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Showing 1 to 12 of 17 entries
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Targeting HER2(+) breast cancer: the TBK1/IKKε axis.

Oncoscience

Jiang Z, Liu JC, Chung PE, Egan SE, Zacksenhaus E.
PMID: 25594009
Oncoscience. 2014 Mar 06;1(2):180-2. doi: 10.18632/oncoscience.18. eCollection 2014.

HER2(+) breast cancer (BC) is a highly aggressive subtype, affecting ~20% of BC patients. Current treatments include adjuvant or neoadjuvant chemotherapy plus anti-HER2 agents such as trastuzumab, a monoclonal antibody directed against HER2. Despite improvement in disease free survival,...

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Jiang Z, Liu JC, Chung PE, et al. Targeting HER2(+) breast cancer: the TBK1/IKKε axis. Oncoscience. 2014;1(2):180-2doi: 10.18632/oncoscience.18.
Jiang, Z., Liu, J. C., Chung, P. E., Egan, S. E., & Zacksenhaus, E. (2014). Targeting HER2(+) breast cancer: the TBK1/IKKε axis. Oncoscience, 1(2), 180-2. https://doi.org/10.18632/oncoscience.18
Jiang, Zhe, et al. "Targeting HER2(+) breast cancer: the TBK1/IKKε axis." Oncoscience vol. 1,2 (2014): 180-2. doi: https://doi.org/10.18632/oncoscience.18
Jiang Z, Liu JC, Chung PE, Egan SE, Zacksenhaus E. Targeting HER2(+) breast cancer: the TBK1/IKKε axis. Oncoscience. 2014 Mar 06;1(2):180-2. doi: 10.18632/oncoscience.18. eCollection 2014. PMID: 25594009; PMCID: PMC4278282.
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CDC25 as a common therapeutic target for triple-negative breast cancer - the challenges ahead.

Molecular & cellular oncology

Zacksenhaus E, Liu JC, Granieri L, Vorobieva I, Wang DY, Ghanbari-Azarnier R, Li H, Ali A, Chung PED, Ju Y, Jiang Z, Shrestha M.
PMID: 30250928
Mol Cell Oncol. 2018 Aug 15;5(4):e1481814. doi: 10.1080/23723556.2018.1481814. eCollection 2018.

The dual phosphatase CDC25 has recently been identified as a target for diverse triple-negative breast cancers including

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Zacksenhaus E, Liu JC, Granieri L, et al. CDC25 as a common therapeutic target for triple-negative breast cancer - the challenges ahead. Mol Cell Oncol. 2018;5(4):e1481814doi: 10.1080/23723556.2018.1481814.
Zacksenhaus, E., Liu, J. C., Granieri, L., Vorobieva, I., Wang, D. Y., Ghanbari-Azarnier, R., Li, H., Ali, A., Chung, P. E. D., Ju, Y., Jiang, Z., & Shrestha, M. (2018). CDC25 as a common therapeutic target for triple-negative breast cancer - the challenges ahead. Molecular & cellular oncology, 5(4), e1481814. https://doi.org/10.1080/23723556.2018.1481814
Zacksenhaus, Eldad, et al. "CDC25 as a common therapeutic target for triple-negative breast cancer - the challenges ahead." Molecular & cellular oncology vol. 5,4 (2018): e1481814. doi: https://doi.org/10.1080/23723556.2018.1481814
Zacksenhaus E, Liu JC, Granieri L, Vorobieva I, Wang DY, Ghanbari-Azarnier R, Li H, Ali A, Chung PED, Ju Y, Jiang Z, Shrestha M. CDC25 as a common therapeutic target for triple-negative breast cancer - the challenges ahead. Mol Cell Oncol. 2018 Aug 15;5(4):e1481814. doi: 10.1080/23723556.2018.1481814. eCollection 2018. PMID: 30250928; PMCID: PMC6149702.
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Associations Between XPD Lys751Gln Polymorphism and Leukemia: A Meta-Analysis.

Frontiers in genetics

Wen M, Zhou B, Lin X, Chen Y, Song J, Li Y, Zacksenhaus E, Ben-David Y, Hao X.
PMID: 30100919
Front Genet. 2018 Jun 14;9:218. doi: 10.3389/fgene.2018.00218. eCollection 2018.

No abstract available.

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Wen M, Zhou B, Lin X, et al. Associations Between XPD Lys751Gln Polymorphism and Leukemia: A Meta-Analysis. Front Genet. 2018;9:218doi: 10.3389/fgene.2018.00218.
Wen, M., Zhou, B., Lin, X., Chen, Y., Song, J., Li, Y., Zacksenhaus, E., Ben-David, Y., & Hao, X. (2018). Associations Between XPD Lys751Gln Polymorphism and Leukemia: A Meta-Analysis. Frontiers in genetics, 9218. https://doi.org/10.3389/fgene.2018.00218
Wen, Min, et al. "Associations Between XPD Lys751Gln Polymorphism and Leukemia: A Meta-Analysis." Frontiers in genetics vol. 9 (2018): 218. doi: https://doi.org/10.3389/fgene.2018.00218
Wen M, Zhou B, Lin X, Chen Y, Song J, Li Y, Zacksenhaus E, Ben-David Y, Hao X. Associations Between XPD Lys751Gln Polymorphism and Leukemia: A Meta-Analysis. Front Genet. 2018 Jun 14;9:218. doi: 10.3389/fgene.2018.00218. eCollection 2018. PMID: 30100919; PMCID: PMC6073102.
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Signal-independent timescale analysis (SITA) and its application for neural coding during reaching and walking.

Frontiers in computational neuroscience

Zacksenhouse M, Lebedev MA, Nicolelis MA.
PMID: 25191263
Front Comput Neurosci. 2014 Aug 19;8:91. doi: 10.3389/fncom.2014.00091. eCollection 2014.

What are the relevant timescales of neural encoding in the brain? This question is commonly investigated with respect to well-defined stimuli or actions. However, neurons often encode multiple signals, including hidden or internal, which are not experimentally controlled, and...

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Zacksenhouse M, Lebedev MA, Nicolelis MA. Signal-independent timescale analysis (SITA) and its application for neural coding during reaching and walking. Front Comput Neurosci. 2014;8:91doi: 10.3389/fncom.2014.00091.
Zacksenhouse, M., Lebedev, M. A., & Nicolelis, M. A. (2014). Signal-independent timescale analysis (SITA) and its application for neural coding during reaching and walking. Frontiers in computational neuroscience, 891. https://doi.org/10.3389/fncom.2014.00091
Zacksenhouse, Miriam, et al. "Signal-independent timescale analysis (SITA) and its application for neural coding during reaching and walking." Frontiers in computational neuroscience vol. 8 (2014): 91. doi: https://doi.org/10.3389/fncom.2014.00091
Zacksenhouse M, Lebedev MA, Nicolelis MA. Signal-independent timescale analysis (SITA) and its application for neural coding during reaching and walking. Front Comput Neurosci. 2014 Aug 19;8:91. doi: 10.3389/fncom.2014.00091. eCollection 2014. PMID: 25191263; PMCID: PMC4137543.
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Methylation data of mouse Rb-deficient pineoblastoma.

Data in brief

Chung PED, Zacksenhaus E.
PMID: 32923545
Data Brief. 2020 Aug 25;32:106229. doi: 10.1016/j.dib.2020.106229. eCollection 2020 Oct.

Methylation profiling is widely used to study tumor biology and perform cluster analysis, particularly in brain cancer research where tissue biopsies are scarce. We have recently reported on the development of novel mouse models for germ line mutations in...

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Chung PED, Zacksenhaus E. Methylation data of mouse Rb-deficient pineoblastoma. Data Brief. 2020;32:106229doi: 10.1016/j.dib.2020.106229.
Chung, P. E. D., & Zacksenhaus, E. (2020). Methylation data of mouse Rb-deficient pineoblastoma. Data in brief, 32106229. https://doi.org/10.1016/j.dib.2020.106229
Chung, Philip E D, and Zacksenhaus, Eldad. "Methylation data of mouse Rb-deficient pineoblastoma." Data in brief vol. 32 (2020): 106229. doi: https://doi.org/10.1016/j.dib.2020.106229
Chung PED, Zacksenhaus E. Methylation data of mouse Rb-deficient pineoblastoma. Data Brief. 2020 Aug 25;32:106229. doi: 10.1016/j.dib.2020.106229. eCollection 2020 Oct. PMID: 32923545; PMCID: PMC7476231.
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SMAD1 as a biomarker and potential therapeutic target in drug-resistant multiple myeloma.

Biomarker research

Wu J, Zhang M, Faruq O, Zacksenhaus E, Chen W, Liu A, Chang H.
PMID: 34134766
Biomark Res. 2021 Jun 16;9(1):48. doi: 10.1186/s40364-021-00296-7.

BACKGROUND: SMAD1, a central mediator in TGF-β signaling, is involved in a broad range of biological activities including cell growth, apoptosis, development and immune response, and is implicated in diverse type of malignancies. Whether SMAD1 plays an important role...

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Wu J, Zhang M, Faruq O, et al. SMAD1 as a biomarker and potential therapeutic target in drug-resistant multiple myeloma. Biomark Res. 2021;9(1):48doi: 10.1186/s40364-021-00296-7.
Wu, J., Zhang, M., Faruq, O., Zacksenhaus, E., Chen, W., Liu, A., & Chang, H. (2021). SMAD1 as a biomarker and potential therapeutic target in drug-resistant multiple myeloma. Biomarker research, 9(1), 48. https://doi.org/10.1186/s40364-021-00296-7
Wu, Jian, et al. "SMAD1 as a biomarker and potential therapeutic target in drug-resistant multiple myeloma." Biomarker research vol. 9,1 (2021): 48. doi: https://doi.org/10.1186/s40364-021-00296-7
Wu J, Zhang M, Faruq O, Zacksenhaus E, Chen W, Liu A, Chang H. SMAD1 as a biomarker and potential therapeutic target in drug-resistant multiple myeloma. Biomark Res. 2021 Jun 16;9(1):48. doi: 10.1186/s40364-021-00296-7. PMID: 34134766; PMCID: PMC8207655.
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Hypophosphorylated pRb knock-in mice exhibit hallmarks of aging and vitamin C-preventable diabetes.

The EMBO journal

Jiang Z, Li H, Schroer SA, Voisin V, Ju Y, Pacal M, Erdmann N, Shi W, Chung PED, Deng T, Chen NJ, Ciavarra G, Datti A, Mak TW, Harrington L, Dick FA, Bader GD, Bremner R, Woo M, Zacksenhaus E.
PMID: 35023164
EMBO J. 2022 Jan 13;e106825. doi: 10.15252/embj.2020106825. Epub 2022 Jan 13.

Despite extensive analysis of pRB phosphorylation in vitro, how this modification influences development and homeostasis in vivo is unclear. Here, we show that homozygous Rb

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Jiang Z, Li H, Schroer SA, et al. Hypophosphorylated pRb knock-in mice exhibit hallmarks of aging and vitamin C-preventable diabetes. EMBO J. 2022;e106825doi: 10.15252/embj.2020106825.
Jiang, Z., Li, H., Schroer, S. A., Voisin, V., Ju, Y., Pacal, M., Erdmann, N., Shi, W., Chung, P. E. D., Deng, T., Chen, N. J., Ciavarra, G., Datti, A., Mak, T. W., Harrington, L., Dick, F. A., Bader, G. D., Bremner, R., Woo, M., & Zacksenhaus, E. (2022). Hypophosphorylated pRb knock-in mice exhibit hallmarks of aging and vitamin C-preventable diabetes. The EMBO journal, e106825. https://doi.org/10.15252/embj.2020106825
Jiang, Zhe, et al. "Hypophosphorylated pRb knock-in mice exhibit hallmarks of aging and vitamin C-preventable diabetes." The EMBO journal vol. (2022): e106825. doi: https://doi.org/10.15252/embj.2020106825
Jiang Z, Li H, Schroer SA, Voisin V, Ju Y, Pacal M, Erdmann N, Shi W, Chung PED, Deng T, Chen NJ, Ciavarra G, Datti A, Mak TW, Harrington L, Dick FA, Bader GD, Bremner R, Woo M, Zacksenhaus E. Hypophosphorylated pRb knock-in mice exhibit hallmarks of aging and vitamin C-preventable diabetes. EMBO J. 2022 Jan 13;e106825. doi: 10.15252/embj.2020106825. Epub 2022 Jan 13. PMID: 35023164.
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The vulnerability of RB loss in breast cancer: Targeting a void in cell cycle control.

Oncotarget

Knudsen ES, Zacksenhaus E.
PMID: 30123416
Oncotarget. 2018 Jul 24;9(57):30940-30941. doi: 10.18632/oncotarget.25797. eCollection 2018 Jul 24.

No abstract available.

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Knudsen ES, Zacksenhaus E. The vulnerability of RB loss in breast cancer: Targeting a void in cell cycle control. Oncotarget. 2018;9(57):30940-30941doi: 10.18632/oncotarget.25797.
Knudsen, E. S., & Zacksenhaus, E. (2018). The vulnerability of RB loss in breast cancer: Targeting a void in cell cycle control. Oncotarget, 9(57), 30940-30941. https://doi.org/10.18632/oncotarget.25797
Knudsen, Erik S, and Zacksenhaus, Eldad. "The vulnerability of RB loss in breast cancer: Targeting a void in cell cycle control." Oncotarget vol. 9,57 (2018): 30940-30941. doi: https://doi.org/10.18632/oncotarget.25797
Knudsen ES, Zacksenhaus E. The vulnerability of RB loss in breast cancer: Targeting a void in cell cycle control. Oncotarget. 2018 Jul 24;9(57):30940-30941. doi: 10.18632/oncotarget.25797. eCollection 2018 Jul 24. PMID: 30123416; PMCID: PMC6089558.
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Oscillatory neural networks for robotic yo-yo control.

IEEE transactions on neural networks

Jin HL, Zacksenhouse M.
PMID: 18238015
IEEE Trans Neural Netw. 2003;14(2):317-25. doi: 10.1109/TNN.2002.806952.

Different networks of coupled oscillators were developed for open-loop control of periodic motion. However, some tasks, like yo-yo playing, are open-loop unstable and require proper phase locking to stabilize. Given the phase-locking property of coupled oscillators, we investigate their...

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Jin HL, Zacksenhouse M. Oscillatory neural networks for robotic yo-yo control. IEEE Trans Neural Netw. 2003;14(2):317-25doi: 10.1109/TNN.2002.806952.
Jin, H. L., & Zacksenhouse, M. (2003). Oscillatory neural networks for robotic yo-yo control. IEEE transactions on neural networks, 14(2), 317-25. https://doi.org/10.1109/TNN.2002.806952
Jin, Hui-Liang, and Zacksenhouse, M. "Oscillatory neural networks for robotic yo-yo control." IEEE transactions on neural networks vol. 14,2 (2003): 317-25. doi: https://doi.org/10.1109/TNN.2002.806952
Jin HL, Zacksenhouse M. Oscillatory neural networks for robotic yo-yo control. IEEE Trans Neural Netw. 2003;14(2):317-25. doi: 10.1109/TNN.2002.806952. PMID: 18238015.
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Robust versus optimal strategies for two-alternative forced choice tasks.

Journal of mathematical psychology

Zacksenhouse M, Bogacz R, Holmes P.
PMID: 23180885
J Math Psychol. 2010 Apr 01;54(2):230-246. doi: 10.1016/j.jmp.2009.12.004. Epub 2010 Jan 13.

It has been proposed that animals and humans might choose a speed-accuracy tradeoff that maximizes reward rate. For this utility function the simple drift-diffusion model of two-alternative forced-choice tasks predicts a parameter-free optimal performance curve that relates normalized decision...

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Zacksenhouse M, Bogacz R, Holmes P. Robust versus optimal strategies for two-alternative forced choice tasks. J Math Psychol. 2010;54(2):230-246doi: 10.1016/j.jmp.2009.12.004.
Zacksenhouse, M., Bogacz, R., & Holmes, P. (2010). Robust versus optimal strategies for two-alternative forced choice tasks. Journal of mathematical psychology, 54(2), 230-246. https://doi.org/10.1016/j.jmp.2009.12.004
Zacksenhouse, M, et al. "Robust versus optimal strategies for two-alternative forced choice tasks." Journal of mathematical psychology vol. 54,2 (2010): 230-246. doi: https://doi.org/10.1016/j.jmp.2009.12.004
Zacksenhouse M, Bogacz R, Holmes P. Robust versus optimal strategies for two-alternative forced choice tasks. J Math Psychol. 2010 Apr 01;54(2):230-246. doi: 10.1016/j.jmp.2009.12.004. Epub 2010 Jan 13. PMID: 23180885; PMCID: PMC3505075.
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Progression to Metastasis of Solid Cancer.

Cancers

Zacksenhaus E, Egan SE.
PMID: 33578666
Cancers (Basel). 2021 Feb 10;13(4). doi: 10.3390/cancers13040717.

Metastatic dissemination of cancer cells, their colonization at distal sites, and ultimate disruption of tissue physiology are the root causes of most deaths from solid cancers, particularly in tumor types where the primary lesion can be easily dissected and...

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Zacksenhaus E, Egan SE. Progression to Metastasis of Solid Cancer. Cancers (Basel). 2021;13(4)doi: 10.3390/cancers13040717.
Zacksenhaus, E., & Egan, S. E. (2021). Progression to Metastasis of Solid Cancer. Cancers, 13(4), . https://doi.org/10.3390/cancers13040717
Zacksenhaus, Eldad, and Egan, Sean E. "Progression to Metastasis of Solid Cancer." Cancers vol. 13,4 (2021). doi: https://doi.org/10.3390/cancers13040717
Zacksenhaus E, Egan SE. Progression to Metastasis of Solid Cancer. Cancers (Basel). 2021 Feb 10;13(4). doi: 10.3390/cancers13040717. PMID: 33578666; PMCID: PMC7916396.
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Optimal feedback control successfully explains changes in neural modulations during experiments with brain-machine interfaces.

Frontiers in systems neuroscience

Benyamini M, Zacksenhouse M.
PMID: 26042002
Front Syst Neurosci. 2015 May 19;9:71. doi: 10.3389/fnsys.2015.00071. eCollection 2015.

Recent experiments with brain-machine-interfaces (BMIs) indicate that the extent of neural modulations increased abruptly upon starting to operate the interface, and especially after the monkey stopped moving its hand. In contrast, neural modulations that are correlated with the kinematics...

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Benyamini M, Zacksenhouse M. Optimal feedback control successfully explains changes in neural modulations during experiments with brain-machine interfaces. Front Syst Neurosci. 2015;9:71doi: 10.3389/fnsys.2015.00071.
Benyamini, M., & Zacksenhouse, M. (2015). Optimal feedback control successfully explains changes in neural modulations during experiments with brain-machine interfaces. Frontiers in systems neuroscience, 971. https://doi.org/10.3389/fnsys.2015.00071
Benyamini, Miri, and Zacksenhouse, Miriam. "Optimal feedback control successfully explains changes in neural modulations during experiments with brain-machine interfaces." Frontiers in systems neuroscience vol. 9 (2015): 71. doi: https://doi.org/10.3389/fnsys.2015.00071
Benyamini M, Zacksenhouse M. Optimal feedback control successfully explains changes in neural modulations during experiments with brain-machine interfaces. Front Syst Neurosci. 2015 May 19;9:71. doi: 10.3389/fnsys.2015.00071. eCollection 2015. PMID: 26042002; PMCID: PMC4436824.
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Showing 1 to 12 of 17 entries