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2,197 results on '"El-Deiry, Wafik S."'

4. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Aqeilan, Rami I, Arama, Eli, Baehrecke, Eric H, Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A, Bartek, Jiri, Bazan, Nicolas G, Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Marco E, Blagosklonny, Mikhail V, Blander, J Magarian, Blandino, Giovanni, Blomgren, Klas, Borner, Christoph, Bortner, Carl D, Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, Thomas, Damgaard, Rune Busk, Calin, George A, Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chen, Guo-Qiang, Chen, Quan, Chen, Youhai H, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M, Dawson, Valina L, De Maria, Ruggero, De Strooper, Bart, Debatin, Klaus-Michael, Deberardinis, Ralph J, Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Engeland, Kurt, Fimia, Gian Maria, Galassi, Claudia, Ganini, Carlo, Garcia-Saez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J Marie, Haupt, Ygal, He, Sudan, Heery, David M, Hengartner, Michael O, Hetz, Claudio, Hildeman, David A, Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J, and Kanneganti, Thirumala-Devi

Subjects
Biochemistry and Cell Biology, Biological Sciences, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Generic health relevance, Good Health and Well Being, Animals, Humans, Apoptosis, Cell Death, Caspases, Carcinogenesis, Mammals, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

5. Molecular Characterization of KRAS Wild-type Tumors in Patients with Pancreatic Adenocarcinoma.

Author

Philip, Philip A, Azar, Ibrahim, Xiu, Joanne, Hall, Michael J, Hendifar, Andrew Eugene, Lou, Emil, Hwang, Jimmy J, Gong, Jun, Feldman, Rebecca, Ellis, Michelle, Stafford, Phil, Spetzler, David, Khushman, Moh'd M, Sohal, Davendra, Lockhart, A Craig, Weinberg, Benjamin A, El-Deiry, Wafik S, Marshall, John, Shields, Anthony F, and Korn, W Michael

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Digestive Diseases, Cancer, Rare Diseases, Pancreatic Cancer, Genetics, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Adenocarcinoma, Aged, Carcinoma, Pancreatic Ductal, DNA Helicases, Female, Humans, Male, Microsatellite Instability, Mutation, Nuclear Proteins, Pancreatic Neoplasms, Proto-Oncogene Proteins B-raf, Proto-Oncogene Proteins p21(ras), Transcription Factors, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

PurposeKRAS mutation (MT) is a major oncogenic driver in pancreatic ductal adenocarcinoma (PDAC). A small subset of PDACs harbor KRAS wild-type (WT). We aim to characterize the molecular profiles of KRAS WT PDAC to uncover new pathogenic drivers and offer targeted treatments.Experimental designTumor tissue obtained from surgical or biopsy material was subjected to next-generation DNA/RNA sequencing, microsatellite instability (MSI) and mismatch repair status determination.ResultsOf the 2,483 patients (male 53.7%, median age 66 years) studied, 266 tumors (10.7%) were KRAS WT. The most frequently mutated gene in KRAS WT PDAC was TP53 (44.5%), followed by BRAF (13.0%). Multiple mutations within the DNA-damage repair (BRCA2, ATM, BAP1, RAD50, FANCE, PALB2), chromatin remodeling (ARID1A, PBRM1, ARID2, KMT2D, KMT2C, SMARCA4, SETD2), and cell-cycle control pathways (CDKN2A, CCND1, CCNE1) were detected frequently. There was no statistically significant difference in PD-L1 expression between KRAS WT (15.8%) and MT (17%) tumors. However, KRAS WT PDAC were more likely to be MSI-high (4.7% vs. 0.7%; P < 0.05), tumor mutational burden-high (4.5% vs. 1%; P < 0.05), and exhibit increased infiltration of CD8+ T cells, natural killer cells, and myeloid dendritic cells. KRAS WT PDACs exhibited gene fusions of BRAF (6.6%), FGFR2 (5.2%), ALK (2.6%), RET (1.3%), and NRG1 (1.3%), as well as amplification of FGF3 (3%), ERBB2 (2.2%), FGFR3 (1.8%), NTRK (1.8%), and MET (1.3%). Real-world evidence reveals a survival advantage of KRAS WT patients in overall cohorts as well as in patients treated with gemcitabine/nab-paclitaxel or 5-FU/oxaliplatin.ConclusionsKRAS WT PDAC represents 10.7% of PDAC and is enriched with targetable alterations, including immuno-oncologic markers. Identification of KRAS WT patients in clinical practice may expand therapeutic options in a clinically meaningful manner.

Published
2022

6. PBRM1 mutations might render a subtype of biliary tract cancers sensitive to drugs targeting the DNA damage repair system

Author

Zimmer, Kai, Kocher, Florian, Untergasser, Gerold, Kircher, Brigitte, Amann, Arno, Baca, Yasmine, Xiu, Joanne, Korn, W. Micheal, Berger, Martin D., Lenz, Heinz-Josef, Puccini, Alberto, Fontana, Elisa, Shields, Anthony F., Marshall, John L., Hall, Michael, El-Deiry, Wafik S., Hsiehchen, David, Macarulla, Teresa, Tabernero, Josep, Pichler, Renate, Khushman, Moh’d, Manne, Upender, Lou, Emil, Wolf, Dominik, Sokolova, Viktorija, Schnaiter, Simon, Zeimet, Alain G., Gulhati, Pat, Widmann, Gerlig, and Seeber, Andreas

Published
2023
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7. Harnessing artificial intelligence for prostate cancer management

Author

Zhu, Lingxuan, Pan, Jiahua, Mou, Weiming, Deng, Longxin, Zhu, Yinjie, Wang, Yanqing, Pareek, Gyan, Hyams, Elias, Carneiro, Benedito A., Hadfield, Matthew J., El-Deiry, Wafik S., Yang, Tao, Tan, Tao, Tong, Tong, Ta, Na, Zhu, Yan, Gao, Yisha, Lai, Yancheng, Cheng, Liang, Chen, Rui, and Xue, Wei

Published
2024
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11. Therapeutic insights for the aggressive subset of high-grade gliomas (HGG) driven by chromosome 1q32 MDM4-containing amplicon and unmethylated MGMT.

Author

El-Deiry, Wafik S., primary, Horowitch, Brooke, additional, Lou, Emil, additional, Subbiah, Vivek, additional, Carneiro, Benedito A., additional, Safran, Howard, additional, Gokaslan, Ziya L., additional, Sobol, Robert W., additional, Mani, Sendurai A., additional, Lawler, Sean E., additional, Chen, Clark C, additional, Wong, Eric T., additional, Kurzrock, Razelle, additional, Xiu, Joanne, additional, Elliott, Andrew, additional, Capelletti, Marzia, additional, Ressler, Steven, additional, Vanderwalde, Ari M., additional, Nabhan, Chadi, additional, and Spetzler, David, additional

Published
2024
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12. Genomic, immunologic, and prognostic associations of TROP2 (TACSTD2) expression in solid tumors.

Author

Morgenstern-Kaplan, Dan, Kareff, Samuel A, Trabolsi, Asaad, Rodriguez, Estelamari, Krause, Harris, Ribeiro, Jennifer R, Tan, Heng, Antonarakis, Emmanuel S, Lou, Emil, Nagasaka, Misako, Algaze, Sandra, Lenz, Heinz-Josef, Liu, Stephen V, Halmos, Balazs, Hoon, Dave S B, Seeber, Andreas, Ma, Patrick C, El-Deiry, Wafik S, Vanderwalde, Ari M, and Lopes, Gilberto

Subjects
PROTEINS, GENOMICS, RESEARCH funding, BREAST tumors, FISHER exact test, DNA, COLORECTAL cancer, DESCRIPTIVE statistics, MANN Whitney U Test, CHI-squared test, GENE expression, IMMUNOHISTOCHEMISTRY, KAPLAN-Meier estimator, PANCREATIC tumors, GENES, GENE expression profiling, TUMORS, TUMOR antigens, GENETIC mutation, SEQUENCE analysis, OVERALL survival, HEPATOCELLULAR carcinoma, CYCLIN-dependent kinases
Abstract

Background TROP2 (TACSTD2) expression is associated with decreased overall survival (OS) in some solid tumors, and the TROP2-targeting antibody-drug conjugate (ADC) sacituzumab govitecan has been approved in breast and urothelial carcinomas. We aimed to explore the multi-omic landscape associated with TACSTD2 gene expression in various solid tumors to identify patients most likely to benefit from this approach. Methods Breast (N  = 11 246), colorectal (N  = 15 425), hepatocellular (N  = 433), pancreatic (N  = 5488), and urothelial (N  = 4125) tumors were stratified into quartiles by TACSTD2 gene expression, analyzed by next-generation DNA sequencing, whole transcriptome sequencing, and immunohistochemistry at Caris Life Sciences (Phoenix, AZ). Survival data were obtained from insurance claims, and Kaplan-Meier estimates were calculated for molecularly defined cohorts. Results Several pathogenic mutations were associated with TACSTD2 -high tumors, including TP53 in breast, colorectal (CRC), pancreatic, and hepatocellular cancers; KRAS in pancreatic and CRC cancers; ARID1A and FGFR3 in urothelial cancer; and CTNNB1 in hepatocellular cancer. TACSTD2-low breast tumors were enriched for copy number amplifications in CCND1 and FGF/R family member genes. TACSTD2 high was generally associated with more immune cell infiltration and greater T-cell inflammation scores. Patients with TACSTD2 -high breast, CRC, and pancreatic cancers demonstrated a significantly shorter OS than TACSTD2 -low tumors. This was restricted to CRC with microsatellite stable tumors and patients with pancreatic cancer with KRAS -mutant tumors. Patients with breast cancer with TACSTD2 -high tumors also experienced significantly worse OS following immune checkpoint inhibitors. Conclusions TACSTD2 expression is associated with key driver alterations and a more active immune microenvironment, suggesting possible combinatorial strategies with TROP2-targeting ADCs plus immunotherapy in various solid tumors. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V, Arama, Eli, Baehrecke, Eric H, Barlev, Nickolai A, Bazan, Nicolas G, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Katiuscia, Blagosklonny, Mikhail V, Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chandel, Navdeep S, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Cohen, Gerald M, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D’Angiolella, Vincenzo, Dawson, Ted M, Dawson, Valina L, De Laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J, Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M, Dixon, Scott J, Duckett, Colin S, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Fimia, Gian Maria, Fulda, Simone, García-Sáez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J Marie, Harris, Isaac S, Hengartner, Michael O, Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, Philipp J, Juin, Philippe P, Kaiser, William J, Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N, Klionsky, Daniel J, Knight, Richard A, Kumar, Sharad, Lee, Sam W, Lemasters, John J, Levine, Beth, Linkermann, Andreas, Lipton, Stuart A, Lockshin, Richard A, López-Otín, Carlos, Lowe, Scott W, Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, and Manic, Gwenola

Subjects
Biochemistry and Cell Biology, Biological Sciences, Animals, Cell Death, Humans, Lysosomes, Mitochondrial Membrane Transport Proteins, Mitochondrial Permeability Transition Pore, Necrosis, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018

14. Efficacy of Larotrectinib in TRK Fusion–Positive Cancers in Adults and Children

Author

Drilon, Alexander, Laetsch, Theodore W, Kummar, Shivaani, DuBois, Steven G, Lassen, Ulrik N, Demetri, George D, Nathenson, Michael, Doebele, Robert C, Farago, Anna F, Pappo, Alberto S, Turpin, Brian, Dowlati, Afshin, Brose, Marcia S, Mascarenhas, Leo, Federman, Noah, Berlin, Jordan, El-Deiry, Wafik S, Baik, Christina, Deeken, John, Boni, Valentina, Nagasubramanian, Ramamoorthy, Taylor, Matthew, Rudzinski, Erin R, Meric-Bernstam, Funda, Sohal, Davendra PS, Ma, Patrick C, Raez, Luis E, Hechtman, Jaclyn F, Benayed, Ryma, Ladanyi, Marc, Tuch, Brian B, Ebata, Kevin, Cruickshank, Scott, Ku, Nora C, Cox, Michael C, Hawkins, Douglas S, Hong, David S, and Hyman, David M

Subjects
Pediatric, Patient Safety, Cancer, Clinical Research, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Adolescent, Adult, Aged, Antineoplastic Agents, Child, Child, Preschool, Disease-Free Survival, Female, Humans, Infant, Kaplan-Meier Estimate, Male, Middle Aged, Neoplasms, Oncogene Proteins, Fusion, Protein Kinases, Pyrazoles, Pyrimidines, Receptor Protein-Tyrosine Kinases, Young Adult, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundFusions involving one of three tropomyosin receptor kinases (TRK) occur in diverse cancers in children and adults. We evaluated the efficacy and safety of larotrectinib, a highly selective TRK inhibitor, in adults and children who had tumors with these fusions.MethodsWe enrolled patients with consecutively and prospectively identified TRK fusion-positive cancers, detected by molecular profiling as routinely performed at each site, into one of three protocols: a phase 1 study involving adults, a phase 1-2 study involving children, or a phase 2 study involving adolescents and adults. The primary end point for the combined analysis was the overall response rate according to independent review. Secondary end points included duration of response, progression-free survival, and safety.ResultsA total of 55 patients, ranging in age from 4 months to 76 years, were enrolled and treated. Patients had 17 unique TRK fusion-positive tumor types. The overall response rate was 75% (95% confidence interval [CI], 61 to 85) according to independent review and 80% (95% CI, 67 to 90) according to investigator assessment. At 1 year, 71% of the responses were ongoing and 55% of the patients remained progression-free. The median duration of response and progression-free survival had not been reached. At a median follow-up of 9.4 months, 86% of the patients with a response (38 of 44 patients) were continuing treatment or had undergone surgery that was intended to be curative. Adverse events were predominantly of grade 1, and no adverse event of grade 3 or 4 that was considered by the investigators to be related to larotrectinib occurred in more than 5% of patients. No patient discontinued larotrectinib owing to drug-related adverse events.ConclusionsLarotrectinib had marked and durable antitumor activity in patients with TRK fusion-positive cancer, regardless of the age of the patient or of the tumor type. (Funded by Loxo Oncology and others; ClinicalTrials.gov numbers, NCT02122913 , NCT02637687 , and NCT02576431 .).

Published
2018

20. First-in-Human Phase 1b Trial of Quinacrine Plus Capecitabine in Patients With Refractory Metastatic Colorectal Cancer

Author

Winer, Arthur, Denlinger, Crystal S., Vijayvergia, Namrata, Cohen, Steven J., Astaturov, Igor, Dotan, Efrat, Gallant, Jean-Nicolas, Wang, Edward W., Kunkel, Miriam, Lim, Bora, Harvey, Harold A., Sivik, Jeffrey, Korzekwa, Kenneth, Ruth, Karen, White, Kevin, Cooper, Harry S., Ross, Eric A., Zhou, Lanlan, and El-Deiry, Wafik S.

Published
2021
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22. ONC201 and imipridones: Anti-cancer compounds with clinical efficacy

Author

Prabhu, Varun Vijay, Morrow, Sara, Rahman Kawakibi, Abed, Zhou, Lanlan, Ralff, Marie, Ray, Jocelyn, Jhaveri, Aakash, Ferrarini, Isacco, Lee, Young, Parker, Cassandra, Zhang, Yiqun, Borsuk, Robyn, Chang, Wen-I, Honeyman, Joshua N., Tavora, Fabio, Carneiro, Benedito, Raufi, Alexander, Huntington, Kelsey, Carlsen, Lindsey, Louie, Anna, Safran, Howard, Seyhan, Attila A., Tarapore, Rohinton S., Schalop, Lee, Stogniew, Martin, Allen, Joshua E., Oster, Wolfgang, and El-Deiry, Wafik S.

Published
2020
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23. Molecular characteristics of BRCA1/2 and PALB2 mutations in pancreatic ductal adenocarcinoma

Author

Seeber, Andreas, Zimmer, Kai, Kocher, Florian, Puccini, Alberto, Xiu, Joanne, Nabhan, Chadi, Elliott, Andrew, Goldberg, Richard M., Grothey, Axel, Shields, Anthony F., Battaglin, Francesca, El-Deiry, Wafik S., Philip, Philip A., Marshall, John L., Hall, Michael, Korn, W. Michael, Lenz, Heinz-Josef, Wolf, Dominik, Feistritzer, Clemens, and Spizzo, Gilbert

Published
2020
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24. Molecular profile of BRCA-mutated biliary tract cancers

Author

Spizzo, Gilbert, Puccini, Alberto, Xiu, Joanne, Goldberg, Richard M., Grothey, Axel, Shields, Anthony F., Arora, Sukeshi Patel, Khushman, Moh’d, Salem, Mohamed E., Battaglin, Francesca, Baca, Yasmine, El-Deiry, Wafik S., Philip, Philip A., Nassem, Madiha, Hall, Michael, Marshall, John L., Kocher, Florian, Amann, Arno, Wolf, Dominik, Korn, W. Michael, Lenz, Heinz-Josef, and Seeber, Andreas

Published
2020
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25. Natural Killer Cell Infiltration in Prostate Cancers Predict Improved Patient Outcomes

Author

Zorko, Nicholas A., primary, Makovec, Allison, additional, Elliott, Andrew, additional, Kellen, Samuel, additional, Lozada, John R., additional, Arafa, Ali T., additional, Felices, Martin, additional, Shackelford, Madison, additional, Barata, Pedro, additional, Zakharia, Yousef, additional, Narayan, Vivek, additional, Stein, Mark N., additional, Zarrabi, Kevin K., additional, Patniak, Akash, additional, Bilen, Mehmet A., additional, Radovich, Milan, additional, Sledge, George, additional, El-Deiry, Wafik S., additional, Heath, Elisabeth I., additional, Hoon, Dave S. B., additional, Nabhan, Chadi, additional, Miller, Jeffrey S., additional, Hwang, Justin H., additional, and Antonarakis, Emmanuel S., additional

Published
2024
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30. Molecular differences between lymph nodes and distant metastases compared with primaries in colorectal cancer patients

Author

Puccini, Alberto, Seeber, Andreas, Xiu, Joanne, Goldberg, Richard M., Soldato, Davide, Grothey, Axel, Shields, Anthony F., Salem, Mohamed E., Battaglin, Francesca, Berger, Martin D., El-Deiry, Wafik S., Tokunaga, Ryuma, Naseem, Madiha, Zhang, Wu, Arora, Sukeshi Patel, Khushman, Moh’d M., Hall, Michael J., Philip, Philip A., Marshall, John L., Korn, W. Michael, and Lenz, Heinz-Josef

Published
2021
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33. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. [0000-0002-4643-0474], Dieter, Adam [0000-0002-5668-5032], Agostini, Massimiliano [0000-0003-3124-2072], Agostinis, Patrizia [0000-0003-1314-2115], Alnemri, Emad S. [0000-0002-7295-3383], Altucci, Lucia [0000-0002-7312-5387], Amelio, Ivano [0000-0002-9126-5391], Andrews, David W. [0000-0002-9266-7157], Aqeilan, Rami I. [0000-0002-6034-023X], Arama, Eli [0000-0001-5953-0629], Balachandran, Siddharth [0000-0003-2084-1803], Bano, Daniele [0000-0002-9617-5504], Bartek, Jiri [0000-0003-2013-7525], Bazan, Nicolas G. [0000-0002-9243-5444], Bernassola, Francesca [0000-0002-8883-8654], Bertrand, Mathieu J. M. [0000-0001-9000-0626], Bianchi, Marco Emilio [0000-0002-5329-6445], Blander, J. Magarian [0000-0001-9207-1700], Blandino, Giovanni [0000-0002-6970-2241], Blomgren, Klas [0000-0002-0476-7271], Bortner, Carl D. [0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. [0000-0002-2915-3970], De Maria, Ruggero [0000-0003-2255-0583], Debatin, Klaus-Michael [0000-0002-8397-1886], Deberardinis, Ralph J. [0000-0002-2705-7432], Degterev, Alexei [0000-0002-8240-7132], Del Sal, Giannino [0000-0003-2185-6003], Deshmukh, Mohanish [0000-0002-2597-5862], Di Virgilio, Francesco [0000-0003-3566-1362], Diederich, Marc [0000-0003-0115-4725], Dixon, Scott J. [0000-0001-6230-8199], El-Deiry, Wafik S. [0000-0002-9577-8266], Elrod, John W. [0000-0003-3925-2224], Engeland, Kurt [0000-0003-3525-0440], Fimia, Gian María [0000-0003-4438-3325], Ganini, Carlo [0000-0002-5839-3965], García-Sáez, Ana J. [0000-0002-3894-5945], Garg, Abhishek D. [0000-0002-9976-9922], Garrido, Carmen [0000-0003-1368-1493], Gavathiotis, Evripidis [0000-0001-6319-8331], Ghosh, Sourav [0000-0001-5990-8708], Green, Douglas R. [0000-0002-7332-1417], Gronemeyer, Hinrich [0000-0001-9454-2449}, Häcker, Georg [0000-0003-1058-5746], Hajnóczky, György [0000-0003-3813-2570], Hardwick, J. Marie [0000-0002-4847-2045], Haupt, Ygal [0000-0001-5925-0096], He, Sudan [0000-0002-0846-1210], Heery, David M. [0000-0002-5035-2392], Hengartner, Michael O. [0000-0002-7584-596X], Hetz, Claudio [0000-0003-1120-7966], Hildeman, David A. [0000-0002-0421-8483], Ichijo, Hidenori [0000-0002-5005-6438], Jäättelä, Marja [0000-0001-5950-7111], Janic, Ana [0000-0002-4200-2560], Joseph, Bertrand [0000-0001-5655-9979], Jost, Philipp J. [0000-0003-2454-0362], Kanneganti, Thirumala-Devi [0000-0002-6395-6443], Karin, Michael [0000-0002-2758-6473], Kashkar, Hamid [0000-0003-2796-1429], Kaufmann, Thomas [0000-0001-9906-874X], Kelly, Gemma L. [0000-0002-6533-1201], Kepp, Oliver [0000-0002-6081-9558], Kimchi, Adi [0000-0002-8236-8989], Klionsky, Daniel J. [0000-0002-7828-8118], Kluck, Ruth [0000-0002-7101-1925], Krysko, Dmitri V. [0000-0002-9692-2047], Kulms, Dagmar [0000-0001-6874-0548], Kumar, Sharad [0000-0001-7126-9814], Lavandero, Sergio [0000-0003-4258-1483], Lavrik, Inna N. 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Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravinchandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strappazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, G, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

35. Preclinical Synergistic Combination Therapy of Lurbinectedin with Irinotecan and 5-Fluorouracil in Pancreatic Cancer

Author

Tummala, Tej, primary, Uruchurtu, Ashley Sanchez Sevilla, additional, De La Cruz, Arielle, additional, Huntington, Kelsey E., additional, George, Andrew, additional, Liguori, Nicholas R., additional, Zhang, Leiqing, additional, Zhou, Lanlan, additional, Abbas, Abbas E., additional, Azzoli, Christopher G., additional, and El-Deiry, Wafik S., additional

Published
2023
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47. GSK-3 Inhibitor Elraglusib Enhances Tumor-Infiltrating Immune Cell Activation in Tumor Biopsies and Synergizes with Anti-PD-L1 in a Murine Model of Colorectal Cancer

Author

Huntington, Kelsey E., primary, Louie, Anna D., additional, Srinivasan, Praveen R., additional, Schorl, Christoph, additional, Lu, Shaolei, additional, Silverberg, David, additional, Newhouse, Daniel, additional, Wu, Zhijin, additional, Zhou, Lanlan, additional, Borden, Brittany A., additional, Giles, Francis J., additional, Dooner, Mark, additional, Carneiro, Benedito A., additional, and El-Deiry, Wafik S., additional

Published
2023
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48. Validation of a whole exome/whole transcriptome liquid biopsy assay with correction for clonal hematopoiesis.

Author

Perdigones Borderias, Nieves, primary, Abraham, Jim, additional, Radovich, Milan, additional, Oberley, Matthew James, additional, Swensen, Jeffrey, additional, Heath, Elisabeth I., additional, Dietrich, Martin Frederik, additional, Liu, Stephen V., additional, Nabhan, Chadi, additional, Hahn-Lowry, Robert, additional, Lou, Emil, additional, El-Deiry, Wafik S., additional, Shields, Anthony F., additional, Marshall, John, additional, Miglarese, Mark Robert, additional, Antani, Sourabh, additional, Sledge, George W., additional, Halbert, David D., additional, Spetzler, David, additional, and Domenyuk, Valeriy, additional

Published
2023
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