scispace - formally typeset
S

Simone Petersen

Researcher at Charité

Publications -  23
Citations -  2762

Simone Petersen is an academic researcher from Charité. The author has contributed to research in topics: Comparative genomic hybridization & Lung cancer. The author has an hindex of 18, co-authored 23 publications receiving 2719 citations. Previous affiliations of Simone Petersen include Humboldt University of Berlin.

Papers
More filters
Journal ArticleDOI

Diversity of gene expression in adenocarcinoma of the lung

TL;DR: Gene expression analysis promises to extend and refine standard pathologic analysis and make possible the subclassification of adenocarcinoma into subgroups that correlated with the degree of tumor differentiation as well as patient survival.
Journal Article

Patterns of Chromosomal Imbalances in Adenocarcinoma and Squamous Cell Carcinoma of the Lung

TL;DR: The study strengthens the notion that different tumor subgroups of the respiratory tract are characterized by distinct patterns of chromosomal alterations.
Journal ArticleDOI

Chromosomal alterations in the clonal evolution to the metastatic stage of squamous cell carcinomas of the lung.

TL;DR: Comparative genomic hybridization was applied to squamous cellcarcinomas of the lung to define chromosomal imbalances that are associated with the metastatic phenotype, and metastasis-associated lesions were frequently detectable in the primary tumour providing a method of identifying patients at risk for tumour dissemination.
Journal ArticleDOI

Genetic imbalances with impact on survival in head and neck cancer patients.

TL;DR: The genomic data being derived from the evaluation of primary HNSCC enabled a stratification of the patients into subgroups with different survival highlighting the necessity of a genetically based tumor classification for refining diagnosis and treatment of H NSCC patients.
Journal ArticleDOI

Chromosomal imbalances of primary and metastatic lung adenocarcinomas

TL;DR: The analysis of the paired samples revealed considerable chromosomal instability, but indicated a clonal relationship in each case, suggesting that loss of function mutations are critical in the initial phase of tumour dissemination, whereas the metastases preferentially acquired DNA gains, probably modulating the metastatic phenotype.