يعرض 1 - 7 نتائج من 7 نتيجة بحث عن '"Aft, R.L."', وقت الاستعلام: 0.89s تنقيح النتائج
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    المؤلفون: Woo, X.Y., Giordano, J., Srivastava, A., Zhao, Z.-., Lloyd, M.W., de Bruijn, R., Suh, Y.-., Patidar, R., Chen, L., Scherer, S., Bailey, M.H., Yang, C.-., Cortes-Sanchez, E., Xi, Y., Wang, J., Wickramasinghe, J., Kossenkov, A.V., Rebecca, V.W., Sun, H., Mashl, R.J., Davies, S.R., Jeon, R., Frech, C., Randjelovic, J., Rosains, J., Galimi, F., Bertotti, A., Lafferty, A., O'Farrell, A.C., Modave, E., Lambrechts, D., ter Brugge, P., Marangoni, E., El Botty, R., Kim, H., Kim, J.-., Yang, H.-., Lee, C., Dean, D.A., Davis-Dusenbery, B., Evrard, Y.A., Doroshow, J.H., Welm, A.L., Welm, B.E., Lewis, M.T., Fang, B., Roth, J.A., Meric-Bernstam, F., Herlyn, M., Davies, M.A., Ding, L., Li, S., Govindan, R., Isella, C., Moscow, J.A., Trusolino, L., Byrne, A.T., Jonkers, J., Bult, C.J., Medico, E., Chuang, J.H., Robinson, P.N., Sanderson, B.J., Neuhauser, S.B., Dobrolecki, L.E., Zheng, X., Majidi, M., Zhang, R., Zhang, X., Akcakanat, A., Evans, K.W., Yap, T.A., Li, D., Yucan, E., Lanier, C.D., Saridogan, T., Kirby, B.P., M. J., H., Chen, H., Kopetz, S., Menter, D.G., Zhang, J., Westin, S.N., Kim, M.P., Dai, B., Gibbons, D.L., Tapia, C., Jensen, V.B., Boning, G., Minna, J.D., Park, H., Timmons, B.C., Girard, L., Fingerman, D., Liu, Q., Somasundaram, R., Xiao, M., Yennu-Nanda, V.G., Tetzlaff, M.T., Xu, X., Nathanson, K.L., Cao, S., Chen, F., Dipersio, J.F., Lim, K.H., C. X., M., Rodriguez, F.M., Van Tine, B.A., Wang-Gillam, A., Wendl, M.C., Wu, Y., Wyczalkowski, M.A., Yao, L., Jayasinghe, R., Aft, R.L., Fields, R.C., Luo, J., Fuh, K.C., Chin, V., Digiovanna, J., Grover, J., Koc, S., Seepo, S., Wallace, T., Pan, C.-., Chen, M.S., Carvajal-Carmona, L.G., Kirane, A.R., Cho, M., Gandara, D.R., Riess, J.W., Le, T., deVere White, R.W., Tepper, C.G., Zhang, H., Coggins, N.B., Lott, P., Estrada, A., Toal, T., Arana, A.M., Polanco-Echeverry, G., Rocha, S., A. -H., M., Mitsiades, N., Kaochar, S., O'Malley, B.W., Ellis, M.J., Hilsenbeck, S.G., Ittmann, M., Corso, S., Fiori, A., Giordano, S., van de Ven, M., Peeper, D.S., Miller, I., Bernado, C., Morancho, B., Ramirez, L., Arribas, J., Palmer, H.G., Piris-Gimenez, A., Soucek, L., Dahmani, A., Montaudon, E., Nemati, F., Dangles-Marie, V., Decaudin, D., Roman-Roman, S., Alferez, D.G., Spence, K., Clarke, R.B., Bentires-Alj, M., Chang, D.K., Biankin, A.V., Bruna, A., O'Reilly, M., Caldas, C., Casanovas, O., Gonzalez-Suarez, E., Munoz, P., Villanueva, A., Conte, N., Mason, J., Thorne, R., Meehan, T.F., Parkinson, H., Dudova, Z., Krenek, A., Stuchlik, D., Elemento, O., Inghirami, G., Golebiewska, A., Niclou, S.P., Wisman, G.B.A., de Jong, S., Kralova, P., Sedlacek, R., Claeys, E., Leucci, E., Borsani, M., Lanfrancone, L., Pelicci, P.G., Maelandsmo, G.M., Norum, J.H., Vinolo, E., Serra, V.

    المساهمون: Leucci, Eleonora

    المصدر: Nature Genetics
    bioRxiv
    PDXNET Consortium, EurOPDX Consortium, Alferez-Castro, D, Spence, K, Clarke, R & et al. 2021, ' Conservation of copy number profiles during engraftment and passaging of patient-derived cancer xenografts ', Nature Genetics, vol. 53, no. 1, pp. 86-99 . https://doi.org/10.1038/s41588-020-00750-6Test

    الوصف: Patient-derived xenografts (PDXs) are resected human tumors engrafted into mice for preclinical studies and therapeutic testing. It has been proposed that the mouse host affects tumor evolution during PDX engraftment and propagation, affecting the accuracy of PDX modeling of human cancer. Here, we exhaustively analyze copy number alterations (CNAs) in 1,451 PDX and matched patient tumor (PT) samples from 509 PDX models. CNA inferences based on DNA sequencing and microarray data displayed substantially higher resolution and dynamic range than gene expression-based inferences, and they also showed strong CNA conservation from PTs through late-passage PDXs. CNA recurrence analysis of 130 colorectal and breast PT/PDX-early/PDX-late trios confirmed high-resolution CNA retention. We observed no significant enrichment of cancer-related genes in PDX-specific CNAs across models. Moreover, CNA differences between patient and PDX tumors were comparable to variations in multiregion samples within patients. Our study demonstrates the lack of systematic copy number evolution driven by the PDX mouse host.
    Analysis of copy number alterations in 1,451 patient-derived xenografts (PDXs) and matched patient tumor samples shows strong conservation from patient tumors through late-passage PDXs and a lack of systematic copy number evolution driven by the mouse host.

    وصف الملف: Print-Electronic; application/pdf

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    دورية أكاديمية
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    دورية أكاديمية

    الوصف: The goal of breast-conserving surgery is to completely remove all of the cancer. Currently, no intraoperative tools can microscopically analyze the entire lumpectomy specimen, which results in 20 to 60% of patients undergoing second surgeries to achieve clearmargins. To address this critical need, we have laid the foundation for the development of a device that could allow accurate intraoperative margin assessment. We demonstrate that by taking advantage of the intrinsic optical contrast of breast tissue, photoacousticmicroscopy (PAM) can achievemultilayered histology-like imaging of the tissue surface. The high correlation of the PAM images to the conventional histologic images allows rapid computations of diagnostic features such as nuclear size and packing density, potentially identifying small clusters of cancer cells. Because PAM does not require tissue processing or staining, it can be performed promptly and intraoperatively, enabling immediate directed re-excision and reducing the number of second surgeries. 2017 © The Authors, some rights reserved;.

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    دورية أكاديمية
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    دورية أكاديمية

    المؤلفون: Aft, R.L., Zhang, F.W., Gius, D.

    المصدر: British Journal of Cancer. 9/23/2002, Vol. 87 Issue 7, p805-812. 8p.

    مصطلحات موضوعية: *DRUG therapy, *CANCER

    مستخلص: Nutrient deprivation has been shown to cause cancer cell death. To exploit nutrient deprivation as anti-cancer therapy, we investigated the effects of the anti-metabolite 2-deoxy-D-glucose on breast cancer cells in vitro. This compound has been shown to inhibit glucose metabolism. Treatment of human breast cancer cell lines with 2-deoxy-D-glucose results in cessation of cell growth in a dose dependent manner. Cell viability as measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide conversion assay and clonogenic survival are decreased with 2-deoxy-D-glucose treatment indicating that 2-deoxy-D-glucose causes breast cancer cell death. The cell death induced by 2-deoxy-D-glucose was found to be due to apoptosis as demonstrated by induction of caspase 3 activity and cleavage of poly (ADP-ribose) polymerase. Breast cancer cells treated with 2-deoxy-D-glucose express higher levels of Glut1 transporter protein as measured by Western blot analysis and have increased glucose uptake compared to non-treated breast cancer cells. From these results we conclude that 2-deoxy-D-glucose treatment causes death in human breast cancer cell lines by the activation of the apoptotic pathway. Our data suggest that breast cancer cells treated with 2-deoxy-D-glucose accelerate their own demise by initially expressing high levels of glucose transporter protein, which allows increased uptake of 2-deoxy-D-glucose, and subsequent induction of cell death. These data support the targeting of glucose metabolism as a site for chemotherapeutic intervention by agents such as 2-deoxy-D-glucose. [ABSTRACT FROM AUTHOR]