Publications by authors named "Monika Prelowska"

4 Publications

  • Page 1 of 1

ALK-rearranged renal cell carcinomas in Polish population.

Pathol Res Pract 2019 Dec 25;215(12):152669. Epub 2019 Sep 25.

Department of Pathomorphology, Medical University of Gdansk, Mariana Smoluchowskiego 17, 80-214 Gdansk, Poland. Electronic address:

Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase, the activation of which is considered an important event in the pathogenesis of several neoplasms and a predictive factor for the targeted therapy with ALK inhibitors. Thus far, ALK rearrangements have been identified in 22 renal cell carcinomas in both pediatric and adult patients. We evaluated the incidence of ALK rearrangement-associated RCC in adult Central European population. An immunohistochemical evaluation of 1019 kidney tumors was performed with use of three different clones of anti-ALK antibodies. None of the tested samples showed positive staining, which suggests that the incidence of ALK rearrangement-associated renal cell carcinomas is significantly lower in the Polish population, and indicates a potential association between ethnicity and occurrence of these rare neoplasms.
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http://dx.doi.org/10.1016/j.prp.2019.152669DOI Listing
December 2019

Upregulation of MLK4 promotes migratory and invasive potential of breast cancer cells.

Oncogene 2019 04 14;38(15):2860-2875. Epub 2018 Dec 14.

Laboratory of Experimental Medicine, Centre of New Technologies, University of Warsaw, Warsaw, Poland.

Metastasis to distant organs is a major cause for solid cancer mortality, and the acquisition of migratory and invasive phenotype is a key factor in initiation of malignancy. In this study we investigated the contribution of Mixed-Lineage Kinase 4 (MLK4) to aggressive phenotype of breast cancer cells. Our TCGA cancer genomic data analysis revealed that amplification or mRNA upregulation of MLK4 occurred in 23% of invasive breast carcinoma cases. To find the association between MLK4 expression and the specific subtype of breast cancer, we performed a transcriptomic analysis of multiple datasets, which showed that MLK4 is highly expressed in triple-negative breast cancer compared to other molecular subtypes. Depletion of MLK4 in cell lines with high MLK4 expression impaired proliferation and anchorage-dependent colony formation. Moreover, silencing of MLK4 expression significantly reduced the migratory potential and invasiveness of breast cancer cells as well as the number of spheroids formed in 3D cultures. These in vitro findings translate into slower rate of tumor growth in mice upon MLK4 knock-down. Furthermore, we established that MLK4 activates NF-κB signaling and promotes a mesenchymal phenotype in breast cancer cells. Immunohistochemical staining of samples obtained from breast cancer patients revealed a strong positive correlation between high expression of MLK4 and metastatic potential of tumors, which was predominantly observed in TNBC subgroup. Taken together, our results show that high expression of MLK4 promotes migratory and invasive phenotype of breast cancer and may represent a novel target for anticancer treatment.
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http://dx.doi.org/10.1038/s41388-018-0618-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6484767PMC
April 2019

4-(Methylthio)butyl isothiocyanate inhibits the proliferation of breast cancer cells with different receptor status.

Pharmacol Rep 2017 Oct 23;69(5):1059-1066. Epub 2017 Apr 23.

Department of Medical Biology and Genetics, University of Gdańsk, Gdańsk, Poland. Electronic address:

Background: Epidemiological studies indicate that the consumption of Brassicaceae plants, a rich source of biologically active isothiocyanates (ITCs), may effectively reduce cancer risk. In the current study, we evaluated the anticancer potential of 4-(methylthio)butyl ITC (erucin, ERN) against three phenotypically different breast cancer cell lines: MDA-MB-231, SKBR-3 and T47D.

Methods: The effect of ERN on the viability of breast cancer cells was evaluated using sulforhodamine B and clonogenic assays, and acridine orange/ethidium bromide staining. Cell cycle was investigated using flow cytometry. The status of signaling molecules was examined by western blot analysis.

Results: ERN decreased the viability of all tested cancer cell lines in a concentration-dependent manner; this effect was much weaker in normal breast cells (MCF-10A). ERN induced cell cycle arrest in the G2/M phase, down-regulated the phosphorylation of S6 ribosomal protein in all tested breast cancer cell lines, and reduced HER2 receptor levels in SKBR-3 cells. A 24-h treatment with lower concentrations of ERN (5-20μM) induced apoptosis; higher ERN concentrations (40μM) induced necrosis. The latter also irreversibly inhibited the proliferative potential of cancer cells.

Conclusion: ERN effectively inhibits proliferation of breast cancer cells irrespectively of their receptor status.
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http://dx.doi.org/10.1016/j.pharep.2017.04.014DOI Listing
October 2017

ALK-positive cancer: still a growing entity.

Future Oncol 2014 Feb;10(2):305-21

Department of Pathomorphology, Medical University of Gdańsk, Mariana Smoluchowskiego 17, 80-214, Gdańsk, Poland.

 Since the discovery of ALK-positive anaplastic large-cell lymphoma in 1994 many other types of tumors showing ALK expression were disclosed. They form a heterogeneous group, including lung, renal and soft tissue tumors. The biological function of ALK, its role in carcinogenesis and impact exerted on the clinical outcome have been studied by many research groups. New drugs specifically dedicated for ALK inhibition, for example, crizotinib, have been synthesized and have become a viable treatment option for ALK-positive lung adenocarcinoma, and potentially for other ALK-positive cancers. This review summarizes the current state of knowledge concerning ALK-positive neoplasms, focusing on the clinical aspects of the subject.
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http://dx.doi.org/10.2217/fon.13.184DOI Listing
February 2014