A model for malignancy-associated humoral hypercalcemia

Abramson, Edith C.; Kukla, Lawrence J.; Shevrin, Daniel H.; Lad, Thomas E.; McGuire, William P.; Kukreja, Subhash C.

doi:10.1007/bf02405367

Cited by 27 publications

(5 citation statements)

References 16 publications

(13 reference statements)

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“…Many of the studies reviewed used standard laboratory chow. Standard laboratory chow diets do not have a standardized macronutrient composition and often vary from batch to batch ( 144 ). Furthermore, the ingredients of laboratory chow are rarely defined, therefore it might contain unknown nutrients that may impact study endpoints.…”

Section: Nutritional Interventions: Gaps and Opportunitiesmentioning

confidence: 99%

Nutritional Interventions in Cancer Cachexia: Evidence and Perspectives From Experimental Models

et al. 2020

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Cancer cachexia is a complex metabolic syndrome characterized by involuntary skeletal muscle loss and is associated with poor clinical outcome, decreased survival and negatively influences cancer therapy. No curative treatments are available for cancer cachexia, but nutritional intervention is recommended as a cornerstone of multimodal therapy. Optimal nutritional care is pivotal in the treatment of cancer cachexia, and the effects of nutrients may extend beyond provision of adequate energy uptake, targeting different mechanisms or metabolic pathways that are affected or deregulated by cachexia. The evidence to support this notion derived from nutritional intervention studies in experimental models of cancer cachexia is systematically discussed in this review. Moreover, experimental variables and readout parameters to determine skeletal muscle wasting and cachexia are methodologically evaluated to allow critical comparison of similar studies. Single- and multinutrient intervention studies including qualitative modulation of dietary protein, dietary fat, and supplementation with specific nutrients, such as carnitine and creatine, were reviewed for their efficacy to counteract muscle mass loss and its underlying mechanisms in experimental cancer cachexia. Numerous studies showed favorable effects on impaired protein turnover and related metabolic abnormalities of nutritional supplementation in parallel with a beneficial impact on cancer-induced muscle wasting. The combination of high quality nutrients in a multitargeted, multinutrient approach appears specifically promising, preferentially as a multimodal intervention, although more studies investigating the optimal quantity and combination of nutrients are needed. During the review process, a wide variation in timing, duration, dosing, and route of supplementation, as well as a wide variation in animal models were observed. Better standardization in dietary design, and the development of experimental models that better recapitulate the etiology of human cachexia, will further facilitate successful translation of experimentally-based multinutrient, multimodal interventions into clinical practice.

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Section: Nutritional Interventions: Gaps and Opportunitiesmentioning

confidence: 99%

Nutritional Interventions in Cancer Cachexia: Evidence and Perspectives From Experimental Models

et al. 2020

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“…We were also interested to apply such specific antisera to the treatment of hypercalcaemia in animal models of HHM. These consisted of two tumours from patients with the HHM syndrome: one a squamous cell carcinoma of the lung, and the other of the larynx and maintained as transplanted tumours in athymic mice (Abramson et al, 1984). In each case, the mice bearing the tumours develop hypercalcaemia, hypophosphataemia and elevated urinary cyclic AMP.…”

Section: Immunology Of Pthrpmentioning

confidence: 99%

Parathyroid Hormone‐related Protein in Hypercalcaemia of Malignancy

Martın

Suva

1989

Clinical Endocrinology

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“…We have established a model for malignancy-associ ated hypercalcemia [7], In this model, a human squamouscell lung cancer has been serially carried in athymic mice. On quantitative histomorphometry of bone, the resorptive parameters are increased in these mice in vivo |8).…”

Section: Introductionmentioning

confidence: 99%

Effects of Hypercalcemia-Producing Tumor Extract and Parathyroid Hormone on Osteoclast Ultrastructure

Barengolts

Buschmann²,

Shevrin³

et al. 1990

Cells Tissues Organs

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Hypercalcemia is a frequent complication of cancer. Recently, parathyroid hormone-related protein has been isolated from tumors associated with this syndrome. In the present study, the effects of tumor-derived hypercalcemic factor and bovine parathyroid hormone (PTH) on bone were compared in an organ culture system using calvarial bones from newborn mice. Mouse calvaria were incubated for 72 h with control medium or media containing 0.15 mg/ml tumor extract (TE) or 2 × 10^–9M PTH. Bone resorption as assessed by the amount of calcium released into the medium and the number of osteoclasts counted on light microscopy, was increased by both PTH and TE. On electron microscopy areas for cytoplasm ruffled border and clear zone were statistically increased in PTH- and TE-treated calvaria as compared to control. These values were not significantly different between PTH- and TE-treated calvaria. The study therefore demonstrates that the ultrastructural changes in osteoclasts induced by the hypercalcemia-producing TE are similar to those induced by PTH.

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A model for malignancy-associated humoral hypercalcemia

Cited by 27 publications

References 16 publications

Nutritional Interventions in Cancer Cachexia: Evidence and Perspectives From Experimental Models

Nutritional Interventions in Cancer Cachexia: Evidence and Perspectives From Experimental Models

Parathyroid Hormone‐related Protein in Hypercalcaemia of Malignancy

Effects of Hypercalcemia-Producing Tumor Extract and Parathyroid Hormone on Osteoclast Ultrastructure

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