reported yet.
  • METHODS: Ultrasound-guided percutaneous alcohol injection in one patient with unresectable parathyroid carcinoma is reported.
  • RESULTS: One male patient with extensive recurrent parathyroid carcinoma suffering from severe hypercalcemia, refractory to all available medical measures has undergone two percutaneous ethanol injections.
  • CONCLUSION: Ultrasound-guided percutaneous ethanol injection may be employed to palliate parathyroid carcinoma in selected cases, with a transitory decrease in PTH and calcium levels.
  • [MeSH-major] Ethanol / administration & dosage. Hypercalcemia / drug therapy. Palliative Care / methods. Parathyroid Neoplasms / drug therapy

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  • (PMID = 18604386.001).
  • [ISSN] 1677-9487
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 3K9958V90M / Ethanol
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4. Käkönen SM, Mundy GR: Mechanisms of osteolytic bone metastases in breast carcinoma. Cancer; 2003 Feb 1;97(3 Suppl):834-9
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  • [Title] Mechanisms of osteolytic bone metastases in breast carcinoma.
  • Osteolytic and osteoblastic metastases are often the cause of considerable morbidity in patients with advanced prostate and breast carcinoma.
  • Breast carcinoma metastasis to bone occurs because bone provides a favorable site for aggressive behavior of metastatic cancer cells.
  • A vicious cycle arises between cancer cells and the bone microenvironment, which is mediated by the production of growth factors such as transforming growth factor beta and insulin growth factor from bone and parathyroid hormone-related protein (PTHrP) produced by tumor cells.
  • Other pharmacologic approaches to inhibit PTHrP produced by breast carcinoma cells in the bone microenvironment also produce similar beneficial effects.
  • Identification of the molecular mechanisms responsible for osteolytic metastases is crucial in designing effective therapy for this devastating complication.
  • [MeSH-minor] Bone and Bones / metabolism. Bone and Bones / physiopathology. Female. Humans. Parathyroid Hormone-Related Protein. Peptide Hormones / metabolism

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  • [Copyright] Copyright 2003 American Cancer Society.DOI 10.1002/cncr.11132
  • (PMID = 12548583.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40035
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Peptide Hormones; 0 / Transforming Growth Factor beta
  • [Number-of-references] 51
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5. Goldner B, Milosević Z, Sadiković S, Stojanović M: [Clinical and radiological manifestations of paraneoplastic syndrome of bronchogenic carcinoma]. Srp Arh Celok Lek; 2005 May-Jun;133(5-6):248-53
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  • [Title] [Clinical and radiological manifestations of paraneoplastic syndrome of bronchogenic carcinoma].
  • The objective of this study was to present some clinical and radiological manifestations of PNS in relation to bronchogenic carcinoma (BC) and to evaluate the usefulness of imaging findings in the diagnosis of asymptomatic BC.
  • In the study group of 204 patients (146 male and 58 female) with proven bronchogenic carcinoma, PNS was present in 18 (8.62%) patients.
  • The predominant disorder was Lambert-Eaton Syndrome, associated with small-cell carcinoma.
  • Endocrine manifestations included: inappropriate antidiuretic hormone production syndrome (small-cell carcinoma), a gonadotropin effect with gynaecomastia and testicular atrophy (planocellular carcinoma, small-cell carcinoma), a case of Cushing Syndrome (small-cell carcinoma), and hypercalcaemia, due to the production of the parathyroid hormone-related peptide, which was associated with planocellular carcinoma.
  • The differences between the two groups were related to the time of PNS appearance.
  • Alternatively, the disappearance of a clinical or a radiological manifestation of PNS after surgery or chemotherapy may be an indicator of an improvement in health or PNS may be the first sign of illness recurrence.
  • In symptomatic patients, it may be an indicator of a higher likelihood of metastatic disease.
  • [MeSH-major] Carcinoma, Bronchogenic / complications. Lung Neoplasms / complications. Paraneoplastic Syndromes / diagnosis

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  • (PMID = 16392281.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia and Montenegro
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6. Kanno K, Hikichi T, Saito K, Watanabe K, Takagi T, Shibukawa G, Wakatsuki T, Imamura H, Takahashi Y, Sato A, Sato M, Irisawa A, Obara K, Ohira H: A case of esophageal small cell carcinoma associated with hypercalcemia causing severe acute pancreatitis. Fukushima J Med Sci; 2007 Jun;53(1):51-60
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  • [Title] A case of esophageal small cell carcinoma associated with hypercalcemia causing severe acute pancreatitis.
  • A 60-year-old woman was diagnosed with esophageal small cell carcinoma in October 2004 and received chemotherapy.
  • Anorexia, nausea, emesis, numbness in both hands, and disturbed consciousness developed at the end of January 2006, and the patient was admitted to Fukushima Medical University Hospital.
  • Because the level of blood parathyroid hormone-related protein was elevated, we considered that esophageal small cell carcinoma caused human hypercalcemia of malignancy and that metastatic bone tumors caused local osteolytic hypercalcemia, eventually leading to severe acute pancreatitis.
  • This is an extremely rare case of esophageal small cell carcinoma associated with hypercalcemia causing severe acute pancreatitis.
  • [MeSH-major] Carcinoma, Small Cell / complications. Esophageal Neoplasms / complications. Hypercalcemia / complications. Pancreatitis / etiology

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  • (PMID = 17957966.001).
  • [ISSN] 0016-2590
  • [Journal-full-title] Fukushima journal of medical science
  • [ISO-abbreviation] Fukushima J Med Sci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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7. Bergkamp FJ, van Berkel AM, van der Linden PW, Gorgels JP: Unexpected prolonged extreme hypocalcaemia and an inadequate PTH response in a patient with metastatic breast carcinoma. Neth J Med; 2003 Nov;61(11):371-5
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  • [Title] Unexpected prolonged extreme hypocalcaemia and an inadequate PTH response in a patient with metastatic breast carcinoma.
  • We describe a 37-year-old patient with metastatic carcinoma of the breast, who developed extreme hypocalcaemia (as low as 0.75 mmol calcium per litre) after chemotherapy.
  • This is caused by a combination of hungry-bone syndrome and an insufficient parathyroid response.
  • The latter may be the result of a direct toxic effect of chemotherapy on parathyroid hormone (PTH) synthesis possibly in combination with microscopic tumour infiltration in the parathyroid glands.
  • [MeSH-major] Bone Neoplasms / secondary. Breast Neoplasms / pathology. Hypocalcemia / etiology. Parathyroid Hormone / blood

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  • (PMID = 14768721.001).
  • [ISSN] 0300-2977
  • [Journal-full-title] The Netherlands journal of medicine
  • [ISO-abbreviation] Neth J Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Parathyroid Hormone
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8. Sillero Sánchez A, Atienza Iglesias MA: [Diagnostic-therapeutic management of parathyroid carcinoma]. An Med Interna; 2002 Dec;19(12):644-8
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  • [Title] [Diagnostic-therapeutic management of parathyroid carcinoma].
  • [Transliterated title] Manejo diagnóstico-terapéutico del carcinoma de paratiroides.
  • Parathyroid carcinoma is an uncommon endocrine malignancy, with difficult diagnosis.
  • There are several presenting clinical and biochemical features that suggest it: much higher serum calcium and PTH levels than parathyroid adenomas, symptoms of severe hypercalcemia, the classical target organs affected and a palpable neck mass.
  • Initial surgical therapy (en bloc dissection) is the only chance for cure it.
  • The management of recurrent and/or metastatic parathyroid carcinoma is also surgical, resulting in significant palliation from hypercalcemia, whereas radiation therapy and chemotherapy are not helpful.
  • Bisphosphonates (drugs that inhibit bone resorption) control acute and chronic hypercalcemia when surgery is not effective or possible.
  • Preoperative localization studies (cervical ultrasound, CT scan, MRI and sestamibi scan) are useful in patients with recurrent or persistent parathyroid cancer.
  • [MeSH-major] Parathyroid Neoplasms / diagnosis. Parathyroid Neoplasms / therapy
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / therapy. Antineoplastic Agents / therapeutic use. Calcium / blood. Humans. Hypercalcemia / diagnosis. Hyperparathyroidism / diagnosis. Parathyroid Hormone / blood. Parathyroidectomy

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  • (PMID = 12593036.001).
  • [ISSN] 0212-7199
  • [Journal-full-title] Anales de medicina interna (Madrid, Spain : 1984)
  • [ISO-abbreviation] An Med Interna
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Parathyroid Hormone; SY7Q814VUP / Calcium
  • [Number-of-references] 62
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9. Szmuilowicz ED, Utiger RD: A case of parathyroid carcinoma with hypercalcemia responsive to cinacalcet therapy. Nat Clin Pract Endocrinol Metab; 2006 May;2(5):291-6; quiz 297
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  • [Title] A case of parathyroid carcinoma with hypercalcemia responsive to cinacalcet therapy.
  • His serum calcium concentration was 4.2 mmol/l and his serum parathyroid hormone concentration was 36 pmol/l.
  • He was referred to our hospital on day 35 for treatment of refractory hypercalcemia.
  • INVESTIGATIONS: Sestamibi parathyroid scan, chest and abdominal CT scans, neck ultrasonography, liver biopsy, fine-needle aspiration of neck mass, and measurement of parathyroid hormone in an aspirate of the neck mass.
  • DIAGNOSIS: Primary hyperparathyroidism caused by metastatic parathyroid carcinoma.
  • MANAGEMENT: Intravenous fluids, intravenous doses of pamidronate and zoledronic acid and oral cinacalcet therapy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Hypercalcemia / drug therapy. Naphthalenes / therapeutic use. Parathyroid Neoplasms / complications. Parathyroid Neoplasms / drug therapy
  • [MeSH-minor] Alcohol Drinking / adverse effects. Biopsy, Fine-Needle. Calcitriol / blood. Calcium / blood. Cinacalcet Hydrochloride. Humans. Hyperparathyroidism, Primary / diagnosis. Hyperparathyroidism, Primary / etiology. Liver Neoplasms / diagnosis. Liver Neoplasms / etiology. Liver Neoplasms / pathology. Male. Middle Aged. Neck / ultrasonography. Neoplasm Metastasis / diagnosis. Neoplasm Metastasis / pathology. Parathyroid Hormone / blood

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  • (PMID = 16932300.001).
  • [ISSN] 1745-8366
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Naphthalenes; 0 / Parathyroid Hormone; 1K860WSG25 / Cinacalcet Hydrochloride; FXC9231JVH / Calcitriol; SY7Q814VUP / Calcium
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10. Yoshida S: Intracranial metastatic parathyroid carcinoma: case report. Surg Neurol; 2006 Jan;65(1):81-3
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  • [Title] Intracranial metastatic parathyroid carcinoma: case report.
  • BACKGROUND: Although parathyroid carcinoma is not frequent, it is a slowly progressive disease characterized by frequent recurrences.
  • A review of the literature revealed only 2 other cases of intracranial metastatic parathyroid carcinoma.
  • We present here the case of cerebral metastases from parathyroid carcinoma that could be treated successfully.
  • She had undergone a parathyroidectomy for parathyroid carcinoma 18 years earlier.
  • Lung metastasis was also detected 6 years earlier, and she has been dialyzed twice a month after chemotherapy.
  • CONCLUSIONS: This case report supports aggressive surgical management to eliminate all parathyroid hormone-secreting malignant tissue and prevent metabolic complications.
  • [MeSH-major] Brain Neoplasms / secondary. Brain Neoplasms / surgery. Parathyroid Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Lung Neoplasms / radiography. Lung Neoplasms / secondary. Middle Aged. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 16378868.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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11. Sekkach Y, Baizri H, Mounach J, Qacif H, El Omri N, Chahdi H, Rkiouak F, Belmejdoub G, Ghafir D, Ohayon V, Algayres JP: [An historical case of malignant hyperparathyroidism with unusual metastatic sites]. Ann Endocrinol (Paris); 2009 Mar;70(1):64-70

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  • [Title] [An historical case of malignant hyperparathyroidism with unusual metastatic sites].
  • We report a historical case of hyperparathyroidism in a young patient hospitalized for an array of osteolytic foci and incomplete fracture associated with a swollen neck, revealing a very special form of a metastatic parathyroid carcinoma with unusual multiple locations and exceptional medullary flooding.
  • Carcinoma of the parathyroid gland produces a malignant hypersecreting tumor particularly difficult to diagnose.
  • Treatment of this rare tumor is primarily surgical.
  • Intraoperatively, the size of the tumor and its local extension to surrounding tissue are highly suggestive.
  • Chemotherapy alone or in combination with radiation has not demonstrated its effectiveness.
  • [MeSH-major] Hyperparathyroidism / pathology. Parathyroid Neoplasms / pathology
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Humans. Radiopharmaceuticals. Technetium Tc 99m Sestamibi. Treatment Outcome

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  • (PMID = 18922512.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 971Z4W1S09 / Technetium Tc 99m Sestamibi
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12. Kalajian AH, Malhotra PS, Callen JP, Parker LP: Calciphylaxis with normal renal and parathyroid function: not as rare as previously believed. Arch Dermatol; 2009 Apr;145(4):451-8
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  • [Title] Calciphylaxis with normal renal and parathyroid function: not as rare as previously believed.
  • BACKGROUND: Calciphylaxis is a life-threatening form of metastatic calcification-induced microvascular occlusion syndrome.
  • Although traditionally observed in patients with end-stage renal disease and/or hyperparathyroidism, the development of calciphylaxis in "nontraditional" patients having both normal renal and parathyroid function has been reported.
  • OBSERVATIONS: A 58-year-old woman with endometrial carcinoma developed extensive calciphylaxis despite the presence of normal renal and parathyroid function.
  • The disease resolved with rapid diagnosis, supportive therapy, and medical management.
  • Analysis of this case and the 13 previously reported cases of nontraditional calciphylaxis identified the following patient characteristics that highlight clinical situations potentially predisposing to calciphylaxis: hypoalbuminemia, malignant neoplasm, systemic corticosteroid use, anticoagulation with warfarin sodium or phenprocoumon, chemotherapy, systemic inflammation, hepatic cirrhosis, protein C or S deficiency, obesity, rapid weight loss, and infection.
  • CONCLUSIONS: Calciphylaxis is becoming increasingly common in patients with normal renal and parathyroid function.
  • The observations from this study may assist dermatologists in the rapid diagnosis and prompt initiation of therapy for this devastating disease.
  • [MeSH-minor] Diagnosis, Differential. Endometrial Neoplasms / complications. Female. Humans. Middle Aged. Parathyroid Diseases / complications. Renal Insufficiency / complications. Risk Factors

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  • (PMID = 19380668.001).
  • [ISSN] 1538-3652
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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13. Kinugasa Y, Morishige K, Kamiura S, Tsukamoto Y, Saji F: Parathyroid hormone-related protein-secreting uterine endometrioid adenocarcinoma. Jpn J Clin Oncol; 2006 Feb;36(2):113-5
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  • [Title] Parathyroid hormone-related protein-secreting uterine endometrioid adenocarcinoma.
  • The diagnosis of parathyroid hormone-related protein (PTHrP)-secreting metastatic uterine endometrioid cancer was made in a 32-year-old Japanese woman with humoral hypercalcemia of malignancy.
  • The primary endometrial cancer had been removed, and the tumor was diagnosed as Grade 1 endometrioid adenocarcinoma with shallow myometrial invasion.
  • Salvage chemotherapy (paclitaxel and calboplatin) was started from 5 months after surgery when recurrent tumors were detected in the peritoneum and liver.
  • Despite the salvage chemotherapy, the tumor progressed and hypercalcemia became evident with elevated PTHrP whereas no bone metastasis was identified.
  • [MeSH-major] Carcinoma, Endometrioid / chemistry. Carcinoma, Endometrioid / pathology. Endometrial Neoplasms / chemistry. Endometrial Neoplasms / pathology. Hypercalcemia / etiology. Parathyroid Hormone-Related Protein / analysis

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  • (PMID = 16418186.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Parathyroid Hormone-Related Protein
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14. Ivanyi P, Winkler T, Grosshennig A, Reuter C, Merseburger AS, Ganser A, Grünwald V: Treatment with tyrosine kinase inhibitors in patients with metastatic renal cell carcinoma is associated with drug-induced hyperparathyroidism: a single center experience in 59 patients. World J Urol; 2010 Jun;28(3):311-7
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  • [Title] Treatment with tyrosine kinase inhibitors in patients with metastatic renal cell carcinoma is associated with drug-induced hyperparathyroidism: a single center experience in 59 patients.
  • PURPOSE: Multi-targeted tyrosine kinase inhibitors (MTKIs) are the standard in the treatment of metastatic renal cell carcinoma (mRCC).
  • Demographics, chemistry, parathyroid and renal function, bone metastasis and clinics were assessed, retrospectively.
  • Parathyroid hormone (PTH), calcium and phosphate were either determined prior to, during or after cessation of MTKI therapy.
  • RESULTS: From evaluable patients, 90% (N = 53) received at least one MTKI treatment, 10% (N = 8) had evaluations without MTKI exposure.
  • The mean PTH value prior to MTKI treatment was 49.4 (range (r):2.5-115), increased during the therapy to 121.2 (r:5-302) (P = 0.003) and returned to its basic values after MTKI cessation.
  • In parallel, mean phosphate significantly decreased during the treatment from 1.10 (r = 0.66-1.59) to 0.87 (r = 0.48-1.45) (P < 0.001) and calcium showed a slight decrease (P = 0.039).
  • Univariate logistic regression analysis of pathologically elevated PTH levels revealed an association with MTKI treatment duration.
  • CONCLUSION: Even though the mechanism of bone mineral alteration remains elusive, the MTKI treatment is associated with a dysregulated parathyroid axis, which may have clinical implications in a number of patients.
  • Furthermore, prospective trials are mandatory, and PTH monitoring should be considered in selected patients during MTKI treatment.
  • [MeSH-major] Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / secondary. Hyperparathyroidism / chemically induced. Kidney Neoplasms / drug therapy. Kidney Neoplasms / pathology. Protein Kinase Inhibitors / adverse effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Analysis of Variance. Bone Density / drug effects. Calcium / metabolism. Cohort Studies. Confidence Intervals. Drug Delivery Systems. Female. Follow-Up Studies. Humans. Incidence. Kidney Function Tests. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Odds Ratio. Parathyroid Hormone / metabolism. Probability. Prognosis. Protein-Tyrosine Kinases / antagonists & inhibitors. Registries. Retrospective Studies. Risk Assessment. Survival Analysis

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  • (PMID = 20443009.001).
  • [ISSN] 1433-8726
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Parathyroid Hormone; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; SY7Q814VUP / Calcium
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15. Clemens P, Gregor M, Lamberts R: Pancreatic neuroendocrine tumor with extensive vascularisation and parathyroid hormone-related protein (PTHrP)--associated hypercalcemia of malignancy. Exp Clin Endocrinol Diabetes; 2001;109(7):378-85
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  • [Title] Pancreatic neuroendocrine tumor with extensive vascularisation and parathyroid hormone-related protein (PTHrP)--associated hypercalcemia of malignancy.
  • We report the case of a 34 year old male presenting with symptomatic hypercalcemia due to excessive PTHrP secretion from a pancreatic neuroendocrine carcinoma with extensive hypervascularization and without any evidence for metastatic disease.
  • In the early phase of the disease conventional chemotherapy with streptozocin and doxorubicin was able to control functional activity as well as tumor growth.
  • However, after 2 years tumor escape was indicated by severe therapy-resistant hypercalcemia.
  • Therapeutic options were reduced due to the excessive tumor vascularization and the patient died from his disease after a short period of intensified therapy.
  • The role of PTHrP in hypercalcemia of malignancy (HHM) and its association with neuroendocrine pancreatic tumors as well as possible therapeutic options are reviewed.
  • [MeSH-major] Carcinoma, Neuroendocrine / secretion. Hypercalcemia / etiology. Neovascularization, Pathologic / physiopathology. Pancreatic Neoplasms / secretion. Proteins / secretion
  • [MeSH-minor] Adult. Fatal Outcome. Humans. Male. Parathyroid Hormone-Related Protein

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  • (PMID = 11573150.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Proteins
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16. Luh JY, Han ES, Simmons JR, Whitehead RP: Poorly differentiated colon carcinoma with neuroendocrine features presenting with hypercalcemia and cutaneous metastases: case report and review of the literature. Am J Clin Oncol; 2002 Apr;25(2):160-3
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  • [Title] Poorly differentiated colon carcinoma with neuroendocrine features presenting with hypercalcemia and cutaneous metastases: case report and review of the literature.
  • Humoral hypercalcemia is rarely associated with colon carcinoma; cutaneous metastases from colon carcinoma are also infrequent.
  • To the authors' knowledge, no cases of colon carcinoma presenting with both hypercalcemia and cutaneous metastases have been reported to date.
  • A case of advanced poorly differentiated colon carcinoma with neuroendocrine features with both humoral hypercalcemia of malignancy (HHM) and cutaneous metastases is presented.
  • A poorly differentiated colon carcinoma with neuroendocrine features occurred in a 42-year-old patient with metastases to the liver, both femurs, left orbit, and scalp.
  • The hypercalcemia was caused by the expression of a parathyroid hormone related peptide by both the primary and cutaneous metastatic tumors.
  • Bisphosphonate treatment helped normalize serum calcium in a few days, but hypercalcemia recurred approximately 3 weeks later.
  • Chemotherapy only mildly reduced the size of the cutaneous metastases.
  • Hypercalcemia and cutaneous metastases are separately associated with a poor prognosis and indicate advanced and widely metastatic disease.
  • Although still unclear, the mechanism by which colon cancer causes cutaneous metastases and hypercalcemia, in light of current theories presented in the literature, is discussed.
  • [MeSH-major] Carcinoma / secondary. Colonic Neoplasms / pathology. Hypercalcemia / etiology. Skin Neoplasms / secondary
  • [MeSH-minor] Adult. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Fatal Outcome. Humans. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Male. Neoplasm Proteins / metabolism. Parathyroid Hormone-Related Protein. Proteins / metabolism

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  • (PMID = 11943894.001).
  • [ISSN] 0277-3732
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Proteins
  • [Number-of-references] 24
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17. Talon I, Lindner V, Sourbier C, Schordan E, Rothhut S, Barthelmebs M, Lang H, Helwig JJ, Massfelder T: Antitumor effect of parathyroid hormone-related protein neutralizing antibody in human renal cell carcinoma in vitro and in vivo. Carcinogenesis; 2006 Jan;27(1):73-83
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  • [Title] Antitumor effect of parathyroid hormone-related protein neutralizing antibody in human renal cell carcinoma in vitro and in vivo.
  • We showed recently that VHL-deficient RCCs expressed large amounts of parathyroid hormone-related protein (PTHrP), and that PTHrP, acting through the PTH1 receptor (PTH1R), plays an essential role in tumor growth.
  • Our goal was to determine whether blocking the PTHrP/PTH1R system might be of therapeutic value against RCC, independent of VHL status and PTHrP expression levels.
  • In vivo, the treatment of nude mice bearing the Caki-1 RCC tumor with the PTHrP antibody inhibited tumor growth by 80%, by inducing apoptosis.
  • Anti-PTHrP treatment induced no side effects as assessed by animal weight and blood chemistries.
  • Current therapeutic strategies are only marginally effective against metastatic RCC, and adverse effects are common.
  • This study provides a rationale for evaluating the blockade of PTHrP signaling as therapy for human RCC in a clinical setting.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Carcinoma, Renal Cell / therapy. Gene Expression Regulation, Neoplastic / drug effects. Parathyroid Hormone-Related Protein / immunology
  • [MeSH-minor] Animals. Apoptosis. Cell Proliferation. Humans. In Vitro Techniques. Kidney Neoplasms / immunology. Kidney Neoplasms / metabolism. Kidney Neoplasms / therapy. Male. Mice. Mice, Nude. Neovascularization, Pathologic

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  • (PMID = 16081513.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Parathyroid Hormone-Related Protein
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18. Ghobrial MW, George J, Mannam S, Henien SR: Severe hypercalcemia as an initial presenting manifestation of hepatocellular carcinoma. Can J Gastroenterol; 2002 Sep;16(9):607-9
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  • [Title] Severe hypercalcemia as an initial presenting manifestation of hepatocellular carcinoma.
  • The patient was given a diagnosis of severe hypercalcemia and was subsequently found to have clinical, roentgenographic and pathological evidence of hepatocellular carcinoma.
  • Further studies revealed a low parathyroid hormone level, excluding the possibility of primary hyperparathyroidism, and a negative bone survey, precluding metastatic bone disease.
  • The patient's hypercalcemia was believed to emanate from the humoral secretion of a parathyroid hormone-related peptide, which was found to be elevated, and was abated with conservative management while her cancer was being treated with chemotherapy.
  • [MeSH-major] Carcinoma, Hepatocellular / complications. Hypercalcemia / etiology. Liver Neoplasms / complications
  • [MeSH-minor] Aged. Calcium / blood. Female. Humans. Parathyroid Hormone / blood. Parathyroid Hormone-Related Protein. Peptide Hormones / blood

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  • (PMID = 12362213.001).
  • [ISSN] 0835-7900
  • [Journal-full-title] Canadian journal of gastroenterology = Journal canadien de gastroenterologie
  • [ISO-abbreviation] Can. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / PTHLH protein, human; 0 / Parathyroid Hormone; 0 / Parathyroid Hormone-Related Protein; 0 / Peptide Hormones; SY7Q814VUP / Calcium
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19. Correale P, Micheli L, Vecchio MT, Sabatino M, Petrioli R, Pozzessere D, Marsili S, Giorgi G, Lozzi L, Neri P, Francini G: A parathyroid-hormone-related-protein (PTH-rP)-specific cytotoxic T cell response induced by in vitro stimulation of tumour-infiltrating lymphocytes derived from prostate cancer metastases, with epitope peptide-loaded autologous dendritic cells and low-dose IL-2. Br J Cancer; 2001 Nov 30;85(11):1722-30
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  • [Title] A parathyroid-hormone-related-protein (PTH-rP)-specific cytotoxic T cell response induced by in vitro stimulation of tumour-infiltrating lymphocytes derived from prostate cancer metastases, with epitope peptide-loaded autologous dendritic cells and low-dose IL-2.
  • Bone metastases are one of the most common events in patients with prostate carcinoma.
  • PTH-rP, a protein produced by prostate carcinoma and other epithelial cancers, is a key agent for the development of bone metastases.
  • In this model, we investigated the in vitro possibility of generating an efficient PTH-rP specific CTL response by cyclical stimulations with IL-2 and PTR-4 peptide-pulsed autologous dendritic cells (DC), of HLA-A2.1(+) tumour infiltrating lymphocytes (TIL) derived from a patient with metastatic prostate carcinoma.
  • A T cell line generated in this way (called TM-PTR-4) had a CD3(+), CD5(+), CD4(-), CD8(+), CD45(Ro+), CD56(-) immunophenotype and a HLA-A2.1 restricted cytotoxic activity to PTR-4-peptide pulsed CIR-A2 (HLA-A2.1(+)) target cells, PTH-rP(+)/HLA-A2.1(+) CIR-A2 transfected with PTH-rP gene, prostate carcinoma LNCaP cells, and autologous metastatic prostate cancer cells (M-CaP).
  • These lymphocytes were not cytotoxic to HLA-A2.1(+) targets not producing PTH-rP, such as peptide-unpulsed CIR-A2 and colon carcinoma SW-1463, cell lines.
  • In conclusion PTR-4 peptide-pulsed autologous DC may be a promising approach for vaccine-therapy and antigen-specific CTL adoptive immunotherapy of hormone-resistant prostrate cancer.
  • [MeSH-major] Dendritic Cells / immunology. Interleukin-2 / pharmacology. Lymphocytes, Tumor-Infiltrating / immunology. Prostatic Neoplasms / therapy. Proteins / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bone Neoplasms / immunology. Bone Neoplasms / secondary. Cytotoxicity Tests, Immunologic. Cytotoxicity, Immunologic / drug effects. Cytotoxicity, Immunologic / immunology. Epitopes / immunology. Flow Cytometry. HLA-A2 Antigen / immunology. Humans. Immunophenotyping. Male. Neoplasm Metastasis. Oligopeptides / immunology. Parathyroid Hormone-Related Protein. Tumor Cells, Cultured

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  • [Copyright] (c) 2001 Cancer Research Campaign
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  • (PMID = 11742494.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Epitopes; 0 / HLA-A2 Antigen; 0 / Interleukin-2; 0 / Oligopeptides; 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Proteins
  • [Other-IDs] NLM/ PMC2363980
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20. Björklund P, Svedlund J, Olsson AK, Akerström G, Westin G: The internally truncated LRP5 receptor presents a therapeutic target in breast cancer. PLoS One; 2009;4(1):e4243
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The internally truncated LRP5 receptor presents a therapeutic target in breast cancer.
  • BACKGROUND: Breast cancer is a common malignant disease, which may be caused by a number of genes deregulated by genomic or epigenomic events.
  • An aberrantly spliced internally truncated LRP5 receptor (LRP5Delta666-809, LRP5Delta) was shown recently to be resistant to DKK1 inhibition, and was required for beta-catenin accumulation in hyperparathyroid tumors and parathyroid tumor growth.
  • METHODOLOGY/PRINCIPAL FINDINGS: Here we show, by reverse transcription PCR and Western blot analysis, that LRP5Delta is frequently expressed in breast tumors of different cancer stage (58-100%), including carcinoma in situ and metastatic carcinoma.
  • LRP5Delta was required in MCF7 breast cancer cells for the non-phosphorylated active beta-catenin level, transcription activity of beta-catenin, cell growth in vitro, and breast tumor growth in a xenograft SCID mouse model.
  • Furthermore, an anti-LRP5 antibody attenuated beta-catenin activity, inhibited cell growth, and induced apoptosis in LRP5Delta-positive MCF7 and T-47D breast cancer cells, but not in control cells.
  • CONCLUSIONS/SIGNIFICANCE: Our results suggest that the LRP5Delta receptor is strongly implicated in mammary gland tumorigenesis and that its aberrant expression present an early event during disease progression.
  • LRP5 antibody therapy may have a significant role in the treatment of breast cancer.
  • [MeSH-major] Breast Neoplasms / metabolism. Breast Neoplasms / therapy. Gene Expression Regulation, Neoplastic. LDL-Receptor Related Proteins / physiology
  • [MeSH-minor] Animals. Carcinoma / metabolism. Cell Line, Tumor. Female. Humans. Low Density Lipoprotein Receptor-Related Protein-5. Mice. Mice, SCID. Neoplasm Transplantation. Receptors, LDL / metabolism. Wnt Proteins / metabolism. Wnt3 Protein. Wnt3A Protein. beta Catenin / metabolism

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  • (PMID = 19158955.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LDL-Receptor Related Proteins; 0 / LRP5 protein, human; 0 / Low Density Lipoprotein Receptor-Related Protein-5; 0 / Lrp4 protein, mouse; 0 / Lrp5 protein, mouse; 0 / Receptors, LDL; 0 / WNT3 protein, human; 0 / WNT3A protein, human; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / Wnt3 protein, mouse; 0 / Wnt3A Protein; 0 / Wnt3a protein, mouse; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC2627768
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21. McMahan J, Linneman T: A case of resistant hypercalcemia of malignancy with a proposed treatment algorithm. Ann Pharmacother; 2009 Sep;43(9):1532-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of resistant hypercalcemia of malignancy with a proposed treatment algorithm.
  • OBJECTIVE: To report and describe a case of refractory hypercalcemia of malignancy (HCM) associated with metastatic, transitional-cell carcinoma of the left ureter.
  • Computed tomography scan and liver biopsy revealed recurrent transitional-cell carcinoma with extensive liver metastasis.
  • Four mechanisms of HCM have been recognized thus far, with ectopic tumor production of parathyroid hormone-related protein (PTHrP) being the leading cause.
  • Treatment of HCM revolves around 2 principles: treatment of the underlying malignancy along with reduction of the serum calcium level.
  • Evidence-based therapies for management include: intravenous crystalloid fluids with or without loop diuretics, bisphosphonates, calcitonin, gallium nitrate, and corticosteroids.
  • Therapies used for this patient included aggressive hydration, calcitonin, and 3 distinct treatment courses of intravenous bisphosphonates with varying success.
  • These therapies remain viable options based on individual patient factors.
  • To our knowledge, no published guidelines or algorithms exist for choosing between additional modalities in the treatment of refractory HCM.
  • CONCLUSIONS: For patients with HCM who do not achieve a response from bisphosphonates, or for those who need repeated dosing more often than expected, changing to a different drug class could be an alternative.
  • The specific mechanism of hypercalcemia should be considered when developing a treatment regimen for patients who have had a suboptimal response to initial therapy with bisphosphonates.
  • Multiple treatment modalities exist for the treatment of hypercalcemia, each with a different mechanism of action.
  • As with the treatment of other disease states, we can use this knowledge to more specifically target the mechanism of the patient's disease.
  • [MeSH-major] Carcinoma, Transitional Cell / complications. Hypercalcemia / drug therapy. Ureteral Neoplasms / complications
  • [MeSH-minor] Aged. Algorithms. Bone Density Conservation Agents / therapeutic use. Calcitonin / therapeutic use. Diphosphonates / therapeutic use. Humans. Imidazoles / therapeutic use. Isotonic Solutions / therapeutic use. Male. Neoplasm Metastasis

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  • (PMID = 19622757.001).
  • [ISSN] 1542-6270
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 0 / Isotonic Solutions; 0 / crystalloid solutions; 6XC1PAD3KF / zoledronic acid; 9007-12-9 / Calcitonin; OYY3447OMC / pamidronate
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22. Nakagawa K, Sasaki Y, Kato S, Kubodera N, Okano T: 22-Oxa-1alpha,25-dihydroxyvitamin D3 inhibits metastasis and angiogenesis in lung cancer. Carcinogenesis; 2005 Jun;26(6):1044-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 22-Oxa-1alpha,25-dihydroxyvitamin D3 inhibits metastasis and angiogenesis in lung cancer.
  • 1alpha,25-Dihydroxyvitamin D(3) (1alpha,25-D(3)) has potent antiproliferative and anti-invasive properties in vitro in cancer cells.
  • However, its calcemic effect in vivo limits its therapeutic applications.
  • Here, we report the efficacy of 22-oxa-1alpha,25-dihydroxyvitamin D(3) (22-oxa-1alpha,25-D(3)), a low calcemic analog of vitamin D, against the development of metastatic lung carcinoma after an intravenous injection of green fluorescent protein-transfected Lewis lung carcinoma (LLC-GFP) cells in C57BL/6 mice.
  • The 1alpha,25-D(3) treatment group had been hypercalcemic, but the 22-oxa-1alpha,25-D(3) and vehicle treatment groups remained normocalcemic for the duration of the experiment.
  • In the in vitro experiment, 1alpha,25-D(3) and 22-oxa-1alpha,25-D(3) reduced the expression of matrix metalloproteinase (MMP)-2, MMP-9, vascular endothelial growth factor and parathyroid hormone-related protein in LLC-GFP cells.
  • Moreover, using a new experimental model of vitamin D receptor (VDR) null mutant (VDR(-/-)) mice with corrected hypocalcemia and hypervitaminosis D, we examine the anti-cancer effect of 22-oxa-1alpha,25-D(3) without other functions induced by 22-oxa-1alpha,25-D(3) in the host.
  • In the VDR(-/-) mice, 22-oxa-1alpha,25-D(3) directly inhibited the metastatic activity of LLC-GFP cells in a dose-dependent manner without exerting a direct influence on the calcemic activity or other actions regulated by 22-oxa-1alpha,25-D(3) in the host.
  • These results indicate that the inhibition of metastasis and angiogenesis-inducing activity in cancer cells seemed to be a major mechanism responsible for the anti-cancer effects of 22-oxa-1alpha,25-D(3).
  • Our findings show that 22-oxa-1alpha,25-D(3) is beneficial for the prevention of metastasis in lung carcinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Calcitriol / analogs & derivatives. Calcitriol / therapeutic use. Carcinoma, Lewis Lung / drug therapy. Lung Neoplasms / drug therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / adverse effects. Angiogenesis Inhibitors / therapeutic use. Animals. Calcium / blood. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 9 / biosynthesis. Matrix Metalloproteinase 9 / genetics. Mice. Mice, Inbred C57BL. Mice, Knockout. Parathyroid Hormone-Related Protein / metabolism. RNA, Messenger / biosynthesis. Receptors, Calcitriol / genetics. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 15718253.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Parathyroid Hormone-Related Protein; 0 / RNA, Messenger; 0 / Receptors, Calcitriol; 0 / Vascular Endothelial Growth Factor A; 103909-75-7 / maxacalcitol; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; FXC9231JVH / Calcitriol; SY7Q814VUP / Calcium
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23. Mundy GR, Yoneda T, Hiraga T: Preclinical studies with zoledronic acid and other bisphosphonates: impact on the bone microenvironment. Semin Oncol; 2001 Apr;28(2 Suppl 6):35-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The propensity for breast cancer cells to metastasize to bone and to induce osteolysis has long been recognized.
  • Breast cancer cells and other tumor types influence osteoclastic bone resorption by increasing the number of osteoclasts and enhancing their resorptive activity.
  • Parathyroid hormone-related peptide, in addition to its role in humorally mediated hypercalcemia, is secreted by metastatic breast cancer cells in bone in which it acts as a paracrine factor to stimulate osteoclasts.
  • Transforming growth factor (TGF)-beta, one of the most abundant of the bone-derived factors, promotes increased production of parathyroid hormone-related peptide by tumor cells, establishing a "vicious cycle" leading to progressive tumor growth and bone destruction.
  • In several animal models of breast cancer metastasis to bone, bisphosphonates decrease the number of new bone metastases and inhibit progression of existing lesions.
  • Tumor volume in bone was decreased by zoledronic acid in a dose-dependent manner in the same model, and tumor cell apoptosis was increased by zoledronic acid in bone metastases in the 4T1 murine model of mammary carcinoma metastasis.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Bone and Bones / drug effects. Diphosphonates / pharmacology. Imidazoles / pharmacology
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Mammary Neoplasms, Experimental. Mice. Models, Animal. Neoplasm Metastasis / pathology. Rats

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  • (PMID = 11346863.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  • [Number-of-references] 75
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24. Gallwitz WE, Guise TA, Mundy GR: Guanosine nucleotides inhibit different syndromes of PTHrP excess caused by human cancers in vivo. J Clin Invest; 2002 Nov;110(10):1559-72
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  • There are two well-described syndromes caused by tumor production of parathyroid hormone-related peptide (PTHrP), namely osteolytic bone disease associated with breast cancer and humoral hypercalcemia of malignancy (HHM) that occurs with or without bone metastasis.
  • We show in nude athymic murine models that these compounds reduce PTHrP-mediated osteolytic lesions associated with metastatic human breast-cancer cells as well as the degree of hypercalcemia caused by excessive PTHrP production by a squamous-cell carcinoma of the lung.

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  • (PMID = 12438453.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA040035; United States / NCI NIH HHS / CA / P01CA40035
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Guanine Nucleotides; 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Peptide Hormones; 0 / Thionucleosides; 12133JR80S / Guanosine; C558LI0K8P / 6-thioguanosine; FTK8U1GZNX / Thioguanine
  • [Other-IDs] NLM/ PMC151806
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25. Zhang H, Yano S, Miki T, Goto H, Kanematsu T, Muguruma H, Uehara H, Sone S: A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice. Clin Exp Metastasis; 2003;20(2):153-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel bisphosphonate minodronate (YM529) specifically inhibits osteolytic bone metastasis produced by human small-cell lung cancer cells in NK-cell depleted SCID mice.
  • In the present study, we examined the effects of a newly developed bisphosphonate, minodronate (YM529), on osteolytic bone metastasis caused by lung cancer.
  • Human small-cell lung cancer (SBC-5) cells, injected intravenously into natural killer cell-depleted SCID mice, produced radiologically detectable bone metastasis by day 18 and macroscopically visible visceral metastases (lung, liver, kidney, systemic lymph node) by day 35.
  • Prophylactic treatment with YM529 on day 1 significantly inhibited the formation of osteolytic bone metastasis evaluated on X-ray photographs in a dose-dependent manner.
  • In addition, treatment with YM529 after establishment of bone metastasis (on day 21) also inhibited bone metastasis, although the treatment was more effective when started earlier.
  • Single administration was as effective as repeated treatment, suggesting a sustained inhibitory effect of YM529 on bone metastasis.
  • YM529 reduced the number of osteoclasts in the bone metastatic lesions in vivo, but had no effect on the proliferation or cytokine production of SBC-5 cells in vitro.
  • These results suggest that YM529 is a potent inhibitor of bone metastasis of human lung cancer, probably by suppressing osteoclastic bone resorption.
  • In contrast, treatment with YM529 had no effect on visceral metastasis, even if started on day 1, and did not prolong the survival of the mice.
  • Therefore, development of a combined modality is necessary for prolonging the survival of small-cell lung cancer patients with multiple-organ metastasis.
  • [MeSH-major] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma, Small Cell / drug therapy. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Killer Cells, Natural / physiology. Lung Neoplasms / drug therapy. Lymphocyte Depletion
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Bone Resorption / drug therapy. Cell Division / drug effects. Cytokines / metabolism. Disease Models, Animal. Dose-Response Relationship, Drug. Endothelial Growth Factors / metabolism. Humans. Immunoenzyme Techniques. Intercellular Signaling Peptides and Proteins / metabolism. Kidney Neoplasms / drug therapy. Kidney Neoplasms / secondary. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Lymphatic Metastasis / prevention & control. Lymphokines / metabolism. Male. Mice. Mice, SCID. Osteolysis. Parathyroid Hormone-Related Protein. Peptide Hormones / metabolism. Severe Combined Immunodeficiency / immunology. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 12705636.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Diphosphonates; 0 / Endothelial Growth Factors; 0 / Imidazoles; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Peptide Hormones; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 127657-42-5 / YM 529
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26. Berruti A, Tucci M, Terrone C, Scarpa RM, Angeli A, Dogliotti L: Re: A randomized, placebo-controlled trial of zoledronic acid in patients with hormone-refractory metastatic prostate carcinoma. J Natl Cancer Inst; 2003 Feb 19;95(4):332-3; author reply 333-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Re: A randomized, placebo-controlled trial of zoledronic acid in patients with hormone-refractory metastatic prostate carcinoma.
  • [MeSH-major] Alkaline Phosphatase / metabolism. Androgens / metabolism. Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / metabolism. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Parathyroid Hormone / blood. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism

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  • [CommentOn] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]
  • (PMID = 12591993.001).
  • [ISSN] 0027-8874
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comment; Letter; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Diphosphonates; 0 / Imidazoles; 0 / Parathyroid Hormone; 6XC1PAD3KF / zoledronic acid; EC 3.1.3.1 / Alkaline Phosphatase
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