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Akademický článek

Extracellular vesicle-mediated macrophage activation: An insight into the mechanism of thioredoxin-mediated immune activation

Autor: Chontida Yarana, Hannah Thompson, Luksana Chaiswing, D. Allan Butterfield, Heidi Weiss, Subbarao Bondada, Sara Alhakeem, Suriyan Sukati, Daret K. St. Clair

Publikováno v: Redox Biology, Vol 26, Iss , Pp - (2019)

Extracellular vesicles (EVs) generated from redox active anticancer drugs are released into the extracellular environment. These EVs contain oxidized molecules and trigger inflammatory responses by macrophages. Using a mouse model of doxorubicin (DOX

Externí odkaz: https://doaj.org/article/98e908279b00465d8862dbf696cd086c

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Akademický článek

PI3K/mTOR Dual Inhibitor PF-04691502 Is a Schedule-Dependent Radiosensitizer for Gastroenteropancreatic Neuroendocrine Tumors

Autor: Zeta Chow, Jeremy Johnson, Aman Chauhan, Tadahide Izumi, Michael Cavnar, Heidi Weiss, Courtney M. Townsend, Lowell Anthony, Carrigan Wasilchenko, Matthew L. Melton, Jörg Schrader, B. Mark Evers, Piotr Rychahou

Publikováno v: Cells, Vol 10, Iss 5, p 1261 (2021)

Patients with advanced-stage gastroenteropancreatic neuroendocrine tumors (GEP-NETs) have a poor overall prognosis despite chemotherapy and radiotherapy (e.g., peptide receptor radionuclide therapy (PRRT)). Better treatment options are needed to impr

Externí odkaz: https://doaj.org/article/6b5223d474e44dc4a6fc947c392a93ae

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Akademický článek

Plasma TNF-α and Soluble TNF Receptor Levels after Doxorubicin with or without Co-Administration of Mesna-A Randomized, Cross-Over Clinical Study.

Autor: John Hayslip, Emily V Dressler, Heidi Weiss, Tammy J Taylor, Mara Chambers, Teresa Noel, Sumitra Miriyala, Jeriel T R Keeney, Xiaojia Ren, Rukhsana Sultana, Mary Vore, D Allan Butterfield, Daret St Clair, Jeffrey A Moscow

Publikováno v: PLoS ONE, Vol 10, Iss 4, p e0124988 (2015)

Chemotherapy-induced cognitive impairment (CICI) is a common sequelae of cancer therapy. Recent preclinical observations have suggested that CICI can be mediated by chemotherapy-induced plasma protein oxidation, which triggers TNF-α mediated CNS dam

Externí odkaz: https://doaj.org/article/8e1bb119d4ac4a6881744d355ef08626

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Supplementary Figure 6 from Cotargeting the PI3K and RAS Pathways for the Treatment of Neuroendocrine Tumors

Autor: B. Mark Evers, Courtney M. Townsend, Lowell Anthony, Jun Song, Chi Wang, Heidi Weiss, Katherine Campbell, Jennifer W. Harris, Ji Tae Kim, Victoria A. Elliott, W. Conan Mustain, Yekaterina Y. Zaytseva, Jing Li, Joseph D. Valentino

PDF file - 1066KB, MEK inhibition alone and combination PI3K + MEK inhibition decreases serotonin secretion, while BEZ235 decreases CgA expression. (A) BON and (B) QGP-1 cells were plated in 24 well plates at a density of 1x105 cells/cm2. After 24h,

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::206d1335cecf375d3bc06e8d45dd8bb7
https://doi.org/10.1158/1078-0432.22448676.v1

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Supplementary Figure 4 from Cotargeting the PI3K and RAS Pathways for the Treatment of Neuroendocrine Tumors

PDF file - 649KB, Combination PI3K and MEK inhibitor treatment results in a more pronounced decrease in NCI-H727 and QGP-1 cell proliferation. (A) NCI-H727 and (B) QGP-1 cells were plated in 24 well plates at a density of 3x104 cells/well. Treatments

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::17be64dfc60bce0063c41dfe8f890fea
https://doi.org/10.1158/1078-0432.22448685

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Supplementary Figure 2 from Cotargeting the PI3K and RAS Pathways for the Treatment of Neuroendocrine Tumors

PDF file - 812 KB, PI3K inhibition decreases cell proliferation in NCI-H727 and QGP-1 cell lines. (A) NCI-H727 and (B) QGP-1 cells were plated in 24 well plates at a density of 3x104 cells/well. Treatments were initiated the following morning with in

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0c9edc5e1a2999209f432255a4fae0d8
https://doi.org/10.1158/1078-0432.22448691.v1

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Supplementary Figure 3 from Cotargeting the PI3K and RAS Pathways for the Treatment of Neuroendocrine Tumors

PDF file - 741KB, PI3K inhibition enhances apoptosis in NCI-H727 and QGP-1 cell lines. (A) NCI-H727 and (B) QGP-1 cells were plated in 24 well plates at a density of 5x104 cells/cm2. Treatments were initiated the following morning with increasing dos

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::98498e8962022dd181ec10e2d29ee1fa
https://doi.org/10.1158/1078-0432.22448688

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Data from Cotargeting the PI3K and RAS Pathways for the Treatment of Neuroendocrine Tumors

Background: The precise involvement of the PI3K/mTOR and RAS/MEK pathways in carcinoid tumors is not well defined. Therefore, the purpose of our study was to evaluate the role these pathways play in carcinoid cell proliferation, apoptosis, and secret

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e5cba95d5276998ff61661a8bf1380b1
https://doi.org/10.1158/1078-0432.c.6521457.v1

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Supplementary Figure 5 from Cotargeting the PI3K and RAS Pathways for the Treatment of Neuroendocrine Tumors

PDF file - 1080KB, Combination PI3K + MEK inhibition enhances apoptosis compared to monotherapy. (A) NCI-H727 and (B) QGP-1 cells were plated in 24 well plates at a density of 5x104 cells/cm2. Treatments were initiated the following morning with eith

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0572ef88fc7591b71483945f0a0c969b
https://doi.org/10.1158/1078-0432.22448682

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