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10. Author Correction: Microphysiological model reveals the promise of memory-like natural killer cell immunotherapy for HIV± cancer

Author

Ayuso, Jose M., Farooqui, Mehtab, Virumbrales-Muñoz, María, Denecke, Katheryn, Rehman, Shujah, Schmitz, Rebecca, Guerrero, Jorge F., Sanchez-de-Diego, Cristina, Campo, Sara Abizanda, Maly, Elizabeth M., Forsberg, Matthew H., Kerr, Sheena C., Striker, Robert, Sherer, Nathan M., Harari, Paul M., Capitini, Christian M., Skala, Melissa C., and Beebe, David J.

Published
2023
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11. Microphysiological model reveals the promise of memory-like natural killer cell immunotherapy for HIV± cancer

Author

Ayuso, Jose M., Farooqui, Mehtab, Virumbrales-Muñoz, María, Denecke, Katheryn, Rehman, Shujah, Schmitz, Rebecca, Guerrero, Jorge F., Sanchez-de-Diego, Cristina, Campo, Sara Abizanda, Maly, Elizabeth M., Forsberg, Matthew H., Kerr, Sheena C., Striker, Robert, Sherer, Nathan M., Harari, Paul M., Capitini, Christian M., Skala, Melissa C., and Beebe, David J.

Published
2023
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12. The NIH Somatic Cell Genome Editing program

Author

Saha, Krishanu, Sontheimer, Erik J, Brooks, PJ, Dwinell, Melinda R, Gersbach, Charles A, Liu, David R, Murray, Stephen A, Tsai, Shengdar Q, Wilson, Ross C, Anderson, Daniel G, Asokan, Aravind, Banfield, Jillian F, Bankiewicz, Krystof S, Bao, Gang, Bulte, Jeff WM, Bursac, Nenad, Campbell, Jarryd M, Carlson, Daniel F, Chaikof, Elliot L, Chen, Zheng-Yi, Cheng, R Holland, Clark, Karl J, Curiel, David T, Dahlman, James E, Deverman, Benjamin E, Dickinson, Mary E, Doudna, Jennifer A, Ekker, Stephen C, Emborg, Marina E, Feng, Guoping, Freedman, Benjamin S, Gamm, David M, Gao, Guangping, Ghiran, Ionita C, Glazer, Peter M, Gong, Shaoqin, Heaney, Jason D, Hennebold, Jon D, Hinson, John T, Khvorova, Anastasia, Kiani, Samira, Lagor, William R, Lam, Kit S, Leong, Kam W, Levine, Jon E, Lewis, Jennifer A, Lutz, Cathleen M, Ly, Danith H, Maragh, Samantha, McCray, Paul B, McDevitt, Todd C, Mirochnitchenko, Oleg, Morizane, Ryuji, Murthy, Niren, Prather, Randall S, Ronald, John A, Roy, Subhojit, Roy, Sushmita, Sabbisetti, Venkata, Saltzman, W Mark, Santangelo, Philip J, Segal, David J, Shimoyama, Mary, Skala, Melissa C, Tarantal, Alice F, Tilton, John C, Truskey, George A, Vandsburger, Moriel, Watts, Jonathan K, Wells, Kevin D, Wolfe, Scot A, Xu, Qiaobing, Xue, Wen, Yi, Guohua, and Zhou, Jiangbing

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Gene Therapy, Biotechnology, Human Genome, 5.2 Cellular and gene therapies, Generic health relevance, Animals, Cells, Gene Editing, Genetic Therapy, Genome, Human, Goals, Humans, National Institutes of Health (U.S.), United States, SCGE Consortium, General Science & Technology
Abstract

The move from reading to writing the human genome offers new opportunities to improve human health. The United States National Institutes of Health (NIH) Somatic Cell Genome Editing (SCGE) Consortium aims to accelerate the development of safer and more-effective methods to edit the genomes of disease-relevant somatic cells in patients, even in tissues that are difficult to reach. Here we discuss the consortium's plans to develop and benchmark approaches to induce and measure genome modifications, and to define downstream functional consequences of genome editing within human cells. Central to this effort is a rigorous and innovative approach that requires validation of the technology through third-party testing in small and large animals. New genome editors, delivery technologies and methods for tracking edited cells in vivo, as well as newly developed animal models and human biological systems, will be assembled-along with validated datasets-into an SCGE Toolkit, which will be disseminated widely to the biomedical research community. We visualize this toolkit-and the knowledge generated by its applications-as a means to accelerate the clinical development of new therapies for a wide range of conditions.

Published
2021

21. Micro blood analysis technology (μBAT): multiplexed analysis of neutrophil phenotype and function from microliter whole blood samples.

Author

Juang, Terry D., Riendeau, Jeremiah, Geiger, Peter G., Datta, Rupsa, Lares, Marcos, Yada, Ravi Chandra, Singh, Anne Marie, Seroogy, Christine M., Gern, James E., Skala, Melissa C., Beebe, David J., and Kerr, Sheena C.

Subjects
BLOOD testing, NEUTROPHILS, BLOOD sampling, PHENOTYPES, PHAGOCYTOSIS, MEDICAL research
Abstract

There is an ongoing need to do more with less and provide highly multiplexed analysis from limited sample volumes. Improved "sample sparing" assays would have a broad impact across pediatric and other rare sample type studies in addition to enabling sequential sampling. This capability would advance both clinical and basic research applications. Here we report the micro blood analysis technology (μBAT), a microfluidic platform that supports multiplexed analysis of neutrophils from a single drop of blood. We demonstrate the multiplexed orthogonal capabilities of μBAT including functional assays (phagocytosis, neutrophil extracellular traps, optical metabolic imaging) and molecular assays (gene expression, cytokine secretion). Importantly we validate our microscale platform using a macroscale benchmark assay. μBAT is compatible with lancet puncture or microdraw devices, and its design facilitates rapid operations without the need for specialized equipment. μBAT offers a new method for investigating neutrophil function in populations with restricted sample amounts. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Autofluorescence lifetime flow cytometry with time‐correlated single photon counting.

Author

Samimi, Kayvan, Pasachhe, Ojaswi, Guzman, Emmanuel Contreras, Riendeau, Jeremiah, Gillette, Amani A., Pham, Dan L., Wiech, Kasia J., Moore, Darcie L., and Skala, Melissa C.

Abstract

Autofluorescence lifetime imaging microscopy (FLIM) is sensitive to metabolic changes in single cells based on changes in the protein‐binding activities of the metabolic co‐enzymes NAD(P)H. However, FLIM typically relies on time‐correlated single‐photon counting (TCSPC) detection electronics on laser‐scanning microscopes, which are expensive, low‐throughput, and require substantial post‐processing time for cell segmentation and analysis. Here, we present a fluorescence lifetime‐sensitive flow cytometer that offers the same TCSPC temporal resolution in a flow geometry, with low‐cost single‐photon excitation sources, a throughput of tens of cells per second, and real‐time single‐cell analysis. The system uses a 375 nm picosecond‐pulsed diode laser operating at 50 MHz, alkali photomultiplier tubes, an FPGA‐based time tagger, and can provide real‐time phasor‐based classification (i.e., gating) of flowing cells. A CMOS camera produces simultaneous brightfield images using far‐red illumination. A second PMT provides two‐color analysis. Cells are injected into the microfluidic channel using a syringe pump at 2–5 mm/s with nearly 5 ms integration time per cell, resulting in a light dose of 2.65 J/cm2 that is well below damage thresholds (25 J/cm2 at 375 nm). Our results show that cells remain viable after measurement, and the system is sensitive to autofluorescence lifetime changes in Jurkat T cells with metabolic perturbation (sodium cyanide), quiescent versus activated (CD3/CD28/CD2) primary human T cells, and quiescent versus activated primary adult mouse neural stem cells, consistent with prior studies using multiphoton FLIM. This TCSPC‐based autofluorescence lifetime flow cytometer provides a valuable label‐free method for real‐time analysis of single‐cell function and metabolism with higher throughput than laser‐scanning microscopy systems. [ABSTRACT FROM AUTHOR]

Published
2024
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29. Label free metabolic imaging to enhance the efficacy of Chimeric Antigen Receptor T cell therapy

Author

Pham, Dan L., primary, Cappabianca, Daniel, additional, Forsberg, Matthew H., additional, Weaver, Cole, additional, Mueller, Katherine P., additional, Tommasi, Anna, additional, Vidugiriene, Jolanta, additional, Lauer, Anthony, additional, Sylvester, Kayla, additional, Bugel, Madison, additional, Capitini, Christian M., additional, Saha, Krishanu, additional, and Skala, Melissa C., additional

Published
2024
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30. Metabolic priming of GD2TRAC-CAR T cells during manufacturing promotes memory phenotypes while enhancing persistence

Author

Cappabianca, Dan, primary, Pham, Dan, additional, Forsberg, Matthew H., additional, Bugel, Madison, additional, Tommasi, Anna, additional, Lauer, Anthony, additional, Vidugiriene, Jolanta, additional, Hrdlicka, Brookelyn, additional, McHale, Alexandria, additional, Sodji, Quaovi, additional, Skala, Melissa C., additional, Capitini, Christian M., additional, and Saha, Krishanu, additional

Published
2024
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36. 87 Monitoringin vivoCD8 T and tumor cell metabolic changes in solid tumors during anin situvaccine using autofluorescence imaging

Author

Heaton, Alexa R, primary, Hoefges, Anna, additional, Burkard, Nathaniel J, additional, Feils, Arika S, additional, Tsarovsky, Noah W, additional, Lublin, Garrett M, additional, Hampton, Alina A, additional, Erbe-Gurel, Amy K, additional, Rakhmilevich, Alexander L, additional, Sondel, Paul M, additional, and Skala, Melissa C, additional

Published
2023
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39. Pharmacological blockade of ASCT2-dependent glutamine transport leads to antitumor efficacy in preclinical models

Author

Schulte, Michael L, Fu, Allie, Zhao, Ping, Li, Jun, Geng, Ling, Smith, Shannon T, Kondo, Jumpei, Coffey, Robert J, Johnson, Marc O, Rathmell, Jeffrey C, Sharick, Joe T, Skala, Melissa C, Smith, Jarrod A, Berlin, Jordan, Washington, M Kay, Nickels, Michael L, and Manning, H Charles

Subjects
Precision medicine -- Genetic aspects -- Research, Glutamine -- Physiological aspects -- Genetic aspects -- Research, Cancer cells -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

The unique metabolic demands of cancer cells underscore potentially fruitful opportunities for drug discovery in the era of precision medicine. However, therapeutic targeting of cancer metabolism has led to surprisingly few new drugs to date. The neutral amino acid glutamine serves as a key intermediate in numerous metabolic processes leveraged by cancer cells, including biosynthesis, cell signaling, and oxidative protection. Herein we report the preclinical development of V-9302, a competitive small molecule antagonist of transmembrane glutamine flux that selectively and potently targets the amino acid transporter ASCT2. Pharmacological blockade of ASCT2 with V-9302 resulted in attenuated cancer cell growth and proliferation, increased cell death, and increased oxidative stress, which collectively contributed to antitumor responses in vitro and in vivo. This is the first study, to our knowledge, to demonstrate the utility of a pharmacological inhibitor of glutamine transport in oncology, representing a new class of targeted therapy and laying a framework for paradigm-shifting therapies targeting cancer cell metabolism., Author(s): Michael L Schulte [1, 2, 3]; Allie Fu [1]; Ping Zhao [1]; Jun Li [1]; Ling Geng [1]; Shannon T Smith [1]; Jumpei Kondo [4]; Robert J Coffey [4, [...]

Published
2018
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42. Light-sheet autofluorescence lifetime imaging with a single-photon avalanche diode array

Author

Samimi, Kayvan, primary, Desa, Danielle E., additional, Lin, Wei, additional, Weiss, Kurt, additional, Li, Joe, additional, Huisken, Jan, additional, Miskolci, Veronika, additional, Huttenlocher, Anna, additional, Chacko, Jenu V., additional, Velten, Andreas, additional, Rogers, Jeremy D., additional, Eliceiri, Kevin W., additional, and Skala, Melissa C., additional

Published
2023
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44. Abstract 2389: In vivo multiphoton autofluorescence imaging is sensitive to CD8 T cell and tumor cell metabolic changes during immunotherapy in a murine melanoma model

Author

Heaton, Alexa R., primary, Hoefges, Anna, additional, Rehani, Peter R., additional, Burkard, Nathaniel J., additional, Feils, Arika S., additional, Spiegelman, Dan V., additional, Tsarovsky, Noah W., additional, Hampton, Alina A., additional, Gurel, Amy K. Erbe, additional, Rakhmilevich, Alexander L., additional, Sondel, Paul M., additional, and Skala, Melissa C., additional

Published
2023
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45. Data from MTORC1/2 Inhibition as a Therapeutic Strategy for PIK3CA Mutant Cancers

Author

Fricke, Stephanie L., primary, Payne, Susan N., primary, Favreau, Peter F., primary, Kratz, Jeremy D., primary, Pasch, Cheri A., primary, Foley, Tyler M., primary, Yueh, Alexander E., primary, Van De Hey, Dana R., primary, Depke, Mitchell G., primary, Korkos, Demetra P., primary, Sha, Gioia Chengcheng, primary, DeStefanis, Rebecca A., primary, Clipson, Linda, primary, Burkard, Mark E., primary, Lemmon, Kayla K., primary, Parsons, Benjamin M., primary, Kenny, Paraic A., primary, Matkowskyj, Kristina A., primary, Newton, Michael A., primary, Skala, Melissa C., primary, and Deming, Dustin A., primary

Published
2023
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46. Supplementary Table S1 from MTORC1/2 Inhibition as a Therapeutic Strategy for PIK3CA Mutant Cancers

Author

Fricke, Stephanie L., primary, Payne, Susan N., primary, Favreau, Peter F., primary, Kratz, Jeremy D., primary, Pasch, Cheri A., primary, Foley, Tyler M., primary, Yueh, Alexander E., primary, Van De Hey, Dana R., primary, Depke, Mitchell G., primary, Korkos, Demetra P., primary, Sha, Gioia Chengcheng, primary, DeStefanis, Rebecca A., primary, Clipson, Linda, primary, Burkard, Mark E., primary, Lemmon, Kayla K., primary, Parsons, Benjamin M., primary, Kenny, Paraic A., primary, Matkowskyj, Kristina A., primary, Newton, Michael A., primary, Skala, Melissa C., primary, and Deming, Dustin A., primary

Published
2023
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47. Supplementary Figure S1 from MTORC1/2 Inhibition as a Therapeutic Strategy for PIK3CA Mutant Cancers

Author

Fricke, Stephanie L., primary, Payne, Susan N., primary, Favreau, Peter F., primary, Kratz, Jeremy D., primary, Pasch, Cheri A., primary, Foley, Tyler M., primary, Yueh, Alexander E., primary, Van De Hey, Dana R., primary, Depke, Mitchell G., primary, Korkos, Demetra P., primary, Sha, Gioia Chengcheng, primary, DeStefanis, Rebecca A., primary, Clipson, Linda, primary, Burkard, Mark E., primary, Lemmon, Kayla K., primary, Parsons, Benjamin M., primary, Kenny, Paraic A., primary, Matkowskyj, Kristina A., primary, Newton, Michael A., primary, Skala, Melissa C., primary, and Deming, Dustin A., primary

Published
2023
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48. Interactions with stromal cells promote a more oxidized cancer cell redox state in pancreatic tumors

Author

Massachusetts Institute of Technology. Department of Biology, Datta, Rupsa, Sivanand, Sharanya, Lau, Allison N, Florek, Logan V, Barbeau, Anna M, Wyckoff, Jeffrey, Skala, Melissa C, Vander Heiden, Matthew G, Massachusetts Institute of Technology. Department of Biology, Datta, Rupsa, Sivanand, Sharanya, Lau, Allison N, Florek, Logan V, Barbeau, Anna M, Wyckoff, Jeffrey, Skala, Melissa C, and Vander Heiden, Matthew G

Abstract

Access to electron acceptors supports oxidized biomass synthesis and can be limiting for cancer cell proliferation, but how cancer cells overcome this limitation in tumors is incompletely understood. Nontransformed cells in tumors can help cancer cells overcome metabolic limitations, particularly in pancreatic cancer, where pancreatic stellate cells (PSCs) promote cancer cell proliferation and tumor growth. However, whether PSCs affect the redox state of cancer cells is not known. By taking advantage of the endogenous fluorescence properties of reduced nicotinamide adenine dinucleotide and oxidized flavin adenine dinucleotide cofactors we use optical imaging to assess the redox state of pancreatic cancer cells and PSCs and find that direct interactions between PSCs and cancer cells promote a more oxidized state in cancer cells. This suggests that metabolic interaction between cancer cells and PSCs is a mechanism to overcome the redox limitations of cell proliferation in pancreatic cancer.

Published
2023

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