Ectopic expression of embryonic stem cell and other developmental genes in cutaneous T-cell lymphoma

Litvinov, Ivan V.; Netchiporouk, Elena; Cordeiro, Brendan; Zargham, Hanieh; Pehr, Kevin; Gilbert, Martin; Zhou, Youwen; Moreau, Linda; Woetmann, Anders; Ødum, Niels; Kupper, Thomas S.; Sasseville, Denis

doi:10.4161/21624011.2014.970025

Cited by 40 publications

(47 citation statements)

References 66 publications

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“…A 5.3-fold increase in CD164 mRNA was noted in skin from psoriasis patients. T plastin mRNA was also increased in skin lesions of CTCL patients, as previously reported by other authors (data not shown) [25]. …”

Section: Resultssupporting

confidence: 88%

CD164 identifies CD4+ T cells highly expressing genes associated with malignancy in Sézary syndrome: the Sézary signature genes, FCRL3, Tox, and miR-214

et al. 2016

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Sézary syndrome (SS), a leukemic variant of cutaneous T-cell lymphoma (CTCL), is associated with a significantly shorter life expectancy compared to skin–restricted mycosis fungoides. Early diagnosis of SS is therefore key to achieving enhanced therapeutic responses. However, the lack of a biomarker (s) highly specific for malignant CD4+ T cells in SS patients has been a serious obstacle in making an early diagnosis. We recently demonstrated the high expression of CD164 on CD4+ T cells from Sézary syndrome patients with a wide range of circulating tumor burdens. To further characterize CD164 as a potential biomarker for malignant CD4+T cells, CD164+ and CD164− CD4+ T cells isolated from patients with high circulating tumor burden, B2 stage, and medium/low tumor burden, B1-B0 stage, were assessed for the expression of genes reported to differentiate SS from normal controls, and associated with malignancy and poor prognosis. The expression of Sézary signature genes: T plastin, GATA-3, along with FCRL3, Tox and miR -214 was significantly higher, whereas STAT-4 was lower, in CD164+ compared with CD164−CD4+ T cells. While Tox was highly expressed in both B2 and B1-B0 patients, the expression of Sézary signature genes, FCRL3 and miR-214 was associated predominantly with advanced B2 disease. High expression of CD164 mRNA and protein was also detected in skin from CTCL patients. CD164 was co-expressed with KIR3DL2 on circulating CD4+ T cells from high tumor burden SS patients, further providing strong support for CD164 as a disease relevant surface biomarker.

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Section: Resultssupporting

confidence: 88%

CD164 identifies CD4+ T cells highly expressing genes associated with malignancy in Sézary syndrome: the Sézary signature genes, FCRL3, Tox, and miR-214

et al. 2016

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“…Chromosomal instability, abnormal gene expression, gene duplication, and epigenetic deregulation have been implicated in CTCL, but no single underlying genetic or epigenetic event has yet been identified as a likely cause of the disease. [3][4][5][6][7][8][9] Persistent activation of signal transducer and activator of transcription 3 (STAT3) 10 has repeatedly been implicated in CTCL pathogenesis as a potent driver of survival and proliferation of malignant T cells. [11][12][13][14][15][16][17] Importantly, STAT3 promotes malignant expression of the proinflammatory cytokine interleukin (IL)-17, including a range of cytokines associated with skin inflammation, immune deregulation, and disease progression.…”

Section: Introductionmentioning

confidence: 99%

Staphylococcal enterotoxin A (SEA) stimulates STAT3 activation and IL-17 expression in cutaneous T-cell lymphoma

Willerslev-Olsen

Krejsgaard

Lindahl

et al. 2016

Blood

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• Staphylococcal enterotoxins activate oncogenic pathways in CTCL.• This discovery implies a novel role of microbes as drivers of disease progression. In conclusion, we demonstrate that SEA induces cell cross talk-dependent activation of STAT3 and expression of IL-17 in malignant T cells, suggesting a mechanism whereby SEA-producing bacteria promote activation of an established oncogenic pathway previously implicated in

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“…Pathways downstream of Chd7 include induction of Bmp signaling in mice (Jiang et al 2012; Liu et al 2014) and inhibition of CHK1 phosphorylation-dependent DNA damage repair in response to gemcitabine in human pancreatic cancer cells (Colbert et al 2014). CHD7 and embryonic stem cell genes are aberrantly upregulated in cutaneous T-cell lymphoma, leading to stem cell-like features (Litvinov et al 2014). Consistent with these findings made using human cells, conditional deletion of Chd7 in mice reveals that Chd7 maintains quiescence, thereby preventing premature depletion of neural stem cells (Jones et al 2015).…”

Section: Subfamily Iii: Chd6 Chd7 Chd8 Chd9mentioning

confidence: 99%

“…Whereas there are loss-of-function mutations in CHD7 (like CHD8 ) in colorectal cancer and these lesions correlate with mutations in BRAF, P53, and KRAS (Tahara et al 2014b), there is enhanced expression of CHD7 in cutaneous T-cell lymphoma (Litvinov et al 2014). Consistent with the concept that CHD7 promotes oncogenesis, low-level CHD7 protein expression correlates with enhanced survival of patients with pancreatic cancer (Colbert et al 2014).…”

Section: Subfamily Iii: Chd6 Chd7 Chd8 Chd9mentioning

confidence: 99%

The Chromodomain Helicase DNA-Binding Chromatin Remodelers: Family Traits that Protect from and Promote Cancer

Mills

2017

Cold Spring Harb Perspect Med

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A plethora of mutations in chromatin regulators in diverse human cancers is emerging, attesting to the pivotal role of chromatin dynamics in tumorigenesis. A recurrent theme is inactivation of the Chromodomain Helicase DNA-binding (CHD) family of proteins—ATP-dependent chromatin remodelers that govern the cellular machinery’s access to DNA, thereby controlling fundamental processes including transcription, proliferation, and DNA damage repair. This review highlights what is currently known about how genetic and epigenetic perturbation of CHD proteins and the pathways they regulate set the stage for cancer, providing new insight for designing more effective anti-cancer therapies.

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Ectopic expression of embryonic stem cell and other developmental genes in cutaneous T-cell lymphoma

Cited by 40 publications

References 66 publications

CD164 identifies CD4+ T cells highly expressing genes associated with malignancy in Sézary syndrome: the Sézary signature genes, FCRL3, Tox, and miR-214

CD164 identifies CD4+ T cells highly expressing genes associated with malignancy in Sézary syndrome: the Sézary signature genes, FCRL3, Tox, and miR-214

Staphylococcal enterotoxin A (SEA) stimulates STAT3 activation and IL-17 expression in cutaneous T-cell lymphoma

The Chromodomain Helicase DNA-Binding Chromatin Remodelers: Family Traits that Protect from and Promote Cancer

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