Transcription profiling of C/EBP targets identifies Per2 as a gene implicated in myeloid leukemia

Gery, Sigal; Gombart, Adrian F.; Yi, William S.; Koeffler, Chloe; Hofmann, Werner; Koeffler, H. Phillip

doi:10.1182/blood-2005-01-0358

Cited by 143 publications

(143 citation statements)

References 56 publications

Supporting

Mentioning

132

Contrasting

Unclassified

Order By: Relevance

“…Results from a mouse model study have indicated that circadian gene CKIdelta plays a role in lymphocyte physiology [36]. Observations from a human study have also demonstrated that expression levels of the circadian gene PER2 were reduced in lymphoma cell lines and in acute myeloid leukemia (AML) patient samples [37].…”

Section: Possible Mechanisms: Clock-controlled Immune Functionmentioning

confidence: 93%

Clock-cancer connection in non-Hodgkin’s lymphoma

Zhu

Zheng

2008

Medical Hypotheses

View full text Add to dashboard Cite

The universal 24-hour circadian clock has a profound impact on many daily biological processes. Disturbance of circadian rhythms has been implicated in the etiologies of many chronic illnesses, including cancer; with correlations most profoundly found among hormone-related breast and prostate cancers. Given the fact that circadian disruption can cause immune deregulation, which is so far the only established risk factor for non-Hodgkin's lymphoma (NHL), we hypothesize that altered circadian rhythms due to environmental factors and/or genetic variations in genes responsible for maintaining circadian rhythms may result in the deregulation of clock-associated biological processes such as immune responses and activities, and consequently influence an individual's risk of developing NHL. Our recent findings provided the first molecular epidemiological evidence linking a major circadian gene to NHL and warrant further investigation. Confirmation of this hypothesis will further add to our understanding of the role of the circadian clock in lymphomagenesis and facilitate the development of novel risk and prognostic biomarkers for NHL.

show abstract

Section: Possible Mechanisms: Clock-controlled Immune Functionmentioning

confidence: 93%

Clock-cancer connection in non-Hodgkin’s lymphoma

Zhu

Zheng

2008

Medical Hypotheses

View full text Add to dashboard Cite

show abstract

“…Thus, impaired expressions of the clock genes Per1, Per2, or Per3 have been reported in human cancers originating from breast, lung, endometrium, pancreas, or colon, as well as in human myeloid leukemia Gery et al 2005Gery et al , 2006Gery et al , 2007aYeh et al 2005;Shih et al 2006;Krugluger et al 2007). Promoter methylation defects may account for such impaired clock gene expression .…”

Section: Implications For Cancer Chronotherapeuticsmentioning

confidence: 99%

Cross-talks between Circadian Timing System and Cell Division Cycle Determine Cancer Biology and Therapeutics

Lévi

Filipski²,

Iurisci³

et al. 2007

Cold Spring Harbor Symposia on Quantitative Biology

View full text Add to dashboard Cite

“…Plasmids of 1 mg pTag1 (empty vector), pTTF-1, and pHNF3b/ FoxA2 were transfected into BHPs cells using Lipofectamine 2000 (Invitrogen). The zinc-inducible pMT-C/EBPb expression plasmid (Gery et al, 2005) was transfected into BHP cells (sublines 2 -7 and 7 -13), which were selected with 500 mg ml À1 G418 for 48 h.…”

Section: Plasmid Transfection and Colony Assaymentioning

confidence: 99%

Induction of sodium iodide symporter gene and molecular characterisation of HNF3β/FoxA2, TTF-1 and C/EBPβ in thyroid carcinoma cells

et al. 2008

View full text Add to dashboard Cite

Thyroid carcinoma cells often do not express thyroid-specific genes including sodium iodide symporter (NIS), thyroperoxidase (TPO), thyroglobulin (TG), and thyrotropin-stimulating hormone receptor (TSHR). Treatment of thyroid carcinoma cells (four papillary and two anaplastic cell lines) with histone deacetylase inhibitors (SAHA or VPA) modestly induced the expression of the NIS gene. The promoter regions of the thyroid-specific genes contained binding sites for hepatocyte nuclear factor 3 b (HNF3b)/forkhead box A2 (FoxA2), thyroid transcription factor 1 (TTF-1), and CCAAT/enhancer binding protein b (C/EBPb). Quantitative reverse transcription-polymerase chain reaction (RT -PCR) showed decreased expression of HNF3b/FoxA2 and TTF-1 mRNA in papillary thyroid carcinoma cell lines, when compared with normal thyroid cells. Forced expression of these genes in papillary thyroid carcinoma cells inhibited their growth. Furthermore, the CpG island in the promoter region of HNF3b/FoxA2 was aberrantly methylated; and treatment with 5-aza-2-deoxycytidine (5-Az) induced its expression. Immunohistochemical staining showed that C/EBPb was localised in the nucleus in normal thyroid cells but was detected in the cytoplasm in papillary thyroid carcinoma cells. Subcellular fractionation of papillary thyroid carcinoma cell lines also demonstrated high levels of expression of C/EBPb in the cytoplasm, suggesting that a large proportion of C/EBPb protein is inappropriately localised in the cytoplasm. In summary, these findings reveal novel abnormalities in thyroid carcinoma cells

show abstract

Transcription profiling of C/EBP targets identifies Per2 as a gene implicated in myeloid leukemia

Cited by 143 publications

References 56 publications

Clock-cancer connection in non-Hodgkin’s lymphoma

Clock-cancer connection in non-Hodgkin’s lymphoma

Cross-talks between Circadian Timing System and Cell Division Cycle Determine Cancer Biology and Therapeutics

Induction of sodium iodide symporter gene and molecular characterisation of HNF3β/FoxA2, TTF-1 and C/EBPβ in thyroid carcinoma cells

Contact Info

Product

Resources

About