Paweł Andrzej Karpiński

Dr. Paweł Andrzej Karpiński

Department of Genetics, Wroclaw Medical University, 50-368 Wroclaw, Poland
orcid

Research Focus & Metrics

Academic Career Length

23Years (2004-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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SSStanislaw Supplitt
Stanislaw Supplitt
Paweł Andrzej KarpińskiPaweł Andrzej Karpiński
Paweł Andrzej Karpiński
MSMaria M. Sasiadek
Maria M. Sasiadek
IŁIzabela Łaczmańska
Izabela Łaczmańska
Over the last decades, transcriptome profiling emerged as one of the most powerful approaches in oncology, providing prognostic and predictive utility for cancer management. The development of novel technologies, such as revolutionary next-generation sequencing, enables the identification of cancer biomarkers, gene signatures, and their aberrant expression affecting oncogenesis, as well as the discovery of molecular targets for anticancer therapies. Transcriptomics contribute to a change in the holistic understanding of cancer, from histopathological and organic to molecular classifications, opening a more personalized perspective for tumor diagnostics and therapy. The further advancement on transcriptome profiling may allow standardization and cost reduction of its analysis, which will be the next step for transcriptomics to become a canon of contemporary cancer medicine.

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WŚWitold Józef Światowy
Witold Józef Światowy
HDHanna Drzewiecka
Hanna Drzewiecka
MKMichalina Kliber
Michalina Kliber
MSMaria M. Sasiadek
Maria M. Sasiadek
Paweł Andrzej KarpińskiPaweł Andrzej Karpiński
Paweł Andrzej Karpiński
PJPaweł Jagodziński
Paweł Jagodziński
Physical activity is a strong stimulus influencing the overall physiology of the human body. Exercises lead to biochemical changes in various tissues and exert an impact on gene expression. Exercise-induced changes in gene expression may be mediated by epigenetic modifications, which rearrange the chromatin structure and therefore modulate its accessibility for transcription factors. One of such epigenetic mark is DNA methylation that involves an attachment of a methyl group to the fifth carbon of cytosine residue present in CG dinucleotides (CpG). DNA methylation is catalyzed by a family of DNA methyltransferases. This reversible DNA modification results in the recruitment of proteins containing methyl binding domain and further transcriptional co-repressors leading to the silencing of gene expression. The accumulation of CpG dinucleotides, referred as CpG islands, occurs at the promoter regions in a great majority of human genes. Therefore, changes in DNA methylation profile affect the transcription of multiple genes. A growing body of evidence indicates that exercise training modulates DNA methylation in muscles and adipose tissue. Some of these epigenetic markers were associated with a reduced risk of chronic diseases. This review summarizes the current knowledge about the influence of physical activity on the DNA methylation status in humans.

11 May 2011 in Molecular Biology Reports
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JGJustyna Gil
Justyna Gil
DRDave Ramsey
Dave Ramsey
ASAgnieszka Stembalska
Agnieszka Stembalska
Paweł Andrzej KarpińskiPaweł Andrzej Karpiński
Paweł Andrzej Karpiński
KPKarolina A. Pesz
Karolina A. Pesz
MSMaria M. Sasiadek
Maria M. Sasiadek

27 October 2017 in Oncotarget
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Paweł Andrzej KarpińskiPaweł Andrzej Karpiński
Paweł Andrzej Karpiński
JRJoanna Rossowska
Joanna Rossowska
MSMaria M. Sasiadek
Maria M. Sasiadek
Immunological landscape of consensus clusters in colorectal cancer Immunological landscape of consensus clusters in colorectal cancer

27 July 2015 in Epigenomics
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Blazej MisiakBlazej Misiak
Blazej Misiak
ESElżbieta Szmida
Elżbieta Szmida
Paweł Andrzej KarpińskiPaweł Andrzej Karpiński
Paweł Andrzej Karpiński
OLOlga Loska
Olga Loska
MSMaria M. Sasiadek
Maria M. Sasiadek
DFDorota Frydecka
Dorota Frydecka
We investigated methylation of DNA repetitive sequences (LINE-1 and BAGE) in peripheral blood leukocytes from first-episode schizophrenia (FES) patients and healthy controls (HCs) with respect to childhood adversities. Patients were divided into two subgroups based on the history of childhood trauma - FES(+) and FES(-) subjects. The majority of HCs had a negative history of childhood trauma - HCs(-) subjects. FES(+) patients had significantly lower LINE-1 methylation in comparison with FES(-) patients or HC(-) subjects. Emotional abuse and total trauma score predicted lower LINE-1 methylation in FES patients, while general trauma score was associated with lower BAGE methylation in HCs. Childhood adversities might be associated with global DNA hypomethylation in adult FES patients.

6 April 2011 in Tumor Biology
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Paweł Andrzej KarpińskiPaweł Andrzej Karpiński
Paweł Andrzej Karpiński
AMAleksander Myszka
Aleksander Myszka
DRDavid Ramsey
David Ramsey
WKWojciech Kielan
Wojciech Kielan
MSMaria M. Sasiadek
Maria M. Sasiadek
There is evidence that insertion of viral DNA into a mammalian genome can lead to alterations of methylation patterns. The aim of the present study was to examine the presence of DNA sequences of five human DNA viruses (assessed by PCR): JC polyoma virus (JCV), human adenovirus (AdV), Epstein–Barr virus (EBV), Kaposi sarcoma-associated herpesvirus (KSHV/HHV8) and human papillomavirus (HPV) in a cohort of 186 sporadic colorectal cancers (CRCs) and related these data with the methylation status of six CpG island methylator phenotype (CIMP)-specific genes (MLH1, CACNA1G, NEUROG1, IGF2, SOCS1, RUNX3) and seven cancer-related genes markers (p16, MINT1, MINT2, MINT31, EN1, SCTR and INHBB) assessed by methylation-specific PCR in 186 and 134 CRC cases, respectively. The AdV, KSHV and HPV were detected in four (2%), two (1%) and zero CRC cases, respectively, and thus were excluded from further analyses. Although 19% and 9% of the CRCs were positive for EBV and JCV, respectively, no associations between virus presence and CpG island methylation were found after correction for multiple testing. Our results demonstrate that the presence of DNA sequences of JCV and EBV in CRC is unrelated to the methylation of the 13 cancer-related CpG islands and CIMP.