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Relevant bibliographies by topics / CCNE2

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Journal articles

Academic literature on the topic 'CCNE2'

Author: Grafiati

Published: 1 April 2023

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Journal articles on the topic "CCNE2"

1

Kondo, Yukio, Eric Wieder, Sijie Lu, and Jeffrey Molldrem. "High Avidity Cyclin E1-Derived Peptide-Specific CTL Kill Lymphoid Leukemia Cells and Cross-Recognize a Homologous Cyclin E2-Derived Peptide." Blood 104, no. 11 (2004): 4498. http://dx.doi.org/10.1182/blood.v104.11.4498.4498.

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Abstract Using a similar strategy that successfully identified PR1 as a leukemia-associated antigen (LAA), we identified two homologous HLA-A2-restricted peptides from cyclin E1 (CCNE1) and cyclin E2 (CCNE2) that could be used to elicit peptide-specific CTL from healthy donors in vitro. Two homologous nonameric peptides from CCNE1 (CCNE1144–152) and CCNE2 (CCNE2144–152), which differ by a single amino acid at position 7, have equal binding affinity for HLA-A2 and each elicited peptide-specific CTL with equal efficiency, as measured by specific lysis of T2 cells pulsed with either peptide (CCNE

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2

Sonntag, Roland, Nives Giebeler, Yulia A. Nevzorova, et al. "Cyclin E1 and cyclin-dependent kinase 2 are critical for initiation, but not for progression of hepatocellular carcinoma." Proceedings of the National Academy of Sciences 115, no. 37 (2018): 9282–87. http://dx.doi.org/10.1073/pnas.1807155115.

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E-type cyclins E1 (CcnE1) and E2 (CcnE2) are regulatory subunits of cyclin-dependent kinase 2 (Cdk2) and thought to control the transition of quiescent cells into the cell cycle. Initial findings indicated that CcnE1 and CcnE2 have largely overlapping functions for cancer development in several tumor entities including hepatocellular carcinoma (HCC). In the present study, we dissected the differential contributions of CcnE1, CcnE2, and Cdk2 for initiation and progression of HCC in mice and patients. To this end, we tested the HCC susceptibility in mice with constitutive deficiency for CcnE1 or

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3

Ishiyama, Ken, Yukio Kondo, Eric Wieder, Sijie Lu, and Jeffrey Molldrem. "High Avidity Cyclin E-Derived Peptide-Specific CTL Contribute to Induction of Remission after Stem Cell Transplantation without Associated Graft-Versus-Host Disease." Blood 106, no. 11 (2005): 1424. http://dx.doi.org/10.1182/blood.v106.11.1424.1424.

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Abstract Cyclin E1 (CCNE1) and cyclin E2 (CCNE2) are cell cycle genes that are overexpressed in AML, ALL, and CML, and in solid tumors such as breast cancer, lung cancer, and gastric cancer. We reported that two homologous nonameric peptides from CCNE1 (CCNE1144-152, ILLDWLMEV) and CCNE2 (CCNE2144-152, ILLDWLLEV), which differ by a single amino acid at position 7, have equal binding affinity for HLA-A2 and that CCNE1- and CCNE2- specific CTL elicited from healthy donors kill ALL and CML cells that overexpress CCNE1 and CCNE2. Interestingly, CCNE1/A2 and CCNE2/A2 tetramers bind to both T-cell r

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4

He, Hong, Ken Ishiyama, Gheath Alatrash, Yukio Kondo, Sijie Lu, and Jeffrey J. Molldrem. "T-Cell Immunity to Two HLA-A2-Restricted Self-Determinants of Cyclin E May Contribute to Remission After Stem Cell Transplantation." Blood 114, no. 22 (2009): 686. http://dx.doi.org/10.1182/blood.v114.22.686.686.

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Abstract Abstract 686 Cyclin E1 (CCNE1) and cyclin E2 (CCNE2) are tightly regulated cell cycle genes in normal cells but are over-expressed and constitutively active in breast cancer and in the majority of hematological malignances. To validate CCNE as a potential target antigen for T-cells in leukemia, we first confirmed aberrant CCNE1 and CCNE2 protein in PBMC from 26 (93%) of 28 patients (CML = 16; AML = 7; ALL =2; NHL = 3) by Western Blot compared to 4 (33%) of 12 healthy controls (p < 0.0005). Next, we screened the sequences of CCNE1 and CCNE2 for HLA-A*0201 binding motifs and identifi

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5

Martín-Garcia, David, Alba Navarro, Rafael Valdés-Mas, et al. "CCND2 and CCND3 hijack immunoglobulin light-chain enhancers in cyclin D1− mantle cell lymphoma." Blood 133, no. 9 (2019): 940–51. http://dx.doi.org/10.1182/blood-2018-07-862151.

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Abstract Mantle cell lymphoma (MCL) is characterized by the t(11;14)(q13;q32) translocation resulting in overexpression of cyclin D1. However, a small subset of cyclin D1− MCL has been recognized, and approximately one-half of them harbor CCND2 translocations while the primary event in cyclin D1−/D2− MCL remains elusive. To identify other potential mechanisms driving MCL pathogenesis, we investigated 56 cyclin D1−/SOX11+ MCL by fluorescence in situ hybridization (FISH), whole-genome/exome sequencing, and gene-expression and copy-number arrays. FISH with break-apart probes identified CCND2 rear

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6

Wu, Lizheng, Kuan Yang, Yajie Gui, and Xiaojing Wang. "Nicotine-upregulated miR-30a arrests cell cycle in G1 phase by directly targeting CCNE2 in human periodontal ligament cells." Biochemistry and Cell Biology 98, no. 3 (2020): 354–61. http://dx.doi.org/10.1139/bcb-2019-0156.

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The consumption of nicotine via smoking tobacco has been reported to stimulate the occurrence and progression of periodontitis. Many studies have demonstrated that nicotine prevents the regeneration of periodontal tissues primarily by inhibiting the proliferation of human periodontal ligament (PDL) cells. However, the mechanisms underlying this process are still unclear. Therefore, we investigated whether nicotine-upregulated miR-30a inhibited the proliferation of human PDL cells by downregulating cyclin E2 (CCNE2), in vitro. Quantitative real-time PCR analysis revealed that nicotine upregulat

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7

Tao, Kaiyi, JinShi Liu, JinXiao Liang, XiaoFang Xu, LiWei Xu, and WeiMin Mao. "Vascular endothelial cell-derived exosomal miR-30a-5p inhibits lung adenocarcinoma malignant progression by targeting CCNE2." Carcinogenesis 42, no. 8 (2021): 1056–67. http://dx.doi.org/10.1093/carcin/bgab051.

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Abstract This study tried to explore the molecular mechanism underlying progression of lung adenocarcinoma (LUAD) and discuss the extracellular communication between cancer cells and vascular endothelial cells. Roughly, differential analysis was carried out to note that miR-30a-5p was lowly expressed in LUAD, whereas CCNE2 was highly expressed. Cell functional experiments demonstrated that overexpressed miR-30a-5p led to suppressed cell abilities in proliferation, migration and invasion. Dual-luciferase reporter gene assay and RNA immunoprecipitation verified the binding of miR-30a-5p and CCNE

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8

Diab, Sami, Matei P. Socoteanu, Carlos A. Encarnacion, et al. "High-risk breast cancer genes at 8q22-24 and their role in over 5,000 patients evaluated with the 70-gene risk of recurrence assay." Journal of Clinical Oncology 38, no. 15_suppl (2020): 3569. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3569.

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3569 Background: Previous studies have shown that CCNE2 expression is higher in patients’ cancers resistant to CDK4/6 inhibitors. Increased expression of CCNE2, MTDH, or TSPYL5, genes contained within the 70-gene risk of distant recurrence signature (70GS), has also been implicated in breast oncogenesis, poor prognosis, and chemoresistance. These genes are located on chromosome region 8q22.1, one of the most recurrently amplified regions out of all 70GS genes in breast tumors (Fatima et al. 2017). MYC, located on 8q24, is overexpressed in 40% of all breast cancers (BC). Here we examined the ex

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9

Lee, Christine, Kristine J. Fernandez, Sarah Alexandrou, et al. "Cyclin E2 Promotes Whole Genome Doubling in Breast Cancer." Cancers 12, no. 8 (2020): 2268. http://dx.doi.org/10.3390/cancers12082268.

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Genome doubling is an underlying cause of cancer cell aneuploidy and genomic instability, but few drivers have been identified for this process. Due to their physiological roles in the genome reduplication of normal cells, we hypothesised that the oncogenes cyclins E1 and E2 may be drivers of genome doubling in cancer. We show that both cyclin E1 (CCNE1) and cyclin E2 (CCNE2) mRNA are significantly associated with high genome ploidy in breast cancers. By live cell imaging and flow cytometry, we show that cyclin E2 overexpression promotes aberrant mitosis without causing mitotic slippage, and i

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10

Kikuchi, Kei, and Daisuke Kaida. "CCNE1 and E2F1 Partially Suppress G1 Phase Arrest Caused by Spliceostatin A Treatment." International Journal of Molecular Sciences 22, no. 21 (2021): 11623. http://dx.doi.org/10.3390/ijms222111623.

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The potent splicing inhibitor spliceostatin A (SSA) inhibits cell cycle progression at the G1 and G2/M phases. We previously reported that upregulation of the p27 cyclin-dependent kinase inhibitor encoded by CDKN1B and its C-terminal truncated form, namely p27*, which is translated from CDKN1B pre-mRNA, is one of the causes of G1 phase arrest caused by SSA treatment. However, the detailed molecular mechanism underlying G1 phase arrest caused by SSA treatment remains to be elucidated. In this study, we found that SSA treatment caused the downregulation of cell cycle regulators, including CCNE1,

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