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825 results on '"Radivoyevitch, Tomas"'

2. Pathophysiologic and clinical implications of molecular profiles resultant from deletion 5q

Author

Adema, Vera, Palomo, Laura, Walter, Wencke, Mallo, Mar, Hutter, Stephan, La Framboise, Thomas, Arenillas, Leonor, Meggendorfer, Manja, Radivoyevitch, Tomas, Xicoy, Blanca, Pellagatti, Andrea, Haferlach, Claudia, Boultwood, Jacqueline, Kern, Wolfgang, Visconte, Valeria, Sekeres, Mikkael, Barnard, John, Haferlach, Torsten, Solé, Francesc, and Maciejewski, Jaroslaw P.

Published
2022
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3. Global immune fingerprinting in glioblastoma patient peripheral blood reveals immune-suppression signatures associated with prognosis

Author

Alban, Tyler J, Alvarado, Alvaro G, Sorensen, Mia D, Bayik, Defne, Volovetz, Josephine, Serbinowski, Emily, Mulkearns-Hubert, Erin E, Sinyuk, Maksim, Hale, James S, Onzi, Giovana R, McGraw, Mary, Huang, Pengjing, Grabowski, Matthew M, Wathen, Connor A, Ahluwalia, Manmeet S, Radivoyevitch, Tomas, Kornblum, Harley I, Kristensen, Bjarne W, Vogelbaum, Michael A, and Lathia, Justin D

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Rare Diseases, Genetics, Immunotherapy, Cancer, Brain Disorders, Brain Cancer, Human Genome, Orphan Drug, Neurosciences, Clinical Research, 2.1 Biological and endogenous factors, 6.1 Pharmaceuticals, Inflammatory and immune system, Good Health and Well Being, Brain Neoplasms, Cell Line, Disease Progression, Female, Flow Cytometry, Glioblastoma, Humans, Longitudinal Studies, Male, Myeloid-Derived Suppressor Cells, Neoplasm Metastasis, Neoplasm Staging, Prognosis, Survival Analysis, Tumor Microenvironment, Brain cancer, Cancer immunotherapy, Oncology, Biomedical and clinical sciences, Health sciences
Abstract

Glioblastoma (GBM) remains uniformly lethal, and despite a large accumulation of immune cells in the microenvironment, there is limited antitumor immune response. To overcome these challenges, a comprehensive understanding of GBM systemic immune response during disease progression is required. Here, we integrated multiparameter flow cytometry and mass cytometry TOF (CyTOF) analysis of patient blood to determine changes in the immune system among tumor types and over disease progression. Utilizing flow cytometry analysis in a cohort of 259 patients ranging from benign to malignant primary and metastatic brain tumors, we found that GBM patients had a significant elevation in myeloid-derived suppressor cells (MDSCs) in peripheral blood but not immunosuppressive Tregs. In GBM patient tissue, we found that increased MDSC levels in recurrent GBM portended poor prognosis. CyTOF analysis of peripheral blood from newly diagnosed GBM patients revealed that reduced MDSCs over time were accompanied by a concomitant increase in DCs. GBM patients with extended survival also had reduced MDSCs, similar to the levels of low-grade glioma (LGG) patients. Our findings provide a rationale for developing strategies to target MDSCs, which are elevated in GBM patients and predict poor prognosis.

Published
2018

5. Machine learning integrates genomic signatures for subclassification beyond primary and secondary acute myeloid leukemia

Author

Awada, Hassan, Durmaz, Arda, Gurnari, Carmelo, Kishtagari, Ashwin, Meggendorfer, Manja, Kerr, Cassandra M., Kuzmanovic, Teodora, Durrani, Jibran, Shreve, Jacob, Nagata, Yasunobu, Radivoyevitch, Tomas, Advani, Anjali S., Ravandi, Farhad, Carraway, Hetty E., Nazha, Aziz, Haferlach, Claudia, Saunthararajah, Yogen, Scott, Jacob, Visconte, Valeria, Kantarjian, Hagop, Kadia, Tapan, Sekeres, Mikkael A., Haferlach, Torsten, and Maciejewski, Jaroslaw P.

Published
2021
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8. Tet2 loss leads to hypermutagenicity in haematopoietic stem/progenitor cells.

Author

Pan, Feng, Wingo, Thomas, Zhao, Zhigang, Gao, Rui, Makishima, Hideki, Qu, Guangbo, Lin, Li, Yu, Miao, Ortega, Janice, Wang, Jiapeng, Nazha, Aziz, Chen, Li, Yao, Bing, Liu, Can, Chen, Shi, Weeks, Ophelia, Ni, Hongyu, Phillips, Brittany, Huang, Suming, Wang, Jianlong, He, Chuan, Li, Guo-Min, Radivoyevitch, Tomas, Aifantis, Iannis, Maciejewski, Jaroslaw, Yang, Feng-Chun, Jin, Peng, and Xu, Mingjiang

Subjects
5-Methylcytosine, Aged, Animals, Cell Line, Tumor, DNA Demethylation, DNA Mutational Analysis, DNA-Binding Proteins, Dioxygenases, Epigenesis, Genetic, Gene Expression Regulation, Neoplastic, Hematologic Neoplasms, Hematopoietic Stem Cells, Humans, Mice, Mice, Knockout, Mutagenesis, Mutation Rate, Proto-Oncogene Proteins, RNA, Small Interfering, Single-Cell Analysis, Exome Sequencing
Abstract

TET2 is a dioxygenase that catalyses multiple steps of 5-methylcytosine oxidation. Although TET2 mutations frequently occur in various types of haematological malignancies, the mechanism by which they increase risk for these cancers remains poorly understood. Here we show that Tet2-/- mice develop spontaneous myeloid, T- and B-cell malignancies after long latencies. Exome sequencing of Tet2-/- tumours reveals accumulation of numerous mutations, including Apc, Nf1, Flt3, Cbl, Notch1 and Mll2, which are recurrently deleted/mutated in human haematological malignancies. Single-cell-targeted sequencing of wild-type and premalignant Tet2-/- Lin-c-Kit+ cells shows higher mutation frequencies in Tet2-/- cells. We further show that the increased mutational burden is particularly high at genomic sites that gained 5-hydroxymethylcytosine, where TET2 normally binds. Furthermore, TET2-mutated myeloid malignancy patients have significantly more mutational events than patients with wild-type TET2. Thus, Tet2 loss leads to hypermutagenicity in haematopoietic stem/progenitor cells, suggesting a novel TET2 loss-mediated mechanism of haematological malignancy pathogenesis.

Published
2017

12. Extracellular Vesicle-Enriched miRNA-Biomarkers Show Improved Utility for Detecting Alzheimer’s Disease Dementia and Medial Temporal Atrophy

Author

Chai, Yuek Ling, primary, Strohm, Lea, additional, Zhu, Yanan, additional, Chia, Rachel S.L., additional, Chong, Joyce Ruifen, additional, Suresh, Danesha Devini, additional, Zhou, Li Han, additional, Too, Heng Phon, additional, Hilal, Saima, additional, Radivoyevitch, Tomas, additional, Koo, Edward H., additional, Chen, Christopher P., additional, and Poplawski, Gunnar Heiko Dirk, additional

Published
2024
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15. BRCC3 mutations in myeloid neoplasms

Author

Huang, Dayong, Nagata, Yasunobu, Grossmann, Vera, Radivoyevitch, Tomas, Okuno, Yusuke, Nagae, Genta, Hosono, Naoko, Schnittger, Susanne, Sanada, Masashi, Przychodzen, Bartlomiej, Kon, Ayana, Polprasert, Chantana, Shen, Wenyi, Clemente, Michael J, Phillips, James G, Alpermann, Tamara, Yoshida, Kenichi, Nadarajah, Niroshan, Sekeres, Mikkael A, Oakley, Kevin, Nguyen, Nhu, Shiraishi, Yuichi, Shiozawa, Yusuke, Chiba, Kenichi, Tanaka, Hiroko, Koeffler, H Phillip, Klein, Hans-Ulrich, Dugas, Martin, Aburatani, Hiroyuki, Miyano, Satoru, Haferlach, Claudia, Kern, Wolfgang, Haferlach, Torsten, Du, Yang, Ogawa, Seishi, and Makishima, Hideki

Subjects
Human Genome, Rare Diseases, Cancer, Genetics, Hematology, Stem Cell Research, Stem Cell Research - Nonembryonic - Non-Human, Aged, Aged, 80 and over, Alleles, Animals, BRCA1 Protein, Chromosome Aberrations, DNA Mutational Analysis, Deubiquitinating Enzymes, Female, Gene Frequency, Gene Knockdown Techniques, Genetic Association Studies, Genotype, Humans, Male, Membrane Proteins, Mice, Middle Aged, Mutation, Myeloproliferative Disorders, Phenotype, RNA, Small Interfering, Immunology
Abstract

Next generation sequencing technologies have provided insights into the molecular heterogeneity of various myeloid neoplasms, revealing previously unknown somatic genetic events. In our cohort of 1444 cases analyzed by next generation sequencing, somatic mutations in the gene BRCA1-BRCA2-containing complex 3 (BRCC3) were identified in 28 cases (1.9%). BRCC3 is a member of the JAMM/MPN+ family of zinc metalloproteases capable of cleaving Lys-63 linked polyubiquitin chains, and is implicated in DNA repair. The mutations were located throughout its coding region. The average variant allelic frequency of BRCC3 mutations was 30.1%, and by a serial sample analysis at two different time points a BRCC3 mutation was already identified in the initial stage of a myelodysplastic syndrome. BRCC3 mutations commonly occurred in nonsense (n=12), frameshift (n=4), and splice site (n=5) configurations. Due to the marginal male dominance (odds ratio; 2.00, 0.84-4.73) of BRCC3 mutations, the majority of mutations (n=23; 82%) were hemizygous. Phenotypically, BRCC3 mutations were frequently observed in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms and associated with -Y abnormality (odds ratio; 3.70, 1.25-11.0). Clinically, BRCC3 mutations were also related to higher age (P=0.01), although prognosis was not affected. Knockdown of Brcc3 gene expression in murine bone marrow lineage negative, Sca1 positive, c-kit positive cells resulted in 2-fold more colony formation and modest differentiation defect. Thus, BRCC3 likely plays a role as tumor-associated gene in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms.

Published
2015

16. Stochastic Process Pharmacodynamics: Dose Timing in Neonatal Gentamicin Therapy as an Example

Author

Radivoyevitch, Tomas, Siranart, Nopphon, Hlatky, Lynn, and Sachs, Rainer

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, 6.1 Pharmaceuticals, Administration, Intravenous, Anti-Bacterial Agents, Colony Count, Microbial, Escherichia coli, Escherichia coli Infections, Gentamicins, Humans, Infant, Newborn, Models, Biological, Probability, Stochastic Processes, Pharmacology and Pharmaceutical Sciences, Pharmacology & Pharmacy, Pharmacology and pharmaceutical sciences
Abstract

We consider dosing regimens designed to cure patients by eradicating colony forming units (CFU) such as bacteria. In the field of "population" pharmaco-kinetics/dynamics (PK/PD), inter-individual variability (IIV) of patients is estimated using model parameter statistical distributions. We consider a more probabilistic approach to IIV called stochastic process theory, motivated by the fact that tumor treatment planning uses both approaches. Stochastic process PD can supply additional insights and suggest different dosing regimens due to its emphasis on the probability of complete CFU eradication and its predictions on "pure chance" fluctuations of CFU number per patient when treatment has reduced this integer to less than ~100. To exemplify the contrast between stochastic process PD models and standard deterministic PD models, which track only average CFU number, we analyze, neglecting immune responses, neonatal intravenous gentamicin dosing regimens directed against Escherichia coli. Our stochastic calculations predict that the first dose is crucial for CFU eradication. For example, a single 6 mg/kg dose is predicted to have a higher eradication probability than four daily 4 mg/kg doses. We conclude: (1) neonatal gentamicin dosing regimens with larger first doses but smaller total doses deserve investigation; (2) in general, if standard PK/PD models predict average CFU number drops substantially below 100, the models should be modified to incorporate stochastic effects more accurately, and will then usually make more favorable, or less unfavorable, predictions for front boosting ("hit hard early"). Various caveats against over-interpreting the calculations are given.

Published
2015

18. Subclonal STAT3 mutations solidify clonal dominance

Author

Kerr, Cassandra M., Clemente, Michael J., Chomczynski, Peter W., Przychodzen, Bartlomiej, Nagata, Yasunobu, Adema, Vera, Visconte, Valeria, Lichtin, Alan E., Mustjoki, Satu, Radivoyevitch, Tomas, Sekeres, Mikkael A., and Maciejewski, Jaroslaw P.

Published
2019
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19. Invariant phenotype and molecular association of biallelic TET2 mutant myeloid neoplasia

Author

Awada, Hassan, Nagata, Yasunobu, Goyal, Abhinav, Asad, Mohammad F., Patel, Bhumika, Hirsch, Cassandra M., Kuzmanovic, Teodora, Guan, Yihong, Przychodzen, Bartlomiej P., Aly, Mai, Adema, Vera, Shen, Wenyi, Williams, Louis, Nazha, Aziz, Abazeed, Mohamed E., Sekeres, Mikkael A., Radivoyevitch, Tomas, Haferlach, Torsten, Jha, Babal K., Visconte, Valeria, and Maciejewski, Jaroslaw P.

Published
2019
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20. Risk of acute myeloid leukemia and myelodysplastic syndrome after autotransplants for lymphomas and plasma cell myeloma

Author

Radivoyevitch, Tomas, Dean, Robert M., Shaw, Bronwen E., Brazauskas, Ruta, Tecca, Heather R., Molenaar, Remco J., Battiwalla, Minoo, Savani, Bipin N., Flowers, Mary E.D., Cooke, Kenneth R., Hamilton, Betty K., Kalaycio, Matt, Maciejewski, Jaroslaw P., Ahmed, Ibrahim, Akpek, Görgün, Bajel, Ashish, Buchbinder, David, Cahn, Jean-Yves, D’Souza, Anita, Daly, Andrew, DeFilipp, Zachariah, Ganguly, Siddhartha, Hamadani, Mehdi, Hayashi, Robert J., Hematti, Peiman, Inamoto, Yoshihiro, Khera, Nandita, Kindwall-Keller, Tamila, Landau, Heather, Lazarus, Hillard, Majhail, Navneet S., Marks, David I., Olsson, Richard F., Seo, Sachiko, Steinberg, Amir, William, Basem M., Wirk, Baldeep, Yared, Jean A., Aljurf, Mahmoud, Abidi, Muneer H., Allewelt, Heather, Beitinjaneh, Amer, Cook, Rachel, Cornell, Robert F., Fay, Joseph W., Hale, Gregory, Chakrabarty, Jennifer Holter, Jodele, Sonata, Kasow, Kimberly A., Mahindra, Anuj, Malone, Adriana K., Popat, Uday, Rizzo, J. Douglas, Schouten, Harry C., Warwick, Anne B., Wood, William A., Sekeres, Mikkael A., Litzow, Mark R., Gale, Robert P., and Hashmi, Shahrukh K.

Published
2018
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24. Erratum: Addressing Therapeutic Inertia: Development and Implementation of an Electronic Health Record–Based Diabetes Intensification Tool. Diabetes Spectrum 2023;36:161–170 (https://doi.org/10.2337/ds22-0031)

Author

Pantalone, Kevin M., primary, Rajpathak, Swapnil, additional, Ji, Xinge, additional, Jin, Jian, additional, Weiss, Tracey, additional, Bauman, Janine, additional, Radivoyevitch, Tomas, additional, Kattan, Michael W., additional, Zimmerman, Robert S., additional, and Misra-Hebert, Anita D., additional

Published
2023
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27. Context dependent effects of ascorbic acid treatment in TET2 mutant myeloid neoplasia

Author

Guan, Yihong, Greenberg, Edward F., Hasipek, Metis, Chen, Shi, Liu, Xiaochen, Kerr, Cassandra M., Gackowski, Daniel, Zarakowska, Ewelina, Radivoyevitch, Tomas, Gu, Xiaorong, Willard, Belinda, Visconte, Valeria, Makishima, Hideki, Nazha, Aziz, Mukherji, Mridul, Sekeres, Mikkael A., Saunthararajah, Yogen, Oliński, Ryszard, Xu, Mingjiang, Maciejewski, Jaroslaw P., and Jha, Babal K.

Published
2020
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28. SBML Level 3: an extensible format for the exchange and reuse of biological models

Author

Keating, Sarah M, Waltemath, Dagmar, König, Matthias, Zhang, Fengkai, Dräger, Andreas, Chaouiya, Claudine, Bergmann, Frank T, Finney, Andrew, Gillespie, Colin S, Helikar, Tomáš, Hoops, Stefan, Malik‐Sheriff, Rahuman S, Moodie, Stuart L, Moraru, Ion I, Myers, Chris J, Naldi, Aurélien, Olivier, Brett G, Sahle, Sven, Schaff, James C, Smith, Lucian P, Swat, Maciej J, Thieffry, Denis, Watanabe, Leandro, Wilkinson, Darren J, Blinov, Michael L, Begley, Kimberly, Faeder, James R, Gómez, Harold F, Hamm, Thomas M, Inagaki, Yuichiro, Liebermeister, Wolfram, Lister, Allyson L, Lucio, Daniel, Mjolsness, Eric, Proctor, Carole J, Raman, Karthik, Rodriguez, Nicolas, Shaffer, Clifford A, Shapiro, Bruce E, Stelling, Joerg, Swainston, Neil, Tanimura, Naoki, Wagner, John, Meier‐Schellersheim, Martin, Sauro, Herbert M, Palsson, Bernhard, Bolouri, Hamid, Kitano, Hiroaki, Funahashi, Akira, Hermjakob, Henning, Doyle, John C, Hucka, Michael, Adams, Richard R, Allen, Nicholas A, Angermann, Bastian R, Antoniotti, Marco, Bader, Gary D, Červený, Jan, Courtot, Mélanie, Cox, Chris D, Dalle Pezze, Piero, Demir, Emek, Denney, William S, Dharuri, Harish, Dorier, Julien, Drasdo, Dirk, Ebrahim, Ali, Eichner, Johannes, Elf, Johan, Endler, Lukas, Evelo, Chris T, Flamm, Christoph, Fleming, Ronan MT, Fröhlich, Martina, Glont, Mihai, Gonçalves, Emanuel, Golebiewski, Martin, Grabski, Hovakim, Gutteridge, Alex, Hachmeister, Damon, Harris, Leonard A, Heavner, Benjamin D, Henkel, Ron, Hlavacek, William S, Hu, Bin, Hyduke, Daniel R, de Jong, Hidde, Juty, Nick, Karp, Peter D, Karr, Jonathan R, Kell, Douglas B, Keller, Roland, Kiselev, Ilya, Klamt, Steffen, Klipp, Edda, Knüpfer, Christian, Kolpakov, Fedor, Krause, Falko, Kutmon, Martina, Laibe, Camille, Lawless, Conor, Li, Lu, Loew, Leslie M, Machne, Rainer, Matsuoka, Yukiko, Mendes, Pedro, Mi, Huaiyu, Mittag, Florian, Monteiro, Pedro T, Natarajan, Kedar Nath, Nielsen, Poul MF, Nguyen, Tramy, Palmisano, Alida, Pettit, Jean‐Baptiste, Pfau, Thomas, Phair, Robert D, Radivoyevitch, Tomas, Rohwer, Johann M, Ruebenacker, Oliver A, Saez‐Rodriguez, Julio, Scharm, Martin, Schmidt, Henning, Schreiber, Falk, Schubert, Michael, Schulte, Roman, Sealfon, Stuart C, Smallbone, Kieran, Soliman, Sylvain, Stefan, Melanie I, Sullivan, Devin P, Takahashi, Koichi, Teusink, Bas, Tolnay, David, Vazirabad, Ibrahim, von Kamp, Axel, Wittig, Ulrike, Wrzodek, Clemens, Wrzodek, Finja, Xenarios, Ioannis, Zhukova, Anna, and Zucker, Jeremy

Published
2020
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30. Leukemogenic nucleophosmin mutation disrupts the transcription factor hub that regulates granulomonocytic fates

Author

Gu, Xiaorong, Ebrahem, Quteba, Mahfouz, Reda Z., Hasipek, Metis, Enane, Francis, Radivoyevitch, Tomas, Rapin, Nicolas, Przychodzen, Bartlomiej, Hu, Zhenbo, Balusu, Ramesh, Cotta, Claudiu V., Wald, David, Argueta, Christian, Landesman, Yosef, Martelli, Maria Paola, Falini, Brunangelo, Carraway, Hetty, Porse, Bo T., Maciejewski, Jaroslaw, Jha, Babal K., and Saunthararajah, Yogen

Subjects
Genetic aspects, Health aspects, Oncogenes -- Health aspects, Gene mutation -- Health aspects, Granulocytes -- Genetic aspects -- Health aspects, Transcription factors -- Health aspects, Gene expression -- Health aspects
Abstract

Introduction Nucleophosmin (NPM1) is one of the most frequently mutated genes in de novo acute myeloid leukemia (AML) (~30% of cases) (1). Only approximately 50% of patients with NPM1-mutated AML [...], Nucleophosmin (NPM1) is among the most frequently mutated genes in acute myeloid leukemia (AML). It is not known, however, how the resulting oncoprotein mutant NPM1 is leukemogenic. To reveal the cellular machinery in which NPM1 participates in myeloid cells, we analyzed the endogenous NPM1 protein interactome by mass spectrometry and discovered abundant amounts of the master transcription factor driver of monocyte lineage differentiation PU.1 (also known as SPI1). Mutant NPM1, which aberrantly accumulates in cytoplasm, dislocated PU.1 into cytoplasm with it. CEBPA and RUNX1, the master transcription factors that collaborate with PU.1 to activate granulomonocytic lineage fates, remained nuclear; but without PU.1, their coregulator interactions were toggled from coactivators to corepressors, repressing instead of activating more than 500 granulocyte and monocyte terminal differentiation genes. An inhibitor of nuclear export, selinexor, by locking mutant NPM1/PU.1 in the nucleus, activated terminal monocytic fates. Direct depletion of the corepressor DNA methyltransferase 1 (DNMT1) from the CEBPA/RUNX1 protein interactome using the clinical drug decitabine activated terminal granulocytic fates. Together, these noncytotoxic treatments extended survival by more than 160 days versus vehicle in a patient-derived xenotransplant model of NPM1/FLT3-mutated AML. In sum, mutant NPM1 represses monocyte and granulocyte terminal differentiation by disrupting PU.1/CEBPA/RUNX1 collaboration, a transforming action that can be reversed by pharmacodynamically directed dosing of clinical small molecules.

Published
2018
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34. Consequences of mutant TET2 on clonality and subclonal hierarchy

Author

Hirsch, Cassandra M., Nazha, Aziz, Kneen, Kassy, Abazeed, Mohamed E., Meggendorfer, Manja, Przychodzen, Bartlomiej P., Nadarajah, Niroshan, Adema, Vera, Nagata, Yasunobu, Goyal, Abhinav, Awada, Hassan, Asad, Mohammad Fahad, Visconte, Valeria, Guan, Yihong, Sekeres, Mikkael A., Olinski, Ryszard, Jha, Babal Kant, LaFramboise, Thomas, Radivoyevitch, Tomas, Haferlach, Torsten, and Maciejewski, Jaroslaw P.

Published
2018
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35. Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

Author

Biswas, Sudipta, primary, Kang, Kai, additional, Ng, Kwok Peng, additional, Radivoyevitch, Tomas, additional, Schalper, Kurt, additional, Zhang, Hua, additional, Lindner, Daniel J., additional, Thomas, Anish, additional, MacPherson, David, additional, Gastman, Brian, additional, Schrump, David S., additional, Wong, Kwok-Kin, additional, Velcheti, Vamsidhar, additional, and Saunthararajah, Yogen, additional

Published
2023
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38. Invariant patterns of clonal succession determine specific clinical features of myelodysplastic syndromes

Author

Nagata, Yasunobu, Makishima, Hideki, Kerr, Cassandra M., Przychodzen, Bartlomiej P., Aly, Mai, Goyal, Abhinav, Awada, Hassan, Asad, Mohammad Fahad, Kuzmanovic, Teodora, Suzuki, Hiromichi, Yoshizato, Tetsuichi, Yoshida, Kenichi, Chiba, Kenichi, Tanaka, Hiroko, Shiraishi, Yuichi, Miyano, Satoru, Mukherjee, Sudipto, LaFramboise, Thomas, Nazha, Aziz, Sekeres, Mikkael A., Radivoyevitch, Tomas, Haferlach, Torsten, Ogawa, Seishi, and Maciejewski, Jaroslaw P.

Published
2019
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41. Data from Radioprotection of IDH1-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198

Author

Molenaar, Remco J., primary, Botman, Dennis, primary, Smits, Myrthe A., primary, Hira, Vashendriya V., primary, van Lith, Sanne A., primary, Stap, Jan, primary, Henneman, Peter, primary, Khurshed, Mohammed, primary, Lenting, Krissie, primary, Mul, Adri N., primary, Dimitrakopoulou, Dionysia, primary, van Drunen, Cornelis M., primary, Hoebe, Ron A., primary, Radivoyevitch, Tomas, primary, Wilmink, Johanna W., primary, Maciejewski, Jaroslaw P., primary, Vandertop, W. Peter, primary, Leenders, William P., primary, Bleeker, Fonnet E., primary, and van Noorden, Cornelis J., primary

Published
2023
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42. Supplementary Figure 1 from Increased CDA Expression/Activity in Males Contributes to Decreased Cytidine Analog Half-Life and Likely Contributes to Worse Outcomes with 5-Azacytidine or Decitabine Therapy

Author

Mahfouz, Reda Z., primary, Jankowska, Ania, primary, Ebrahem, Quteba, primary, Gu, Xiaorong, primary, Visconte, Valeria, primary, Tabarroki, Ali, primary, Terse, Pramod, primary, Covey, Joseph, primary, Chan, Kenneth, primary, Ling, Yonghua, primary, Engelke, Kory J., primary, Sekeres, Mikkael A., primary, Tiu, Ramon, primary, Maciejewski, Jaroslaw, primary, Radivoyevitch, Tomas, primary, and Saunthararajah, Yogen, primary

Published
2023
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43. Supplements from IDH1/2 Mutations Sensitize Acute Myeloid Leukemia to PARP Inhibition and This Is Reversed by IDH1/2-Mutant Inhibitors

Author

Molenaar, Remco J., primary, Radivoyevitch, Tomas, primary, Nagata, Yasunobu, primary, Khurshed, Mohammed, primary, Przychodzen, Bartolomiej, primary, Makishima, Hideki, primary, Xu, Mingjiang, primary, Bleeker, Fonnet E., primary, Wilmink, Johanna W., primary, Carraway, Hetty E., primary, Mukherjee, Sudipto, primary, Sekeres, Mikkael A., primary, van Noorden, Cornelis J.F., primary, and Maciejewski, Jaroslaw P., primary

Published
2023
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44. Supplementary Table S1 from Radioprotection of IDH1-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198

Author

Molenaar, Remco J., primary, Botman, Dennis, primary, Smits, Myrthe A., primary, Hira, Vashendriya V., primary, van Lith, Sanne A., primary, Stap, Jan, primary, Henneman, Peter, primary, Khurshed, Mohammed, primary, Lenting, Krissie, primary, Mul, Adri N., primary, Dimitrakopoulou, Dionysia, primary, van Drunen, Cornelis M., primary, Hoebe, Ron A., primary, Radivoyevitch, Tomas, primary, Wilmink, Johanna W., primary, Maciejewski, Jaroslaw P., primary, Vandertop, W. Peter, primary, Leenders, William P., primary, Bleeker, Fonnet E., primary, and van Noorden, Cornelis J., primary

Published
2023
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45. Supplementary Data from Preclinical Modeling of Surgery and Steroid Therapy for Glioblastoma Reveals Changes in Immunophenotype that are Associated with Tumor Growth and Outcome

Author

Otvos, Balint, primary, Alban, Tyler J., primary, Grabowski, Matthew M., primary, Bayik, Defne, primary, Mulkearns-Hubert, Erin E., primary, Radivoyevitch, Tomas, primary, Rabljenovic, Anja, primary, Johnson, Sarah, primary, Androjna, Charlie, primary, Mohammadi, Alireza M., primary, Barnett, Gene H., primary, Ahluwalia, Manmeet S., primary, Vogelbaum, Michael A., primary, Fecci, Peter E., primary, and Lathia, Justin D., primary

Published
2023
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46. Data from Increased CDA Expression/Activity in Males Contributes to Decreased Cytidine Analog Half-Life and Likely Contributes to Worse Outcomes with 5-Azacytidine or Decitabine Therapy

Author

Mahfouz, Reda Z., primary, Jankowska, Ania, primary, Ebrahem, Quteba, primary, Gu, Xiaorong, primary, Visconte, Valeria, primary, Tabarroki, Ali, primary, Terse, Pramod, primary, Covey, Joseph, primary, Chan, Kenneth, primary, Ling, Yonghua, primary, Engelke, Kory J., primary, Sekeres, Mikkael A., primary, Tiu, Ramon, primary, Maciejewski, Jaroslaw, primary, Radivoyevitch, Tomas, primary, and Saunthararajah, Yogen, primary

Published
2023
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47. GATA4 loss of function in liver cancer impedes precursor to hepatocyte transition

Author

Enane, Francis O., Shuen, Wai Ho, Gu, Xiaorong, Quteba, Ebrahem, Przychodzen, Bartlomiej, Makishima, Hideki, Bodo, Juraj, Ng, Joanna, Chee, Chit Lai, Ba, Rebecca, Koh, Lip Seng, Lim, Janice, Cheong, Rachael, Teo, Marissa, Hu, Zhenbo, Ng, Kwok Peng, Maciejewski, Jaroslaw, Radivoyevitch, Tomas, Chung, Alexander, Ooi, London Lucien, Tan, Yu Meng, Cheow, Peng-Chung, Chow, Pierce, Chan, Chung Yip, Lim, Kiat Hon, Yerian, Lisa, Hsi, Eric, Toh, Han Chong, and Saunthararajah, Yogen

Subjects
Physiological aspects, Health aspects, Liver cancer -- Physiological aspects, Hepatocytes -- Health aspects
Abstract

Introduction Hepatocellular carcinoma (HCC) is the world's second leading cause of cancer death. In the effort to understand the molecular mechanisms of HCC genesis, a relevant lead is that the [...], The most frequent chromosomal structural loss In hepatocellular carcinoma (HCC) Is of the short arm of chromosome 8 (8p). Genes on the remaining homologous chromosome, however, are not recurrently mutated, and the identity of key 8p tumor-suppressor genes (TSG) is unknown. In this work, analysis of minimal commonly deleted 8p segments to identify candidate TSG implicated GATA4, a master transcription factor driver of hepatocyte epithelial lineage fate. In a murine model, liver-conditional deletion of 1 Gata4 allele to model the haploinsufficiency seen in HCC produced enlarged livers with a gene expression profile of persistent precursor proliferation and failed hepatocyte epithelial differentiation. HCC mimicked this gene expression profile, even in cases that were morphologically classified as well differentiated. HCC with intact chromosome 8p also featured GATA4 loss of function via GATA4 germline mutations that abrogated GATA4 interactions with a coactivator, MED12, or by inactivating mutations directly in GATA4 coactivators, including ARID1A. GATA4 reintroduction into GATA4-haploinsufficient HCC cells or ARID1A reintroduction into ARID1A-mutant/GATA4-intact HCC cells activated hundreds of hepatocyte genes and quenched the proliferative precursor program. Thus, disruption of GATA4-mediated transactivation in HCC suppresses hepatocyte epithelial differentiation to sustain replicative precursor phenotype.

Published
2017
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49. p53-Independent Epigenetic Treatment for Chemo-Refractory Small Cell Lung Cancer: Bio-Rationale and in vivo Proof-of-Principle

Author

Biswas, Sudipta, primary, Kang, Kai, additional, Ng, Kwok Peng, additional, Radivoyevitch, Tomas, additional, Schalper, Kurt, additional, Zhang, Hua, additional, Lindner, Daniel, additional, Thomas, Anish, additional, MacPherson, David, additional, Gastman, Brian, additional, Schrump, David, additional, Wong, Kwok-Kin, additional, Velcheti, Vamsi, additional, and Saunthararajah, Yogen, additional

Published
2023
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