Search

Your search keyword '"Tapinos, Nikos"' showing total 143 results
Start Over Author "Tapinos, Nikos" Search Limiters Peer Reviewed
143 results on '"Tapinos, Nikos"'

6. Data from Chi3l1 Is a Modulator of Glioma Stem Cell States and a Therapeutic Target in Glioblastoma

Author

Guetta-Terrier, Charlotte, primary, Karambizi, David, primary, Akosman, Bedia, primary, Zepecki, John P., primary, Chen, Jia-Shu, primary, Kamle, Suchitra, primary, Fajardo, J. Eduardo, primary, Fiser, Andras, primary, Singh, Ritambhara, primary, Toms, Steven A., primary, Lee, Chun Geun, primary, Elias, Jack A., primary, and Tapinos, Nikos, primary

Published
2023
Full Text
View/download PDF

7. Supplementary Table 2 from Chi3l1 Is a Modulator of Glioma Stem Cell States and a Therapeutic Target in Glioblastoma

Author

Guetta-Terrier, Charlotte, primary, Karambizi, David, primary, Akosman, Bedia, primary, Zepecki, John P., primary, Chen, Jia-Shu, primary, Kamle, Suchitra, primary, Fajardo, J. Eduardo, primary, Fiser, Andras, primary, Singh, Ritambhara, primary, Toms, Steven A., primary, Lee, Chun Geun, primary, Elias, Jack A., primary, and Tapinos, Nikos, primary

Published
2023
Full Text
View/download PDF

8. Supplementary Figures from Chi3l1 Is a Modulator of Glioma Stem Cell States and a Therapeutic Target in Glioblastoma

Author

Guetta-Terrier, Charlotte, primary, Karambizi, David, primary, Akosman, Bedia, primary, Zepecki, John P., primary, Chen, Jia-Shu, primary, Kamle, Suchitra, primary, Fajardo, J. Eduardo, primary, Fiser, Andras, primary, Singh, Ritambhara, primary, Toms, Steven A., primary, Lee, Chun Geun, primary, Elias, Jack A., primary, and Tapinos, Nikos, primary

Published
2023
Full Text
View/download PDF

9. Supplementary Data from Chi3l1 Is a Modulator of Glioma Stem Cell States and a Therapeutic Target in Glioblastoma

Author

Guetta-Terrier, Charlotte, primary, Karambizi, David, primary, Akosman, Bedia, primary, Zepecki, John P., primary, Chen, Jia-Shu, primary, Kamle, Suchitra, primary, Fajardo, J. Eduardo, primary, Fiser, Andras, primary, Singh, Ritambhara, primary, Toms, Steven A., primary, Lee, Chun Geun, primary, Elias, Jack A., primary, and Tapinos, Nikos, primary

Published
2023
Full Text
View/download PDF

10. Supplementary Table 1 from Chi3l1 Is a Modulator of Glioma Stem Cell States and a Therapeutic Target in Glioblastoma

Author

Guetta-Terrier, Charlotte, primary, Karambizi, David, primary, Akosman, Bedia, primary, Zepecki, John P., primary, Chen, Jia-Shu, primary, Kamle, Suchitra, primary, Fajardo, J. Eduardo, primary, Fiser, Andras, primary, Singh, Ritambhara, primary, Toms, Steven A., primary, Lee, Chun Geun, primary, Elias, Jack A., primary, and Tapinos, Nikos, primary

Published
2023
Full Text
View/download PDF

12. Chi3l1 is a modulator of glioma stem cell states and a therapeutic target in glioblastoma

Author

Guetta-Terrier, Charlotte, primary, Karambizi, David, additional, Akosman, Bedia, additional, Zepecki, John P., additional, Chen, Jia-Shu, additional, Kamle, Suchitra, additional, Fajardo, J. Eduardo, additional, Fiser, Andras, additional, Singh, Ritambhara, additional, Toms, Steven A., additional, Lee, Chun Geun, additional, Elias, Jack A., additional, and Tapinos, Nikos, additional

Published
2023
Full Text
View/download PDF

20. The germline factor DDX4 contributes to the chemoresistance of small cell lung cancer cells

Author

Noyes, Christopher, primary, Kitajima, Shunsuke, additional, Li, Fengkai, additional, Suita, Yusuke, additional, Miriyala, Saradha, additional, Isaac, Shakson, additional, Ahsan, Nagib, additional, Knelson, Erik, additional, Vajdi, Amir, additional, Tani, Tetsuo, additional, Thai, Tran C., additional, Xu, Derek, additional, Murai, Junko, additional, Tapinos, Nikos, additional, Takahashi, Chiaki, additional, Barbie, David A., additional, and Yajima, Mamiko, additional

Published
2022
Full Text
View/download PDF

21. Chi3l1 is a modulator of glioma stem cell states and a therapeutic vulnerability for glioblastoma

Author

Guetta-Terrier, Charlotte, primary, Karambizi, David, additional, Akosman, Bedia, additional, Chen, Jia-Shu, additional, Kamle, Suchitra, additional, Fajardo, Eduardo, additional, Fiser, Andras, additional, Singh, Ritambhara, additional, Toms, Steven A., additional, Lee, Chun Geun, additional, Elias, Jack A., additional, and Tapinos, Nikos, additional

Published
2021
Full Text
View/download PDF

22. Potent preclinical sensitivity to imipridone-based combination therapies in oncohistone H3K27M-mutant diffuse intrinsic pontine glioma is associated with induction of the integrated stress response, TRAIL death receptor DR5, reduced ClpX and apoptosis

Author

Borsuk, Robyn, Zhou, Lanlan, Chang, Wen-I, Zhang, Yiqun, Sharma, Aditi, Prabhu, Varun V, Tapinos, Nikos, Lulla, Rishi R, and El-Deiry, Wafik S

Subjects
Original Article
Abstract

The H3K27M oncohistone mutation, identified in approximately 80% of diffuse intrinsic pontine gliomas (DIPG), is a potential target for therapy. Imipridone ONC201/TIC10 (TRAIL-Inducing Compound #10) induces apoptosis of cancer cells, and has clinical efficacy against H3K27M-mutant DIPG. We demonstrate synergy between ONC201, ONC206 and ONC212, and targeted therapies with known preclinical activity against DIPG. We hypothesized that imipridone combinations with HDAC or proteasome inhibitors may be superior to single agent ONC201 treatment in H3K27M mutant DIPG. Six patient-derived DIPG cell lines (SU-DIPG-IV, SU-DIPG-13, SU-DIPG-25, SU-DIPG-27, SU-DIPG-29, SU-DIPG-36) were exposed to imipridones alone or combinations with histone de-acetylase inhibitors [HDACi], marizomib, etoposide, and temozolomide. Dose-dependent response to imipridones was observed in DIPG cells with half-maximal inhibitory concentration (IC(50)) of 1.46 µM, 0.11 µM, and 0.03 µM, for ONC201, ONC206, and ONC212, respectively. Upon treatment with the imipridones, DIPG cell lines engaged CLpP/CLPX, the integrated stress response with ATF4 activation, and TRAIL death receptor 5 (DR5) induction. Strong synergy was identified between ONC201 and HDACi panobinostat (combination index [CI] 0.01), romidepsin (CI 0.08) and proteasome inhibitor marizomib (CI 0.19). Synergy was demonstrated between ONC201 and etoposide (CI 0.54), although to a lesser degree than with panobinostat, romidepsin, and marizomib. ONC206 and ONC212 showed similar synergistic effects with panobinostat, romidepsin, and marizomib. Induction of apoptosis was demonstrated with imipridones and panobinostat or romidepsin combinations. Our results suggest increased sensitivity of H3K27M-mutant DIPG cell lines to second generation imipridone therapies, as compared to ONC201. Additionally, there is synergistic cell death with combination of imipridones and panobinostat, romidepsin, or marizomib, which may be further tested in vivo and in clinical trials.

Published
2021

30. miRNA-mediated loss of m6A increases nascent translation in glioblastoma

Author

Zepecki, John P., primary, Karambizi, David, additional, Fajardo, J. Eduardo, additional, Snyder, Kristin M., additional, Guetta-Terrier, Charlotte, additional, Tang, Oliver Y., additional, Chen, Jia-Shu, additional, Sarkar, Atom, additional, Fiser, Andras, additional, Toms, Steven A., additional, and Tapinos, Nikos, additional

Published
2021
Full Text
View/download PDF

33. miRNA-mediated loss of m6A increases nascent translation in glioblastoma

Author

Zepecki, John P., primary, Karambizi, David, additional, Fajardo, J. Eduardo, additional, Snyder, Kristin M., additional, Guetta-Terrier, Charlotte, additional, Tang, Oliver Y., additional, Chen, Jia-Shu, additional, Sarkar, Atom, additional, Fiser, Andras, additional, Toms, Steven A., additional, and Tapinos, Nikos, additional

Published
2020
Full Text
View/download PDF

40. The Dynamic m6A Epitranscriptome in Glioma Stem Cell Plasticity and Function

Author

Tapinos, Nikos and Karambizi, David

Subjects
Medical
Abstract

Glioblastoma multiforme is one of the most aggressive tumors of the central nervous system. The current standard-of-care includes maximal resection followed by chemotherapy, radiation and more recently, tumor treating fields (TTFs). Despite this multimodal approach, glioblastoma remains refractory to therapy. Glioblastoma resistance, recurrence and malignancy are believed to be driven by a subpopulation of glioma stem cells (GSCs) within the tumor bulk which are characterized by the retention of self-renewal potential as well as the capacity to recapitulate tumor heterogeneity. Within the dynamic intratumoral niche, GSCs demonstrate a high degree of cellular plasticity, reversibly interconverting between stem-like states and more differentiated states as a result of environmental cues/signaling fluctuations. Such plastic adaptive properties are mostly driven by multiple dynamic, reversible epigenetic modifications. We posit that reversible post-transcriptional methylation of RNA transcripts at the m6A position may be one such regulatory mechanism employed by GSCs to efficiently maintain plasticity and adaptive phenotypic transitions. In this section, we discuss the concept of cellular plasticity, introduce dynamic m6a epitranscriptomic mechanisms as potential key regulators of GSC plasticity and finally propose epigenetic based therapeutics as a mean of attenuating glioblastoma plasticity to improve patient outcome.

Published
2019

42. miRNA-mediated loss of m6A increases nascent translation in glioblastoma.

Author

Zepecki, John P., Karambizi, David, Fajardo, J. Eduardo, Snyder, Kristin M., Guetta-Terrier, Charlotte, Tang, Oliver Y., Chen, Jia-Shu, Sarkar, Atom, Fiser, Andras, Toms, Steven A., and Tapinos, Nikos

Subjects
GLIOBLASTOMA multiforme, TUMOR suppressor genes, GENETIC translation, HUMAN stem cells, RNA methylation, TUMOR growth
Abstract

Within the glioblastoma cellular niche, glioma stem cells (GSCs) can give rise to differentiated glioma cells (DGCs) and, when necessary, DGCs can reciprocally give rise to GSCs to maintain the cellular equilibrium necessary for optimal tumor growth. Here, using ribosome profiling, transcriptome and m6A RNA sequencing, we show that GSCs from patients with different subtypes of glioblastoma share a set of transcripts, which exhibit a pattern of m6A loss and increased protein translation during differentiation. The target sequences of a group of miRNAs overlap the canonical RRACH m6A motifs of these transcripts, many of which confer a survival advantage in glioblastoma. Ectopic expression of the RRACH-binding miR-145 induces loss of m6A, formation of FTO/AGO1/ILF3/miR-145 complexes on a clinically relevant tumor suppressor gene (CLIP3) and significant increase in its nascent translation. Inhibition of miR-145 maintains RRACH m6A levels of CLIP3 and inhibits its nascent translation. This study highlights a critical role of miRNAs in assembling complexes for m6A demethylation and induction of protein translation during GSC state transition. Author summary: Cellular plasticity and epigenetic adaptation of human glioblastoma stem cells to the tumor microenvironment is a hallmark of this devastating disease. With our present work, we discover the relationship between miRNAs and the RNA methylation machinery in human glioblastoma and show how miRNA-induced loss of m6A results in increase in protein translation of clinically important transcripts during glioblastoma stem cell differentiation. Leveraging the dynamic functions of these miRNAs can be important in the design of optimal therapeutics targeted at cancer cell plasticity. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

47. Sustained Local Release of Methylprednisolone From a Thiol-Acrylate Poly(Ethylene Glycol) Hydrogel for Treating Chronic Compressive Radicular Pain

Author

Slotkin, Jonathan R., primary, Ness, Jennifer K., additional, Snyder, Kristin M., additional, Skiles, Amanda A., additional, Woodard, Eric J., additional, OʼShea, Timothy, additional, Layer, Rick T., additional, Aimetti, Alex A., additional, Toms, Steven A., additional, Langer, Robert, additional, and Tapinos, Nikos, additional

Published
2016
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results