Joanna Wietrzyk

Prof. Joanna Wietrzyk

Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, R. Weigla 12, 53-114 Wrocław, Poland
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orcid

Research Focus & Metrics

Academic Career Length

29Years (1998-Present)

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

Representative Publications

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26 September 2016 in International Journal of Oncology
Verified
Journal Article
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EMEwa Maj
Ewa Maj
DPDiana Papiernik
Diana Papiernik
JWJoanna Wietrzyk
Joanna Wietrzyk
The discovery of tumor angiogenesis opened a new path in fighting cancer. The approval of different antiangiogenic agents, most targeting vascular endothelial growth factor (VEGF) signaling, has either increased the effectiveness of standard chemotherapy or even replaced it by offering better patient outcomes. However, an increasing number of preclinical and clinical observations have shown that the process of angiogenesis is far from clearly understood. Apart from targeting the VEGF pathway, novel strategies aim to influence other molecular factors that are involved in tumor angiogenesis. In addition, naturally occurring compounds seem to offer additional agents for influencing angiogenesis. The first concept of antiangiogenic therapy aimed to destroy tumor vessels, while it turned out that, paradoxically, antiangiogenic drugs normalized vasculature and as a result offered an improvement in chemotherapeutic delivery. In order to design an effective treatment schedule, methods for detecting the time window of normalization and biomarkers predicting patient response are needed. The initial idea that antiangiogenic therapy would be resistance-free failed to materialize and currently we still face the obstacle of resistance to antiangiogenic therapy.

14 April 2020 in Molecules
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Journal Article
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JKJulia Krzywik
Julia Krzywik
WMWitold Mozga
Witold Mozga
MAMaral Aminpour
Maral Aminpour
Jan JanczakJan Janczak
Jan Janczak
EMEwa Maj
Ewa Maj
AHAdam Huczyński
Adam Huczyński
Colchicine is a well-known compound with strong antiproliferative activity that has had limited use in chemotherapy because of its toxicity. In order to create more potent anticancer agents, a series of novel colchicine derivatives have been obtained by simultaneous modification at C7 (amides and sulfonamides) and at C10 (methylamino group) positions and characterized by spectroscopic methods. All the synthesized compounds have been tested in vitro to evaluate their cytotoxicity toward A549, MCF-7, LoVo, LoVo/DX and BALB/3T3 cell lines. Additionally, the activity of the studied compounds was investigated using computational methods involving molecular docking of the colchicine derivatives to β-tubulin. The majority of the obtained derivatives exhibited higher cytotoxicity than colchicine, doxorubicin or cisplatin against tested cancer cell lines. Furthermore, molecular modeling studies of the obtained compounds revealed their possible binding modes into the colchicine binding site of tubulin.

1 April 2014 in European Journal of Medicinal Chemistry
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Journal Article
Closed access
Michał AntoszczakMichał Antoszczak
Michał Antoszczak
KPKatarzyna Popiel
Katarzyna Popiel
JSJoanna Stefańska
Joanna Stefańska
JWJoanna Wietrzyk
Joanna Wietrzyk
EMEwa Maj
Ewa Maj
AHAdam Huczyński
Adam Huczyński

1 December 2004 in Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Verified
Journal Article
Closed access
ANAnna Nasulewicz-Goldeman
Anna Nasulewicz-Goldeman
JWJoanna Wietrzyk
Joanna Wietrzyk
Federica I. WolfFederica I. Wolf
Federica I. Wolf
Stanisław DzimiraStanisław Dzimira
Stanisław Dzimira
JMJanusz Madej
Janusz Madej
AOAdam Opolski
Adam Opolski

9 November 2018 in Molecules
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Journal Article
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ABAgnieszka Bartmańska
Agnieszka Bartmańska
Tomasz TroninaTomasz Tronina
Tomasz Tronina
JPJarosław Popłoński
Jarosław Popłoński
MMMagdalena Milczarek
Magdalena Milczarek
BFBeata Filip-Psurska
Beata Filip-Psurska
JWJoanna Wietrzyk
Joanna Wietrzyk
Xanthohumol (XN) and four minor hops prenylflavonoids: α,β-dihydroxanthohumol (2HXN), isoxanthohumol (IXN), 8-prenylnaringenin (8PN), and 6-prenylnaringenin (6PN), were tested for antiproliferative activity towards human cancer and normal cell lines. Nonprenylated naringenin (NG) was used as a model compound. Xanthohumol, α,β-dihydroxanthohumol and 6-prenylnaringenin were the most active compounds. Xanthohumol exhibited higher antiproliferative activity than cisplatin (CP) against five cancer cell lines: ovarian resistant to cisplatin A2780cis, breast MDA-MB-231 and T-47D, prostate PC-3, and colon HT-29. Isoxanthohumol was more potent than cisplatin against breast cancer cell lines MDA-MB-231 and T-47D whereas 6-prenylnaringenin was stronger than cisplatin against breast cancer cell line T-47D. It was found that tested chalcones possessed highly selective antiproliferative activity towards all tested breast cancer lines compared to the normal breast MCF 10A cell line (the calculated selectivity index ranged from 5 to 10). Low antiproliferative activity of naringenin indicates the importance of the prenyl group with respect to antiproliferative activity.

17 April 2013 in Molecules
Verified
Journal Article
Open access
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SBStanisław Boryczka
Stanisław Boryczka
EBEwa Bębenek
Ewa Bębenek
JWJoanna Wietrzyk
Joanna Wietrzyk
KKKatarzyna Kempinska
Katarzyna Kempinska
MJMaria Jastrzębska
Maria Jastrzębska
MNMaria Nowak
Maria Nowak
A new series of betulin derivatives containing one or two pharmacophores bearing an acetylenic and carbonyl function at the C-3 and/or C-28 positions has been synthesized and characterized by 1H- and 13C-NMR, IR, MS and elemental analyses. The crystal structure of 28-O-propynoylbetulin was determined by X-ray structural analysis. All new compounds, as well as betulin, were tested in vitro for their antiproliferative activity against human SW707 colorectal, CCRF/CEM leukemia, T47D breast cancer, and against murine P388 leukemia and Balb3T3 normal fibroblasts cell lines. Most of the compounds showed better cytotoxicity than betulin and cisplatin used as reference agent. 28-O-Propynoylbetulin was the most potent derivative, being over 500 times more potent than betulin and about 100 times more cytotoxic than cisplatin against the human leukemia (CCRF/CEM) cell line, with an ID50 value of 0.02 μg/mL.