Effects of corticosteroid use on treatment of solid tumours

Rutz, Hans

doi:10.1016/s0140-6736(02)11922-2

Cited by 104 publications

(80 citation statements)

References 18 publications

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“…In fact, the authors detected around 40% cortisol levels in knockout mice relative to control mice after cortisone challenge 40 . In addition, Dex has been reported to render non-haematological cancer cells more resistant to antitumour drugs [41][42][43][44] . However, clinical evidence for this drug resistance induction remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Switch of glycolysis to gluconeogenesis by dexamethasone for treatment of hepatocarcinoma

et al. 2013

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Gluconeogenesis is a fundamental feature of hepatocytes. Whether this gluconeogenic activity is also present in malignant hepatocytes remains unexplored. A better understanding of this biological process may lead to novel therapeutic strategies. Here we show that gluconeogenesis is not present in mouse or human malignant hepatocytes. We find that two critical enzymes 11b-HSD1 and 11b-HSD2 that regulate glucocorticoid activities are expressed inversely in malignant hepatocytes, resulting in the inactivation of endogenous glucocorticoids and the loss of gluconeogenesis. In patients' hepatocarcinoma, the expression of 11b-HSD1 and 11b-HSD2 is closely linked to prognosis and survival. Dexamethasone, an active form of synthesized glucocorticoids, is capable of restoring gluconeogenesis in malignant cells by bypassing the abnormal regulation of 11b-HSD enzymes, leading to therapeutic efficacy against hepatocarcinoma. These findings clarify the molecular basis of malignant hepatocyte loss of gluconeogenesis and suggest new therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Switch of glycolysis to gluconeogenesis by dexamethasone for treatment of hepatocarcinoma

et al. 2013

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“…3 GCs are also widely used as comedication in cancer therapy of solid malignant tumors due for their effectiveness in treating the malignant tumor or treatment-related oedema, inflammation, pain, electrolyte imbalance, to stimulate appetite, to prevent nausea and emesis or toxic reactions caused by cytotoxic treatment. 1,4 Before, during and after chemotherapy of solid malignant tumors GCs are given at varying doses to reduce acute toxicity, particularly hyperemesis and to protect normal tissue, e.g., bone marrow progenitor cells, 5 of cancer patients against the long-term effects of genotoxic drugs. 4 The cell type-specific and GC-mediated protection of normal tissues and solid tumors from apoptosis induction by cytotoxic agents and its potential clinical implications have been mostly unknown so far and are just about to be recognized as a more common phenomenon.…”

Section: Introductionmentioning

confidence: 99%

“…1,4 Before, during and after chemotherapy of solid malignant tumors GCs are given at varying doses to reduce acute toxicity, particularly hyperemesis and to protect normal tissue, e.g., bone marrow progenitor cells, 5 of cancer patients against the long-term effects of genotoxic drugs. 4 The cell type-specific and GC-mediated protection of normal tissues and solid tumors from apoptosis induction by cytotoxic agents and its potential clinical implications have been mostly unknown so far and are just about to be recognized as a more common phenomenon. 6,7 However, little is known about how GCs might affect the response of solid, nonhematological tumors in patients undergoing cancer chemo-or radiotherapy.…”

Section: Introductionmentioning

confidence: 99%

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

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ABBrevIAtIons DEX ABstrActGlucocorticoids have been widely used as cotreatment for patients with cancer due to potent pro-apoptotic properties in lymphoid cells, reduction of nausea and diminishing acute toxicity on normal tissue. There are now data from preclinical and, to some extent, clinical studies, demonstrating that these medicaments are highly suspicious to induce therapy resistance in the majority of malignant solid tumors-irrespective of tumor origin and the nature of specific anticancer drugs or irradiation used for treatment. Despite these huge amounts of data, the underlying mechanisms of cell type-specific signaling by these steroid hormones are just beginning to be described. This review summarizes our present understanding of a relationship between glucocorticoid-induced reversible cell cycle arrest and therapy resistance in solid tumors. We give a summary of our current knowledge of decreased proliferation rates in response to glucocorticoid pre and combination treatment which are suspicious to be involved not only in protection of normal tissues, but also in protection of solid tumors from cytotoxic effects of anticancer agents. The inhibition of cell cycle progression by pretreatment with GCs may be crucially involved in switching the balance of several interacting pathways to survival upon treatment with GCs.

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“…The role of PET in the diagnosis of pancreatic cancer is unclear with significant false positives and negatives 5. The improved oxygenation following methylprednisolone therapy may have related to decreased oedema and secretions such as seen when used with lymphangitis carcinomatosis 6 or to the anti‐inflammatory and tumour angiogenesis suppressive effects of corticosteroids 7.…”

Section: Discussionmentioning

confidence: 99%

Metastatic pancreatic carcinoma masquerading as cystic lung disease: a rare presentation

Stern

Huseini

Kuok

et al. 2017

Respirology Case Reports

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This 52‐year‐old male ex‐smoker presented with a six‐month history of progressive breathlessness and weight loss. He deteriorated acutely, and was admitted with severe type 1 respiratory failure. Apart from diffuse coarse crackles on chest auscultation, physical examination was unremarkable. High‐resolution computed tomography (HRCT) showed diffuse cystic changes throughout the lungs. A diagnosis of pulmonary Langerhans cell histiocytosis (PLCH) was considered. Further workup identified a coincidental pancreatic lesion of uncertain significance, which remained indeterminate on magnetic resonance imaging (MRI) and on positron emission tomography (PET). Transbronchial biopsy revealed enteric differentiated adenocarcinoma exhibiting lepidic spread, and autopsy later confirmed primary pancreatic malignancy. This case demonstrates that metastatic pancreatic malignancy can present with severe respiratory failure and masquerade as cystic lung disease.

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Effects of corticosteroid use on treatment of solid tumours

Cited by 104 publications

References 18 publications

Switch of glycolysis to gluconeogenesis by dexamethasone for treatment of hepatocarcinoma

Switch of glycolysis to gluconeogenesis by dexamethasone for treatment of hepatocarcinoma

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Metastatic pancreatic carcinoma masquerading as cystic lung disease: a rare presentation

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