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Your search keyword '"Taylor, Kristin"' showing total 4 results
Start Over Author "Taylor, Kristin" Topic antineoplastic agents
4 results on '"Taylor, Kristin"'

1. FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy.

Author

Diaz Osterman CJ, Ozmadenci D, Kleinschmidt EG, Taylor KN, Barrie AM, Jiang S, Bean LM, Sulzmaier FJ, Jean C, Tancioni I, Anderson K, Uryu S, Cordasco EA, Li J, Chen XL, Fu G, Ojalill M, Rappu P, Heino J, Mark AM, Xu G, Fisch KM, Kolev VN, Weaver DT, Pachter JA, Győrffy B, McHale MT, Connolly DC, Molinolo A, Stupack DG, and Schlaepfer DD

Subjects
Animals, Cisplatin pharmacology, Disease Models, Animal, Female, Humans, Mice, Proto-Oncogene Proteins c-myc metabolism, Proto-Oncogene Proteins p21(ras) metabolism, Signal Transduction, Stem Cells, Antineoplastic Agents pharmacology, Drug Resistance, Neoplasm, Focal Adhesion Kinase 1 metabolism, Ovarian Neoplasms drug therapy, Platinum pharmacology
Abstract

Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in K ras , M yc and F AK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance., Competing Interests: CD, DO, EK, KT, AB, SJ, LB, FS, CJ, IT, KA, SU, EC, JL, XC, GF, MO, PR, JH, AM, GX, KF, BG, MM, DC, AM, DS, DS No competing interests declared, VK Former employee at Verastem Inc, DW, JP employee of Verastem Inc, (© 2019, Diaz Osterman et al.)

Published
2019
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2. FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy.

Author

Diaz Osterman, Carlos J, Ozmadenci, Duygu, Kleinschmidt, Elizabeth G, Taylor, Kristin N, Barrie, Allison M, Jiang, Shulin, Bean, Lisa M, Sulzmaier, Florian J, Jean, Christine, Tancioni, Isabelle, Anderson, Kristen, Uryu, Sean, Cordasco, Edward A, Li, Jian, Chen, Xiao Lei, Fu, Guo, Ojalill, Marjaana, Rappu, Pekka, Heino, Jyrki, Mark, Adam M, Xu, Guorong, Fisch, Kathleen M, Kolev, Vihren N, Weaver, David T, Pachter, Jonathan A, Győrffy, Balázs, McHale, Michael T, Connolly, Denise C, Molinolo, Alfredo, Stupack, Dwayne G, and Schlaepfer, David D

Subjects
Stem Cells, Animals, Humans, Mice, Ovarian Neoplasms, Disease Models, Animal, Cisplatin, Platinum, Proto-Oncogene Proteins c-myc, Antineoplastic Agents, Signal Transduction, Drug Resistance, Neoplasm, Female, Proto-Oncogene Proteins p21(ras), Focal Adhesion Kinase 1, beta-catenin, cancer biology, focal adhesion kinase FAK, mouse, ovarian cancer, platinum chemotherapy, pluripotency, tumorspheres, Rare Diseases, Genetics, Stem Cell Research, Ovarian Cancer, Cancer, 2.1 Biological and endogenous factors, Biochemistry and Cell Biology
Abstract

Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance.

Published
2019

3. FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy

Author

Osterman, Carlos J Diaz, Ozmadenci, Duygu, Kleinschmidt, Elizabeth G, Taylor, Kristin N, Barrie, Allison M, Jiang, Shulin, Bean, Lisa M, Sulzmaier, Florian J, Jean, Christine, Tancioni, Isabelle, Anderson, Kristen, Uryu, Sean, Cordasco, Edward A, Li, Jian, Chen, Xiao Lei, Fu, Guo, Ojalill, Marjaana, Rappu, Pekka, Heino, Jyrki, Mark, Adam M, Xu, Guorong, Fisch, Kathleen M, Kolev, Vihren N, Weaver, David T, Pachter, Jonathan A, Győrffy, Balázs, McHale, Michael T, Connolly, Denise C, Molinolo, Alfredo, Stupack, Dwayne G, and Schlaepfer, David D

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Ovarian Cancer, Genetics, Rare Diseases, Cancer, Clinical Research, Women's Health, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Animals, Antineoplastic Agents, Cisplatin, Disease Models, Animal, Drug Resistance, Neoplasm, Female, Focal Adhesion Kinase 1, Humans, Mice, Ovarian Neoplasms, Platinum, Proto-Oncogene Proteins c-myc, Proto-Oncogene Proteins p21(ras), Signal Transduction, Stem Cells, beta-catenin, cancer biology, focal adhesion kinase FAK, mouse, ovarian cancer, platinum chemotherapy, pluripotency, tumorspheres, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance.

Published
2019

4. PARP inhibitors Choosing what to use in epithelial ovarian cancer: Across different drugs and clinical settings, use of PARPi has resulted in a prolonged period without cancer recurrence

Author

Taylor, Kristin N. and Scott, Marla

Subjects
United States. Food and Drug Administration, Antineoplastic agents, Diseases -- Relapse, Drug approval, Chemotherapy, Cancer -- Chemotherapy, Ovarian cancer -- Drug therapy, Antimitotic agents, Health
Abstract

Since the discovery of PARP inhibitors (PARPi) in 2005, there has been rapid clinical development of five different agents (olaparib, rucaparib, niraparib, veliparib, talazoparib), leading to seven indications approved by [...]

Published
2020

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