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Your search keyword '"Baranowska‐Kortylewicz, Janina"' showing total 165 results
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165 results on '"Baranowska‐Kortylewicz, Janina"'

11. Tolerable limits to whole liver irradiation in non-human primates: 1674

Author

Yannam, Govardhana R., Han, Bing, Setoyama, Kentaro, Yamamoto, Toshiyuki, Ito, Ryotaro, Brooks, Jenna M., Guzman-Lepe, Jorge, Galambos, Csaba, Fong, Jason V., Deutsch, Melvin, Quader, Mubina A., Yamanouchi, Kosho, Mehta, Keyur, Soto-Gutierrez, Alejandro, Roy-Chowdhury, Jayanta, Locker, Joseph, Abe, Michio, Enke, Charles A., Baranowska-Kortylewicz, Janina, Solberg, Timothy D., Guha, Chandan, and Fox, Ira J.

Published
2012

19. Multifarious Functions of Butyrylcholinesterase in Neuroblastoma: Impact of BCHEDeletion on the Neuroblastoma Growth In Vitro and In Vivo

Author

Baranowska-Kortylewicz, Janina, Kortylewicz, Zbigniew P., McIntyre, Erin M., Sharp, John G., and Coulter, Don W.

Abstract

The physiological functions of butyrylcholinesterase (BChE) and its role in malignancy remain unexplained. Our studies in children newly diagnosed with neuroblastoma indicated that BChE expressions is proportional to MYCNamplification suggesting that pathogenesis of high-risk disease may be related to the persistent expression of abnormally high levels of tumor-associated BChE. BChE-deficient neuroblastoma cells (KO [knockout]) were produced from MYCN-amplified BE(2)-C cells (WT [wild-type]) by the CRISPR-Cas9 targeted disruption of the BCHElocus. KO cells have no detectable BChE activity. The compensatory acetylcholinesterase activity was not detected. The average population doubling time of KO cells is 47.0±2.4 hours, >2× longer than WT cells. Reduced proliferation rates of KO cells were accompanied by the loss of N-Myc protein and a significant deactivation of tyrosine kinase receptors associated with the aggressive neuroblastoma phenotype including Ros1, TrkB, and Ltk. Tumorigenicity of WT and KO cells in male mice was essentially identical. In contrast, KO xenografts in female mice were very small (0.37±0.10 g), ~3× smaller compared with WT xenografts (1.11±0.30 g). Unexpectedly, KO xenografts produced changes in plasma BChE similarly to WT tumors but lesser in magnitude. The disruption of BCHElocus in MYCN-amplified neuroblastoma cells decelerates proliferation and produces neuroblastoma cells that are less aggressive in female mice.

Published
2022
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23. In vitro and in vivo evaluation of radiolabeled methyl N‐[5‐(3′‐halobenzoyl)‐1H‐benzimidazol‐2‐yl]carbamate for cancer radiotherapy.

Author

Kortylewicz, Zbigniew P., Coulter, Don W., and Baranowska‐Kortylewicz, Janina

Subjects
CANCER radiotherapy, TUMOR growth, CANCER cells, CELL lines, DRUG administration, PHARMACOKINETICS, RADIOACTIVE tracers
Abstract

The role of theranostics in cancer management is growing so is the selection of vectors used to deliver these modalities to cancer cells. We describe biological evaluation of a novel theranostic agent targeted to microtubules. Methyl N‐[5‐(3′‐[131I]iodobenzoyl)‐1H‐benzimidazol‐2‐yl]carbamate (1) and methyl N‐[5‐(3′‐[125I]iodobenzoyl)‐1H‐benzimidazol‐2‐yl]carbamate (2) were synthesized from a common precursor 3′‐stannylated derivative (4). Antiproliferative effects and radiotoxicity of 131I‐labeled β‐particle emitting 1 were examined in vitro in human neuroblastoma and glioblastoma cells lines. The therapeutic potential of 1 was also examined in a subcutaneous mouse model of human glioblastoma U‐87 MG. Compound 1 at the extracellular radioactive concentration of 0.35 MBq/mL, easily achievable in vivo, kills >90% of neuroblastoma cells and >60% glioblastoma cells as measured in a clonogenic assay. D10 doses established for 1 indicate that as few as 3,000 decays are sufficient to kill 90% of BE(2)‐C cells. Even U‐87 MG cells, the least sensitive of the tested cell lines, require <20,000 decays of intracellular 131I to reduce number of clonogenic cells by 90%. Biodistribution studies of 2 delivered either intratumorally or intraperitoneally show a similar tissue distribution for both routes of the drug administration. The whole body clearance half‐lives were on average 6 hr. Intratumor administration of 1 produces significant tumor growth delay. After a single dose of 8.4 ± 0.3 MBq of compound 1, the tumor doubling times were 3.2 ± 0.1 and 7.9 ± 0.6 days in control and treated mice, respectively. Methyl N‐[5‐(3′‐radiohalobenzoyl)‐1H‐benzimidazol‐2‐yl]carbamates have properties compatible with a theranostic approach to cancer management. [ABSTRACT FROM AUTHOR]

Published
2020
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28. Norepinephrine-Transporter-Targeted and DNA-Co-Targeted Theranostic Guanidines

Author

Kortylewicz, Zbigniew P., Coulter, Donald W., Han, Guang, and Baranowska-Kortylewicz, Janina

Abstract

High risk neuroblastoma often recurs, even with aggressive treatments. Clinical evidence suggests that proliferative activities are predictive of poor outcomes. This report describes syntheses, characterization, and biological properties of theranostic guanidines that target norepinephrine transporter and undergo intracellular processing, and subsequently their catabolites are efficiently incorporated into DNA of proliferating neuroblastoma cells. Radioactive guanidines are synthesized from 5-radioiodo-2′-deoxyuridine, a molecular radiotherapy platform with clinically proven minimal toxicities and DNA-targeting properties. The transport of radioactive guanidines into neuroblastoma cells is active as indicated by the competitive suppression of cellular uptake by meta-iodobenzylguanidine. The rate of intracellular processing and DNA uptake is influenced by the agent’s catabolic stability and cell population doubling times. The radiotoxicity is directly proportional to DNA uptake and duration of exposure. Biodistribution of 5-[125I]iodo-3′-O-(ε-guanidinohexanoyl)-2′-deoxyuridine in a mouse neuroblastoma model shows significant tumor retention of radioactivity. Neuroblastoma xenografts regress in response to the clinically achievable doses of this agent.

Published
2020
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29. Abstract A127: Butyrylcholinesterase (BChE) expression as a marker of cellular proliferation across neuroblastoma cells lines: new prognostic marker and therapeutic target

Author

Greenwood, Katie, primary, McGuire, Timothy R., additional, Coulter, Donald, additional, McIntyre, Erin, additional, Chaturvedi, Nagendra K., additional, Kortylewicz, Paul, additional, Joshi, Shantaram S., additional, Chen, Xiaoyu, additional, Sharp, John G., additional, and Baranowska-Kortylewicz, Janina, additional

Published
2015
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32. A Nonhuman Primate Model of Human Radiation-Induced Venocclusive Liver Disease and Hepatocyte Injury

Author

Yannam, Govardhana Rao, primary, Han, Bing, additional, Setoyama, Kentaro, additional, Yamamoto, Toshiyuki, additional, Ito, Ryotaro, additional, Brooks, Jenna M., additional, Guzman-Lepe, Jorge, additional, Galambos, Csaba, additional, Fong, Jason V., additional, Deutsch, Melvin, additional, Quader, Mubina A., additional, Yamanouchi, Kosho, additional, Kabarriti, Rafi, additional, Mehta, Keyur, additional, Soto-Gutierrez, Alejandro, additional, Roy-Chowdhury, Jayanta, additional, Locker, Joseph, additional, Abe, Michio, additional, Enke, Charles A., additional, Baranowska-Kortylewicz, Janina, additional, Solberg, Timothy D., additional, Guha, Chandan, additional, and Fox, Ira J., additional

Published
2014
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33. Effect of platelet-derived growth factor receptor-beta inhibition with STI571 on radioimmunotherapy

Author

Baranowska-Kortylewicz, Janina, Abe, Michio, Pietras, Kristian, Kortylewicz, Zbigniew P, Kurizaki, Takashi, Nearman, Jessica, Paulsson, Janna, Mosley, R Lee, Enke, Charles A, Östman, Arne, Baranowska-Kortylewicz, Janina, Abe, Michio, Pietras, Kristian, Kortylewicz, Zbigniew P, Kurizaki, Takashi, Nearman, Jessica, Paulsson, Janna, Mosley, R Lee, Enke, Charles A, and Östman, Arne

Abstract

Whereas radioimmunotherapy of hematologic malignancies has evolved into a viable treatment option, the responses of solid tumors to radioimmunotherapy are discouraging. The likely cause of this problem is the interstitial hypertension inherent to all solid tumors. Remarkable improvements in tumor responses to radioimmunotherapy were discovered after the inclusion of STI571 in the therapy regimen. A combination of the tumor stroma-reactive STI571, a potent platelet-derived growth factor receptor-beta (PDGFr-beta) antagonist, and the tumor-seeking radiolabeled antibody B72.3 yielded long-lasting growth arrest of the human colorectal adenocarcinoma LS174T grown as s.c. xenografts in athymic mice. The interaction of STI571 with the stromal PDGFr-beta reduced tumor interstitial fluid pressure (P(IF)) by >50% and in so doing improved the uptake of B72.3. The attenuation of P(IF) also had a positive effect on the homogeneity of antibody distribution. These effects were dose-dependent and under optimized dosing conditions allowed for a 2.45 times increase in the tumor uptake of B72.3 as determined in the biodistribution studies. Single-photon emission computed tomography imaging studies substantiated these results and indicated that the homogeneity of the radioisotope distribution was also much improved when compared with the control mice. The increased uptake of radioimmunotherapy into the tumor resulted in >400% increase in the tumor absorbed radiation doses in STI571 + radioimmunotherapy-treated mice compared with PBS + radioimmunotherapy-treated mice. The improved antibody uptake in response to the attenuation of tumor P(IF) was identified as the primary reason for the growth arrest of the STI571 + radioimmunotherapy-treated tumors. Two related causes were also identified: (a) the improved homogeneity of monoclonal antibody distribution in tumor and (b) the increased tumor radiosensitivity resulting from the improved tumor oxygenation.

Published
2005
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35. Antigen-Independent Methods to Improve Radioimmunotherapy of Prostate Cancer

Author

NEBRASKA UNIV MEDICAL CENTER OMAHA, Baranowska-Kortylewicz, Janina, NEBRASKA UNIV MEDICAL CENTER OMAHA, and Baranowska-Kortylewicz, Janina

Abstract

These studies were designed to improve the outcome of radioimmunotherapy (RIT) in prostate adenocarcinoma by the inclusion of vasoactive peptides in the RIT protocol. To date three peptides able to modify vascular permeability (VP) were tested. Cytotoxicity studies indicated dose-dependent changes in cell metabolic activities after treatment with two agonists interacting with CD88 (C5aAP peptides); whereas one peptide interactive with a formyl peptide receptor-like I did not seem to have any effect on the growth of these cells in vitro. In vivo results confirmed that at least two of these peptides significantly augmented RIT with 131ICC49. The principal reason for improvements was identified as the increased tumor uptake of the radiotracer. However, there is also an indication that the generation of reactive oxygen species play a significant role. The effect of the C5aAP peptide N2's effect on VP and tumor uptake is virtually identical to the effects of the N1 peptide. The N2, however, considerably reduces the radiosensitivity of LNCaP, PC3 and DU145 cells in vitro. The in vivo studies of N2 with and without thiol group modification are in progress.

Published
2004

37. Antigen-Independent Methods to Improve Radioimmunotherapy of Prostate Cancer

Author

NEBRASKA UNIV MEDICAL CENTER OMAHA, Baranowska-Kortylewicz, Janina, NEBRASKA UNIV MEDICAL CENTER OMAHA, and Baranowska-Kortylewicz, Janina

Abstract

Radioimmunolocalization of prostate cancer with radiolabeled antibodies is widely used in a clinic but radioimmunotherapy (RIT) fails to produce objective responses. Physiological barriers to the delivery of macromolecules to solid tumors are usually blamed for these failures. These studies are designed to improve the outcome of RIT in prostate adenocarcinoma by the inclusion of the antigen-independent peptides in the RIT protocol. To date two peptides able to modify vascular permeability were tested. Cytotoxicity studies indicate dose-dependent changes in cell metabolic activities after treatment with the C5aAP peptide; whereas peptide able to interact with a formyl peptide receptor-like 1 (FPRL1) does not seem to have any effect on the growth of these cells in vitro. In vivo results indicate that both peptides significantly augment RIT with 131ICC49. Three xenografts were tested to date: LNCaP, PC3 and DU145. These xenografts do not show differences in the growth pattern between the untreated tumors and peptide only-treated tumors, but there is a considerable delay in the tumor growth when peptides are combined with 131ICC49. The mechanism of this effect is more complicated than observed for LS174T tumors evaluated in the pilot studies and appears to vary depending on the tumor model and the peptide. The pattern of dependence on to key two factors emerged from these studies: (1) the improved vascular permeability and (2) the generation of reactive oxygen species., The original document contains color images. All DTIC reproductions will be in black and white.

Published
2003

44. WITHDRAWN: Prolonged Survival of Porcine Hepatocytes in Cynomolgus Monkeys

Author

Nagata, Hideo, primary, Nishitai, Ryuta, additional, Shirota, Chiyoe, additional, Zhang, Jia-lin, additional, Koch, Cody A., additional, Cai, Jin, additional, Awwad, Michel, additional, Schuurman, Henk-Jan, additional, Christians, Uwe, additional, Abe, Michio, additional, Baranowska-Kortylewicz, Janina, additional, Platt, Jeffrey L., additional, and Fox, Ira J., additional

Published
2006
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49. Biochemical Modulation by 5-Fluorouracil and 1-Folinic Acid of Tumor Uptake of Intra-Arterial 5-[123I]Iodo-2'-Deoxyuridine in Patients with Liver Metastases from Colorectal Cancer

Author

Mariani, Giuliano, primary, Sacco, Sonia Di, additional, Bonini, Rita, additional, Luca, Lorella Di, additional, Buralli, Simona, additional, Bonora, Danilo, additional, Ricci, Sergio, additional, Baranowska-Kortylewicz, Janina, additional, Adelstein, S. James, additional, Falcone, Alfredo, additional, and Kassis, Amin I., additional

Published
1996
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