Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extra-abdominal fibromatosis in the neck may occasionally cause serious sequelae when aggressive invasion of the vital structures occurs. However, the principle of wide excision is difficult to apply in some patients because of the important organs surrounding the tumor. We report herein, a woman followed up for 22 years, in whom testolactone showed a definite effect during the course of observation. She first presented, at the age of 52, with a painful tumor in the neck, located behind the right thyroid lobe and fixed to the adjacent structures. Incomplete excision of the tumor was followed by a local recurrence accompanied with recurrent laryngeal nerve palsy and Horner's syndrome on the right side. Prednisolone was administered for 2 1/2 months and external irradiation of 8,000 RAD was given. Enlargement of the recurrent tumor stopped but 2 months later an emergency tracheostomy was required for an airway obstruction. Over the next 3 years, the local findings remained unchanged, but then a painful tumor growth reappeared cephalad which gradually attained a size of 5 cm in diameter, and was fixed to the base. Testolactone 150 to 200 mg was given to the patient daily for 2 months, resulting in marked regression of the tumor. During the last 13 years the patient has been well with the tumor still decreasing in size.
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PMID:Aggressive fibromatosis in the neck. A case treated effectively by testolactone with a long follow-up study. 238 45

Glucocorticoids can inhibit solid tumor growth possibly due to an inhibitory effect on angiogenesis. The antitumor effects of the free drugs have only been observed using treatment schedules based on high and frequent dosing for prolonged periods of time. As long-circulating liposomes accumulate at sites of malignancy, we investigated the tumor-inhibiting potential of liposome-encapsulated prednisolone phosphate. Liposomal prednisolone phosphate could inhibit tumor growth dose-dependently, with 80% to 90% tumor growth inhibition of subcutaneous B16.F10 melanoma and C26 colon carcinoma murine tumor models at 20 mg/kg by single or weekly doses. Prednisolone phosphate in the free form was completely ineffective at this low-frequency treatment schedule, even when administered at a dose of 50 mg/kg. In vitro studies did not show an inhibitory effect of prednisolone (phosphate) on tumor cell, nor on endothelial cell proliferation. Histologic evaluation revealed that liposomal prednisolone phosphate-treated tumors contained a center with areas of picnotic/necrotic cells, which were not apparent in untreated tumors or tumors treated with the free drug. In conclusion, the present study shows potent antitumor effects of liposomal formulations of glucocorticoids in a low dose and low-frequency schedule, offering promise for liposomal glucocorticoids as novel antitumor agents.
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PMID:Liposome-encapsulated prednisolone phosphate inhibits growth of established tumors in mice. 1580 17

Prednisolone phosphate (PLP) encapsulated in long-circulating liposomes can inhibit tumor growth after intravenous administration (i.v.). These antitumor effects of liposomal PLP are the result of the tumor-targeting property of the liposome formulation. The mechanism by which liposomal PLP inhibits tumor growth is unclear. We investigated the effects of liposome-encapsulated PLP versus free PLP on angiogenic protein production in tumor tissue in vivo and on viability and proliferation of tumor and endothelial cells in vitro. In vivo, liposomal PLP had a stronger reducing effect on pro-angiogenic protein levels than free PLP, whereas levels of anti-angiogenic proteins were hardly affected. Cell viability was only slightly affected with either treatment. Liposomal PLP had strong anti-proliferative effects on human umbilical vein endothelial cells, whereas free PLP had hardly any effect. Taken together, the present study points to a strong inhibitory effect of liposomal PLP on tumor angiogenesis by reduction of the intratumoral production of the majority of pro-angiogenic factors studied and direct inhibition of endothelial cell proliferation, which is the result of high prolonged levels of prednisolone in the tumor by liposomal delivery.
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PMID:Anti-angiogenic effects of liposomal prednisolone phosphate on B16 melanoma in mice. 1670 87

Prednisolone phosphate (PLP) encapsulated in long-circulating liposomes (LCLs) (LCL-PLP) exerts antitumor activity through the inhibition of tumor angiogenesis. It is known that tumor-associated macrophages (TAMs) play a crucial role in tumor growth as they are actively involved in promoting and maintaining tumor angiogenesis. To gain more insight into the antiangiogenic mechanisms of LCL-PLP, this study aimed to investigate the role of TAM in the antitumor mode of action of LCL-PLP in B16.F10 melanoma-bearing mice. Our results show that TAMs have a pivotal function in the growth of B16.F10 melanoma through the production of pro-angiogenic/pro-inflammatory factors. One of the major inhibitory actions of LCL-PLP on tumor growth is the reduction of the TAM-mediated production of pro-angiogenic factors, whereas production of anti-angiogenic factors by these cells is hardly affected.
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PMID:Antitumor activity of liposomal prednisolone phosphate depends on the presence of functional tumor-associated macrophages in tumor tissue. 1828 32

Prednisolone disodium phosphate (PLP) encapsulated in long-circulating liposomes (LCL) (LCL-PLP) inhibited tumor growth by 80-90% after a single dose of 20 mg/kg, whereas PLP in the free form was completely ineffective at the same single dose. To generalize our findings with LCL-PLP, the antitumor activity and side effects of LCL containing synthetic glucocorticoids (LCL-GC) other than PLP were investigated. In addition to PLP, budesonide disodium phosphate, dexamethasone disodium phosphate, and methylprednisolone disodium phosphate were selected based on the difference in their potency to activate the human glucocorticoid receptor. The present study shows that the tumor localization of each GC is governed by the transport capacity of the LCL composed of dipalmitoylphosphatidylcholine, cholesterol, and polyethylene glycol 2000-distearoylphosphatidylethanolamine in a molar ratio of 1.85:1.0:0.15. The antitumor potency of the LCL-GC strongly depends on the potency of the type of GC encapsulated. LCL-encapsulated budesonide disodium phosphate (LCL-BUP) had the highest antitumor activity which is likely due to the much higher potency of BUP encapsulated in LCL versus the other three GC types. The high potency of LCL-BUP confers the risk for occurrence of strong side effects. However, at the dose of 3 mg/kg, LCL-BUP was highly efficacious without the occurrence of adverse effects.
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PMID:Antitumor activity and tumor localization of liposomal glucocorticoids in B16 melanoma-bearing mice. 1829 48