Prof. Dr. Anna M. Czarnecka, MBA
Maria Sklodowska-Curie National Research Institute of Oncology, Warsaw, Poland
Head of Department of Outpatient Chemotherapy
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Academic Career Length
21Years (2006-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
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Journal Article
Anna M. Czarnecka, MBAKSKamil Synoradzki
Kamil SynoradzkiWFWiktoria Firlej
Wiktoria Firlej
Ewa BartnikPSPaweł Sobczuk
Paweł Sobczuk
Piotr Rutkowski +2
Osteosarcoma (OS) is the most frequent primary bone cancer in children and adolescents and the third most frequent in adults. Many inherited germline mutations are responsible for syndromes that predispose to osteosarcomas including Li Fraumeni syndrome, retinoblastoma syndrome, Werner syndrome, Bloom syndrome or Diamond–Blackfan anemia. TP53 is the most frequently altered gene in osteosarcoma. Among other genes mutated in more than 10% of OS cases, c-Myc plays a role in OS development and promotes cell invasion by activating MEK–ERK pathways. Several genomic studies showed frequent alterations in the RB gene in pediatric OS patients. Osteosarcoma driver mutations have been reported in NOTCH1, FOS, NF2, WIF1, BRCA2, APC, PTCH1 and PRKAR1A genes. Some miRNAs such as miR-21, -34a, -143, -148a, -195a, -199a-3p and -382 regulate the pathogenic activity of MAPK and PI3K/Akt-signaling pathways in osteosarcoma. CD133+ osteosarcoma cells have been shown to exhibit stem-like gene expression and can be tumor-initiating cells and play a role in metastasis and development of drug resistance. Although currently osteosarcoma treatment is based on adriamycin chemoregimens and surgery, there are several potential targeted therapies in development. First of all, activity and safety of cabozantinib in osteosarcoma were studied, as well as sorafenib and pazopanib. Finally, novel bifunctional molecules, of potential imaging and osteosarcoma targeting applications may be used in the future.
19 December 2016 in Molecular Cancer
Journal Article
KBKlaudia K. Brodaczewska
Klaudia K. Brodaczewska
CSCezary Szczylik
Cezary SzczylikMFMichal Fiedorowicz
Michal FiedorowiczCPCamillo Porta
Camillo Porta
Anna M. Czarnecka, MBACell lines are still a tool of choice for many fields of biomedical research, including oncology. Although cancer is a very complex disease, many discoveries have been made using monocultures of established cell lines. Therefore, the proper use of in vitro models is crucial to enhance our understanding of cancer. Therapeutics against renal cell cancer (RCC) are also screened with the use of cell lines. Multiple RCC in vitro cultures are available, allowing in vivo heterogeneity in the laboratory, but at the same time, these can be a source of errors. In this review, we tried to sum up the data on the RCC cell lines used currently. An increasing amount of data on RCC shed new light on the molecular background of the disease; however, it revealed how much still needs to be done. As new types of RCC are being distinguished, novel cell lines and the re-exploration of old ones seems to be indispensable to create effective in vitro tools for drug screening and more.
Journal Article
Anna M. Czarnecka, MBAEwa BartnikMFMichal Fiedorowicz
Michal FiedorowiczPiotr RutkowskiThe common mutation BRAFV600 in primary melanomas activates the mitogen-activated protein kinase/extracellular-signal-regulated kinase (MAPK/ERK) pathway and the introduction of proto-oncogene B-Raf (BRAF) and mitogen-activated protein kinase kinase (MEK) inhibitors (BRAFi and MEKi) was a breakthrough in the treatment of these cancers. However, 15–20% of tumors harbor primary resistance to this therapy, and moreover, patients develop acquired resistance to treatment. Understanding the molecular phenomena behind resistance to BRAFi/MEKis is indispensable in order to develop novel targeted therapies. Most often, resistance develops due to either the reactivation of the MAPK/ERK pathway or the activation of alternative kinase signaling pathways including phosphatase and tensin homolog (PTEN), neurofibromin 1 (NF-1) or RAS signaling. The hyperactivation of tyrosine kinase receptors, such as the receptor of the platelet-derived growth factor β (PDFRβ), insulin-like growth factor 1 receptor (IGF-1R) and the receptor for hepatocyte growth factor (HGF), lead to the induction of the AKT/3-phosphoinositol kinase (PI3K) pathway. Another pathway resulting in BRAFi/MEKi resistance is the hyperactivation of epidermal growth factor receptor (EGFR) signaling or the deregulation of microphthalmia-associated transcription factor (MITF).
4 March 2020 in Cancer
Journal Article
LDLorenzo D'Ambrosio
Lorenzo D'AmbrosioNTNathan Touati
Nathan Touati
Jaen-Yves BlayGGGiovanni Grignani
Giovanni GrignaniRFRonan Flippot
Ronan Flippot
TGthe European Organization for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Group
the European Organization for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Group
+23
1 July 2006 in Cancer Biology & Therapy
Journal Article
Anna M. Czarnecka, MBACCClaudia Campanella
Claudia Campanella
GZGiovanni Zummo
Giovanni Zummo
Francesco CappelloMitochondria are cell organelles involved in processes of cell life and death, and therefore also in tumoral transformation. Indeed, mitochondria dysfunction is a prominent feature of cancer cells....
19 January 2015 in Journal of Cellular and Molecular Medicine
Journal Article
KKKatarzyna Kamińska
Katarzyna KamińskaCSCezary Szczylik
Cezary SzczylikZBZofia F. Bielecka
Zofia F. Bielecka
EBEwa Bartnik
Ewa Bartnik
CPCamillo Porta
Camillo PortaAnna M. Czarnecka, MBA +1
In the field of cancer research, scientific investigations are based on analysing differences in the secretome, the proteome, the transcriptome, the expression of cell surface molecules, and the deregulation of signal transduction pathways between neoplastic and normal cells. Accumulating evidence indicates a crucial role in carcinogenesis concerning not only stromal cells but also normal cells from target organs and tissue where tumours emerge. The tumour microenvironment (TME) definitively plays an important role in regulating neighbouring cell behaviour. To date, limited attention has been focused upon interactions between cancer cells and normal cells. This review concentrates on the interactions between stromal and healthy cells from the TME in cancer development. In the article, the authors also describe mutations, genes and proteins expression pattern that are involved in tumour development in target organ.
About Me
Prof. Dr. Anna M. Czarnecka is a full professor of Medical Oncology and head of Department of Outpatient Chemotherapy at the Maria-Sklodowska Curie National Research Institute of Oncology in Warsaw and a molecular biology expert in the Department of Experimental Pharmacology of the Institute of Experimental and Clinical Medicine at the Polish Academy of Sciences. In the years 2009–2017, she worked at the Oncology Department of the Military Medical Institute in Warsaw and was also the PI of the research teams of the Molecular Oncology Laboratory. She served as the Deputy Director of the NIO-PIB for Research (2020–2021). She obtained her PhD (2010) based on the thesis “Tumors as Mitochondrial Disorders” and a DSc degree with a series of publications entitled: “Clinical and molecular markers of the effectiveness of treating renal cell carcinoma with Tyrosine kinase inhibitors”. In addition,
she is a graduate of Master of Business Administration (MBA) studies, Innovation Management in the Health Sector Studies (Kozminski University, Warsaw) and Innovation Management Studies (Warsaw School of Economics), and Biostatistics in Medical Research (Collegium Medicum of the Jagiellonian University, Krakow). She has been honored with multiple awards, including scholarships from the Goldman Sachs Foundation, Kościuszko Foundation, and Fulbright Foundation, as well as the Foundation for Polish Science. She received a national L’Oreal Scholarship for the Women and Science award.