Analyses of the genomic methylation status of the human cyclin A1 promoter by a novel real‐time PCR‐based methodology

Müller‐Tidow, Carsten; Bornemann, Christina; Diederichs, Sven; Westermann, Annette; Klümpen, S.; Zuo, Peijun; Wang, Wenbing; Berdel, Wolfgang E.

doi:10.1016/s0014-5793(01)02128-7

Cited by 19 publications

(13 citation statements)

References 11 publications

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“…Aberrant methylation of CpG dinucleotides occurs frequently in acute leukemia. Recently, we introduced a real-time PCR method to quantitatively analyze DNA methylation patterns of specific gene promoters with high sensitivity (27).…”

Section: Resultsmentioning

confidence: 99%

“…Due to the high frequency of DNA methylation in acute leukemias and its involvement in leukemia pathogenesis, we investigated whether sensitive and specific analysis of DNA methylation patterns could serve as reliable markers for MRD quantitation and as a predictor for leukemia relapse in remission. Recently, we introduced a rapid and quantitative methylation detection methodology based on real-time PCR (27). Here, we show increased estrogen receptor a (ERa) and p15 INK4B methylation levels in bone marrow from leukemia patients in clinical remission.…”

Section: Introductionmentioning

confidence: 92%

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DNA Methylation of Tumor Suppressor Genes in Clinical Remission Predicts the Relapse Risk in Acute Myeloid Leukemia

et al. 2007

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Epigenetic changes play an important role in leukemia pathogenesis. DNA methylation is among the most common alterations in leukemia. The potential role of DNA methylation as a biomarker in leukemia is unknown. In addition, the lack of molecular markers precludes minimal residual disease (MRD) estimation for most patients with hematologic malignancies. We analyzed the potential of aberrant DNA promoter methylation as a biomarker for MRD in acute leukemias. Quantitative real-time PCR methods with bisulfite-modified DNA were established to quantify MRD based on estrogen receptor A (ERA) and/or p15 INK4B methylation. Methylation analyses were done in >370 DNA specimens from 180 acute leukemia patients and controls. Methylation of ERA and/or p15 INK4B occurred frequently and specifically in acute leukemia but not in healthy controls or in nonmalignant hematologic diseases. Aberrant DNA methylation was detectable in >20% of leukemia patients during clinical remission. In pediatric acute lymphoblastic leukemia, methylation levels during clinical remission correlated closely with T-cell receptor/immunoglobulin MRD levels (r = +0.7, P < 0.01) and were associated with subsequent relapse. In acute myelogenous leukemia patients in clinical remission, increased methylation levels were associated with a high relapse risk and significantly reduced relapse-free survival (P = 0.003). Many patients with acute leukemia in clinical remission harbor increased levels of aberrant DNA methylation. Analysis of methylation MRD might be used as a novel biomarker for leukemia patients' relapse risk. [Cancer Res 2007;67(3):1370-7]

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

DNA Methylation of Tumor Suppressor Genes in Clinical Remission Predicts the Relapse Risk in Acute Myeloid Leukemia

et al. 2007

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“…For stable transfection, MCF-7 cells were transfected with control pcDNA vector and pcDNA vector containing full-length human cyclin A1 cDNA using the electroporation system with Nucleofection kit (Amaxa Biosystems). The cyclin A1-pcDNA vector was kindly provided by Dr. Carsten Muller-Tidow (Department of Medicine, University of Munster, Munster, Germany) and was described previously [21]. 2–5 µg vectors were used in transfection experiments.…”

Section: Methodsmentioning

confidence: 99%

“…Cyclin A1 has been previously shown to play an important role in tumorigenesis. In normal tissues, cyclin A1 expression has mainly been detected in testes, hematopoietic cells and brain [21–24]. Only low level of cyclin A1 transcript is observed in the developing mammary gland, but its level becomes undetectable in adult gland during pregnancy [25].…”

Section: Introductionmentioning

confidence: 99%

Cyclin A1 Modulates the Expression of Vascular Endothelial Growth Factor and Promotes Hormone-Dependent Growth and Angiogenesis of Breast Cancer

et al. 2013

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Alterations in cellular pathways related to both endocrine and vascular endothelial growth factors (VEGF) may contribute to breast cancer progression. Inhibition of the elevated levels of these pathways is associated with clinical benefits. However, molecular mechanisms by which endocrine-related pathways and VEGF signalling cooperatively promote breast cancer progression remain poorly understood. In the present study, we show that the A-type cyclin, cyclin A1, known for its important role in the initiation of leukemia and prostate cancer metastasis, is highly expressed in primary breast cancer specimens and metastatic lesions, in contrasting to its barely detectable expression in normal human breast tissues. There is a statistically significant correlation between cyclin A1 and VEGF expression in breast cancer specimens from two patient cohorts (p<0.01). Induction of cyclin A1 overexpression in breast cancer cell line MCF-7 results in an enhanced invasiveness and a concomitant increase in VEGF expression. In addition, there is a formation of protein–protein complexes between cyclin A1 and estrogen receptor ER-α cyclin A1 overexpression increases ER-α expression in MCF-7 and T47D cells. In mouse tumor xenograft models in which mice were implanted with MCF-7 cells that overexpressed cyclin A1 or control vector, cyclin A1 overexpression results in an increase in tumor growth and angiogenesis, which is coincident with an enhanced expression of VEGF, VEGFR1 and ER-α Our findings unravel a novel role for cyclin A1 in growth and progression of breast cancer, and suggest that multiple cellular pathways, including cell cycle regulators, angiogenesis and estrogen receptor signalling, may cooperatively contribute to breast cancer progression.

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“…This fragment can induce expression of a reporter gene mediated by GC boxes that can bind Sp1 in HeLa cells (Muller et al, 1999) and by coexpression with B-myb and cyclin A1 in CV-1 cells (Muller et al, 2000b). Although it was initially suggested that the tissue-specific expression of mouse cyclin A1 correlates with methylation of its CpG-rich proximal promoter (Muller et al, 2000a), subsequent studies revealed that this is not likely (Muller-Tidow et al, 2001). Cyclin A1 frequently is overexpressed in human acute promyelocytic leukemia, a subtype of acute myeloid leukemia that is characterized by the presence of the PML-RAR␣ fusion protein .…”

Section: Regulation Of Expression Of the A-type Cyclinsmentioning

confidence: 99%

Regulation of the Mitotic and Meiotic Cell Cycles in the Male Germ Line

Wolgemuth¹

2002

Recent Progress in Hormone Research

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Mammalian gametogenesis provides a unique system in which to study cell-cycle regulation. Furthermore, understanding the genetic program controlling the mitotic and meiotic divisions of the germ line will provide insight into understanding infertility and new directions for contraception. Male and female germ cells have stages of cell-cycle regulation in common, including a mitotic proliferative stage, entry into meiosis, completion of a reductive division, and entry into a quiescent state awaiting signals at fertilization. However, the timing of these events -and, indeed, even the stage of development at which these events occurs -differs in the two sexes. The genes involved in controlling these specialized mitotic and meiotic cycles of mammalian germ cell differentiation are only now being identified. They include a complex array of kinases, phosphatases, regulatory proteins (e.g., cyclins), and an equally complex array of substrates, including components of the nuclear and cytoplasmic structures involved in cell division. This chapter provides an overview of our current understanding of cell-cycle regulation in mammalian mitotic cells and the importance of restriction points. A summary of observations regarding the expression of various cell-cycle regulatory genes in mouse gametes is provided, along with comments on interesting differences between mitotic and meiotic cells. Finally, the role of the novel A-type cyclin, cyclin A1, during male meiosis is discussed in depth.

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Analyses of the genomic methylation status of the human cyclin A1 promoter by a novel real‐time PCR‐based methodology

Cited by 19 publications

References 11 publications

DNA Methylation of Tumor Suppressor Genes in Clinical Remission Predicts the Relapse Risk in Acute Myeloid Leukemia

DNA Methylation of Tumor Suppressor Genes in Clinical Remission Predicts the Relapse Risk in Acute Myeloid Leukemia

Cyclin A1 Modulates the Expression of Vascular Endothelial Growth Factor and Promotes Hormone-Dependent Growth and Angiogenesis of Breast Cancer

Regulation of the Mitotic and Meiotic Cell Cycles in the Male Germ Line

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