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Antoaneta Mincheva

Researcher at German Cancer Research Center

Publications -  36
Citations -  1582

Antoaneta Mincheva is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Gene & Exon. The author has an hindex of 20, co-authored 36 publications receiving 1530 citations.

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Molecular characterization of a slowly gating human hyperpolarization-activated channel predominantly expressed in thalamus, heart, and testis

TL;DR: The characteristic expression pattern and the sluggish gating suggest that hHCN4 controls the rhythmic activity in both thalamocortical neurons and pacemaker cells of the heart.
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Adrenocortical carcinoma is characterized by a high frequency of chromosomal gains and high-level amplifications.

TL;DR: Interestingly, the adenomas larger than 4 cm contained gained material of regions also overrepresented in carcinomas, indicating that the larger adrenal lesions need to be carefully considered in the diagnosis of adrenocortical tumors, and that genetic aberrations might provide useful markers for a better diagnostic differentiation.
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Chromosomal integration sites of human papillomavirus DNA in three cervical cancer cell lines mapped by in situ hybridization

TL;DR: Metaphase chromosomes of three cervical cancer cell lines were subjected to in situ hybridizations with the DNA of human papillomaviruses (HPV) types 16 and 18 and indirectly support a trans-acting function of HPV-mediated cell transformation.
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Comprehensive genomic analysis of desmoplastic medulloblastomas: identification of novel amplified genes and separate evaluation of the different histological components.

TL;DR: Several novel genetic alterations in DMBs are identified and genetic evidence for a monoclonal origin of their different tissue components is provided, and common chromosomal imbalances in five of six informative tumours are identified.
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Clustered arrangement of winged helix genes fkh-6 and MFH-1: possible implications for mesoderm development.

TL;DR: It is suggested that a mutation in MFH-1, not fkh-6 is the possible cause for the amputated phenotype, and the close physical linkage of these two winged helix genes is conserved in man, where the two genes map to chromosome 16q22-24.