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Book ; Online ; E-Book: Molecular targeted radiosensitizers

Willers, Henning / Eke, Iris

opportunities and challenges

(Cancer drug discovery and development)

2020

Author's details	Henning Willers, Iris Eke editors
Series title	Cancer drug discovery and development
Keywords	Cancer research ; Radiotherapy ; Pharmacology
Subject code	614.5999
Language	English
Size	1 Online-Ressource (xi, 364 Seiten), Illustrationen
Publisher	Humana Press
Publishing place	Cham
Publishing country	Switzerland
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT020573292
ISBN	978-3-030-49701-9 ; 9783030497002 ; 3-030-49701-1 ; 3030497003
DOI	10.1007/978-3-030-49701-9
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Unilateral Diaphragmatic Paralysis After Stereotactic Ablative Radiation Therapy to a Lung Tumor Abutting the Course of the Phrenic Nerve.

Eke, Iris / Guo, H Henry / Loo, Billy W / Sung, Arthur W / Diehn, Maximilian / Vitzthum, Lucas / Chin, Alexander L / Gensheimer, Michael F

Practical radiation oncology

2023 Volume 13, Issue 5, Page(s) e383–e388

Abstract: We present the case of a woman with metastatic adenoid cystic carcinoma who received stereotactic ablative radiation therapy with a total dose of 50 Gy in 4 fractions to 2 lung metastases and developed symptomatic left phrenic nerve injury 2 years after ... ...

Abstract	We present the case of a woman with metastatic adenoid cystic carcinoma who received stereotactic ablative radiation therapy with a total dose of 50 Gy in 4 fractions to 2 lung metastases and developed symptomatic left phrenic nerve injury 2 years after radiation. The maximum dose to the approximate location of the phrenic nerve was 57.7 Gy, which corresponds to a biologically effective dose for late effects (using α/β ratio = 3) of 335.14 Gy. Here, we discuss the case, planning considerations by radiation oncologists and medical physicists, and the multidisciplinary medical management of this patient.
MeSH term(s)	Female ; Humans ; Phrenic Nerve/pathology ; Respiratory Paralysis/etiology ; Lung Neoplasms/pathology ; Radiosurgery/adverse effects ; Disease Progression
Language	English
Publishing date	2023-05-06
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2655748-4
ISSN	1879-8519 ; 1879-8500
ISSN (online)	1879-8519
ISSN	1879-8500
DOI	10.1016/j.prro.2023.04.010
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Article ; Online: Focal adhesion signaling and therapy resistance in cancer.

Eke, Iris / Cordes, Nils

Seminars in cancer biology

2015 Volume 31, Page(s) 65–75

Abstract: Interlocking gene mutations, epigenetic alterations and microenvironmental features perpetuate tumor development, growth, infiltration and spread. Consequently, intrinsic and acquired therapy resistance arises and presents one of the major goals to solve ...

Abstract	Interlocking gene mutations, epigenetic alterations and microenvironmental features perpetuate tumor development, growth, infiltration and spread. Consequently, intrinsic and acquired therapy resistance arises and presents one of the major goals to solve in oncologic research today. Among the myriad of microenvironmental factors impacting on cancer cell resistance, cell adhesion to the extracellular matrix (ECM) has recently been identified as key determinant. Despite the differentiation between cell adhesion-mediated drug resistance (CAMDR) and cell adhesion-mediated radioresistance (CAMRR), the underlying mechanisms share great overlap in integrin and focal adhesion hub signaling and differ further downstream in the complexity of signaling networks between tumor entities. Intriguingly, cell adhesion to ECM is per se also essential for cancer cells similar to their normal counterparts. However, based on the overexpression of focal adhesion hub signaling receptors and proteins and a distinct addiction to particular integrin receptors, targeting of focal adhesion proteins has been shown to potently sensitize cancer cells to different treatment regimes including radiotherapy, chemotherapy and novel molecular therapeutics. In this review, we will give insight into the role of integrins in carcinogenesis, tumor progression and metastasis. Additionally, literature and data about the function of focal adhesion molecules including integrins, integrin-associated proteins and growth factor receptors in tumor cell resistance to radio- and chemotherapy will be elucidated and discussed.
MeSH term(s)	Cell Adhesion ; Disease Progression ; Extracellular Matrix/metabolism ; Focal Adhesions ; Humans ; Integrins/metabolism ; Models, Biological ; Neoplasm Metastasis ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Signal Transduction
Chemical Substances	Integrins
Language	English
Publishing date	2015-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2014.07.009
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Article ; Online: Microarray analysis of hub genes, non-coding RNAs and pathways in lung after whole body irradiation in a mouse model.

Aryankalayil, Molykutty J / Bylicky, Michelle A / Martello, Shannon / Chopra, Sunita / Sproull, Mary / May, Jared M / Shankardass, Aman / MacMillan, Laurel / Vanpouille-Box, Claire / Eke, Iris / Scott, Kevin M K / Dalo, Juan / Coleman, C Norman

International journal of radiation biology

2023 Volume 99, Issue 11, Page(s) 1702–1715

Abstract: Purpose: Previous research has highlighted the impact of radiation damage, with cancer patients developing acute disorders including radiation induced pneumonitis or chronic disorders including pulmonary fibrosis months after radiation therapy ends. We ... ...

Abstract	Purpose: Previous research has highlighted the impact of radiation damage, with cancer patients developing acute disorders including radiation induced pneumonitis or chronic disorders including pulmonary fibrosis months after radiation therapy ends. We sought to discover biomarkers that predict these injuries and develop treatments that mitigate this damage and improve quality of life. Materials and methods: Six- to eight-week-old female C57BL/6 mice received 1, 2, 4, 8, 12 Gy or sham whole body irradiation. Animals were euthanized 48 h post exposure and lungs removed, snap frozen and underwent RNA isolation. Microarray analysis was performed to determine dysregulation of messenger RNA (mRNA), microRNA (miRNA), and long non-coding RNA (lncRNA) after radiation injury. Results: We observed sustained dysregulation of specific RNA markers including: mRNAs, lncRNAs, and miRNAs across all doses. We also identified significantly upregulated genes that can indicate high dose exposure, including Conclusions: These RNA biomarkers might be highly relevant in the development of treatments and in predicting normal tissue injury in patients undergoing radiation treatment. We are conducting further experiments in our laboratory, which includes a human lung-on-a-chip model, to develop a decision tree model using RNA biomarkers.
MeSH term(s)	Mice ; Animals ; Humans ; Whole-Body Irradiation/adverse effects ; Quality of Life ; Mice, Inbred C57BL ; Lung/radiation effects ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Biomarkers/metabolism ; Oligonucleotide Array Sequence Analysis ; Disease Models, Animal ; Xedar Receptor/genetics ; Xedar Receptor/metabolism
Chemical Substances	MicroRNAs ; Biomarkers ; Eda2r Protein, mouse ; Xedar Receptor ; Mirn142 microRNA, mouse
Language	English
Publishing date	2023-06-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
ZDB-ID	3065-x
ISSN	1362-3095 ; 0020-7616 ; 0955-3002
ISSN (online)	1362-3095
ISSN	0020-7616 ; 0955-3002
DOI	10.1080/09553002.2023.2214205
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Article: The lncRNAs

Eke, Iris / Bylicky, Michelle A / Sandfort, Veit / Chopra, Sunita / Martello, Shannon / Graves, Edward E / Coleman, C Norman / Aryankalayil, Molykutty J

Molecular therapy. Nucleic acids

2021 Volume 24, Page(s) 175–187

Abstract: Long non-coding RNAs (lncRNAs) have been shown to impact important biological functions such as proliferation, survival, and genomic stability. To analyze radiation-induced lncRNA expression in human tumors, we irradiated prostate cancer cells with a ... ...

Abstract	Long non-coding RNAs (lncRNAs) have been shown to impact important biological functions such as proliferation, survival, and genomic stability. To analyze radiation-induced lncRNA expression in human tumors, we irradiated prostate cancer cells with a single dose of 10 Gy or a multifractionated radiotherapeutic regimen of 10 fractions with a dose of 1 Gy (10 × 1 Gy) during 5 days. We found a stable upregulation of the lncRNA
Language	English
Publishing date	2021-02-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2662631-7
ISSN	2162-2531
ISSN	2162-2531
DOI	10.1016/j.omtn.2021.02.024
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Article ; Online: 3D matrix-based cell cultures: Automated analysis of tumor cell survival and proliferation.

Eke, Iris / Hehlgans, Stephanie / Sandfort, Veit / Cordes, Nils

International journal of oncology

2016 Volume 48, Issue 1, Page(s) 313–321

Abstract: Three-dimensional ex vivo cell cultures mimic physiological in vivo growth conditions thereby significantly contributing to our understanding of tumor cell growth and survival, therapy resistance and identification of novel potent cancer targets. In the ... ...

Abstract	Three-dimensional ex vivo cell cultures mimic physiological in vivo growth conditions thereby significantly contributing to our understanding of tumor cell growth and survival, therapy resistance and identification of novel potent cancer targets. In the present study, we describe advanced three-dimensional cell culture methodology for investigating cellular survival and proliferation in human carcinoma cells after cancer therapy including molecular therapeutics. Single cells are embedded into laminin-rich extracellular matrix and can be treated with cytotoxic drugs, ionizing or UV radiation or any other substance of interest when consolidated and approximating in vivo morphology. Subsequently, cells are allowed to grow for automated determination of clonogenic survival (colony number) or proliferation (colony size). The entire protocol of 3D cell plating takes ~1 h working time and pursues for ~7 days before evaluation. This newly developed method broadens the spectrum of exploration of malignant tumors and other diseases and enables the obtainment of more reliable data on cancer treatment efficacy.
MeSH term(s)	Carcinoma/drug therapy ; Carcinoma/pathology ; Carcinoma/radiotherapy ; Cell Culture Techniques/methods ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/radiation effects ; Cell Survival/drug effects ; Cell Survival/radiation effects ; Extracellular Matrix/drug effects ; Extracellular Matrix/radiation effects ; Humans ; Laminin/chemistry
Chemical Substances	Laminin
Language	English
Publishing date	2016-01
Publishing country	Greece
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1154403-x
ISSN	1791-2423 ; 1019-6439
ISSN (online)	1791-2423
ISSN	1019-6439
DOI	10.3892/ijo.2015.3230
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Article: Comprehensive analysis of signal transduction in three-dimensional ECM-based tumor cell cultures.

Eke, Iris / Hehlgans, Stephanie / Zong, Yaping / Cordes, Nils

Journal of biological methods

2015 Volume 2, Issue 4

Abstract: Analysis of signal transduction and protein phosphorylation is fundamental to understanding physiological and pathological cell behavior and identifying novel therapeutic targets. Despite the fact that the use of physiological three-dimensional cell ... ...

Abstract	Analysis of signal transduction and protein phosphorylation is fundamental to understanding physiological and pathological cell behavior and identifying novel therapeutic targets. Despite the fact that the use of physiological three-dimensional cell culture assays is increasing, 3D proteomics and phosphoproteomics remain challenging due to difficulties with easy, robust and reproducible sample preparation. Here, we present an easy-to-perform, reliable and time-efficient method for the production of 3D cell lysates that does not compromise cell adhesion before cell lysis. The samples can be used for western blotting as well as phosphoproteome array technology. This technique will be of interest for researchers working in all fields of biology and drug development.
Language	English
Publishing date	2015-11-17
Publishing country	United States
Document type	Journal Article
ISSN	2326-9901
ISSN	2326-9901
DOI	10.14440/jbm.2015.96
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Article ; Online: ILKAP, ILK and PINCH1 control cell survival of p53-wildtype glioblastoma cells after irradiation.

Hausmann, Christina / Temme, Achim / Cordes, Nils / Eke, Iris

Oncotarget

2015 Volume 6, Issue 33, Page(s) 34592–34605

Abstract: The prognosis is generally poor for patients suffering from glioblastoma multiforme (GBM) due to radiation and drug resistance. Prosurvival signaling originating from focal adhesion hubs essentially contributes to therapy resistance and tumor ... ...

Abstract	The prognosis is generally poor for patients suffering from glioblastoma multiforme (GBM) due to radiation and drug resistance. Prosurvival signaling originating from focal adhesion hubs essentially contributes to therapy resistance and tumor aggressiveness. As the underlying molecular mechanisms remain largely elusive, we addressed whether targeting of the focal adhesion proteins particularly interesting new cysteine-histidine-rich 1 (PINCH1), integrin-linked kinase (ILK) and ILK associated phosphatase (ILKAP) modulates GBM cell radioresistance. Intriguingly, PINCH1, ILK and ILKAP depletion sensitized p53-wildtype, but not p53-mutant, GBM cells to radiotherapy. Concomitantly, these cells showed inactivated Glycogen synthase kinase-3β (GSK3β) and reduced proliferation. For PINCH1 and ILKAP knockdown, elevated levels of radiation-induced γH2AX/53BP1-positive foci, as a marker for DNA double strand breaks, were observed. Mechanistically, we identified radiation-induced phosphorylation of DNA protein kinase (DNAPK), an important DNA repair protein, to be dependent on ILKAP. This interaction was fundamental to radiation survival of p53-wildtype GBM cells. Conclusively, our data suggest an essential role of PINCH1, ILK and ILKAP for the radioresistance of p53-wildtype GBM cells and provide evidence for DNAPK functioning as a central mediator of ILKAP signaling. Strategies for targeting focal adhesion proteins in combination with radiotherapy might be a promising approach for patients with GBM.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Blotting, Western ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Brain Neoplasms/radiotherapy ; Cell Survival ; DNA-Activated Protein Kinase/metabolism ; Fluorescent Antibody Technique ; Gene Knockdown Techniques ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Glioblastoma/radiotherapy ; Humans ; LIM Domain Proteins/metabolism ; Membrane Proteins/metabolism ; Nuclear Proteins/metabolism ; Phosphoprotein Phosphatases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; RNA, Small Interfering ; Radiation Tolerance/physiology ; Transfection ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Adaptor Proteins, Signal Transducing ; LIM Domain Proteins ; LIMS1 protein, human ; Membrane Proteins ; Nuclear Proteins ; RNA, Small Interfering ; TP53 protein, human ; Tumor Suppressor Protein p53 ; integrin-linked kinase (EC 2.7.1.-) ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; PRKDC protein, human (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; ILKAP protein, human (EC 3.1.3.-) ; Phosphoprotein Phosphatases (EC 3.1.3.16)
Language	English
Publishing date	2015-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.5423
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Article ; Online: Multiomic-Based Molecular Landscape of FaDu Xenograft Tumors in Mice after a Combinatorial Treatment with Radiation and an HSP90 Inhibitor Identifies Adaptation-Induced Targets of Resistance and Therapeutic Intervention.

Bylicky, Michelle A / Shankavaram, Uma / Aryankalayil, Molykutty J / Chopra, Sunita / Naz, Sarwat / Sowers, Anastasia L / Choudhuri, Rajani / Calvert, Valerie / Petricoin, Emanuel F / Eke, Iris / Mitchell, James B / Coleman, C Norman

Molecular cancer therapeutics

2022 Volume 23, Issue 4, Page(s) 577–588

Abstract: Treatments involving radiation and chemotherapy alone or in combination have improved patient survival and quality of life. However, cancers frequently evade these therapies due to adaptation and tumor evolution. Given the complexity of predicting ... ...

Abstract	Treatments involving radiation and chemotherapy alone or in combination have improved patient survival and quality of life. However, cancers frequently evade these therapies due to adaptation and tumor evolution. Given the complexity of predicting response based solely on the initial genetic profile of a patient, a predetermined treatment course may miss critical adaptation that can cause resistance or induce new targets for drug and immunotherapy. To address the timescale for these evasive mechanisms, using a mouse xenograft tumor model, we investigated the rapidity of gene expression (mRNA), molecular pathway, and phosphoproteome changes after radiation, an HSP90 inhibitor, or combination. Animals received radiation, drug, or combination treatment for 1 or 2 weeks and were then euthanized along with a time-matched untreated group for comparison. Changes in gene expression occur as early as 1 week after treatment initiation. Apoptosis and cell death pathways were activated in irradiated tumor samples. For the HSP90 inhibitor and combination treatment at weeks 1 and 2 compared with Control Day 1, gene-expression changes induced inhibition of pathways including invasion of cells, vasculogenesis, and viral infection among others. The combination group included both drug-alone and radiation-alone changes. Our data demonstrate the rapidity of gene expression and functional pathway changes in the evolving tumor as it responds to treatment. Discovering these phenotypic adaptations may help elucidate the challenges in using sustained treatment regimens and could also define evolving targets for therapeutic efficacy.
MeSH term(s)	Animals ; Humans ; Heterografts ; Multiomics ; Quality of Life ; Antineoplastic Agents/pharmacology ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/radiotherapy ; HSP90 Heat-Shock Proteins ; Cell Line, Tumor ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; HSP90 Heat-Shock Proteins
Language	English
Publishing date	2022-11-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-23-0796
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Article ; Online: Targeting of the EGFR/β1 integrin connecting proteins PINCH1 and Nck2 radiosensitizes three-dimensional SCC cell cultures.

Rossow, Lydia / Eke, Iris / Dickreuter, Ellen / Cordes, Nils

Oncology reports

2015 Volume 34, Issue 1, Page(s) 469–476

Abstract: Epidermal growth factor receptor (EGFR) signaling plays an important role in tumor cell resistance to therapy. In addition to ligand binding, mutual and cooperative interactions of EGFR with integrin cell adhesion receptors critically influence proper ... ...

Abstract	Epidermal growth factor receptor (EGFR) signaling plays an important role in tumor cell resistance to therapy. In addition to ligand binding, mutual and cooperative interactions of EGFR with integrin cell adhesion receptors critically influence proper downstream signaling through a number of bridging adapter proteins. In the present study, we analyzed the role of two of these adapter proteins, called PINCH1 and Nck2, for cellular radioresistance in combination with EGFR-targeting using the monoclonal antibody cetuximab. siRNA-mediated knockdown of PINCH1 or Nck2 resulted in enhanced radiosensitivity of 3D grown human squamous cell carcinoma cell lines FaDu (head and neck) and A431 (epidermis) comparable with effects seen after cetuximab treatment. Combination of knockdown and cetuximab did not result in additive nor synergistic effects regarding clonogenic radiation survival. Modifications in MAPK, Akt and FAK phosphorylation occurred upon cetuximab treatment as well as PINCH1 or Nck2 depletion. We further found this tumor cell radiosensitization to be due to attenuated repair of DNA double strand breaks and altered Rad50 and Nbs1 expression but without changes in other DNA repair proteins such as ATM, DNA-PK and Mre11. Our data suggest that the adaptor proteins PINCH1 and Nck2 critically contribute to cellular radioresistance and proper EGFR signaling in 3D lrECM grown human squamous cell carcinoma cells. Further investigations are warranted to identify the intracellular signaling network controlled by EGFR, PINCH1 and Nck2.
MeSH term(s)	Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Antineoplastic Agents/pharmacology ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/radiotherapy ; Cell Culture Techniques ; Cell Line, Tumor ; Cetuximab/pharmacology ; Humans ; Hypopharyngeal Neoplasms/genetics ; Hypopharyngeal Neoplasms/metabolism ; Hypopharyngeal Neoplasms/radiotherapy ; Integrin beta1/metabolism ; LIM Domain Proteins/antagonists & inhibitors ; LIM Domain Proteins/genetics ; LIM Domain Proteins/metabolism ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Oncogene Proteins/antagonists & inhibitors ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; RNA, Small Interfering/pharmacology ; Radiation Tolerance/drug effects ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Signal Transduction/drug effects ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/radiotherapy
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antineoplastic Agents ; Integrin beta1 ; LIM Domain Proteins ; LIMS1 protein, human ; Membrane Proteins ; NCK2 protein, human ; Oncogene Proteins ; RNA, Small Interfering ; EGFR protein, human (EC 2.7.10.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Cetuximab (PQX0D8J21J)
Language	English
Publishing date	2015-07
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1222484-4
ISSN	1791-2431 ; 1021-335X
ISSN (online)	1791-2431
ISSN	1021-335X
DOI	10.3892/or.2015.4006
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