In-Vitro Glucocorticoid Studies for Predicting Response to Glucocorticoid Therapy in Adults With Malignant Lymphoma

Bloomfield, Clara D.; Peterson, Bruce A.; Zaleskas, J.; Frizzerà, Glauco; Smith, Kendall A.; Hildebrandt, Laurie; Gajl‐Peczalska, Kazimiera J.; Munck, Allan

doi:10.1016/s0140-6736(80)91405-1

Cited by 55 publications

(15 citation statements)

References 10 publications

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“…2 specifically induce apoptosis in several types of leukemia and lymphoma, and they are used routinely in treating T-cell acute lymphoblastic leukemia (T-ALL) (1)(2)(3)(4)(5)(6). The cellular function of GCs is mediated by the glucocorticoid receptor (GR) protein, which is widely expressed in most tissues and cell lines (7)(8)(9)(10).…”

Section: Glucocorticoids (Gcs)mentioning

confidence: 99%

c-Myb and Members of the c-Ets Family of Transcription Factors Act as Molecular Switches to Mediate Opposite Steroid Regulation of the Human Glucocorticoid Receptor 1A Promoter

Geng

Vedeckis

2005

Journal of Biological Chemistry

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Section: Glucocorticoids (Gcs)mentioning

confidence: 99%

c-Myb and Members of the c-Ets Family of Transcription Factors Act as Molecular Switches to Mediate Opposite Steroid Regulation of the Human Glucocorticoid Receptor 1A Promoter

Geng

Vedeckis

2005

Journal of Biological Chemistry

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“…Aside from the well-established therapeutic targeting of AR and ERs there are established roles to target GR as a pro-apoptotic therapeutic approach in lymphoma(43–45). However ligand-activation of the GR has been less effective in other cancers and suggests the biology of the GR is more nuanced with regards to cancer biology.…”

Section: Introductionmentioning

confidence: 99%

Pan-Cancer Analyses of the Nuclear Receptor Superfamily

Long

Campbell

2015

Nuclear Receptor Research

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Nuclear receptors (NR) act as an integrated conduit for environmental and hormonal signals to govern genomic responses, which relate to cell fate decisions. We review how their integrated actions with each other, shared co-factors and other transcription factors are disrupted in cancer. Steroid hormone nuclear receptors are oncogenic drivers in breast and prostate cancer and blockade of signaling is a major therapeutic goal. By contrast to blockade of receptors, in other cancers enhanced receptor function is attractive, as illustrated initially with targeting of retinoic acid receptors in leukemia. In the post-genomic era large consortia, such as The Cancer Genome Atlas, have developed a remarkable volume of genomic data with which to examine multiple aspects of nuclear receptor status in a pan-cancer manner. Therefore to extend the review of NR function we have also undertaken bioinformatics analyses of NR expression in over 3000 tumors, spread across six different tumor types (bladder, breast, colon, head and neck, liver and prostate). Specifically, to ask how the NR expression was distorted (altered expression, mutation and CNV) we have applied bootstrapping approaches to simulate data for comparison, and also compared these NR findings to 12 other transcription factor families. Nuclear receptors were uniquely and uniformly downregulated across all six tumor types, more than predicted by chance. These approaches also revealed that each tumor type had a specific NR expression profile but these were most similar between breast and prostate cancer. Some NRs were down-regulated in at least five tumor types (e.g. NR3C2/MR and NR5A2/LRH-1)) whereas others were uniquely down-regulated in one tumor (e.g. NR1B3/RARG). The downregulation was not driven by copy number variation or mutation and epigenetic mechanisms maybe responsible for the altered nuclear receptor expression.

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“…Corticosteroid-induced cytolysis in activated T-cell populations appears to be the result of corticosteroid suppression of a lymphokine (IL- 2) responsible for proliferation of the activated T-cell clone [11,12]. In the absence of IL-2, such clones die.…”

Section: Discussionmentioning

confidence: 99%

Response rate and survival in myeloma patients receiving prednisone alone

McIntyre¹,

Pajak²,

Kyle³

et al. 1985

Med. Pediatr. Oncol.

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Thirty-two evaluable good risk patients with multiple myeloma received a 70-day tapering course of prednisone beginning at a dose of 1.2 mg/kg/day. Forty-four percent of the patients demonstrated objective evidence of response to this treatment. Although the median time to disease progression for the prednisone-treated group was shorter than for patients randomized to receive prednisone with alkylating agents or who were treated with alkylating agent alone, the results from this trial indicate that prednisone, by itself, may produce objective responses. Caution must be used interpreting trials of new agents in myeloma when such treatments are combined with corticosteroid administration.

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In-Vitro Glucocorticoid Studies for Predicting Response to Glucocorticoid Therapy in Adults With Malignant Lymphoma

Cited by 55 publications

References 10 publications

c-Myb and Members of the c-Ets Family of Transcription Factors Act as Molecular Switches to Mediate Opposite Steroid Regulation of the Human Glucocorticoid Receptor 1A Promoter

c-Myb and Members of the c-Ets Family of Transcription Factors Act as Molecular Switches to Mediate Opposite Steroid Regulation of the Human Glucocorticoid Receptor 1A Promoter

Pan-Cancer Analyses of the Nuclear Receptor Superfamily

Response rate and survival in myeloma patients receiving prednisone alone

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