Dastin Langner - PhD Student

Tel.: +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: dlangner[at]bio.uni-kl.de
Room: 24-109

Project description:

Aneuploid cells, meaning cells with an aberrant chromosome number, usually show proliferation defects in vitro compared to euploid cells with a natural set of chromosomes. However, aneuploid phenotypes show an adapted behavior regarding the proliferation rate under selective conditions of a stressful and frequently changing environment, as is the case in cancer. My goal is to investigate which adaptations aneuploid and especially monosomic cells undergo in order to be able to outgrow healthy, euploid cells and what specific vulnerabilities or resistances are associated with them.

Karen Barthel - PhD Student

Tel.: +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email: kbarthel[at]bio.uni-kl.de
Room: 24-101A

Project description:

Healthy human cells have a diploid set of chromosomes and alterations are rarely tolerated. However, aneuploidy – an aberrant chromosome number – is a hallmark of cancer. In laboratory strains proliferation defects occur as a consequence of both gains (polyploidy) as well as losses (monosomy) of chromosomes. Yet, some cellular phenotypes seem to differ dependent on ploidy status and identity of the specific chromosome. My research focuses on the cellular consequences of monosomy as well as identifying factors that allow proliferation after chromosome loss.

Antonius Bröhl - PhD Student

Tel.: +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email: broehl[at]rhrk.uni-kl.de
Room: 24-101A

Project description:

Healthy human cells typically contain 46 chromosomes, and rarely tolerate changes of this number. However, around 90% of solid tumors exhibit alterations in chromosome count, so called aneuploidy. Most research has focused on understanding the gain of chromosomes (polysomy), as full chromosome loss (monosomy) is generally not viable for cells. In our recent studies we have found that loss of p53 function allows monosomic cells to survive. My research aims to investigate the impact of monosomy on chromosomal stability and identify potential pathways that enable cell survival under these conditions.

Anna-Luisa Hertel - PhD Student

Tel.:+49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: hertela[at]rptu.de
Room: 24-109

Project description:

Aneuploidy, chromosomal instability (CIN) and whole genome doubling (WGD) are key factors in cancer development. WGD is defined by the duplication of the entire set of chromosomes and can promote tumorigenesis in cells with permissive genetic backgrounds, such as lack or mutation of the TP53 gene. The transcription factor p53 is crucial for tumor suppression by controlling passage through the cell cycle under stress conditions. The loss of the p53 function leads to accumulation of non-diploid cells. Interestingly, some mutations of p53 has been proposed to lead to changes in the regulatory functions of this important protein.

In my project I will identify deregulations of genomic instability in response to the type of p53 mutation in human cells. Specifically, I intend to induce whole genome doubling in various cell lines with p53 alterations and analyze proteome and transcriptome data derived from these model cells to determine the effect of p53 function on cellular response to chromosome copy number changes. Moreover, I will analyze data sets derived from large cell line collections of cancer cell lines with altered chromosome numbers and p53 status.

Jan-Eric Bökenkamp - PhD Student

Tel. +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: boekenka[at]biologie.uni-kl.de
Raum: 24-109

Project description:

Chromosomal copy number aberrations are a well-established hallmark of cancer cells. Yet, adding extra chromosomes to cells in-vitro often has an initially detrimental effect on cell survival and proliferation. Through statistical analysis of data from various models of evolving cells with altered chromosome numbers, I aim to derive robust and comprehensive characterizations of multi-omic changes that facilitate the tolerance and adaption to aneuploidy.

Leah Johnson - PhD Student

Tel. +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email: leahj[at]bio.uni-kl.de
Raum: 24-101A

Project description:

Aneuploidy, a karyotype characterized by the uneven gain or loss of whole chromosomes or regions of chromosomes, is frequently observed in cancer. My project aims to engineer a complete trisomy collection in near-diploid cancer cell lines using Microcell-Mediated Chromosome Transfer (MMCT). The trisomic cells will be analyzed by  transcriptomics and proteomics, and by phenotypic characterization, to identify the changes caused by the gain of a chromosome. The trisomy collection cell lines will serve as a tool to better understand why certain chromosomes are gained more frequently than the others in cancer.

Olha Kurpa - PhD Student

Tel. +49 (0)631-205-4385
Fax: +49 (0)631-205-4090
Email: 
Raum: 24-101

Project description:

Aneuploidy, defined as alterations in the number of whole chromosomes or chromosome segments, is a common feature in cancer cells. Chromosomal gain leads to the overexpression of unnecessary proteins. It induces proteotoxic stress, when protein folding is disrupted, while protein aggregation and degradation increase.

In response to proteotoxic stress, aneuploid cells upregulate the autophagy receptor p62, which sequesters mitochondrial proteins and localizes to mitochondria. Cells with chromosomal gains also exhibit impaired mitochondrial structure and import. However, the specific mechanisms linking disrupted protein homeostasis to mitochondrial dysfunction in aneuploidy remain unclear.

My project aims to analyze the impact of chromosomal gains on mitochondrial structure and function and to explore the link between proteotoxic stress and mitochondrial alterations in aneuploidy.

Bastian Hinkel - PhD Student

Tel. +49 (0)631-205-5919
Fax: +49 (0)631-205-4090
Email: bhinkel[at]rptu.de
Raum: 24-101A

Project description:

Aneuploidy, a condition in which the number of chromosomes deviates from the normal diploid karyotype, is common in cancer, with an incidence of over 90 % in solid tumors and 75 % in hematopoietic cancers. Understanding the effects of aneuploidies is critical to uncover mechanisms leading to tumorigenesis and to develop effective treatments for cancer patients. The key focus of my research is the analysis of chromosome loss (monosomy), which is much less understood than chromosome gain (polysomy). In particular, my research focuses on pathways and proteins that facilitate the replication and repair of under-replicated, difficult-to-replicate, or damaged DNA regions in monosomic cells compared to diploid cells. The goal is to determine the effects of chromosome loss on these processes and to understand the underlying mechanisms.

Tamara Hamann - PhD Student

Tel. +49 (0)631-205-5920
Fax: +49 (0)631-205-4090
Email: thamann[at]rptu.de
Raum: 24-109

Project description:

Glioblastoma multiforme is the most aggressive brain cancer, well known for its high plasticity enabling it to evade therapy by transitioning to less vulnerable cell states. As of yet plasticity in cancer cells is poorly understood, however, research suggests that aneuploidy – the cellular state of an abnormal chromosome copy number – is one key benefactor. Indeed, nearly 90% of GBM tumors display a non-random aneuploid karyotype at an early stage, with specific chromosome gains and losses. Despite this, its role in tumorigenesis and treatment resistance remains unclear. We hypothesize that an aneuploid karyotype provides a reservoir of potentially resistant cell states, giving it a selective advantage in challenging microenvironments. I aim to address this proposition by combining both experimental and computational approaches.