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Maciej Rosolowski

About Maciej Rosolowski:
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LHA-ID: 7WATJM05G3-0

Location:  Germany

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LIFE- Leipzig Research Center for Civilization Diseases: inactive since

Goal of the Leipzig Research Center for Civilization Diseases (LIFE) is the investigation of civilization diseases like depression, diabetes, allergies or cardiovascular diseases. For this purpose we collect as much data as possible regarding health and living conditions of the population in Leipzig and provide these data for scientists of the University of Leipzig and other research institutions.

Programme: Epidemiology

Public web page: http://life.uni-leipzig.de/

Start date: 1st Jan 2009

LIFE Head and Neck Cancer Group

The aim of the Head and Neck Group within the Leipzig Research Center for Civilization Diseases (LIFE) is to facilitate improvements in the treatment and care of head and neck cancer patients through insights from molecular studies.

The Head and Neck Group within the Leipzig Research Center for Civilization Diseases (LIFE) investigates the molecular mechanisms and the diagnostic and prognostic factors of head and neck cancer. For this purpose, we collected phenotypic information from about 300
...

Programme: This Project is not associated with a Programme

Public web page: http://life.uni-leipzig.de/

Start date: 1st Jan 2012

End date: 31st Dec 2012

head and neck squamous cell carcinomas
LIFE Head and Neck Cancer Group

Stratification of head and neck squamous cell carcinomas (HNSCC) based on HPV16 DNA and RNA status

Snapshots: No snapshots

HNSCC
LIFE Head and Neck Cancer Group

Stratification of head and neck squamous cell carcinomas (HNSCC) based on HPV16 DNA and RNA status

Person responsible: Maciej Rosolowski

Snapshots: No snapshots

Study type: Clinical study (Phase 1)

HNSCC Clinical Dataset
LIFE Head and Neck Cancer Group
No description specified

Contributor: René Hänsel

Assay type: Experimental Assay Type

Technology type: Technology Type

Snapshots: No snapshots

HNSCC OMICS Data
LIFE Head and Neck Cancer Group
No description specified

Contributor: René Hänsel

Assay type: Experimental Assay Type

Technology type: Technology Type

Snapshots: No snapshots

GSE 65858 ODM
LIFE Head and Neck Cancer Group

Our first objective was to compare the molecular features of subgroups of HNSCC defined by their HPV16 DNA and RNA status. The second objective was to identify gene expression subtypes in HNSCC and to correlate them with other characteristics of the patients.

HPV DNA and RNA status, mutations of 50 genes, survival and other clinical characteristics of 270 patients with head and neck cancer.

Creators: René Hänsel, Maciej Rosolowski

Contributor: René Hänsel

Data file type: ODM Data

Download
GSE 65858 CSV
LIFE Head and Neck Cancer Group

Our first objective was to compare the molecular features of subgroups of HNSCC defined by their HPV16 DNA and RNA status. The second objective was to identify gene expression subtypes in HNSCC and to correlate them with other characteristics of the patients.

HPV DNA and RNA status, mutations of 50 genes, survival and other clinical characteristics of 270 patients with head and neck cancer.

Creators: René Hänsel, Maciej Rosolowski

Contributor: René Hänsel

Data file type: Clinical Data

Download
GSE 65858 XLS
LIFE Head and Neck Cancer Group

Our first objective was to compare the molecular features of subgroups of HNSCC defined by their HPV16 DNA and RNA status. The second objective was to identify gene expression subtypes in HNSCC and to correlate them with other characteristics of the patients.

HPV DNA and RNA status, mutations of 50 genes, survival and other clinical characteristics of 270 patients with head and neck cancer.

Creators: René Hänsel, Maciej Rosolowski

Contributor: René Hänsel

Data file type: Clinical Data

Download
Gene expression patterns and TP53 mutations are associated with HPV RNA status, lymph node metastasis, and survival in head and neck cancer (clinical Dataset)
LIFE Head and Neck Cancer Group

Our first objective was to compare the molecular features of subgroups of HNSCC defined by their HPV16 DNA and RNA status. The second objective was to identify gene expression subtypes in HNSCC and to correlate them with other characteristics of the patients.

HPV DNA and RNA status, mutations of 50 genes, survival and other clinical characteristics of 270 patients with head and neck cancer.

Creator: Maciej Rosolowski

Contributor: Christoph Beger

Data file type: Clinical Data

Download
SOM Analysis Results of Head and Neck Squamous Cell Carcinomas
LIFE Head and Neck Cancer Group
No description specified

Creator: Maciej Rosolowski

Contributors: Maciej Rosolowski, Christoph Beger

Data file type: SOM Data

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Genomic and transcriptomic heterogeneity of colorectal tumours arising in Lynch syndrome.
LIFE- Leipzig Research Center for Civilization Diseases

Abstract (Expand)

Colorectal cancer (CRC) arising in Lynch syndrome (LS) comprises tumours with constitutional mutations in DNA mismatch repair genes. There is still a lack of whole-genome and transcriptome studies of … LS-CRC to address questions about similarities and differences in mutation and gene expression characteristics between LS-CRC and sporadic CRC, about the molecular heterogeneity of LS-CRC, and about specific mechanisms of LS-CRC genesis linked to dysfunctional mismatch repair in LS colonic mucosa and the possible role of immune editing. Here, we provide a first molecular characterization of LS tumours and of matched tumour-distant reference colonic mucosa based on whole-genome DNA-sequencing and RNA-sequencing analyses. Our data support two subgroups of LS-CRCs, G1 and G2, whereby G1 tumours show a higher number of somatic mutations, a higher amount of microsatellite slippage, and a different mutation spectrum. The gene expression phenotypes support this difference. Reference mucosa of G1 shows a strong immune response associated with the expression of HLA and immune checkpoint genes and the invasion of CD4+ T cells. Such an immune response is not observed in LS tumours, G2 reference and normal (non-Lynch) mucosa, and sporadic CRC. We hypothesize that G1 tumours are edited for escape from a highly immunogenic microenvironment via loss of HLA presentation and T-cell exhaustion. In contrast, G2 tumours seem to develop in a less immunogenic microenvironment where tumour-promoting inflammation parallels tumourigenesis. Larger studies on non-neoplastic mucosa tissue of mutation carriers are required to better understand the early phases of emerging tumours. Copyright (c) 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Authors: Hans Binder, Lydia Hopp, M. R. Schweiger, S. Hoffmann, F. Juhling, M. Kerick, B. Timmermann, S. Siebert, C. Grimm, L. Nersisyan, A. Arakelyan, M. Herberg, P. Buske, Henry Löffler-Wirth, Maciej Rosolowski, Christoph Engel, J. Przybilla, M. Peifer, N. Friedrichs, G. Moeslein, M. Odenthal, M. Hussong, S. Peters, S. Holzapfel, J. Nattermann, R. Hueneburg, W. Schmiegel, B. Royer-Pokora, S. Aretz, M. Kloth, M. Kloor, R. Buettner, J. Galle, Markus Löffler

Date Published: 21st Jul 2017

Journal: J Pathol

Human Diseases: Lynch syndrome, colorectal cancer

The role of HPV RNA transcription, immune response-related gene expression and disruptive TP53 mutations in diagnostic and prognostic profiling of head and neck cancer.
LIFE Head and Neck Cancer Group

Abstract (Expand)

Stratification of head and neck squamous cell carcinomas (HNSCC) based on HPV16 DNA and RNA status, gene expression patterns, and mutated candidate genes may facilitate patient treatment decision. We … characterize head and neck squamous cell carcinomas (HNSCC) with different HPV16 DNA and RNA (E6*I) status from 290 consecutively recruited patients by gene expression profiling and targeted sequencing of 50 genes. We show that tumors with transcriptionally inactive HPV16 (DNA+ RNA-) are similar to HPV-negative (DNA-) tumors regarding gene expression and frequency of TP53 mutations (47%, 8/17 and 43%, 72/167, respectively). We also find that an immune response-related gene expression cluster is associated with lymph node metastasis, independent of HPV16 status and that disruptive TP53 mutations are associated with lymph node metastasis in HPV16 DNA- tumors. We validate each of these associations in another large data set. Four gene expression clusters which we identify differ moderately but significantly in overall survival. Our findings underscore the importance of measuring the HPV16 RNA (E6*I) and TP53-mutation status for patient stratification and identify associations of an immune response-related gene expression cluster and TP53 mutations with lymph node metastasis in HNSCC.

Authors: G. Wichmann, Maciej Rosolowski, K. Krohn, Markus Kreuz, A. Boehm, A. Reiche, U. Scharrer, D. Halama, J. Bertolini, U. Bauer, D. Holzinger, M. Pawlita, J. Hess, Christoph Engel, D. Hasenclever, Markus Scholz, P. Ahnert, Toralf Kirsten, A. Hemprich, C. Wittekind, O. Herbarth, F. Horn, A. Dietz, Markus Löffler

Date Published: 15th Dec 2015

Journal: Int J Cancer

Human Diseases: head and neck cancer

The PCBP1 gene encoding poly(rC) binding protein I is recurrently mutated in Burkitt lymphoma.
LIFE- Leipzig Research Center for Civilization Diseases

Abstract (Expand)

The genetic hallmark of Burkitt lymphoma is the translocation t(8;14)(q24;q32), or one of its light chain variants, resulting in IG-MYC juxtaposition. However, these translocations alone are insufficient … to drive lymphomagenesis, which requires additional genetic changes for malignant transformation. Recent studies of Burkitt lymphoma using next generation sequencing approaches have identified various recurrently mutated genes including ID3, TCF3, CCND3, and TP53. Here, by using similar approaches, we show that PCBP1 is a recurrently mutated gene in Burkitt lymphoma. By whole-genome sequencing, we identified somatic mutations in PCBP1 in 3/17 (18%) Burkitt lymphomas. We confirmed the recurrence of PCBP1 mutations by Sanger sequencing in an independent validation cohort, finding mutations in 3/28 (11%) Burkitt lymphomas and in 6/16 (38%) Burkitt lymphoma cell lines. PCBP1 is an intron-less gene encoding the 356 amino acid poly(rC) binding protein 1, which contains three K-Homology (KH) domains and two nuclear localization signals. The mutations predominantly (10/12, 83%) affect the KH III domain, either by complete domain loss or amino acid changes. Thus, these changes are predicted to alter the various functions of PCBP1, including nuclear trafficking and pre-mRNA splicing. Remarkably, all six primary Burkitt lymphomas with a PCBP1 mutation expressed MUM1/IRF4, which is otherwise detected in around 20-40% of Burkitt lymphomas. We conclude that PCBP1 mutations are recurrent in Burkitt lymphomas and might contribute, in cooperation with other mutations, to its pathogenesis.

Authors: R. Wagener, S. M. Aukema, M. Schlesner, A. Haake, B. Burkhardt, A. Claviez, H. G. Drexler, Michael Hummel, Markus Kreuz, Markus Löffler, Maciej Rosolowski, C. Lopez, P. Moller, J. Richter, M. Rohde, M. J. Betts, R. B. Russell, S. H. Bernhart, S. Hoffmann, P. Rosenstiel, M. Schilhabel, M. Szczepanowski, L. Trumper, W. Klapper, R. Siebert

Date Published: 16th Jul 2015

Journal: Genes Chromosomes Cancer

Human Diseases: lymphoma

Characterization of genomic imbalances in diffuse large B-cell lymphoma by detailed SNP-chip analysis.
Molecular mechanisms in malignant lymphoma

Abstract (Expand)

The pathogenesis of diffuse large B-cell lymphomas (DLBCL) is only partly understood. We analyzed 148 DLBCL by single nucleotide polymorphism (SNP)-chips to characterize genomic imbalances. Seventy-nine … cases were of the germinal center B-cell like (GCB) type of DLBCL, 49 of the activated B-cell like (ABC) subtype and 20 were unclassified DLBCL. Twenty-four regions of recurrent genomic gains and 38 regions of recurrent genomic losses were identified over the whole cohort, with a median of 25 imbalances per case for ABC-DLBCL and 19 per case for GCB-DLBCL. Several recurrent copy number changes showed differential frequencies in the GCB- and ABC-DLBCL subgroups, including gains of HDAC7A predominantly in GCB-DLBCL (38% of cases) and losses of BACH2 and CASP8AP2 predominantly in ABC-DLBCL (35%), hinting at disparate pathogenetic mechanisms in these entities. Correlating gene expression and copy number revealed a strong gene dosage effect in all tumors, with 34% of probesets showing a concordant expression change in affected regions. Two new potential tumor suppressor genes emerging from the analysis, CASP3 and IL5RA, were sequenced in ten and 16 candidate cases, respectively. However, no mutations were found, pointing to a potential haploinsufficiency effect of these genes, considering their reduced expression in cases with deletions. Our study thus describes differences and similarities in the landscape of genomic aberrations in the DLBCL subgroups in a large collection of cases, confirming already known targets, but also discovering novel copy number changes with possible pathogenetic relevance.

Authors: R. Scholtysik, Markus Kreuz, Michael Hummel, Maciej Rosolowski, M. Szczepanowski, W. Klapper, Markus Löffler, L. Trumper, R. Siebert, R. Kuppers

Date Published: 1st Mar 2015

Journal: Int J Cancer

Human Diseases: diffuse large B-cell lymphoma

Genomic and epigenomic co-evolution in follicular lymphomas.
LIFE Adult

Abstract (Expand)

Follicular lymphoma (FL) with a t(14;18) is a B-cell neoplasm clinically characterized by multiple recurrencies. In order to investigate the clonal evolution of this lymphoma, we studied paired primary … and relapse tumor samples from 33 patients with recurrent non-transformed t(14;18)-positive FL. We reconstructed phylogenetic trees of the evolution by taking advantage of the activation-induced cytidine deaminase (AID)-mediated somatic hypermutation (SHM) active in the germinal center reaction using sequences of the clonal VHDHJH rearrangements of the immunoglobulin heavy chain (IGH) locus. Mutational analysis of the IGH locus showed evidence for ongoing somatic mutation and for counter-selection of mutations affecting the BCR conformation during tumor evolution. We further followed evolutionary divergence by targeted sequencing of gene loci affected by aberrant SHM as well as of known driver genes of lymphomagenesis, and by array-based genome-wide chromosomal imbalance and DNA methylation analysis. We observed a wide spectrum of evolutionary patterns ranging from almost no evolution to divergent evolution within recurrent non-transformed t(14;18) FL. Remarkably, we observed a correlation of the magnitude of evolutionary divergence across all genetic and epigenetic levels suggesting co-evolution. The distribution of coding mutations in driver genes and the correlation with SHM suggest CREBBP and AID to be potential modifiers of genetic and epigenetic co-evolution in FL.

Authors: Markus Löffler, Markus Kreuz, A. Haake, D. Hasenclever, H. Trautmann, C. Arnold, K. Winter, K. Koch, W. Klapper, R. Scholtysik, Maciej Rosolowski, S. Hoffmann, O. Ammerpohl, M. Szczepanowski, D. Herrmann, R. Kuppers, C. Pott, R. Siebert

Date Published: 17th Jul 2014

Journal: Leukemia

Human Diseases: follicular lymphoma

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