Dexamethasone reduces tumor recurrence and metastasis after pancreatic tumor resection in SCID mice

Egberts, Jan‐Hendrik; Schniewind, Bodo; Pätzold, Miriam; Kettler, Bastian; Tepel, Jürgen; Kalthoff, Holger; Trauzold, Anna

doi:10.4161/cbt.7.7.6099

Cited by 29 publications

(32 citation statements)

References 38 publications

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“…Surgery causes inevitable inflammatory response in tumor microenvironment; therefore, GCs might be beneficial in reducing acute phase inflammatory reaction, even though GCs may possibly suppress immune response against cancer. One study has shown beneficial results of DEX treatment for the host after resection of pancreatic cancer (25). DEX was found to reduce metastasis and size of local tumor recurrence (25).…”

Section: Discussionmentioning

confidence: 99%

“…One study has shown beneficial results of DEX treatment for the host after resection of pancreatic cancer (25). DEX was found to reduce metastasis and size of local tumor recurrence (25). Therefore, to maximize the efficacy of cancer therapy, more specific understanding of the cancer cells themselves and the tumor microenvironment is necessary, because the effect of DEX on solid tumor can be still double-edged.…”

Section: Discussionmentioning

confidence: 99%

“…To understand the effects of GCs, we focused on the relationship among three molecules DEX, STAT3 and VEGF. By ONCOLOGY REPORTS 23: 1139-1143, 2010 Dexamethasone treatment inhibits VEGF production via suppression of STAT3 in a head and neck cancer cell line SEON Western blot analysis. Cultured cells were rinsed with PBS, suspended in lysis buffer (0.5% NP40, 50 mM Tris-Cl, 150 mM NaCl, 1 mM dithiothreitol, 1% sodium deoxycholate, 0.1% SDS, 1 mM EDTA, 1 mM phenylmethylsulfonyl fluoride, 0.1 M aprotinin and 1 M pepstatin A).…”

Section: Introductionmentioning

confidence: 99%

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Dexamethasone treatment inhibits VEGF production via suppression of STAT3 in a head and neck cancer cell line

Shim

Hah²,

Hwang³

et al. 2010

Oncol Rep

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Abstract. Glucocorticoids (GCs) modulate the synthesis of many pro-inflammatory cytokines and influence multiple transduction pathways. GCs negatively or positively influence the transcription factors of their target genes. All of these transcription signals are closely connected to cancer survival or death. We investigated the action of dexamethasone (DEX) on head and neck cancer cell lines. When SNU-1041 and SNU-1076 were treated with DEX, the cell lines showed different patterns of responses. DEX inhibition of cell growth depended on concentration in SNU-1041, but not in SNU-1076. Furthermore, DEX suppressed vascular endothelial growth factor (VEGF) secretion from SNU-1041, but not from SNU-1076. We explored the mechanism that explains these distinct differences. After DEX treatment, the differences of NF-κB (p65), glucocorticoid receptor and p-AKT were not observed between the cell lines. However, phospho-signal transducer and activator of transcription 3 (STAT3) decreased in SNU-1041 only. Moreover, STAT3 inhibition using si-RNA suppressed VEGF secretion. When STAT3 was overexpressed after DEX treatment, the level of VEGF in the culture media was restored. Taken together, we suggest that p-STAT3 can be a mediating factor which regulates VEGF secretion in the DEX treatment. Because the relationship between the three molecules DEX, STAT3 and VEGF is scarcely known, our findings clarified one of the signaling pathways of DEX, which is often used in clinical conditions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Dexamethasone treatment inhibits VEGF production via suppression of STAT3 in a head and neck cancer cell line

Shim

Hah²,

Hwang³

et al. 2010

Oncol Rep

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“…Therefore, this steroid results in a profound influence on the malignant phenotype but it is not clear whether this effect is due to direct action or inhibition of proinflammatory singals [45].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Glucocorticoid Receptor in Human Pancreatic Cancer and in Xenografts. An Immunohistochemical Study

Bekasi

Zalatnai

2009

Pathol. Oncol. Res.

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Glucocorticoid receptor overexpression has been reported in a variety of human solid tumors, but much less in known about its presence in pancreatic cancer. Only one report is available in the literature, back to 1994, since that no peculiar attention has been paid to this issue. Immunohistochemical analysis of paraffin-embedded tissue sections was performed in human normal pancreata and well differentiated pancreatic adenocarcinomas (monoclonal primary antibody, ABCAM, Cambridge, UK). As positive control invasive ductal adenocarcinoma of the breast was used. In the normal non-tumorous pancreas a strong positivity was detected in all acinar cells, typically in the cytoplasm. Nuclear staining was not visible. The distribution of the positive reaction was homogenous. The ductal pancreatic carcinoma cells also displayed a strong positivity. The location of the immune reaction was mainly cytoplasmic but in some tumors a strong nuclear reaction was also noticed. In some slides acini remained also positive in the close vicinity of the tumor. Although the positivity of the ductal tumor cells was a constant finding in our samples, surprisingly, the liver metastasis was completely negative. Strong glucocorticoid receptor expression was also found in xenografted human pancreatic cancer showing a diffuse, mainly cytoplasmic positivity. Our studies have shown that the human pancreatic carcinomas do overexpress a strong glucocorticoid receptor positivity, but its significance is not clear. However, this finding might have a clinical relevance.

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“…Therefore, hMSH2 and hPMS1 could be immunogenic antigens in patients with pancreatic adenocarcinoma. Additionally Egberts et al showed that dexamethasone treatment had profound influence of pancreatic duct adenocarcinoma cells in vitro in terms of inhibition of invasiveness and activation of NFκB which was approved in vivo by reduced metastasing capability and reduced size of local tumour recurrence in an experimental model of pancreatic cancer[15]. These observations indicate that the link between malignancy and inflammatory myopathy relates possibly to the expression of common autoantigens between cancer tissue and muscle tissue in some patients with polymyositis.…”

Section: Discussionmentioning

confidence: 99%

Pancreatic adenocarcinoma-associated polymyositis treated with corticosteroids along with cancer specific treatment: case report

et al. 2011

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BackgroundAdenocarcinoma of the pancreas only rarely is associated with inflammatory myopathy. In this setting, polymyositis may be treated with glucocorticoids in combination with cancer specific treatment.Case presentationWe present the case of a 52-year-old man with stage IIA pancreatic tail adenocarcinoma who underwent surgical treatment and six months into therapy with gemcitabine he developed symmetrical, painful, proximal muscle weakness with peripheral oedema. Re-evaluation with imaging modalities, muscle histology and biochemistry conferred the diagnosis of polymyositis associated with pancreatic cancer progression. The patient was treated with glucocorticoids along with gemcitabine and erlotinib which resulted in complete remission within six months. He remained in good health for a further six months on erlotinib maintenance therapy when a new computer tomography scan showed pancreatic cancer relapse and hence prompted 2nd line chemotherapy with gemcitabine.ConclusionsPolymyositis associated with pancreatic cancer may respond to glucocorticoids along with cancer specific treatment.

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Dexamethasone reduces tumor recurrence and metastasis after pancreatic tumor resection in SCID mice

Cited by 29 publications

References 38 publications

Dexamethasone treatment inhibits VEGF production via suppression of STAT3 in a head and neck cancer cell line

Dexamethasone treatment inhibits VEGF production via suppression of STAT3 in a head and neck cancer cell line

Overexpression of Glucocorticoid Receptor in Human Pancreatic Cancer and in Xenografts. An Immunohistochemical Study

Pancreatic adenocarcinoma-associated polymyositis treated with corticosteroids along with cancer specific treatment: case report

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