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Gunilla Chebil

Researcher at Lund University

Publications -  37
Citations -  2857

Gunilla Chebil is an academic researcher from Lund University. The author has contributed to research in topics: Bladder cancer & Breast cancer. The author has an hindex of 21, co-authored 37 publications receiving 2503 citations.

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A Molecular Taxonomy for Urothelial Carcinoma

TL;DR: The molecular subtypes cut across pathologic classification, and class-defining gene signatures show coordinated expression irrespective of pathologic stage and grade, suggesting the molecular phenotypes as intrinsic properties of the tumors.
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Combined gene expression and genomic profiling define two intrinsic molecular subtypes of urothelial carcinoma and gene signatures for molecular grading and outcome.

TL;DR: The combination of molecular and histopathologic classification systems might provide a strong improvement for bladder cancer classification and produce new insights into the development of this tumor type.
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MiRNA expression in urothelial carcinomas: Important roles of miR-10a, miR-222, miR-125b, miR-7 and miR-452 for tumor stage and metastasis, and frequent homozygous losses of miR-31.

TL;DR: In this paper, the authors analyzed 34 cases of urothelial carcinomas by miRNA, mRNA and genomic profiling and identified muscle invasive tumors with high precision and sensitivity using hierarchical clustering using expression information for 300 miRNAs.
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Molecular classification of familial non-BRCA1/BRCA2 breast cancer

TL;DR: It is shown that gene expression profiling can discover novel classes among BRCAx tumors, and differentiate them from BRCA1 and BRC a2 tumors, illustrating that, when gene expression-based classifications are used, BRC Ax families can be grouped into homogeneous subsets, thereby potentially increasing the power of conventional genetic analysis.
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Integrated genomic and gene expression profiling identifies two major genomic circuits in urothelial carcinoma.

TL;DR: The integrative approach revealed at least two separate networks of genomic alterations linked to the molecular diversity seen in UC, and that these circuits may reflect distinct pathways of tumor development.