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  1. Article ; Online: Alectinib treatment improves photodynamic therapy in cancer cell lines of different origin.

    Gillissen, Bernhard / Richter, Antje / Essmann, Frank / Kemmner, Wolfgang

    BMC cancer

    2021  Volume 21, Issue 1, Page(s) 971

    Abstract: Background: Photodynamic therapy with a photosensitizer such as protoporphyrin-IX, a light sensitive metabolite of heme synthesis, is a highly selective treatment for various carcinomas. In previous studies, we found a significant down regulation of the ...

    Abstract Background: Photodynamic therapy with a photosensitizer such as protoporphyrin-IX, a light sensitive metabolite of heme synthesis, is a highly selective treatment for various carcinomas. In previous studies, we found a significant down regulation of the relevant enzyme ferrochelatase in gastrointestinal carcinomas leading to an accumulation of protoporphyrin-IX within the tumor cells. Recent studies showed that a novel anti-cancer drug, Alectinib, an orally available, highly selective, potent second-generation inhibitor of anaplastic lymphoma tyrosinkinase binds to ferrochelatase. Therefore, we were interested to see whether Alectinib treatment might lead to an accumulation of protoporphyrin IX.
    Methods: Tumor cells of different origin were cultured, treated with LED-light and Alectinib. Results were gained by flow cytometry, immunohistochemistry and western blotting. Apoptosis was determined by flow cytometric analysis of Annexin V-FITC stained cells. In addition, cells were counterstained with propidium iodide to distinguish early apoptotic cells and late apoptotic/necrotic cells.
    Results: Here, we report that photodynamic treatment of tumor cell lines of different origin in combination with Alectinib increased protoporphyrin-IX specific fluorescence and concomitantly cell death.
    Conclusions: The usage of Alectinib could be another step for enhancing the effectiveness of photodynamic therapy. Further experiments will show whether photodynamic therapy in combination with Alectinib could be a new strategy for the treatment of e.g. peritoneal disseminated carcinomas.
    MeSH term(s) Aminolevulinic Acid/pharmacology ; Carbazoles/pharmacology ; Fluorescence ; Humans ; Light ; Neoplasms/drug therapy ; Neoplasms/pathology ; Photochemotherapy/methods ; Photosensitizing Agents/pharmacology ; Piperidines/pharmacology ; Protoporphyrins/metabolism ; Tumor Cells, Cultured
    Chemical Substances Carbazoles ; Photosensitizing Agents ; Piperidines ; Protoporphyrins ; Aminolevulinic Acid (88755TAZ87) ; protoporphyrin IX (C2K325S808) ; alectinib (LIJ4CT1Z3Y)
    Language English
    Publishing date 2021-08-30
    Publishing country England
    Document type Journal Article
    ISSN 1471-2407
    ISSN (online) 1471-2407
    DOI 10.1186/s12885-021-08667-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Indolyl-chalcone derivatives trigger apoptosis in cisplatin-resistant mesothelioma cells through aberrant tubulin polymerization and deregulation of microtubule-associated proteins.

    Steinlein, Sophia / Essmann, Frank / Ghilardi, Amanda Franceschini / Horn, Heike / Schüler, Julia / Hausser, Angelika / Sun, Lijun / Ott, German / Kalla, Claudia

    Frontiers in oncology

    2023  Volume 13, Page(s) 1190988

    Abstract: Introduction: Malignant pleural mesothelioma (MPM) is a neoplasm with dismal prognosis and notorious resistance to the standard therapeutics cisplatin and pemetrexed. Chalcone derivatives are efficacious anti-cancer agents with minimal toxicity and have, ...

    Abstract Introduction: Malignant pleural mesothelioma (MPM) is a neoplasm with dismal prognosis and notorious resistance to the standard therapeutics cisplatin and pemetrexed. Chalcone derivatives are efficacious anti-cancer agents with minimal toxicity and have, therefore, gained pharmaceutical interest. Here, we investigated the efficacy of CIT-026 and CIT-223, two indolyl-chalcones (CITs), to inhibit growth and viability of MPM cells and defined the mechanism by which the compounds induce cell death.
    Methods: The effects of CIT-026 and CIT-223 were analyzed in five MPM cell lines, using viability, immunofluorescence, real-time cell death monitoring, and tubulin polymerization assays, along with siRNA knockdown. Phospho-kinase arrays and immunoblotting were used to identify signaling molecules that contribute to cell death.
    Results: CIT-026 and CIT-223 were toxic in all cell lines at sub-micromolar concentrations, in particular in MPM cells resistant to cisplatin and pemetrexed, while normal fibroblasts were only modestly affected. Both CITs targeted tubulin polymerization
    Discussion: CIT-026 and CIT-223 are highly effective inducers of tumor cell apoptosis by disrupting microtubule assembly, with only modest effects on non-malignant cells. CITs are potent anti-tumor agents against MPM cells, in particular cells resistant to standard therapeutics, and thus warrant further evaluation as potential small-molecule therapeutics in MPM.
    Language English
    Publishing date 2023-05-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2023.1190988
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: ATF3 characterizes aggressive drug-tolerant persister cells in HGSOC.

    Böpple, Kathrin / Oren, Yaara / Henry, Whitney S / Dong, Meng / Weller, Sandra / Thiel, Julia / Kleih, Markus / Gaißler, Andrea / Zipperer, Damaris / Kopp, Hans-Georg / Aylon, Yael / Oren, Moshe / Essmann, Frank / Liang, Chunguang / Aulitzky, Walter E

    Cell death & disease

    2024  Volume 15, Issue 4, Page(s) 290

    Abstract: High-grade serous ovarian cancer (HGSOC) represents the most common and lethal subtype of ovarian cancer. Despite initial response to platinum-based standard therapy, patients commonly suffer from relapse that likely originates from drug-tolerant ... ...

    Abstract High-grade serous ovarian cancer (HGSOC) represents the most common and lethal subtype of ovarian cancer. Despite initial response to platinum-based standard therapy, patients commonly suffer from relapse that likely originates from drug-tolerant persister (DTP) cells. We generated isogenic clones of treatment-naïve and cisplatin-tolerant persister HGSOC cells. In addition, single-cell RNA sequencing of barcoded cells was performed in a xenograft model with HGSOC cell lines after platinum-based therapy. Published single-cell RNA-sequencing data from neo-adjuvant and non-treated HGSOC patients and patient data from TCGA were analyzed. DTP-derived cells exhibited morphological alterations and upregulation of epithelial-mesenchymal transition (EMT) markers. An aggressive subpopulation of DTP-derived cells showed high expression of the stress marker ATF3. Knockdown of ATF3 enhanced the sensitivity of aggressive DTP-derived cells to cisplatin-induced cell death, implying a role for ATF3 stress response in promoting a drug tolerant persister cell state. Furthermore, single cell lineage tracing to detect transcriptional changes in a HGSOC cell line-derived xenograft relapse model showed that cells derived from relapsed solid tumors express increased levels of EMT and multiple endoplasmic reticulum (ER) stress markers, including ATF3. Single cell RNA sequencing of epithelial cells from four HGSOC patients also identified a small cell population resembling DTP cells in all samples. Moreover, analysis of TCGA data from 259 HGSOC patients revealed a significant progression-free survival advantage for patients with low expression of the ATF3-associated partial EMT genes. These findings suggest that increased ATF3 expression together with partial EMT promote the development of aggressive DTP, and thereby relapse in HGSOC patients.
    MeSH term(s) Humans ; Activating Transcription Factor 3/metabolism ; Activating Transcription Factor 3/genetics ; Female ; Cisplatin/pharmacology ; Cisplatin/therapeutic use ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Drug Resistance, Neoplasm/drug effects ; Epithelial-Mesenchymal Transition/drug effects ; Epithelial-Mesenchymal Transition/genetics ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Ovarian Neoplasms/metabolism ; Animals ; Mice ; Xenograft Model Antitumor Assays ; Gene Expression Regulation, Neoplastic/drug effects
    Chemical Substances Activating Transcription Factor 3 ; Cisplatin (Q20Q21Q62J) ; ATF3 protein, human
    Language English
    Publishing date 2024-04-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-024-06674-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Book ; Conference proceedings: Nachhaltigkeit und Prävention

    Eßmann, Frank / Kaiser, Roswitha

    Konzepte für die dauerhafte Bauwerkserhaltung ; [Tagungsband zur Veranstaltung am 20. November 2010 im Rahmen der Messe "denkmal"]

    2011  

    Event/congress Symposium (2010.11.20, Leipzig)
    Author's details Frank Eßmann; Roswitha Kaiser (Hrsg.)
    Keywords Erhaltung ; Bausubstanz ; Denkmalpflege ; Nachhaltigkeit
    Language German
    Size 125 S, zahlr. Ill., graph. Darst
    Publisher Fraunhofer IRB Verl
    Publishing place Stuttgart
    Document type Book ; Conference proceedings
    ISBN 9783816784234 ; 3816784232
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  5. Article ; Online: BH3-only protein expression determines hepatocellular carcinoma response to sorafenib-based treatment.

    Busche, Stephanie / John, Katharina / Wandrer, Franziska / Vondran, Florian W R / Lehmann, Ulrich / Wedemeyer, Heiner / Essmann, Frank / Schulze-Osthoff, Klaus / Bantel, Heike

    Cell death & disease

    2021  Volume 12, Issue 8, Page(s) 736

    Abstract: Hepatocellular carcinoma (HCC) represents a global health challenge with limited therapeutic options. Anti-angiogenic immune checkpoint inhibitor-based combination therapy has been introduced for progressed HCC, but improves survival only in a subset of ... ...

    Abstract Hepatocellular carcinoma (HCC) represents a global health challenge with limited therapeutic options. Anti-angiogenic immune checkpoint inhibitor-based combination therapy has been introduced for progressed HCC, but improves survival only in a subset of HCC patients. Tyrosine-kinase inhibitors (TKI) such as sorafenib represent an alternative treatment option but have only modest efficacy. Using different HCC cell lines and HCC tissues from various patients reflecting HCC heterogeneity, we investigated whether the sorafenib response could be enhanced by combination with pro-apoptotic agents, such as TNF-related apoptosis-inducing ligand (TRAIL) or the BH3-mimetic ABT-737, which target the death receptor and mitochondrial pathway of apoptosis, respectively. We found that both agents could enhance sorafenib-induced cell death which was, however, dependent on specific BH3-only proteins. TRAIL augmented sorafenib-induced cell death only in NOXA-expressing HCC cells, whereas ABT-737 enhanced the sorafenib response also in NOXA-deficient cells. ABT-737, however, failed to augment sorafenib cytotoxicity in the absence of BIM, even when NOXA was strongly expressed. In the presence of NOXA, BIM-deficient HCC cells could be in turn strongly sensitized for cell death induction by the combination of sorafenib with TRAIL. Accordingly, HCC tissues sensitive to apoptosis induction by sorafenib and TRAIL revealed enhanced NOXA expression compared to HCC tissues resistant to this treatment combination. Thus, our results suggest that BH3-only protein expression determines the treatment response of HCC to different sorafenib-based drug combinations. Individual profiling of BH3-only protein expression might therefore assist patient stratification to certain TKI-based HCC therapies.
    MeSH term(s) Apoptosis/drug effects ; Bcl-2-Like Protein 11/metabolism ; Biphenyl Compounds/pharmacology ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Caspases/metabolism ; Cell Death/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Enzyme Activation/drug effects ; Humans ; Ki-67 Antigen/metabolism ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Mitochondrial Membrane Transport Proteins/metabolism ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Nitrophenols/pharmacology ; Piperazines/pharmacology ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Sorafenib/pharmacology ; Sorafenib/therapeutic use ; Sulfonamides/pharmacology ; TNF-Related Apoptosis-Inducing Ligand/pharmacology
    Chemical Substances ABT-737 ; Bcl-2-Like Protein 11 ; Biphenyl Compounds ; Ki-67 Antigen ; MCL1 protein, human ; Mitochondrial Membrane Transport Proteins ; Myeloid Cell Leukemia Sequence 1 Protein ; Nitrophenols ; PMAIP1 protein, human ; Piperazines ; Proto-Oncogene Proteins c-bcl-2 ; RTL10 protein, human ; Sulfonamides ; TNF-Related Apoptosis-Inducing Ligand ; Sorafenib (9ZOQ3TZI87) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2021-07-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-021-04020-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Book: Modellhafte Qualifizierung von Energieberatern für Baudenkmale

    Kaiser, Roswitha / Eßmann, Frank / Garrecht, Harald

    (Förderschwerpunkt: Zukunftsfähige Sanierung denkmalgeschützter Altbausubstanz) ; Abschlussbericht über ein Forschungsprojekt

    2015  

    Author's details von: Roswitha Kaiser; Frank Eßmann; Harald Garrecht
    Language German
    Size 47 Bl., Ill., graph. Darst., Kt.
    Publisher WTA - Wiss.-Technische Arbeitsgemeinschaft für Bauwerkserhaltung und Denkmalpflege e.V. u.a.
    Publishing place Stuttgart
    Document type Book
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  7. Article: The BCL-2 inhibitor ABT-199/venetoclax synergizes with proteasome inhibition via transactivation of the MCL-1 antagonist NOXA.

    Weller, Sandra / Toennießen, Astrid / Schaefer, Benjamin / Beigl, Tobias / Muenchow, Alina / Böpple, Kathrin / Hofmann, Ute / Gillissen, Bernhard F / Aulitzky, Walter E / Kopp, Hans-Georg / Essmann, Frank

    Cell death discovery

    2022  Volume 8, Issue 1, Page(s) 215

    Abstract: Enhanced expression of anti-apoptotic B-cell lymphoma 2 (BCL-2) protein is frequent in cancer. Targeting of BCL-2 with the specific inhibitor ABT-199 (Venetoclax) has significant clinical activity in malignant diseases such as chronic lymphocytic ... ...

    Abstract Enhanced expression of anti-apoptotic B-cell lymphoma 2 (BCL-2) protein is frequent in cancer. Targeting of BCL-2 with the specific inhibitor ABT-199 (Venetoclax) has significant clinical activity in malignant diseases such as chronic lymphocytic leukemia and multiple myeloma. The small molecule drug ABT-199 mimics the pro-apoptotic BCL-2 homology domain 3 of BH3-only proteins and blocks the hydrophobic BC-groove in BCL-2. We have previously shown that ABT-199 synergizes with the proteasome inhibitor (PI) bortezomib in soft tissue sarcoma derived cells and cell lines to induce apoptosis. Synergistic apoptosis induction relies on the pore-forming effector BAX and expression of the pro-apoptotic BH3-only protein NOXA. Bortezomib augments expression of NOXA by blocking its proteasomal degradation. Interestingly, shown here for the first time, expression of NOXA is strongly enhanced by ABT-199 induced integrated stress response (ISR). ISR transcription factors ATF3 & ATF4 mediate transactivation of the BH3-only protein NOXA which specifically inhibits the anti-apoptotic MCL-1. Thus, NOXA potentiates the efficacy of the BCL-2 inhibitor ABT-199 by simultaneous inhibition of MCL-1. Hence, ABT-199 has a double impact by directly blocking anti-apoptotic BCL-2 and inhibiting MCL-1 via transactivated NOXA. By preventing degradation of NOXA PIs synergize with ABT-199. Synergism of ABT-199 and PIs therefore occurs on several, previously unexpected levels. This finding should prompt clinical evaluation of combinatorial regimens in further malignancies.
    Language English
    Publishing date 2022-04-20
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-022-01009-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Translational approaches targeting the p53 pathway for anti-cancer therapy.

    Essmann, Frank / Schulze-Osthoff, Klaus

    British journal of pharmacology

    2011  Volume 165, Issue 2, Page(s) 328–344

    Abstract: The p53 tumour suppressor blocks cancer development by triggering apoptosis or cellular senescence in response to oncogenic stress or DNA damage. Consequently, the p53 signalling pathway is virtually always inactivated in human cancer cells. This ... ...

    Abstract The p53 tumour suppressor blocks cancer development by triggering apoptosis or cellular senescence in response to oncogenic stress or DNA damage. Consequently, the p53 signalling pathway is virtually always inactivated in human cancer cells. This unifying feature has commenced tremendous efforts to develop p53-based anti-cancer therapies. Different strategies exist that are adapted to the mechanisms of p53 inactivation. In p53-mutated tumours, delivery of wild-type p53 by adenovirus-based gene therapy is now practised in China. Also, remarkable progress has been made in the development of p53-binding drugs that can rescue and reactivate the function of mutant or misfolded p53. Other biologic approaches include the development of oncolytic viruses that are designed to specifically replicate in and kill p53-defective cells. Inactivation of wt-p53 frequently results from dysregulation of MDM2, an E3 ligase that regulates p53 levels. Small-molecule drugs that inhibit the interaction of MDM2 and p53 and block p53 degradation are currently tested in clinical trials. This survey highlights the recent developments that attempt to modulate the function of p53 and outlines strategies that are being investigated for pharmacological intervention in the p53 pathway.
    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Humans ; Indoles/therapeutic use ; Mutation ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Protein Biosynthesis ; Proto-Oncogene Proteins c-mdm2/antagonists & inhibitors ; Pyrrolidinones/therapeutic use ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Antineoplastic Agents ; Indoles ; PXN822 ; Pyrrolidinones ; Tumor Suppressor Protein p53 ; MDM2 protein, human (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
    Language English
    Publishing date 2011-06-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/j.1476-5381.2011.01570.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Book ; Online ; Thesis: Regulationsebenen der Apoptose

    Eßmann, Frank [Verfasser]

    vom DNA-Schaden zur Proteinspaltung

    2008  

    Author's details von Frank Essmann
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  10. Article: Identification of the kinesin KifC3 as a new player for positioning of peroxisomes and other organelles in mammalian cells

    Dietrich, Denise / Seiler, Florian / Essmann, Frank / Dodt, Gabriele

    Biochimica et biophysica acta. Molecular cell research. 2013 Dec., v. 1833, no. 12

    2013  

    Abstract: The attachment of organelles to the cytoskeleton and directed organelle transport is essential for cellular morphology and function. In contrast to other cell organelles like the endoplasmic reticulum or the Golgi apparatus, peroxisomes are evenly ... ...

    Abstract The attachment of organelles to the cytoskeleton and directed organelle transport is essential for cellular morphology and function. In contrast to other cell organelles like the endoplasmic reticulum or the Golgi apparatus, peroxisomes are evenly distributed in the cytoplasm, which is achieved by binding of peroxisomes to microtubules and their bidirectional transport by the microtubule motor proteins kinesin-1 (Kif5) and cytoplasmic dynein. KifC3, belonging to the group of C-terminal kinesins, has been identified to interact with the human peroxin PEX1 in a yeast two-hybrid screen. We investigated the potential involvement of KifC3 in peroxisomal transport. Interaction of KifC3 and the AAA-protein (ATPase associated with various cellular activities) PEX1 was confirmed by in vivo colocalization and by coimmunoprecipitation from cell lysates. Furthermore, knockdown of KifC3 using RNAi resulted in an increase of cells with perinuclear-clustered peroxisomes, indicating enhanced minus-end directed motility of peroxisomes. The occurrence of this peroxisomal phenotype was cell cycle phase independent, while microtubules were essential for phenotype formation. We conclude that KifC3 may play a regulatory role in minus-end directed peroxisomal transport for example by blocking the motor function of dynein at peroxisomes. Knockdown of KifC3 would then lead to increased minus-end directed peroxisomal transport and cause the observed peroxisomal clustering at the microtubule-organizing center.
    Keywords Golgi apparatus ; RNA interference ; adenosinetriphosphatase ; cell cycle ; dynein ATPase ; endoplasmic reticulum ; humans ; kinesin ; microtubules ; molecular motor proteins ; peroxisomes ; phenotype ; two hybrid system techniques
    Language English
    Dates of publication 2013-12
    Size p. 3013-3024.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 283444-3
    ISSN 0167-4889
    ISSN 0167-4889
    DOI 10.1016/j.bbamcr.2013.08.002
    Database NAL-Catalogue (AGRICOLA)

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