1,25 Dihydroxyvitamin D and Dexamethasone Decrease<i>In Vivo</i>Walker Carcinoma Growth, But Not Parathyroid Hormone Related Protein Secretion

Cohen-Solal, M.; Bouizar, Zhor; Ma, Denne; Am, Graulet; Guéris, J; Bracq, S.; Jullienne, A.; Vernejoul, de

doi:10.1055/s-2007-979988

Cited by 14 publications

(5 citation statements)

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“…The W256 cells are the original line and are lacking estrogen receptors. They produce PTHrP allowing them to be a model of hypercalcemia [36,[48][49][50]. They were also used for the induction of bone metastases.…”

Section: Walker 256mentioning

confidence: 99%

Rat Models of Bone Metastases

Blouin

Basle

Chappard

2005

Clin Exp Metastasis

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Bone metastases occur frequently in patients with advanced breast or prostate cancer. Bone metastases can be predominantly osteolytic, osteoblastic or mixed. Studies with animal models allow advances in understanding the molecular basis for bone metastases and provide new targets for therapy. Several animal models have been developed in rat with different pathophysiologies; they required injection or implantation of neoplastic cells into orthotopic locations, bones or the left ventricle of the heart. Several specific strains of rat have an increased incidence of spontaneous tumors. Carcinomas can be induced by either chemicals or physical agents. However, the most used and convenient way to induce bone metastases is a syngeneic transmission. MAT-Ly-Lu cells have been used in several models using Copenhagen rats to induce osteoblastic bone lesions. PA-III cells derived from Pollard tumors can also produce a combination of osteolytic and osteoblastic reactions at the site of transplantation. Osteolytic bone lesions can be obtained with an injection of Walker cells. The use of 13762 or c-SST2 cells allows also leads to osteolysis. Human xenografts can only be used in nude animals. It is essential to validate and correctly interpret the lesions in several models of bone metastasis. No animal model is sufficient by itself to represent the clinical findings observed in humans. The use of models developed in different species should be more predictive and bring a beam of arguments for a better knowledge of pathophysiological and therapeutic mechanisms.

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Section: Walker 256mentioning

confidence: 99%

Rat Models of Bone Metastases

Blouin

Basle

Chappard

2005

Clin Exp Metastasis

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“…International Journal of Toxicology 29(5) 262 ; decreased growth of Dunn OS (osteosarcoma) tumors in mice 263 ; decreased growth of C6 and G9 (gliosarcoma) tumors in rats 264 ; decreased growth of B16 (melanoma) tumors in mice 138…”

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confidence: 99%

Critical Review of Preclinical Approaches to Evaluate the Potential of Immunosuppressive Drugs to Influence Human Neoplasia

Bugelski¹,

Volk²,

Walker³

et al. 2010

Int J Toxicol

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Many immunosuppressive drugs are associated with an increased risk of B-cell lymphoma, squamous cell carcinoma, and Kaposi sarcoma. Thirteen immunosuppressive drugs have been tested in 2-year carcinogenicity studies (abatacept; azathioprine; busulfan; cyclophosphamide; cyclosporine; dexamethasone; everolimus; leflunomide; methotrexate; mycophenolate mofetil; prednisone; sirolimus; and tacrolimus) and in additional models including neonatal and genetically modified mice; chemical, viral, ultraviolet, and ionizing radiation co-carcinogenesis, and in models with transplanted tumor cells. The purpose of this review is to outline the mechanisms by which immunosuppressive drugs can influence neoplasia, to summarize the available preclinical data on the 13 drugs, and to critically review the performance of the models. A combination of primary tumor and metastasis assays conducted with transplanted cells may provide the highest value for hazard identification and can be applied on a case-by-case basis. However, for both small molecules and therapeutic proteins, determining the relative risk to patients from preclinical data remains problematic. Classifying immunosuppressive drugs based on their mechanism of action and hazard identification from preclinical studies and a prospective pharmacovigilance program to monitor carcinogenic risk may be a feasible way to manage patient safety during the clinical development program and postmarketing.

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“…PTH and PTH-RP markedly raise cyclic adenosine monophosphate (cAMP) and inositol trisphosphate (IP3) production from adrenocortical cells; the secretory effect of PTH and PTH-RP is partially suppressed by either the adenylate cyclase inhibitor SQ-22536 or the PLC inhibitor U-73122 at a concentration capable of abolishing cAMP and IP3 responses of adrenocortical cells to both hormones and is annulled by the simultaneous exposure to the two inhibitors [12]. A strong negative relationship between blood plasma levels of PTH-RP and cortisol was found in a study on fish [22]; in contrast, other studies carried out in vivo, using rat models, failed to demonstrate a cortisol-related reduction in PTH-RP production and secretion from tumors [23,24]. The possible role of the stimulating effect of PTH and PTH-RP in the physiological regulation of the human adrenal gland remains to be demonstrated.…”

Section: Discussionmentioning

confidence: 99%