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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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  • [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.
  • We report a patient with i.c. metastasis.
  • 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

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  • [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
  • [MeSH-minor] Biomarkers, Tumor. Disease Progression. Humans. Hypercalcemia / etiology. Mutation. Parathyroidectomy. Prognosis. Tumor Suppressor Proteins / analysis. Tumor Suppressor Proteins / genetics

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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. 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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  • A 60-year-old woman was diagnosed with esophageal small cell carcinoma in October 2004 and received chemotherapy.
  • However, the tumor grew gradually and multiple bone metastases occurred.
  • 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.

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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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4. Muff R, Nigg N, Gruber P, Walters D, Born W, Fuchs B: Altered morphology, nuclear stability and adhesion of highly metastatic derivatives of osteoblast-like SAOS-2 osteosarcoma cells. Anticancer Res; 2007 Nov-Dec;27(6B):3973-9
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  • [Title] Altered morphology, nuclear stability and adhesion of highly metastatic derivatives of osteoblast-like SAOS-2 osteosarcoma cells.
  • BACKGROUND: Metastasis is the leading cause of death in patients with osteosarcoma (OS).
  • High alkaline phosphatase (ALP) activity and resistance to chemotherapy are independent predictors of poor clinical outcome of osteosarcoma.
  • Here, the osteoblastic phenotype, cell and nuclear morphology, cell adhesion and drug resistance of the SAOS-2 cell line and two in vivo selected highly metastatic derivatives, LM5 and LM7, were compared.
  • RESULTS: ALP activity and deposition of mineralized extracellular matrix were the same in the parental SAOS-2 and the LM5 and LM7 cells, but parathyroid hormone (PTH)-stimulated cAMP accumulation was lost in the LM7 cells.
  • CONCLUSION: The increased metastatic potential of LM5 and LM7 as compared to SAOS-2 cells is not associated with a substantial change of the osteoblastic phenotype or of the cytotoxic response to current chemotherapeutic drugs.
  • The decrease in cell size and altered cell adhesion, reflecting cytoskeletal rearrangement, together with increased nuclear instability and partial dedifferentiation, as revealed by the loss of PTH responsiveness in LM7 cells, may account for the higher metastatic potential of the LM5 and LM7 sublines as compared to the parental SAOS-2 cells.
  • [MeSH-minor] Alkaline Phosphatase / metabolism. Cell Adhesion / physiology. Cell Line, Tumor. Cell Nucleus / pathology. Cisplatin / pharmacology. Cyclic AMP / biosynthesis. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Etoposide / pharmacology. Humans. Neoplasm Invasiveness. Osteoblasts / pathology

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  • (PMID = 18225558.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; E0399OZS9N / Cyclic AMP; EC 3.1.3.1 / Alkaline Phosphatase; Q20Q21Q62J / Cisplatin
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5. O'Donoghue LE, Ptitsyn AA, Kamstock DA, Siebert J, Thomas RS, Duval DL: Expression profiling in canine osteosarcoma: identification of biomarkers and pathways associated with outcome. BMC Cancer; 2010;10:506
SciCrunch. OMIA - Online Mendelian Inheritance in Animals: Data: Gene Expression .

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  • The standard treatment for OSA in both species is amputation or limb-sparing surgery, followed by chemotherapy.
  • Unfortunately, OSA is an aggressive cancer with a high metastatic rate.
  • Characterization of OSA with regard to its metastatic potential and chemotherapeutic resistance will improve both prognostic capabilities and treatment modalities.
  • METHODS: We analyzed archived primary OSA tissue from dogs treated with limb amputation followed by doxorubicin or platinum-based drug chemotherapy.
  • Pathway analysis revealed alterations in pathways associated with oxidative phosphorylation, hedgehog and parathyroid hormone signaling, cAMP/Protein Kinase A (PKA) signaling, immune responses, cytoskeletal remodeling and focal adhesion.
  • CONCLUSIONS: This profiling study has identified potential new biomarkers to predict patient outcome in OSA and new pathways that may be targeted for therapeutic intervention.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Bone Neoplasms / metabolism. Bone Neoplasms / veterinary. Osteosarcoma / metabolism. Osteosarcoma / veterinary
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Biomarkers / metabolism. Cyclic AMP / metabolism. Disease Models, Animal. Disease-Free Survival. Dogs. Female. Male. Neoplasm Metastasis. Oligonucleotide Array Sequence Analysis. Phosphorylation. Prognosis. Signal Transduction. Treatment Outcome

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  • (PMID = 20860831.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers; 0 / Biomarkers, Tumor; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ PMC2955038
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6. Saito H, Tsunenari T, Onuma E, Sato K, Ogata E, Yamada-Okabe H: Humanized monoclonal antibody against parathyroid hormone-related protein suppresses osteolytic bone metastasis of human breast cancer cells derived from MDA-MB-231. Anticancer Res; 2005 Nov-Dec;25(6B):3817-23
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  • [Title] Humanized monoclonal antibody against parathyroid hormone-related protein suppresses osteolytic bone metastasis of human breast cancer cells derived from MDA-MB-231.
  • BACKGROUND: Parathyroid hormone-related protein (PTHrP) has been implicated in bone metastasis.
  • However, the effects on bone metastasis of blocking the PTHrP function have not been tested in the clinic.
  • Here, the effects of a humanized anti-PTHrP monoclonal antibody (mAb) on bone metastasis in a human xenograft model are shown.
  • MATERIALS AND METHODS: Subline MDA-5a, with high bone metastatic activity, was established from the human breast cancer cell line MDA-MB-231.
  • Mice were injected with MDA-5a and an anti-PTHrP monoclonal antibody (mAb) raised against human PTHrP (1-34); bone metastasis was evaluated by X-ray photography.
  • Administration of the humanized anti-PTHrP mAb significantly suppressed osteolytic bone metastasis of MDA-5a and caused osteogenesis at the sites of metastasis.
  • CONCLUSION: The humanized anti-PTHrP mAb was effective against bone metastasis by inducing osteogenesis and, therefore, will provide a new treatment option for bone metastasis in breast cancer.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Bone Neoplasms / prevention & control. Breast Neoplasms / drug therapy. Parathyroid Hormone-Related Protein / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Gene Expression Profiling. Humans. Interleukins / biosynthesis. Interleukins / genetics. Matrix Metalloproteinase 1 / biosynthesis. Matrix Metalloproteinase 1 / genetics. Mice. Mice, Inbred BALB C. Mice, Nude. Oligonucleotide Array Sequence Analysis. Xenograft Model Antitumor Assays


7. 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.
  • 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).
  • 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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8. 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-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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9. 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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10. 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.
  • The diagnosis is strengthened in the presence of associated Schantz and Castelman criteria.
  • In some cases, very aggressive complementary postoperative radiotherapy is likely to improve locoregional control of the tumor.
  • 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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11. Generali D, Berruti A, Tampellini M, Dovio A, Tedoldi S, Bonardi S, Tucci M, Allevi G, Aguggini S, Milani M, Bottini A, Dogliotti L, Angeli A: The circadian rhythm of biochemical markers of bone resorption is normally synchronized in breast cancer patients with bone lytic metastases independently of tumor load. Bone; 2007 Jan;40(1):182-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The circadian rhythm of biochemical markers of bone resorption is normally synchronized in breast cancer patients with bone lytic metastases independently of tumor load.
  • METHODS: Twenty post-menopausal women with breast cancer (BC) at first disease relapse and at least one bone metastasis were consecutively recruited.
  • Patients were free from concomitant chemotherapy/endocrine therapy.
  • Serum osteocalcin (OC), total and bone-alkaline phosphatase (tALP and bALP, respectively) and C-terminal telopeptide of type I collagen (CTX), and urinary NTX and free deoxypyridinoline (fDPD) were measured together with serum parathyroid hormone (PTH) and serum and urinary calcium and phosphorus.
  • The rhythmicities in cancer patients were normally synchronized, and rhythmic parameters were independent of tumor load in the skeleton, age and menopausal status.
  • CONCLUSIONS: This is the first study to yield information on the maintenance of the temporal program of bone turnover in bone metastatic cancer patients.
  • [MeSH-major] Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Bone Resorption / metabolism. Breast Neoplasms / pathology. Circadian Rhythm
  • [MeSH-minor] Adult. Aged. Biomarkers / analysis. Biomarkers / metabolism. Female. Humans. Middle Aged. Tumor Burden


12. Endo I, Inoue D: [Treatment of malignancy-associated hypercalcemia]. Clin Calcium; 2006 Apr;16(4):665-69
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  • [Title] [Treatment of malignancy-associated hypercalcemia].
  • Malignancy-associated hypercalcemia (MAH) is caused by tumor over-production of parathyroid hormone-related protein (PTHrP), or by locally enhanced bone resorption in metastatic lesions of solid cancers.
  • Medical treatment of MAH includes hydration by saline infusion, loop diuretics to promote urinary calcium excretion and anti-resorptives such as calcitonin and bisphosphonates.
  • Particularly, bisphosphonates are the current mainstay for MAH treatment : they not only inhibit osteoclastic bone resorption to ameliorate hypercalcemia but can also alleviate bone pain and can even prevent cancer cell expansion in bone metastatic lesions.
  • [MeSH-major] Hypercalcemia / etiology. Hypercalcemia / therapy. Neoplasms / complications
  • [MeSH-minor] Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Bone Resorption. Calcitonin / therapeutic use. Diphosphonates / therapeutic use. Drug Design. Drug Therapy, Combination. Fluid Therapy. Glycoproteins / therapeutic use. Humans. Osteoprotegerin. Parathyroid Hormone-Related Protein. Receptors, Cytoplasmic and Nuclear / therapeutic use. Receptors, Tumor Necrosis Factor / therapeutic use. Sodium Chloride / administration & dosage. Sodium Potassium Chloride Symporter Inhibitors / therapeutic use

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  • (PMID = 16582519.001).
  • [ISSN] 0917-5857
  • [Journal-full-title] Clinical calcium
  • [ISO-abbreviation] Clin Calcium
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Glycoproteins; 0 / Osteoprotegerin; 0 / Parathyroid Hormone-Related Protein; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / Sodium Potassium Chloride Symporter Inhibitors; 0 / TNFRSF11B protein, human; 451W47IQ8X / Sodium Chloride; 9007-12-9 / Calcitonin
  • [Number-of-references] 18
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13. 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.
  • Functional inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene occurs in 40-80% of human conventional renal cell carcinomas (RCCs).
  • 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 vitro, tumor cell growth and viability was decreased by up to 80% by the antibody in all cell lines.
  • 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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14. Hortobagyi GN: Novel approaches to the management of bone metastases. Semin Oncol; 2003 Oct;30(5 Suppl 16):161-6
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  • Standard management of breast cancer metastatic to bone includes systemic chemotherapy and, if applicable, hormone therapy, as well as radiotherapy for control of pain or prevention of pathologic fractures.
  • The clinical evaluation of several osteoprotegerin preparations has shown therapeutic effects as measured by significant reductions in biochemical markers of bone resorption.
  • Monoclonal antibodies to RANK ligand and parathyroid hormone-related protein, as well as Src kinase inhibitors, are also currently under clinical evaluation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Neoplasms / secondary. Bone Neoplasms / therapy. Enzyme Inhibitors / therapeutic use. Osteoclasts / drug effects. Radiopharmaceuticals / therapeutic use
  • [MeSH-minor] Bone Resorption. Breast Neoplasms / pathology. Carrier Proteins. Cytokines. Glycoproteins / antagonists & inhibitors. Humans. Ligands. Membrane Glycoproteins. Osteoprotegerin. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Receptor, Parathyroid Hormone, Type 1. Receptors, Cytoplasmic and Nuclear / antagonists & inhibitors. Receptors, Tumor Necrosis Factor. Signal Transduction. src-Family Kinases / antagonists & inhibitors

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  • (PMID = 14613037.001).
  • [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 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Glycoproteins; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Radiopharmaceuticals; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptor, Parathyroid Hormone, Type 1; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11A protein, human; 0 / TNFRSF11B protein, human; 0 / TNFSF11 protein, human; EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 53
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15. 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.
  • 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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16. 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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17. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • Osteolysis and tumor cell accumulation can be interrupted by inhibiting any of these limbs of the vicious cycle.
  • For example, bisphosphonates (e.g., pamidronate, ibandronate, risedronate, clodronate, and zoledronate) inhibit both bone lesions and tumor cell burden in bone in experimental models of breast carcinomametastasis.
  • Neutralizing antibodies to PTHrP, which inhibit PTHrP effects on osteoclastic bone resorption, also reduce osteolytic bone lesions and tumor burden in bone.
  • 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-major] Bone Neoplasms / physiopathology. Bone Neoplasms / secondary. Breast Neoplasms / pathology. Osteoclasts / physiology. Transforming Growth Factor beta / metabolism
  • [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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18. Ehata S, Hanyu A, Fujime M, Katsuno Y, Fukunaga E, Goto K, Ishikawa Y, Nomura K, Yokoo H, Shimizu T, Ogata E, Miyazono K, Shimizu K, Imamura T: Ki26894, a novel transforming growth factor-beta type I receptor kinase inhibitor, inhibits in vitro invasion and in vivo bone metastasis of a human breast cancer cell line. Cancer Sci; 2007 Jan;98(1):127-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ki26894, a novel transforming growth factor-beta type I receptor kinase inhibitor, inhibits in vitro invasion and in vivo bone metastasis of a human breast cancer cell line.
  • Transforming growth factor (TGF)-beta signaling has been shown to promote tumor growth and metastasis in advanced cancer.
  • Use of inhibitors of TGF-beta signaling may thus be a novel strategy for treatment of patients with such cancers.
  • In this study, we investigated the effects of a novel TGF-beta type I receptor (TbetaR-I) kinase inhibitor, Ki26894, on bone metastasis of a highly bone-metastatic variant of human breast cancer MDA-MB-231 cells, termed MDA-MB-231-5a-D (MDA-231-D).
  • Ki26894 also suppressed transcription of plasminogen activator inhibitor-1 (PAI-1), parathyroid hormone-related protein (PTHrP), and interleukin-11 (IL-11) mRNA of MDA-231-D cells, which were stimulated by TGF-beta.
  • X-ray radiography revealed that systemic Ki26894 treatment initiated 1 day before the inoculation of MDA-231-D cells into the left ventricle of BALB/cnu/nu female mice resulted in decreased bone metastasis of breast cancer cells.
  • [MeSH-major] Activin Receptors, Type I / pharmacokinetics. Antineoplastic Agents / pharmacology. Bone Neoplasms / drug therapy. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / pathology. Neoplasm Metastasis / prevention & control. Protein Kinase Inhibitors / pharmacology
  • [MeSH-minor] Animals. Female. Humans. Immunoblotting. In Vitro Techniques. Mice. Neoplasm Invasiveness / prevention & control. Protein-Serine-Threonine Kinases. Receptors, Transforming Growth Factor beta / drug effects. Reverse Transcriptase Polymerase Chain Reaction


19. Yang M, Burton DW, Geller J, Hillegonds DJ, Hastings RH, Deftos LJ, Hoffman RM: The bisphosphonate olpadronate inhibits skeletal prostate cancer progression in a green fluorescent protein nude mouse model. Clin Cancer Res; 2006 Apr 15;12(8):2602-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Metastatic bone disease is one of the major causes of morbidity and mortality in prostate cancer patients.
  • Bisphosphonates are currently used to inhibit bone resorption and reduce tumor-induced skeletal complications.
  • The in vivo effects of four bisphosphonates, including pamidronate, etidronic acid, and olpadronate, on bone tumor burden in mice intratibially inoculated with PC-3-GFP human prostate cancer cells were visualized by whole-body fluorescence imaging and X-ray.
  • We showed that 3,3-dimethylaminopropane-1-hydroxy-1,1-diphosphonic acid (olpadronate) was the most effective bisphosphonate treatment in reducing tumor burden as assessed by GFP imaging and radiography.
  • The GFP tumor area and X-ray score significantly correlated.
  • Reduced tumor growth in the bone was accompanied by reduced serum calcium, parathyroid hormone-related protein, and osteoprotegerin.
  • CONCLUSIONS: The serum calcium, parathyroid hormone-related protein, and osteoprotegerin levels were significantly correlated with GFP area and X-ray scores.
  • Treatment with olpadronate reduced tumor growth in the bone measured by GFP and X-ray imaging procedures.
  • Imaging of GFP expression enables monitoring of tumor growth in the bone and the GFP results complement the X-ray assessment of bone disease.
  • [MeSH-major] Bone Neoplasms / prevention & control. Diphosphonates / therapeutic use. Green Fluorescent Proteins / metabolism. Prostatic Neoplasms / drug therapy. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Bone Density Conservation Agents / therapeutic use. Calcium / blood. Cell Line, Tumor. Disease Progression. Glycoproteins / blood. Humans. Male. Mice. Mice, Nude. Osteoprotegerin. Parathyroid Hormone-Related Protein / blood. Receptors, Cytoplasmic and Nuclear / blood. Receptors, Tumor Necrosis Factor / blood. Time Factors. Treatment Outcome

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  • (PMID = 16638872.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR47347; United States / NIDDK NIH HHS / DK / DK-60586; United States / NIEHS NIH HHS / ES / ES-09227
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Glycoproteins; 0 / Osteoprotegerin; 0 / Parathyroid Hormone-Related Protein; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11B protein, human; 0 / Tnfrsf11b protein, mouse; 147336-22-9 / Green Fluorescent Proteins; 874HHB2V3S / olpadronic acid; OYY3447OMC / pamidronate; SY7Q814VUP / Calcium
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20. 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.
  • 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 mice injected with tumor cells were implanted simultaneously with osmotic minipumps containing either 1alpha,25-D(3), 22-oxa-1alpha,25-D(3) or vehicle.
  • 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.
  • Furthermore, in the angiogenesis assay, the number of tumor cells or basic fibroblast growth factor-induced angiogenesis was reduced in 1alpha,25-D(3) and 22-oxa-1alpha,25-D(3)-treated mice.
  • 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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21. 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.
  • Characteristics of both the tumor cells and the bone microenvironment contribute to this phenomenon.
  • The presence of tumor in bone is associated with activation of osteoclasts, resulting in excessive bone resorption and subsequent osteolysis.
  • 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.
  • A single 3 microg intravenous injection of zoledronic acid (Zometa; Novartis Pharmaceuticals Corp, East Hanover, NJ), a new highly potent bisphosphonate, prevented destruction of trabecular bone in an orthotopic mouse mammary tumor model.
  • 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.
  • Although bisphosphonates, including zoledronic acid, are able to induce apoptosis in tumor cells in vitro, studies in animal models to date have generally not shown a reduction in nonosseous tumor.
  • Therefore, bisphosphonate-associated tumor reduction in bone is most likely mediated by osteoclast inhibition or is related to high local concentrations of bisphosphonates in the bone compartment.
  • [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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22. Rucci N, Recchia I, Angelucci A, Alamanou M, Del Fattore A, Fortunati D, Susa M, Fabbro D, Bologna M, Teti A: Inhibition of protein kinase c-Src reduces the incidence of breast cancer metastases and increases survival in mice: implications for therapy. J Pharmacol Exp Ther; 2006 Jul;318(1):161-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of protein kinase c-Src reduces the incidence of breast cancer metastases and increases survival in mice: implications for therapy.
  • In this study, we tested the hypothesis that c-Src could promote breast cancer metastasis acting on several cell types and that pharmacological disruption of its kinase activity could be beneficial for the treatment of metastases.
  • These were pharmacologically reduced by treatment with the c-Src inhibitor [7-{4-[2-(2-methoxy-ethylamino-ethoxy]-phenyl}-5-(3-methoxy-phenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-ylamine] CGP76030 (100 mg/kg/day p.o.
  • Metastases were more severe in mice injected with MDA-231 cells stably transfected with wild-type c-Src (MDA-231-SrcWT), whereas transfection in injected cells of a c-Src kinase-dead dominant-negative construct (MDA-231-SrcDN) resulted in reduced morbidity, lethality, and incidence of metastases similar to the mice treated with the inhibitor.
  • It also impaired osteoclast bone resorption both directly and by reducing expression by osteoblasts of the osteoclastogenic cytokines interleukin-1beta and interleukin-6, whereas parathyroid hormone-related peptide was not implicated. c-Src was also modestly but consistently involved in the enhancement of endothelial cell proliferation in vitro and angiogenesis in vivo.
  • In conclusion, we propose that c-Src disruption affects the metastatic process and thus is a therapeutic target for the treatment of breast cancer.
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Female. Humans. Incidence. Mice. Mice, Inbred BALB C. Mice, Nude. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. Pyrroles / pharmacology. Pyrroles / therapeutic use. Survival Rate. Xenograft Model Antitumor Assays / methods. src-Family Kinases

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  • (PMID = 16627750.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CGP 76030; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.13 / Protein Kinase C
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23. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • In a search for small-molecule inhibitors of PTHrP production or effects, we have identified guanine-nucleotide analogs as compounds that inhibit PTHrP expression by human tumor cells associated with these syndromes.
  • 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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24. 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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  • [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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25. Riccardi A, Grasso D, Danova M: Bisphosphonates in oncology: physiopathologic bases and clinical activity. Tumori; 2003 May-Jun;89(3):223-36
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  • Osteoclastic activation is the ultimate way of bone resorption in neoplasia, induced by the combined effects of tumor-secreted humoral factors (especially parathyroid hormone-related peptides) and osteoclastic-osteoblastic interaction.
  • Intravenous clodronate and, especially, pamidronate and zoledronate are the first-choice drugs for hypercalcemia, and they play a significant role in reducing metastatic bone pain.
  • [MeSH-major] Bone Neoplasms / prevention & control. Diphosphonates / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Humans. Hypercalcemia / drug therapy. Hypercalcemia / physiopathology. Neoplasms / pathology. Osteoporosis / physiopathology. Osteoporosis / prevention & control. Pain / physiopathology. Pain / prevention & control

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  • (PMID = 12908775.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphosphonates
  • [Number-of-references] 169
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