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The Merkel Cell Polyomavirus T Antigens Function as Tumor Promoters in Murine Skin.

Cancers

Spurgeon ME, Liem A, Buehler D, Cheng J, DeCaprio JA, Lambert PF.
PMID: 33435392
Cancers (Basel). 2021 Jan 09;13(2). doi: 10.3390/cancers13020222.

Merkel cell polyomavirus (MCPyV) causes the majority of human Merkel cell carcinomas (MCC), a rare but highly aggressive form of skin cancer. We recently reported that constitutive expression of MCC tumor-derived MCPyV tumor (T) antigens in the skin of...

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Spurgeon ME, Liem A, Buehler D, et al. The Merkel Cell Polyomavirus T Antigens Function as Tumor Promoters in Murine Skin. Cancers (Basel). 2021;13(2)doi: 10.3390/cancers13020222.
Spurgeon, M. E., Liem, A., Buehler, D., Cheng, J., DeCaprio, J. A., & Lambert, P. F. (2021). The Merkel Cell Polyomavirus T Antigens Function as Tumor Promoters in Murine Skin. Cancers, 13(2), . https://doi.org/10.3390/cancers13020222
Spurgeon, Megan E, et al. "The Merkel Cell Polyomavirus T Antigens Function as Tumor Promoters in Murine Skin." Cancers vol. 13,2 (2021). doi: https://doi.org/10.3390/cancers13020222
Spurgeon ME, Liem A, Buehler D, Cheng J, DeCaprio JA, Lambert PF. The Merkel Cell Polyomavirus T Antigens Function as Tumor Promoters in Murine Skin. Cancers (Basel). 2021 Jan 09;13(2). doi: 10.3390/cancers13020222. PMID: 33435392; PMCID: PMC7827793.
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Merkel cell polyomavirus activates LSD1-mediated blockade of non-canonical BAF to regulate transformation and tumorigenesis.

Nature cell biology

Park DE, Cheng J, McGrath JP, Lim MY, Cushman C, Swanson SK, Tillgren ML, Paulo JA, Gokhale PC, Florens L, Washburn MP, Trojer P, DeCaprio JA.
PMID: 32284543
Nat Cell Biol. 2020 May;22(5):603-615. doi: 10.1038/s41556-020-0503-2. Epub 2020 Apr 13.

Merkel cell carcinoma (MCC)-a neuroendocrine cancer of the skin-is caused by the integration of Merkel cell polyomavirus and persistent expression of large T antigen and small T antigen. We report that small T antigen in complex with MYCL and...

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Park DE, Cheng J, McGrath JP, et al. Merkel cell polyomavirus activates LSD1-mediated blockade of non-canonical BAF to regulate transformation and tumorigenesis. Nat Cell Biol. 2020;22(5):603-615doi: 10.1038/s41556-020-0503-2.
Park, D. E., Cheng, J., McGrath, J. P., Lim, M. Y., Cushman, C., Swanson, S. K., Tillgren, M. L., Paulo, J. A., Gokhale, P. C., Florens, L., Washburn, M. P., Trojer, P., & DeCaprio, J. A. (2020). Merkel cell polyomavirus activates LSD1-mediated blockade of non-canonical BAF to regulate transformation and tumorigenesis. Nature cell biology, 22(5), 603-615. https://doi.org/10.1038/s41556-020-0503-2
Park, Donglim Esther, et al. "Merkel cell polyomavirus activates LSD1-mediated blockade of non-canonical BAF to regulate transformation and tumorigenesis." Nature cell biology vol. 22,5 (2020): 603-615. doi: https://doi.org/10.1038/s41556-020-0503-2
Park DE, Cheng J, McGrath JP, Lim MY, Cushman C, Swanson SK, Tillgren ML, Paulo JA, Gokhale PC, Florens L, Washburn MP, Trojer P, DeCaprio JA. Merkel cell polyomavirus activates LSD1-mediated blockade of non-canonical BAF to regulate transformation and tumorigenesis. Nat Cell Biol. 2020 May;22(5):603-615. doi: 10.1038/s41556-020-0503-2. Epub 2020 Apr 13. PMID: 32284543; PMCID: PMC7336275.
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Association of Programmed Death 1 Protein Ligand (PD-L1) Expression With Prognosis in Merkel Cell Carcinoma.

Frontiers in medicine

Hanna GJ, Kacew AJ, Tanguturi AR, Grote HJ, Vergara V, Brunkhorst B, Rabinowits G, Thakuria M, LeBoeuf NR, Ihling C, DeCaprio JA, Lorch JH.
PMID: 32582722
Front Med (Lausanne). 2020 Jun 05;7:198. doi: 10.3389/fmed.2020.00198. eCollection 2020.

No abstract available.

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Hanna GJ, Kacew AJ, Tanguturi AR, et al. Association of Programmed Death 1 Protein Ligand (PD-L1) Expression With Prognosis in Merkel Cell Carcinoma. Front Med (Lausanne). 2020;7:198doi: 10.3389/fmed.2020.00198.
Hanna, G. J., Kacew, A. J., Tanguturi, A. R., Grote, H. J., Vergara, V., Brunkhorst, B., Rabinowits, G., Thakuria, M., LeBoeuf, N. R., Ihling, C., DeCaprio, J. A., & Lorch, J. H. (2020). Association of Programmed Death 1 Protein Ligand (PD-L1) Expression With Prognosis in Merkel Cell Carcinoma. Frontiers in medicine, 7198. https://doi.org/10.3389/fmed.2020.00198
Hanna, Glenn J, et al. "Association of Programmed Death 1 Protein Ligand (PD-L1) Expression With Prognosis in Merkel Cell Carcinoma." Frontiers in medicine vol. 7 (2020): 198. doi: https://doi.org/10.3389/fmed.2020.00198
Hanna GJ, Kacew AJ, Tanguturi AR, Grote HJ, Vergara V, Brunkhorst B, Rabinowits G, Thakuria M, LeBoeuf NR, Ihling C, DeCaprio JA, Lorch JH. Association of Programmed Death 1 Protein Ligand (PD-L1) Expression With Prognosis in Merkel Cell Carcinoma. Front Med (Lausanne). 2020 Jun 05;7:198. doi: 10.3389/fmed.2020.00198. eCollection 2020. PMID: 32582722; PMCID: PMC7291775.
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An analysis of the use of targeted therapies in patients with advanced Merkel cell carcinoma and an evaluation of genomic correlates of response.

Cancer medicine

Knepper TC, Panchaud RA, Muradova E, Cohen L, DeCaprio JA, Khushalani NI, Tsai KY, Brohl AS.
PMID: 34269527
Cancer Med. 2021 Sep;10(17):5889-5896. doi: 10.1002/cam4.4138. Epub 2021 Jul 16.

BACKGROUND: The use of targeted therapy remains a treatment consideration for some patients with advanced Merkel cell carcinoma (MCC). However, supportive data on the use of targeted therapy approaches are limited. Thus, we sought to evaluate the responsiveness of...

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Knepper TC, Panchaud RA, Muradova E, et al. An analysis of the use of targeted therapies in patients with advanced Merkel cell carcinoma and an evaluation of genomic correlates of response. Cancer Med. 2021;10(17):5889-5896doi: 10.1002/cam4.4138.
Knepper, T. C., Panchaud, R. A., Muradova, E., Cohen, L., DeCaprio, J. A., Khushalani, N. I., Tsai, K. Y., & Brohl, A. S. (2021). An analysis of the use of targeted therapies in patients with advanced Merkel cell carcinoma and an evaluation of genomic correlates of response. Cancer medicine, 10(17), 5889-5896. https://doi.org/10.1002/cam4.4138
Knepper, Todd C, et al. "An analysis of the use of targeted therapies in patients with advanced Merkel cell carcinoma and an evaluation of genomic correlates of response." Cancer medicine vol. 10,17 (2021): 5889-5896. doi: https://doi.org/10.1002/cam4.4138
Knepper TC, Panchaud RA, Muradova E, Cohen L, DeCaprio JA, Khushalani NI, Tsai KY, Brohl AS. An analysis of the use of targeted therapies in patients with advanced Merkel cell carcinoma and an evaluation of genomic correlates of response. Cancer Med. 2021 Sep;10(17):5889-5896. doi: 10.1002/cam4.4138. Epub 2021 Jul 16. PMID: 34269527; PMCID: PMC8419775.
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Simultaneous expression of MMB-FOXM1 complex components enables efficient bypass of senescence.

Scientific reports

Kumari R, Hummerich H, Shen X, Fischer M, Litovchick L, Mittnacht S, DeCaprio JA, Jat PS.
PMID: 34728711
Sci Rep. 2021 Nov 02;11(1):21506. doi: 10.1038/s41598-021-01012-z.

Cellular senescence is a stable cell cycle arrest that normal cells undergo after a finite number of divisions, in response to a variety of intrinsic and extrinsic stimuli. Although senescence is largely established and maintained by the p53/p21

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Kumari R, Hummerich H, Shen X, et al. Simultaneous expression of MMB-FOXM1 complex components enables efficient bypass of senescence. Sci Rep. 2021;11(1):21506doi: 10.1038/s41598-021-01012-z.
Kumari, R., Hummerich, H., Shen, X., Fischer, M., Litovchick, L., Mittnacht, S., DeCaprio, J. A., & Jat, P. S. (2021). Simultaneous expression of MMB-FOXM1 complex components enables efficient bypass of senescence. Scientific reports, 11(1), 21506. https://doi.org/10.1038/s41598-021-01012-z
Kumari, Ruchi, et al. "Simultaneous expression of MMB-FOXM1 complex components enables efficient bypass of senescence." Scientific reports vol. 11,1 (2021): 21506. doi: https://doi.org/10.1038/s41598-021-01012-z
Kumari R, Hummerich H, Shen X, Fischer M, Litovchick L, Mittnacht S, DeCaprio JA, Jat PS. Simultaneous expression of MMB-FOXM1 complex components enables efficient bypass of senescence. Sci Rep. 2021 Nov 02;11(1):21506. doi: 10.1038/s41598-021-01012-z. PMID: 34728711; PMCID: PMC8563780.
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MMB-FOXM1-driven premature mitosis is required for CHK1 inhibitor sensitivity.

Cell reports

Branigan TB, Kozono D, Schade AE, Deraska P, Rivas HG, Sambel L, Reavis HD, Shapiro GI, D'Andrea AD, DeCaprio JA.
PMID: 33657372
Cell Rep. 2021 Mar 02;34(9):108808. doi: 10.1016/j.celrep.2021.108808.

To identify genes whose loss confers resistance to CHK1 inhibitors, we perform genome-wide CRISPR-Cas9 screens in non-small-cell lung cancer (NSCLC) cell lines treated with the CHK1 inhibitor prexasertib (CHK1i). Five of the top six hits of the screens, MYBL2...

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Branigan TB, Kozono D, Schade AE, et al. MMB-FOXM1-driven premature mitosis is required for CHK1 inhibitor sensitivity. Cell Rep. 2021;34(9):108808doi: 10.1016/j.celrep.2021.108808.
Branigan, T. B., Kozono, D., Schade, A. E., Deraska, P., Rivas, H. G., Sambel, L., Reavis, H. D., Shapiro, G. I., D'Andrea, A. D., & DeCaprio, J. A. (2021). MMB-FOXM1-driven premature mitosis is required for CHK1 inhibitor sensitivity. Cell reports, 34(9), 108808. https://doi.org/10.1016/j.celrep.2021.108808
Branigan, Timothy B, et al. "MMB-FOXM1-driven premature mitosis is required for CHK1 inhibitor sensitivity." Cell reports vol. 34,9 (2021): 108808. doi: https://doi.org/10.1016/j.celrep.2021.108808
Branigan TB, Kozono D, Schade AE, Deraska P, Rivas HG, Sambel L, Reavis HD, Shapiro GI, D'Andrea AD, DeCaprio JA. MMB-FOXM1-driven premature mitosis is required for CHK1 inhibitor sensitivity. Cell Rep. 2021 Mar 02;34(9):108808. doi: 10.1016/j.celrep.2021.108808. PMID: 33657372; PMCID: PMC7970065.
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