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505 results on '"Wood, Kris C."'

1. Targeting a lineage-specific PI3Kɣ–Akt signaling module in acute myeloid leukemia using a heterobifunctional degrader molecule

Author

Kelly, Lois M., Rutter, Justine C., Lin, Kevin H., Ling, Frank, Duchmann, Matthieu, Latour, Emmanuelle, Arang, Nadia, Pasquer, Hélène, Ho Nhat, Duong, Charles, Juliette, Killarney, Shane T., Ang, Hazel X., Namor, Federica, Culeux, Cécile, Lombard, Bérangère, Loew, Damarys, Swaney, Danielle L., Krogan, Nevan J., Brunel, Luc, Carretero, Élodie, Verdié, Pascal, Amblard, Muriel, Fodil, Sofiane, Huynh, Tony, Sebert, Marie, Adès, Lionel, Raffoux, Emmanuel, Fenouille, Nina, Itzykson, Raphaël, Lobry, Camille, Benajiba, Lina, Forget, Antoine, Martin, Anthony R., Wood, Kris C., and Puissant, Alexandre

Published
2024
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2. Mediator kinase inhibition impedes transcriptional plasticity and prevents resistance to ERK/MAPK-targeted therapy in KRAS-mutant cancers

Author

Nussbaum, Daniel P., Martz, Colin A., Waters, Andrew M., Barrera, Alejandro, Liu, Annie, Rutter, Justine C., Cerda-Smith, Christian G., Stewart, Amy E., Wu, Chao, Cakir, Merve, Levandowski, Cecilia B., Kantrowitz, David E., McCall, Shannon J., Pierobon, Mariaelena, Petricoin, III, Emanuel F., Joshua Smith, J., Reddy, Timothy E., Der, Channing J., Taatjes, Dylan J., and Wood, Kris C.

Published
2024
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4. Challenges and Emerging Opportunities for Targeting mTOR in Cancer.

Author

Wood, Kris C and Gutkind, J Silvio

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Clinical Research, Immunization, Clinical Trials and Supportive Activities, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Good Health and Well Being, Humans, Sirolimus, Protein Kinase Inhibitors, TOR Serine-Threonine Kinases, Neoplasms, Signal Transduction, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

The mechanistic target of rapamycin (mTOR) plays a key role in normal and malignant cell growth. However, pharmacologic targeting of mTOR in cancer has shown little clinical benefit, in spite of aberrant hyperactivation of mTOR in most solid tumors. Here, we discuss possible reasons for the reduced clinical efficacy of mTOR inhibition and highlight lessons learned from recent combination clinical trials and approved indications of mTOR inhibitors in cancer. We also discuss how the emerging systems level understanding of mTOR signaling in cancer can be exploited for the clinical development of novel multimodal precision targeted therapies and immunotherapies aimed at achieving tumor remission.

Published
2022

5. Small-molecule targeted therapies induce dependence on DNA double-strand break repair in residual tumor cells

Author

Ali, Moiez, Lu, Min, Ang, Hazel Xiaohui, Soderquist, Ryan S, Eyler, Christine E, Hutchinson, Haley M, Glass, Carolyn, Bassil, Christopher F, Lopez, Omar M, Kerr, D Lucas, Falcon, Christina J, Yu, Helena A, Hata, Aaron N, Blakely, Collin M, McCoach, Caroline E, Bivona, Trever G, and Wood, Kris C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Cancer, Ataxia Telangiectasia, Rare Diseases, Neurodegenerative, Genetics, Lung, Lung Cancer, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Aetiology, Animals, Carcinoma, Non-Small-Cell Lung, DNA, DNA Repair, Humans, Lung Neoplasms, Mice, Neoplasm, Residual, Biological Sciences, Medical and Health Sciences, Medical biotechnology, Biomedical engineering
Abstract

Residual cancer cells that survive drug treatments with targeted therapies act as a reservoir from which eventual resistant disease emerges. Although there is great interest in therapeutically targeting residual cells, efforts are hampered by our limited knowledge of the vulnerabilities existing in this cell state. Here, we report that diverse oncogene-targeted therapies, including inhibitors of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), KRAS, and BRAF, induce DNA double-strand breaks and, consequently, ataxia-telangiectasia mutated (ATM)-dependent DNA repair in oncogene-matched residual tumor cells. This DNA damage response, observed in cell lines, mouse xenograft models, and human patients, is driven by a pathway involving the activation of caspases 3 and 7 and the downstream caspase-activated deoxyribonuclease (CAD). CAD is, in turn, activated through caspase-mediated degradation of its endogenous inhibitor, ICAD. In models of EGFR mutant non-small cell lung cancer (NSCLC), tumor cells that survive treatment with small-molecule EGFR-targeted therapies are thus synthetically dependent on ATM, and combined treatment with an ATM kinase inhibitor eradicates these cells in vivo. This led to more penetrant and durable responses in EGFR mutant NSCLC mouse xenograft models, including those derived from both established cell lines and patient tumors. Last, we found that rare patients with EGFR mutant NSCLC harboring co-occurring, loss-of-function mutations in ATM exhibit extended progression-free survival on first generation EGFR inhibitor therapy relative to patients with EGFR mutant NSCLC lacking deleterious ATM mutations. Together, these findings establish a rationale for the mechanism-based integration of ATM inhibitors alongside existing targeted therapies.

Published
2022

11. P2RY2-AKT activation is a therapeutically actionable consequence of XPO1 inhibition in acute myeloid leukemia

Author

Lin, Kevin H., Rutter, Justine C., Xie, Abigail, Killarney, Shane T., Vaganay, Camille, Benaksas, Chaima, Ling, Frank, Sodaro, Gaetano, Meslin, Paul-Arthur, Bassil, Christopher F., Fenouille, Nina, Hoj, Jacob, Washart, Rachel, Ang, Hazel X., Cerda-Smith, Christian, Chaintreuil, Paul, Jacquel, Arnaud, Auberger, Patrick, Forget, Antoine, Itzykson, Raphael, Lu, Min, Lin, Jiaxing, Pierobon, Mariaelena, Sheng, Zhecheng, Li, Xinghai, Chilkoti, Ashutosh, Owzar, Kouros, Rizzieri, David A., Pardee, Timothy S., Benajiba, Lina, Petricoin, Emanuel, Puissant, Alexandre, and Wood, Kris C.

Published
2022
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12. Cancer genes disfavoring T cell immunity identified via integrated systems approach

Author

Kishton, Rigel J., Patel, Shashank J., Decker, Amy E., Vodnala, Suman K., Cam, Maggie, Yamamoto, Tori N., Patel, Yogin, Sukumar, Madhusudhanan, Yu, Zhiya, Ji, Michelle, Henning, Amanda N., Gurusamy, Devikala, Palmer, Douglas C., Stefanescu, Roxana A., Girvin, Andrew T., Lo, Winifred, Pasetto, Anna, Malekzadeh, Parisa, Deniger, Drew C., Wood, Kris C., Sanjana, Neville E., and Restifo, Nicholas P.

Published
2022
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26. Bayesian Approximate Kernel Regression with Variable Selection

Author

Crawford, Lorin, Wood, Kris C., Zhou, Xiang, and Mukherjee, Sayan

Subjects
Statistics - Methodology, Quantitative Biology - Quantitative Methods, Statistics - Applications, Statistics - Machine Learning
Abstract

Nonlinear kernel regression models are often used in statistics and machine learning because they are more accurate than linear models. Variable selection for kernel regression models is a challenge partly because, unlike the linear regression setting, there is no clear concept of an effect size for regression coefficients. In this paper, we propose a novel framework that provides an effect size analog of each explanatory variable for Bayesian kernel regression models when the kernel is shift-invariant --- for example, the Gaussian kernel. We use function analytic properties of shift-invariant reproducing kernel Hilbert spaces (RKHS) to define a linear vector space that: (i) captures nonlinear structure, and (ii) can be projected onto the original explanatory variables. The projection onto the original explanatory variables serves as an analog of effect sizes. The specific function analytic property we use is that shift-invariant kernel functions can be approximated via random Fourier bases. Based on the random Fourier expansion we propose a computationally efficient class of Bayesian approximate kernel regression (BAKR) models for both nonlinear regression and binary classification for which one can compute an analog of effect sizes. We illustrate the utility of BAKR by examining two important problems in statistical genetics: genomic selection (i.e. phenotypic prediction) and association mapping (i.e. inference of significant variants or loci). State-of-the-art methods for genomic selection and association mapping are based on kernel regression and linear models, respectively. BAKR is the first method that is competitive in both settings., Comment: 22 pages, 3 figures, 3 tables; theory added; new simulations presented; references added

Published
2015

27. Low-Dose Vertical Inhibition of the RAF-MEK-ERK Cascade Causes Apoptotic Death of KRAS Mutant Cancers

Author

Ozkan-Dagliyan, Irem, Diehl, J. Nathaniel, George, Samuel D., Schaefer, Antje, Papke, Bjoern, Klotz-Noack, Kathleen, Waters, Andrew M., Goodwin, Craig M., Gautam, Prson, Pierobon, Mariaelena, Peng, Sen, Gilbert, Thomas S.K., Lin, Kevin H., Dagliyan, Onur, Wennerberg, Krister, Petricoin, Emanuel F., III, Tran, Nhan L., Bhagwat, Shripad V., Tiu, Ramon V., Peng, Sheng-Bin, Herring, Laura E., Graves, Lee M., Sers, Christine, Wood, Kris C., Cox, Adrienne D., and Der, Channing J.

Published
2020
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29. Using antagonistic pleiotropy to design a chemotherapy-induced evolutionary trap to target drug resistance in cancer

Author

Lin, Kevin H., Rutter, Justine C., Xie, Abigail, Pardieu, Bryann, Winn, Emily T., Bello, Reinaldo Dal, Forget, Antoine, Itzykson, Raphael, Ahn, Yeong-Ran, Dai, Ziwei, Sobhan, Raiyan T., Anderson, Gray R., Singleton, Katherine R., Decker, Amy E., Winter, Peter S., Locasale, Jason W., Crawford, Lorin, Puissant, Alexandre, and Wood, Kris C.

Published
2020
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30. Cellphone enabled point-of-care assessment of breast tumor cytology and molecular HER2 expression from fine-needle aspirates

Author

Joh, Daniel Y., Heggestad, Jacob T., Zhang, Shengwei, Anderson, Gray R., Bhattacharyya, Jayanta, Wardell, Suzanne E., Wall, Simone A., Cheng, Amy B., Albarghouthi, Faris, Liu, Jason, Oshima, Sachi, Hucknall, Angus M., Hyslop, Terry, Hall, Allison H. S., Wood, Kris C., Shelley Hwang, E., Strickland, Kyle C., Wei, Qingshan, and Chilkoti, Ashutosh

Published
2021
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31. Author Correction: Cellphone enabled point-of-care assessment of breast tumor cytology and molecular HER2 expression from fine-needle aspirates

Author

Joh, Daniel Y., Heggestad, Jacob T., Zhang, Shengwei, Anderson, Gray R., Bhattacharyya, Jayanta, Wardell, Suzanne E., Wall, Simone A., Cheng, Amy B., Albarghouthi, Faris, Liu, Jason, Oshima, Sachi, Hucknall, Angus M., Hyslop, Terry, Hall, Allison H. S., Wood, Kris C., Shelley Hwang, E., Strickland, Kyle C., Wei, Qingshan, and Chilkoti, Ashutosh

Published
2021
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40. A p300/GATA6 axis determines differentiation and Wnt dependency in pancreatic cancer models

Author

Zhong, Zheng, Harmston, Nathan, Wood, Kris C., Madan, Babita, and Virshup, David M.

Subjects
Oncology, Experimental, Drug resistance -- Research, Cellular signal transduction -- Research, Genetic transcription -- Research, Cancer -- Research, Transcription factors -- Health aspects, Pancreatic cancer -- Genetic aspects -- Development and progression -- Drug therapy, Wnt proteins -- Genetic aspects -- Health aspects, Health care industry
Abstract

Wnt signaling regulates the balance between sternness and differentiation in multiple tissues and in cancer. RNF43-mutant pancreatic cancers are dependent on Wnt production, and pharmacologic blockade of the pathway, e.g., by PORCN inhibitors, leads to tumor differentiation. However, primary resistance to these inhibitors has been observed. To elucidate potential mechanisms, we performed in vivo CRISPR screens in PORCN inhibitor-sensitive RNF43-mutant pancreatic cancer xenografts. As expected, genes in the Wnt pathway whose loss conferred drug resistance were identified, including APC, AXIN1, and CTNNBIP1. Unexpectedly, the screen also identified the histone acetyltransferase EP300 (p300), but not its paralog, CREBBP (CBP). We found that EP300 is silenced due to genetic alterations in all the existing RNF43-mutant pancreatic cancer cell lines that are resistant to PORCN inhibitors. Mechanistically, loss of EP300 directly downregulated GATA6 expression, thereby silencing the GATA6-regulated differentiation program and leading to a phenotypic transition from the classical subtype to the dedifferentiated basal-like/squamous subtype of pancreatic cancer. EP300 mutation and loss of GATA6function bypassed the antidifferentiation activity of Wnt signaling, rendering these cancer cells resistant to Wnt inhibition., Introduction Pancreatic cancer (pancreatic ductal adenocarcinoma [PDAC]) is a lethal disease with a 5-year survival of less than 10%. Most individuals with pancreatic cancer are diagnosed when they have locally [...]

Published
2022
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42. IntegrativePTENEnhancer Discovery Reveals a New Model of Enhancer Organization

Author

Cerda-Smith, Christian G., primary, Hutchinson, Haley M., additional, Liu, Annie, additional, Goel, Viraat Y., additional, Sept, Corriene, additional, Kim, Holly, additional, Casaní-Galdón, Salvador, additional, Burkman, Katherine G., additional, Bassil, Christopher F., additional, Hansen, Anders S., additional, Aryee, Martin J., additional, Johnstone, Sarah E., additional, Eyler, Christine E., additional, and Wood, Kris C., additional

Published
2023
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43. Cooperative regulation of coupled oncoprotein synthesis and stability in triple-negative breast cancer by EGFR and CDK12/13

Author

Ang, Hazel X., primary, Sutiman, Natalia, additional, Deng, Xinyue L., additional, Liu, Annie, additional, Cerda-Smith, Christian G., additional, Hutchinson, Haley M., additional, Kim, Holly, additional, Bartelt, Luke C., additional, Chen, Qiang, additional, Barrera, Alejandro, additional, Lin, Jiaxing, additional, Sheng, Zhecheng, additional, McDowell, Ian C., additional, Reddy, Timothy E., additional, Nicchitta, Christopher V., additional, and Wood, Kris C., additional

Published
2023
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46. Melanoma Therapeutic Strategies that Select against Resistance by Exploiting MYC-Driven Evolutionary Convergence

Author

Singleton, Katherine R., Crawford, Lorin, Tsui, Elizabeth, Manchester, Haley E., Maertens, Ophelia, Liu, Xiaojing, Liberti, Maria V., Magpusao, Anniefer N., Stein, Elizabeth M., Tingley, Jennifer P., Frederick, Dennie T., Boland, Genevieve M., Flaherty, Keith T., McCall, Shannon J., Krepler, Clemens, Sproesser, Katrin, Herlyn, Meenhard, Adams, Drew J., Locasale, Jason W., Cichowski, Karen, Mukherjee, Sayan, and Wood, Kris C.

Published
2017
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47. A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution

Author

Anderson, Grace R., Winter, Peter S., Lin, Kevin H., Nussbaum, Daniel P., Cakir, Merve, Stein, Elizabeth M., Soderquist, Ryan S., Crawford, Lorin, Leeds, Jim C., Newcomb, Rachel, Stepp, Priya, Yip, Catherine, Wardell, Suzanne E., Tingley, Jennifer P., Ali, Moiez, Xu, Mengmeng, Ryan, Meagan, McCall, Shannon J., McRee, Autumn J., Counter, Christopher M., Der, Channing J., and Wood, Kris C.

Published
2017
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49. ABL kinases regulate the stabilization of HIF-1α and MYC through CPSF1

Author

Mayro, Benjamin, primary, Hoj, Jacob P., additional, Cerda-Smith, Christian G., additional, Hutchinson, Haley M., additional, Caminear, Michael W., additional, Thrash, Hannah L., additional, Winter, Peter S., additional, Wardell, Suzanne E., additional, McDonnell, Donald P., additional, Wu, Colleen, additional, Wood, Kris C., additional, and Pendergast, Ann Marie, additional

Published
2023
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50. Figure S1 from The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies

Author

Su, Angela, primary, Ling, Frank, primary, Vaganay, Camille, primary, Sodaro, Gaetano, primary, Benaksas, Chaïma, primary, Dal Bello, Reinaldo, primary, Forget, Antoine, primary, Pardieu, Bryann, primary, Lin, Kevin H., primary, Rutter, Justine C., primary, Bassil, Christopher F., primary, Fortin, Gael, primary, Pasanisi, Justine, primary, Antony-Debré, Iléana, primary, Alexe, Gabriela, primary, Benoist, Jean-François, primary, Pruvost, Alain, primary, Pikman, Yana, primary, Qi, Jun, primary, Schlageter, Marie-Hélène, primary, Micol, Jean-Baptiste, primary, Roti, Giovanni, primary, Cluzeau, Thomas, primary, Dombret, Hervé, primary, Preudhomme, Claude, primary, Fenouille, Nina, primary, Benajiba, Lina, primary, Golan, Hava M., primary, Stegmaier, Kimberly, primary, Lobry, Camille, primary, Wood, Kris C., primary, Itzykson, Raphael, primary, and Puissant, Alexandre, primary

Published
2023
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